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RC 006 143

Biomedical Challenges Presented by the AmericanIndiah, Proceedings of the Special Session of thePAHO Advisory Committee on Medical Research (7th,Washington, D.C., June 25, 1968).Pan American Health Organization, Washington, D.C.Sci-Pub-165Sep 68188p.

MF-$0.65 HC-$6.58*American Indians; Anthropology; Biochemistry;*Biological Influences; Conference Reports;*Genetics; *Health; *Human Geography; Tables(Data)

At each meeting of the Pan American HealthOrganization Advisory Committee on Medical Research, a special 1-daysession is held on a topic chosen by the committee as being ofparticular interest. At the 7th meeting, which convened in June of1969 in Washington, D.C., the session surveyed the origin, presentiistribvtion, and principal bioJogical and medical issues of theAmerican Indian--including the Lroblems of newly contacted Indiangroups and those of groups well along in transition. Recorded in thisvolume are the following papers and ensuing discussions: (1) TheOrigin and Dispersion of American Indians in North America; (2)

Theses for Meditation on the Orijin and Dispersion of Man in SouthAmerica; (3) Biological Subdivisions of the Indian on the Basis ofPhysical Anthropology; (4) Biological Subdivisions of the Indian onthe Basis of Genetic Traits; (5) The American Indian in theInternational Biological Program; (6) Survey of the UnacculturatedIndians of Central and South America; (7) Medical Problems of NewlyContacted Indian Groups; (8) The Problem of Gallbladder Disease amongPima Inlians; (9) Hyperglycemia in Pima Indians; (10) Malaria in theAmerican Indian; (11) Food and Nutrition of the Maya Before theConquest and at the Present Time; (12) Iodine Deficiency WithoutGoiter in Isolated Yanomama Indians; and (13) Study of Endemic Goiterin the American Indian. (Author/LS)

BIOMEDICAL CHALLENGES PRESENTED

BY THE AMERICAN INDIAN

F roceedings of the Special Sessionheld during the Seventh Meeting of the

PAHO Advisory Committeeon Medical Research

25 June 1968

U.S. DEPARTMENT OF HEALTH,EDUCATION WELFAREOFFICE OF EDUCATION

THIS DOCUMENT HAS BEEN REPRO-DUCED EXACTLY AS RECEIVED FROM(HE PERSON OR ORGANIZATION ORIG-INATING IT. POINTS OF VIEW OR OPIN-IONS STATED DO NOT NECESSARILY

,RORESENT OFFICIAL OFFICE OF EDU-CAT)ON POSITION OR POLICY.

Scientific Publication No. 165 September 1968

PAN AMERICAN HEALTH ORGANIZATIONPan American Sanitary Bureau, Regional Office of the

WORLD HEALTH ORGANIZATION525 Twenty-third Street, N.W.

Washington, D.C., 20037

NOTE

At each meeting of the Pan American Health Organization AdvisoryCommittee on Medical Research, a special one zy session is held on atopic chosen by the Committee as being of particular interest. At theSeventh Meeting, which convened in lune 1968 in Washington, D.C., the'session surveyed the origin, present distribution, and principal biologicalsubdivisions of the American Indian and considered the specific scientificand medical issues calling for clarification, including the problems of newlycontacted Indian groups and those of groups well along in transition. Thisvolume records the papers presented and the ensuing discussions.

PAHO ADVISORY COMMITTEE ON MEDICAL RESEARCH

Dr. Herr& AlessandriEx-Decano, Facultad de MedicinaUniversidad de ChileSantiago, Chile

Dr. Otto G. BierDiretor, Departamento de Microbiologia e Imu-

nologiaEscola Pau lista de MedicinaSão Paulo, Brasil

Dr. Roberto Caldeyro-BarciaJefe, Departamento de FisiopatologiaFacultad de MedicinaUniversidad de la RepUblicaMontevideo, Uruguay

Dr. Crtr los ChagasChief, Brazilian Delegat ion to UNESCOParis, France

Dr. Philip P. CohenChairman, Department of Physiologicri Chemis-

tryThe University of WisconsinK-?dison, Wisconsin, U.S.A.

Dr. Rene Dubos (Chairman)Member and ProfessorThe Rockefeller UniversityNew York, New York, U.S.A.

Dr Hermon E. HilleboeDirector, Division of Public He5ith PracticeSchool of Public Health and Administrative

McdicineColumbia UniversityNew York, New York, U.S.A.

Dr. Bernard, HoussayDirector, Instituto de Biologfa y Medicina ;Ex-

perimentalBuenos Aires, Argentina

Dr. Alberto HurtadoRector, Universidad Peruana Cayetano HerediaLimq, Perti

Dr. Walsh McDermottChairman, Department of Public HealthCornell University Medical CollegeNew York, New York, J S.A.

Dr. James V. NeelChairman, Department of Human GeneticsUniversity of Michigan Medical SchoolAnn Arbor, Michigan, U.S.A.

Dr. Marcel Roche ( Vice-Chairman)Director, Instituto Venezolano de Investigacio-

nes CientificasCaracas, Venezuela

Dr. James A. ShannonDirector, National Institutes of HealthBethesda, Maryland, U.S.A.

Dr. John C. WaterlowDirector, Tropical Metabolism Research UnitUniversity of the West IndiesKing:-.ton, Jamaica

Profe' sor Abel WolmanEmeritus Professor of Sanitary Engineering and

Water ResourcesThe Johns Hopkins UniversityBaltimore, Maryland, U.S.A.

Dr. Salvador ZubirainDirector, Instituto Nacional de la NutriciónMexico, D.F., Mexico

Dr. Mauricio Martins da Silva, SecretaryChief, Office of Research CoordinationPan American Health OrganizationWashington, D.C., U.S.A.

PAN AMERICAN HEALTH ORGANIZATIONPan American Sanitary Bureau

Dr. Abraham Horwit7,, Director

Special Session on

BIOMEDICAL CHALLENGES PRESENTED BY THE AMERICAN INDIAN

Moderator: Dr. James V. Neel

PARTICIPANTS

Dr. Tulio ArendsHematologia ExperimentalInstituto Venezolano de Investigaciones

tificasCaracas, Venezuela

Dr. Jose BarzdattoHospital del SalvadorUniversidad de ChileSantiago, Chile

Dr. Moises BeharInstituto de Nutrición de

PanamáGuatemala, Guatemala

Dr. Thomas A. BurchClinical Field Studies UnitNational Institute of Arthritis and Metabolic

DiseasesPhoenix, Arizona, U.S.A.

Dr. William CenterwallD Tartment of Human GeneticsThe University of MichiganAnn Arbor, Michigan, U.S.A.

Dr. Napoleon A. ChagnonDepartment of AnthropologyThe University of MichiganAnn Arbor, Michigan, U.S.A.

Dr. Juan Comas *Sección de AntropologiaInstituto de Investigaciones HistóricasUniversidad Nacional Autónoma de WY iCoMexico, D.F., Mexico

Dr. Edmundo CovamibiasDepartamento de GeneticaFacultad de MedicinaUniversidad de ChileSantiago, Chile

Dr. Jose M. CruxentSección de AntropologiaInstituto Venezolano de Investigaciones Cien-


Dr. George Giglio liMalaria LaboratoryMinistry of HealthGeorgetown, Guyana

Unable to attend.

Cien-

Centro America y

iv

Dr. James B. GriffinMuseum of AnthropologyThe University of MichiganAnn Arbor, Michigan, U.S.A.

Dr. William S. LaughlinDepartment of AnthropologyThe University of WisconsinMadison, Wisconsin, U.S.A.

Dr. Miguel A. LayrisseSecciOn de Fisiopatologianstituto Venezolano de Investigaciones Cien-


Dr. Ruben LiskerInstituto Nacional de la NutriciónMexico, D.F., Mexico

Dr. Max MillerDepanment of MedicineWestern Reserve UniversityCleveland, Ohio, U.S.A.

Dr. Jerry D. NiswanderHuman Genetics BranchNational Institute of Dental HealthBethesda, Maryland, U.S.A.

Dr. Noel NutelsServiço Nacional de TuberculoseMinisterio de SaiideRio de Janeiro, Brasil

Dr. Marcel Rochekstituto Venezolano de Investigaciones Cien-


Dr. Francisco M. SalzanoDepartamento de GeniticaUniversidade Federal do Rio Grande do SulPôrto Alegre, Brasil

Dr. William J. SchullDepartment of Human GeneticsThe University of MichiganAnn Arbor, Michigan, U.S.A.

CONTENTS

Opening Statement lames V. Ned 1

The a igin and Dispersion of AmericanIndians in North America James B. Griffin 2

Theses for Meditation on the Origin and Dispersionof Man in South America Jose M. Cruxent 11

riscussion William S. Laughlin 17

General Discussion 19

Biological Subdivisions of the Indian on theBasis of Physical Anthropology Juan Comas 22

Biological Subdivisions of the Indian on theBasis of Genetic Traits Miguel Layrisse 35

Discussion Tulio Arends 40

Ruben LiAer 43


The American Indian in the InternationalBiological Program fames 17 Ned 47

Discussion 55

Survey of the Unaccultufated Indians ofCentral and South America Francisco M. Salzono 59

Discussion 67

Medical Problems of Newly Contacted Indian Gro,..ps Noel ZVutds 68

Discussion Willard R. Centerwall: A Recent Experience withMeasles in a "Virgin-Soil" Population 77


The Problem of Gallbladder Disease amongPima Indians Thomas A. Burch, Leonard 1. Comets,and Peter H. Bennett 82

Hyperglycemia in Pima Indians: A PreliminaryAppraisal of Its Significana Max Miller,Peter W. Bennett, and Thomas A. Burch 89

Malaria in the American Indian George G. Giglioli 104

Food and Nutrition of the Maya Before the Conquestand at the Present Time Moises Behar 114

Iodine Deficiency Without Goiter in Isolated -

Yanomama Indians: Preliminary Note René Ritnere,Dominique Comar, Mentech Colonomas, Jean Desenne,and Marcel Roche 120

Study of 7I:ndemic Goiter in the American IndianJosé Barzelatto and Edumundo Couarrubias 124

Discussion 1. D. Nistvander 133

Edtnundo Covarrublas 136


Appendix: Tabulations of Phenotype and GeneFrequencies for 11 Different Genetiz SystemsStudied in the American Indian R. H. Post,J. V. Ned, and W. I. Schull 141

vi

OPENING STATEMENT

James V. Neel, Moderator

The American Indian continues today, as hehas ever since the discovery of the Americas, topresent a wide variety of questions and chal-lenges ranging from the purely scientific to theintensely humanitarian. In today's Special Ses-sion, we shall be abie to consider only a few ofthese many challenges.

Specifically, we shall deal first with some ofthe unusual opportunities the Indian still offersfor the investigation of basic problems in ge-netics and anthropology. These oppottunitiesinclude studies of the nature and rate of humandispersion, of the emergence of human diversity,and of the biology of primitive man, wi-h allits ramifications.

In the latter half of the program, we shall turnour attention to some of the more medical andhumanitarian problems presented by the Indian.In many respects, these problems are similar tothose of the cam penno or caboclo throughoutSouth America, to whose gene pool the Indianhas made a significant contribution.

However, the Indian also presents some spe-cial problems. One of these is the transition, inthe relatively unacculturated Indian, from "smallband" epidemiology to "large herd" epidemi-ology. As we are all aware, this transition hasrepeatedly had a fatal impact on Indian groups.

The medical challenge to blunt this impact isclear ane, persistent. In addition, by taking it upwe preserve at least temporarily one of the lastgreat resources for the study of primitive man,one of the last opportunities to attempt to fathom

the nature of the forces to which man was re-sponding during the course of human evolution.

1

Further, it begins to appear as if once thattransition is accomplished the Indian may pre-sent some rather special disease problems,

whose satisfactory solution will challenge allour medical ingenuity.'

There is one important biomedical problemof the Indian that this session will leave com-pletely untouchedthe problem of high-altitudepopulations. This subject was covered both atthe Special Session of 19661 and at a WHO/PAHO/IBP conference held here in November1967. Under these circumstances, a further brieftreatment at this time was deemed redundant.

The number of participants in the Session issomewhat greater than usual, thanks to thegenerous financial assistance of both the U.S.Nationql Committee for the International I3io-logical Program and the Human AdaptabilitySection of the Commi.tee for the InternationalBiological Program of the International Unionof Biological Sciences.

Today's formal presentations will be followedtomorrow by an informal session at which prob-

lems of common interest to the participants heretoday will be discussed, with particular referenceto the International Biological Program.

It is customary at such a session to designatetwo rapporteurs. This year Dr. Napoleon Chag-

non and Dr. Edmund Covarrubias have kindlyagreed to discharge that function.

The proceedings appear in Lik at High Altitudes,PAHO Scicntifi, Publication 140.

THE ORIGIN AND DISPERSION OF AMERICAN INDIANS

IN NORTH AMERICA

James B. Griffin

The historically effective discovery of the New

World by Europeans in 1492 opened the Ameri-

cas to large-scale colonization and to a long

period of speculation on the ultimate origin ofthe New World peoples. For almost four hun-

dred years the chronological framework wasbased on biblical sources and was not adeo,uate

to explain the cultural diversity of New Worldculture. Prominent among the speculations on

origins were the multiple-migration hypotheses,

which provided civilized Mediterranean, Euro-

pean, and even Southeast As;an groups to bring

a level of higher culture into the Americas andproduce the more complex civilizations of Meso-

america and the Andes. Such explanations were

also employed to explain a presumed multiracial

origin of the American Indian.As early as the sixteenth century some writers

recognized the predominantly Asiatic relation-

ships of the native American populations and

postulated that the movement of people took

place from northeast Asia to northwestern North

America. This is, of course, the only routeof entry seriously considered by contemporaryscholars, but there is considerable room fordisagreement in many phases of the origin and

dispersion of American Indian populations. For

this paper I have chosen to refrain from present-

ing many reference citations to support thepoints of view included in the paper and from

directly citing other views. Instead I have in-cluded in the references a list of books and otherarticles that afford a wide spectrum of interpre-

2

tations and can be read by those who care to

do so.

The temporal framew ork for early Indian groups

The time of arrival of the first human groups

is far from settled and is likely to remain aresearch problem for some time. For purposesof this paper I shall refer to the period of timefrom the first arrival of man to about 8000 B.C.

as the Paleo-Indian period, and all cultural

complexes and skeletal material of this age, ifany, will be included within this period. A rapid

review of evidence from the United States and

Canada includes only one fairly homogeneous

and widely dispersed complex, a few examples

of other early Paleo-Indian period peoples, and

a number of purported sites that are not re-garded in this paper as soundly established.

The Fluted Point Hunters are the sole recog-

nizable group with a continent-wide occupancyin the latter part of the Paleo-Indian period from

about 10,000 to 8000 B.C. The earliest radio-carbon dates in association with an established

cultural context are about 9300 to 9000 B.c.,

from sites in Arizona, New Mexico, Colorado,and Oklahoma. This is referred to as the Llanocomplex, with the Clovis fluted point as a major

diagnostic tool. The Sandia finds are regarded

as a potential predecessor, with an uncertain ageprobably within a thousand years of Clovis. In

the western plains the later Folsom assemblages

at several sites have been dated between 9000and 8000 B.C. In the eastern United States andCanada, fluted points are known from thc South

Atlantic and Gulf coasts to the Great Lakes andOntario and into New England, and as farnortheast as Nova Scotia. At the Debert site inNova Scotia, a series of radiocarbon dates sug-gest that man occupied the area between 9000and 8500 B.C. Provisional correlations of the dis-tribution of fluted points in the Great Lakesarea have proposed an age of from 10,000 to8000 B.C. for that area, and the evidence fromthe Southeast also suggests an antiquity forfluted points of abuut the same order.

In the area west of the Rocky Mountains thereare a number of complexes that may beginbefore 8000 B.c., but as yet this has not beenadequately demonstrated. Among these are theDesert Culture, Lake Mohave and the SanDieguito culture of southern California, and anumber of sites and complexes from Oregon toBritish Columbia and Washington compressedby some archaeologists into an Old Cordilleranculture. In extreme northwest Canada, the Brit-ish Mountain complex is assigned considerableantiquity, but its age, except on typologicalgrounds, is not known, and no archaeologicalassemblage from Alaska is as old as 8000 B.C.

The oldest radiocarbon dates in associationwith human habitation in the United States arefrom Wilson Butte Cave in south-central Idaho,where from the lower zone of Stratum C thereis a date of 12,550 -± 500 B.C. (M-1409) andfrom Stratum E a date of 13,050 ± 800 B.C.

(M-1410). The context of the material in thecave indicates the presence of man with extinctfauna such as camel and horse and some Boreal-.zone microfauna, but the few artifacts foundare not particularly diagnostic (7).

Fluted points are known from Mexico and asfar south as Guatemala and perhaps Costa Rica.In none of these instances, however, is there anassociated industry. Most of the few fluted pointsare found in northern Mexico, where they areon the southern fringe of the Llano and Folsomconcentrations in the Southwest and westernTexas. There are no soundly established cultu-ral assemblages in Mexico and Central Americadirectly dated by radiocarbon before 8000 B.C.

There are a large number of locations in

3

North America for which considerable antiquityhas been claimed as places inhabited by earlyIndians. Even whole books have been publishedon non-sites. The reasons why it is now difficultor impossible to include such "finds" here variesfrom location to location; a detailed dissent isnot within the scope of this paper. In this cate-gory I would include the claims for occupationat Tule Springs, Nevada, of the order of 20,000to 30,000 years ago; on Santa Rosa Island, muchbefore 8000 B.c.; at the Scripps Institute bluff atLa Jolla, California, slightly over 20,000 B.C.;

at Lewisville, Texas, more than 37,000 B.C.; atSheguiandah, Manitoulin Island, Ontario, fora cultural complex much before 7000 B.c.; fora completely pebble-tool culture in northernAlabama of extreme antiquity; for a chopper/chopping-tool complex of an interglacial orinterstadial period, or of a simple bone-tool tra-dition of any age; or for Pleistocene man in theTrenton, New Jersey, gravels.

In Mexico particularly and also in CentralAmerica, there are indications of the presenceof man before 8000 B.c., but many of theseidentifications were made quite a number ofyears ago and suffer from a lack of sound datesor are isolated artifacts inadequate for the re-construction of a cultural assemblage. Some ofthese finds from the Late Pleistocene Upper Be-cerra formation may well record human occupa-tion, and continuing excavations in Mexico willeventually place the temporal position and in-dustrial activities during the Pa leo-Indian periodon a firmer basis. At present investigations arebeing conducted in the Valsequillo gravels ofPuebla and at Tlapacoya in the Valley ofMexico. As usual, there is some uncertaintyabout the temporal correlation of gravel depositsbetween one area and another, about radio-carbon dates of 35,000 to 24,000 years ago ofhigh antiquity but not directly associated withadequate artifacts, or about the precise age of acultural complex on a buried living surface.

While the South American evidence for earlyIndian occupations is to be evaluated by Profes-sor J. M. Cruxent at this session, I shall includesome observations on this area because of its

importance in assessing the probable age of thcfirst inhabitants of North America. On thenorth side of the Strait of Mar flan, in FellsCave, there is a date of 8760 B.C. (W-915) ob-tained by Junius Bird. From eastern Brazil, atLagoa Santa, there is evidence of occupationaround 8000 to 7000 B.c., and a sambaquis onthe southeastern Brazilian coast has provided adate close to 6000 B.C. In northeastern Vene-zuela, at the Muaco site, there is a possible asso-ciation of man and extinct fauna in the periodaom 14,500 to 12,000 .J.c. In the northern An-dean area, artifact complexes have been givenages in the neighborhood of 8000 B.C.

The South American data, with their widegeographic spread of early man around or be-fore 9000 to 8000 B.C., imply the arrival of manon that continent substantially before the knowndated complexes. Similarly, in Mexico and Cen-tral America the wide distribution of humanoccupations just before or after 8000 B.C. impliesthat the arrival of the first human groups VIM

substantially before this date. If the proposeddates for man in the Valley of Puebla and theValley of Mexico are confirmed to be between40,000 and 24,000 years ago, there will be muchwork for archaeologists to do in the future tofind substantiating evidence in the rest of theNew World. The North American geographicalspread of dated evidence and the considerablediversity of assemblages shortly after 8000 B.C.imply an antiquity of man in North Americaconsiderably greater than thc known agc of theFluted Point Hunters or of the occupants ofWilson Butte Cave. In summary, an agc of about15,000 years for man in thc New World isviewed as reasonable, with thc possibility thatit may be considerably greater.

The temporal framework for northeast Asia

Sound dating of the Late Pleistocene occupa-tions of Siberia is just beginning; in fact, ade-quate investigation of ancient man in north-eastern Siberia has only recently been initiated.Most of the sites with an agc of morc than fouror five thousand years are along the southcrnborders of Siberia from Russia to the Japancsc

4

islands. A radiocarbon date of 12,800-± 120 B.C.

(GIN-97) has recently been obtained on fossilbone from the lower cultural level of Martanear Irkutsk, often attributed to the older UpperPaleolithic of the Irkutsk area. A date of 18,950-± 300 B.C. was obtained on charcoal from thelower cultural level of Afontova Gora II in theUpper Yenesei Valley near Krasnoyarsk (TO.From Kamchatka there is a date of close to18,000 B.C. on charcoal irom the Uski I site.Other sites in southwest Siberia are presumed todate substantially earlier, and sites in Japan ofan Upper Paleolithic cast date well back towardthe 20,000-year range.

The southern Siberian complexes of about30,000 to 12,000 B.C. have a strong early rela-tionship to the late Mousterian stone industriesof eastern Europe. As the Upper Paleolithicdeveloped, there was corresponding modificationin Siberia, but the patterns of change in Siberiaare sufficiently different from those of the better-known areas to the west that an easy alignmenthas not been possible. The industrial develop-ment of these Siberian populations was the re-sult of the long Eurasian cultural development,which became adapted to the late Pleistocene.The level of occupation is attributed to thelower section of deposits on Terrace II of theYenesei. The faunal composition represet* coldperiglacial conditions, and the date corrwondsto about the maximum of the last major Siberianglaciation, called the Sartan. Also in the MiddleYenesei, at the Kokorevo sites, radiocarbondates range from about 14,000 to 11.000 B.C.

In the same arca at the Marta site, a datc ofabout 7000 B.C. was obtained on a Mesolithic-like complex located on the higher areas of theTerrace I floodplain deposits.

In these Siberian sites there are crude heavychopping tools, a variety of flake implementsincluding scrapers and knives, discoidal corcs,and some bifacially flaked poims or knives.There is a trcnd toward greatc 'se trueblades made from prepared cores t? r., J thefashioning of end and sidc sccar rs,

perforators, gravers and burins, and an increin bone tools and ornaments. The animals on

which the people fed are those from arctic tosubarctic and cold arid steppe environments.They made skin clothing and had substantialhouses in the construction of which they usedthe bones of large mammals such as woollyrhinocerus and i. mmoth. Probably the mostimportant animal was the reindeer in the tundraarea. It might be said that the spread of maninto North America awaited the presence ofarctic-alpine tundra species, during the latePleistocene, on which man could live as hehunted his way across northeastern Siberia intoNorth America.

While the extent of the mountain glaciers ineastern Siberia is not satisfactorily known, it is

certain that only a small part of the land masswas glaciated and that most of the area wasoccupied by xerophytic arctic tundra or alpinetundra. A long tongue of steppe or periglacialsteppe extended from southwest Siberia east-ward between the Central Siberian Plateau andLake Baikal as far as Yakutsk on the MiddleLena. From this area the best access route to thenorth was down the Lena Valley to the ArcticOcean.

The fall of the sea level during the last majorglacial advance of the Wisconsin-Wurm is esti-mated to have produced a land bridge at theBering Strait from about 24,000 to 8000 ex., withtwo periods of submersion of the highest partof the shelf correspcnding to major ice-meltingphases of the retreat of the Wisconsin ice. Thesize of the exposed land was considerable. Mostof it was not forested but was occupied bytundra vegetation similar to that of tne Siberianarid-steppe tundra. During the last glacial domi-nance, betwcen 23,000 and 10,000 Lc., the arctictrees and shrubs were more restricted in theirdistribution than they are today and the climatewas colder than it is now.

The movement of early man intoNorth America

Keeping in mind the lack of direct evidencefor the presence of early man in northwesternNorth America and northeastern Siberia, wecan still present an acceptable hypothesis for aspread of hunting bands from west to east.

5

Their way of life was developed from southernRussia to south-central Siberia during the latterpart of the Pleistocene; it was based on a lateMousterian industry, modified by the initial ele-ments of Upper Paleolithic emphasis on bladetools and the beginnings of a bone industry thatwas an aid in the production of skin clothingand shelter. This gradaal expansion northwardinto new territories from northeastern Siberiato Alaska would have taken place without resis-tance from resident hunters. If it took place inthe time period suggested, then a substantialnumber of hunting camps must now be underocean water, but some will eventually be foundin favorable areas such as elevations overlookingpasses followed by game animals in movingfrom one feeding ground to another.

This early population spread is believed tohave been diverted south along the west side ofthe McKenzie Valley. A number of recentpapers (9, 11 , 28) have emphasized the difficultyof passing from the Lower McKenzie Valleyinto the eastern Rocky Mountain slopes of theUnited States because of the presence of thecoalesced continental and cordilleran ice fromMontana to the Yukon Territory along theeastern margin of the Canadian Rockies. Theevidence for the closing and opening of thecorridor between these sheets is not so firmlyestablished that sound datings for these eventsare available. The position adopted in this paperis that the corridor would have been closed onlyat the maximum of the Wisconsin glaciation fora few thousand years, about 19,000 to 15,000years ago.

If the early hunters came into the UnitedStates before 17,000 B.c., then archaeologists inthe United States either have been unlucky orhave not been able to correctly evaluate the evi-dence for his occupancy before the 13,000 Lc.date mentioned at Wilson Butte Cave. Entryshortly before 17,000 B.c. would allow ampletime for penetration into extreme southernSouth America for the known occupancy there,but would not accommodate the proposed Valse.-quillo and Tlapacoya occupations in CentralMexico. If the corridor was closed between

21,000 and 10,000 p.c., archaeologists are facedwith at least as impressive dilemmas in the formof an absence of sound data representing man inNorth Amerka before 21,000 B.C. and the longperiod from then to 13,000 B.c., or in acceptingthe speed with which man moved from Albertato Tierra del Fuego.

The environmental changes in North Americaas a result of the retizat of the Wisconsin icewould have had an effect upon the way of lifeof ancient man thrlugh the shift of climaticzones, vegetation, and animal life. The expan-sions of the Canadian continental ice sheetseffectively obliterated the vegetation and animallife from much of Canada. The expansion of theice into the northern sections of the UnitedStates markedly altered the biota, and com-pressed and interdigitated elements of previousperiods into assemblages distinctive to late Wis-consin times. The climatic conditions during thelife of the western mountain glaciers lowered thetree line, changed the faunal associations anddistributions, and produced thousands of lakesin the now-dry basins of the western Plains, inthe Southwest, in the intermontane plateau re-gion, and in the Pacific Coast states and Mexico.The lowered forest zones and more extensiveand effective grasslands supported the largegrazing and browsing animals of the late

Pleistocene fauna. There were more streams,with corridors of pine and spruce crossing thegrassland.

The changes in climatic regime accompanyingthe withdrawal of the Wisconsin ice had alreadyproduced notable shifts from the full glacialenvironments by the time of the early FlutedPoint Hunters of 10,000 to 9000 B.C. The shiftin vegetation and accompanying animal life tookplace on a large scale over North America,causing some shifts in hunting and collectingareas, and assisted in the displacement or dis-appearance of a small number of game animals.The northward movement of musk ox andmammoth is thought to have been in a park-tundra vegetation zone which initially occupiedthe soils left free of glacial ice in the GreatLakes area. It has been suggested that there was

an early post-Valders invasion of the east byanimal forms now associated with westernprairie environments, and this would correlatewith recent similar hypotheses of prairie vegeta-tion movement eastward at an early period (8).The park-tundra and cool prairie would besuitable for barren-ground caribou, which havebeen identified in Michigan and New York. Didthey penetrate this far south before the lastWisconsin advance, or did they arrive with the"reopening" of the corridor?

The Fluted Point Hunters of North America

By 10,000 to 8000 p.c. the people of the LatePa leo-Indian period had occupied sparsely mostof the area south of the present Canadian borealforest to South America and from the Pacific tothe Atlantic. Most of these populations werestrongly dependent on hunting, as we knowfrom the spear and dart points, knives, andscrapers of various kinds to work skins andfrom the fact that these tools have been found inassociation with a small number of large gameanimals. This latter fact gave rise for a time tothe idea of almost a limitation of diet to biggame animals. Data from sites such as Linden-meier in Colorado, Graham Cave in centralMissouri, and others prove that the meat dietwas quite varied, and at least in the east thereis very little evidence of early man killing themammott and mastodon. In addition, the earlyFluted Point Hunters would have recognized alarge variety of the plant foods available, fromnuts to berries and tubers. The diet of early manwas not likely to stay restricted to a few classesof foods when he entered environments with awide variety of them. It should be possible todiscover sites that will reflect varieties of foodgathering and processing activities that werepart of the life of the Fluted Point Hunters.They should have had some seasonal activitypatterns. A number of students of the Pa leo-Indian cultures are beginning to recognize re-gional tool and behavior complexes that will aidour understanding of this earliest known com-plex.

The wide distribution of Fluted Point bands

6

12.

and the relative homogeneity of the implementsrecovered implies a rather rapid spread of theseearly hunting people, and apparently into areasnot hitherto occupied. There is also the implica-tion that there would have been continuing con-tact between neighboring bands, perhaps forgroup hunting or other food-procuring activitiesat favorable seasonal locations or at locationsfavorable for shelter during the winter seasons.Such collective activity would have permittedexchanges of new cultural developmentsinterms of sources of food, raw materials, manu-facturing techniques, hunting technologyandof people. It is doubtful that individual bandswouid have been isolated from other groups forextensive periods or that peoples moving intonew regional environments would have been cutoff by those environments from culture-sharingwith peoples in their former territory.

Archaic-period adaptations in North America

In the long Archaic period in the UnitedStates between 8000 B.C. and the effective intro-duction of agriculture around 1 B.c., many re-gional cultural developments occurred as theIndian groups became mcre familiar with localresources and develov.c., the knowledge forsuccessfully exploiting _hem. As they did so,successful adaptations lo particular environmentstended to restrict band and group activity tothese environments and to produce a higherlevel of exchange c; culture and people withinthese areas than between them. This is reflectedarchaeologically by the growth of distinguishableregional cultural traditions.

One of the best-documented cultural continui-ties from the Pa!eo-Indian period Fluted PointHunters to later complexes is in the westernPlains states. The production of fluted pointswas gradually abandoned and nonfluted pointsand knives of essentially the same basic formcontinued in use along with the rest of the stonetools. New tools appe r. such as the specializedCody knife, and new techniques such as theparallel flaking of the Scottsbluff and Edenforms. All the evidence from sites in this region,from the Rio Grande north into the Canadian

7

I

prairie provinces, continues to reflect the exis-tence of a hunting economy with bison as animportant supplier of food, tools, and clothes.At some locations there is clear evidence of masskillings, evidently the result of communal drives.Indications of variability of animal food comesfrom sites where giant beaver, pronghorn ante-lope, elk, deer, raccoon, coyote, and smallermammals as well as bison were part of the foodsupply. At other sites there are indications ofgrinding and milling stones, burins, sandstoneabraders, and whetstones.

West of the Rocky Mountains from around8000 B.C., and continuing for many millenia,archaeologists recognize the Desert Culture,which has a number of named regional variantsfrom Mexico into Oregon and Washington.These variants emphasize the gathering andpreparation of small seeds by hand and millingstones; the hunting of a wide variety of animals;and the extensive utilization of wood, bone,hide, and vegetational sources for tools, orna-ments, and containers. It was a gradually de-veloping adjustment to the essentially desertenvironment, which supported only small bandsand in which population density remained lowup to the historic period. It was not, howeva, astatic complex, for many significant changestook place in the technology, some of them rep-resenting almost continent-wide shifts in toolforms, and new weapons, and shifts in thetechniques of manufacturing baskets. Importantvariants are recognized in areas along streamsand lakes, in upland forested or alpine areas,and where minor shifting climatic patternsallowed the expansion of desert bands into some-times better watered areas or the penetration offoreign groups into the Desert Culture region.

Between 8000 and 6000 B.C. along the North-west Coast and into the interior along the majorrivers, at least some part of the year was spentin obtaining food from the spawning runs andin otherwise exploiting the food supply asso-ciated with the streams and coastal areas. Thelatter is a reasonable inference, for some partsof what was then the coast are now under water.It was to be a long time, however, before the

striking Northwest Coast sea-adapted complexwould develop between Washington and theAlaskan peninsula.

In the interior, from the Yukon territory toIdaho, there is an Old Cordilleran complex thatmay be viewed as an Asiatic-derived parent tothe Fluted Point, as a collateral contemporane-ous variant, or as the result of the northern andwestern expansion of the Llano to Plano tradi-tion. At present there would seem to be a basicrelationship, and current radiocarbon dates indi-cate the time period of Old Cordilleran as notover 8000 B.C.

In southern California the San Dieguitohunting culture with percussion-flaked lanceo-late points, knives, scrapers, and choppers isknown from about 8000 B.C. to 6000 B.C. Shortlyafterward there is a development of a numberof areal specializations in coastal, desert, andforest environments, which during the last fewthousand years resulted in an unusually densepOpulation for a hunting-gathering populationin the oak-forest area of central California.

Southwestern Alaska was sparsely populatalby around 8000 to 6000 B.C. by people with aunifacial core and blade industry whose move-ment into Alaska is likely to have been from thePacific side of the Chuckchi peninsula intocoastal Alaska and south to the eastern Aleutianarea. If these early coastal-adapted groups werethe first Aleuts, as is implied, it would suggestthat the Bering Strait area was occupied byEskimoan-speaking peoples longer ago than hasbeen thought. In interior and northern Alaskathere is a considerable variety of assemblagesreflecting inland and coastal developments withcontinuing ties with Siberia, and also influencesfrom northward-spreading groups primarilymoving with the expansion of bison and othergame animals.

Between 3000 and 2000 B.C. the DenbighFlint Complex, with a marked coastal adapta-tion, spread with surprising speed eastwird toprovide the first successful occupation of theeastern Arctic. The first Eskinio bands reachednorthern Greenland by 2000 B.C. Eskimo cul-tural traditions have a considerable time depth,

8

14

and a main hearth area was the Bering Strait onboth sides of the International Date Line, wherepeople have been moving across in both direc-tions for many millenia.

In the woodland area of the eastern UnitedStates a gradual transition is recognized inseveral areas from the Fluted Point Hunterscomplex to assemblages maintaining the samebasic manufacturing stone-working techniquesand tools, but with the dt:velopment or adoptionof nonfluted projectile forms very similar tosome of the early Plano forms of the Plains. By7000 to 6000 B.C. stemmed and notched pro-jectile forms become common, and an increasingdiversity of regional areas through time reflectsthe increasing specialization of groups learningto exploit the resources of these local regions.Many oi the changes are related in form andfunction to those of areas to the west, but theeast acquires a distinctive flavor of its ownthrough the development of a series of wood-working tools and ground and polished stoneforms. While regional specializations are presentin the eastern Archaic complexes, there is alsoevidence of increasing exchange of raw materialsor manufactured objects as travel or trade routesbecome established.

Many archaeologists view most of the culturalcomplexes of Mexico from about 8000 to 4000B.C. as a southern extension of the Desert Cul-ture. Certainly the general hunting-gatheringpattern is similar, and there arc some tool formsthat are held in common with early Archaic andDesert Culture groups from California to Texas.The most important feature of the Mesoamen-can scene is the early domestication of plants,from Tamaulipas to Chiapas, which has beendemonstrated where systematic efforts havebeen expended to search for such evidence. Thisarea shows a very gradual increase in the num-ber of plants domesticated in the several regionsand in the proportion of domesticates consumed.Marked population increase in some areas suchas the Valley of Mexico, the Valley of Oaxaca,the coastal lowland of southern Vera Cruz andTabasco, and the Pacific Coast of adjacentChiapas and Guatemala is observed by 1000 B.C.,

when agricultural practices were well developedand the Early Formative cultures were becom-ing established.

Summary

All the supportable evidence available indi-cates that the first human occupants of NorthAmerica came from northeastern Asia. Somearchaeologists support the view that this firstoccurred from 30,000 to 40,000 or more yearsago, others believe it was from about 25,000 to20,000 years ago, and some have contended thatit could not have been until about 12,000 yearsago. The time of arrival has not been settled.

Some archaeologists emphasize the Mouste-rian origins of the first emigrants, believing thatthe earliest American cuhural complexes indi-cate a spread into North America before ele-ments of Upper Paleolithic origin had reachedeastern Asia. Many archaeologists, however, be-lieve that Upper Paleolithic developments werea part of the cultural mechanisms that allowed

man to move into North America and spreadthroughout the New World.

The main access route into interior NorthAmeri.ca was east of the Rocky Mountains, anddispersion into most of the Americas was bythis route. Population increase and any physicaldillerentiation of human groups south of theArctic area is derived primarily from the popula-tions of the Pa leo-Indian period. There arc noindications in the prehistoric record of any latersubstantial migrating groups influencing thecultural life of the residents of North Americasouth of the Alaskan and Canadian Arcticregion.

The archaeological evidence, except in rareinstances, supports the view that, in spite ofregional adaptations to food supplies and rawmaterials, there was a continuous exchange ofnew developments between regions, with theadditional implication of population interactionas well.

REFERENCES

1. AVELEYRA ARROYO DE ANDA, L. El SegundoMamzet FoK1 de Santa Isabel Iztapan, Mexico, yArtektos Asociados. Mexico, D. F., Instituto Na-cional de Antropoligia e Historia, 1955. 61 pp.(DirecciOn de Prehistoria, PublicaciOn 1)

2. AVELEYRA ARROYO DE ANDA, L. Antigfiedad delHombre en Mexico y Centroamerica: Cata logoRazonado de Localidades y Bibliografia Selecta(1867-1961). Mexico, D. F., Universidad NationalAutOnoma de Mexico, 1962. 72 pp. (Cuadernos delInstituto de 'Astoria, Serie Antropologica, 14)

3. CUSHING, E. J., and H. E. WRIGHT, JR., eds.Quaternary Paleoecology. Nein Haven and London,Yale University Press, 1967. 443 pp.

4. GOODLIFFE, E. M. Un sitio pleistocenica enTlapacoya, Estado de Mexico. Mexico, D. F., Insti-two Nacional de Antropologia c Historia, Eolethi23, 1966, pp. 30-32.

5. GRIFFIN, J. B. Some prehistoric connectionsbetween Siberia and America. Science 131:801-812,1960.

6. GRIFFIN, J. B. Eastern North American archae-ology: A summary. Science 156:175?191, 1967.

7. GRUHN, R. Two early radiocarbon dates fromthe lower levels of Wilson Butte Cave, SouthCentral Idaho. Tebiwa (Idaho State Museum) 8:57,1965.

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8. GUILDAY, J. Grizzly bears from eastern NorthAmerica. Amer. Midland Nat. 79:247-250, 1968.

9. HAYNES, C. V., JR. Fluted projectile points:Their age and dispersion. Science 145:1408-1413,1964.

10. HAYNES, C. V., JR. Muestras de C-14, deTlapacoya, Estado de Mexico. Mexico, D. F., Insti-tuto Nacional de Antropologia y Historia, Boletin29, 1967, pp. 49-52.

11. HOPKINS, D. M., ed. The Bering Land Bridge.Stanford, California, Stanford University Press,1967. 495 pp.

12. IRWIN, C. lnfornie preliminar sobre las exca-vaciones en Valsequillo. Mexico, D. F., Archivosdel Instituto Nacional de Antropologia c Historia,1965.

13. JENNINGS, J. D., and E. NORBECK, eds. Primi-tive Man in the New World. Chicago, Universityof Chicago Press, 1964. 633 pp.

14. KLEIN, R. G. Radiocarbon dates on occupationsites of Pleistocene age in the U.S.S.R. Arctic An-thropology 1V:224-226, 1967.

15. LORENZO, J. L. A fluted point from Durango,Mexico. Amer. Antiquity 18:394-395, 1953.

16. LORENZO, J. L. Dos puntas acanaladas en laregion de Chapala, Mexico. Mexico, D. F., JnstitutoNacional de Antropologla e Historia, Boletin 18,1964, pp. 1-6.

17. LORENZO, J. L. La etapa Utica en Mexico.Mexico D. F., Instituto Nacioval de Antropologiae Historia, 1967. 49 pp. (Depat tamento de Prehis-toria, Publicaci6n 20)

18. MACDONALD, G. F. Debert: A Paleo-lndianSite in Central Nova Scotia. Ottawa, National Mu-

seum of Canada, 1968. 207 pp. (AnthropologicalPapers, 16)

19. MACNEISH, R. S. Preliminary archaeologicalinvestigations in the Sierra de Tamaulipas, Mexico.Amer. Philo. Soc. Trans. 48, 1958.

20. MACNEISH, R. S. Ancient Mesoamerican Civi-lization. Science 143: 531-537, 1964.

21. MARTIN, P. S., and H. E. WRIGHT, JR., eds.Pleistocene Extinctions: The Search for a Cause.New Haven and London, Yale University Press,1967.

22. MARTINEZ DEL Rio, P. Los origenes ameri-canos. 3a. ed. Mexico, D. F., PAginas del Siglo XX,

1953.23. MASON, R. J. The Paleo-Thdian Tradition in

Eastern North America. Current Anthropology 3:227-278, 1962.

24. MAYER-OAKES, W. J. Life, Land and Water.Proceedings of the 1966 Conference on Environ-mental Studies of the Glacial Lake' Agassiz Region.Winnipeg, University of Manitoba, 1967, 414 pp.(Occasional Papers, Department of Anthropology, 1)

25. MIRAMBEI L, L. Excavaciones en un sitio pleis-

tocen-.:o de Tlapacoya, Mexico. Mexico, D. F., Insti-tituto Nacional de Antropologia c Historia, Boletin29, 1967, pp. 37-41.

26. MOOSER, F. Tefracronologia de la Cuenca deMexico para los tiltimos treinta mil aiios. Mexico,D. F. Instituto Nacional dc Antropologia e His-toria, Boletin 30, 1967, pp. 12-15.

27. WAUCHOPE, R. Lost Tribes and Sunken Conti-nents: Myth and Method in the Sttuly of theAmerican Indian. Chicago, University of ChicagoPress, 1962. 155 pp.

28. WENDORP, F. Early man in the New World:Problems of migration. Amer. Nat. 100253-270,1966.

29. WEST, F. H., ed. Early Man in the WesternAmerican Arctic: A Symposium. College, Anthropo-logical Papers of the University of Alaska 10(2),1963.

30. WEST, R. C. Handbook of Middle AmericanIndians, Vol. I. Natural Environment and EarlyCultures. Austin, University of Texas Press, 1964.

570 pp.31. WILLEY, G. R. An introduction to American

Archaeology. Vol. 1. North and Middle America.Englewood Cliffs, New Jersey, Prentice-Hall, 1966.526 pp.

32. WRIGHT, H. E., JR, and D. G. FREY, eds. TheQuaternary of the United States. Princeton, Prince-ton University Press, 1964. 922 pp.

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164,

MESES FOR MEDITATION ON THE ORIGIN AND DISTRIBUTION OF

MAN IN SOUTH AMERICA

José M. Cruxent

This paper does not constitute an extensivestudy of the origin and early settlement ofSouth America. So many important works onthe subject have been published that I am re-lieved of that duty. I need only cite Hester (10),Krieger (12), Comas (3), Lanning and Patter-son (13), Lynch (14), and Bosch Gimpera (8).

Unfortunately, despite all the valuable recentdocumentation, we still cannot really prove justhow South America was peopled.

As we all know, concern over the problem ofthe origin of American man goes back to thetime of Columbus. The conquistadors evenwondered whether Indians were human, and soit is understandable that Pope Paul III shouldhave issued a papal bull explaining that theIndians were in fact human and could receivethe Faith (18).

Since the sixteenth century numerous hy-potheses about the origin of American manhave been suggested, and most of them havebeen discarded as fantastic. Today we feel thatwe have long outlived that era, that -ur workis imbued with a scientific spirit and our hy-potheses are based on valid archaeological docu-ments. Nevertheless, I find it difficult to acceptthat all this vast ancient documentation is worth-less. I say this in full awareness of how difficultit is for a present-day archaeologist to consultand study this copious literature, which not onlyis hard to find but is sometimes available onlyin archaic languages. But I wonder whetherprejudging all those ancient studies without

even knowing anything about them is a respon-sible thing to do. In many cases I think it maybe precipitate. I am convinced that a review ofthe old literature in the light of modern researchmight be very useful and might lead to surpris-ing conclusions.

Out of the great variety of working hy-potheses on the origin and dispersion of man inSouth America, which I consider of little helpto those concerned with human biology, I findone positive fact: even today we cannot be surethat man in South America came uniquely byland and by way of Panama.

After years of trying to find an answer inarchaeology and other sciences, I believe thatSouth America was peopled not only overlandbut also, and to a large extent, by sea and riverroutes, primitive though the means of naviga-tion must have been. I do not see how mencould otherwise have crossed so many rivers,swamps, and lakes with their entire familieswomen, children, and the agedto occupy thewhole of the South American continent.

If the route was terrestrial, the only entranceis through the Darien jungle in Panama andthe Atrato region in Colombia. I know that areawell; I have crossed it on foot from the Pacificto the Atlantic and back again. In this labyrinththere is no sun, only a weak green light. Atevery step is a river or a marsh. Whetherthrough the low ground or along the mountaincrests, walking is extremely difficult; huntingwould have been practically impossible. In the

"winter" or rainy season no one could havemoved. And there are many other Dariens, andmany rivers to cross. From my travels in SouthAmerica I suspect that Pa leo-Indian man musthave had to go at least part of the way by water(and I make bold to suggest eaat he may haveknown how even before he entered the NewWorld); if so, this would explain many of thegaps we find when we try to trace his migration.Unfortunately, a great deal of the possible evi-dence has disappeared under rising water levelssince Pa leo-Indian times (10).

The immigrants were unquestionably requiredto adapt themselves to a great variety of en-vironments, but if they traveled by water thecultural changes would be less strong and vio-lent than if they came only by land, becausethere would be fewer stages to their journey.Genetically, they might have had fewer contactsor mixtures with other migratory groups becausethe continent was so sparsdy populated at therime. But if we accept the possibility of a waterroute, we must also accept the possibility thatsome groups reached South America some otherway than through Darien.

The "autochthonous" theory of Americanman, which originated in a misreading of Qua-.ternary fossil remains and in the belief thatPa leo-Indian immigration would have been im-possibly difficult, seems now to have been re-jectedamong other reasons because there isno convincing evidence to support it. I shouldlike to make the point that a good way of layingit to rest once and for all would he to prove thatman came from elsewhere and to prove how hecame. I may say in this respect that, eventhough I cannot prove the contrary, I am notat all satisfied with the Bering Strait as the soleentrance route. How could man have spreadover such a vast territory and created such amosaic of cultures and ethnic groups in so shorta time, 20,000 years at most, if he had enteredby a single route?

I have the impression that not enough atten-tion has been paid to the ancient accounts of thetravels of such navigators as the Phoenicians,the Romans, the Arabs, the Vikings, and the

12

Normans. Apart from the reasons I mentionedabove, there is the general discredit to whichthese theories are subject because they have beenput forward by untn ined persons guided byignorance or by a desire to sell books. The scornof responsible archaeologists, and their unwill-ingness to risk their prestige by examining themcritically, is understandable. But there are somerecent finds that if verified would be of greatinterest. I do not believe that the seriousness ofsuch studies as those of Hui-lin Li (11) orSauer (22) can be doubted.

One of the old chronicles tells of finding OldWorld coins in America, and I myself know ofa North American who bought a pot full ofRoman coins, which seems to have been foundin a cave, from a farm worker in Falcon State,Venezuela. The coins are now in the Smith-sonian Institution. I have also seen in the Ja-maica Museum a pedestal with a Roman inscrip-tion that was found off the Jamaican coast. Ihave heard that a Mexican publication, whkI have not seen, mentions a small Roman statueunearthed in that country. The newspapers areforever reporting discoveries of ancient objectsof European and African origindiscoveries,however, that are seldom controlled or studiedby professional archaeologists. I bring all this upmerely to inquire whether it is proper for us toconsider such information a priori false and ofno interest.

Many colleagues have asked me: "If thesearrivals did occur, where is the evidence? Wheredoes archaeology find any appreciable traces inthe indigenous cultures?" This is the problemto which we must find an answer, not only fromthe cultural standpoint but also from the bio-logical.

As to the former, let me say that the culturalimpact of a small immigrant group on anAmerican aboriginal population is in most casespractically nil. We have an example in Balboa'ssiege of Careta: ". . . the chroniclers agree . . .

that Balboa found helpful compatriots alreadyinstalled there. . . They had adapted them-selves to their new environment without reserve,and . . all were 'as naked as the Indians and

4

as plump as the capons that housewives fattenin their cellars' " (20). This probably happenedon many other occasions, and not only at thetime of the Conquest. When I was exploringthe Orinoco Delta region I came upon a French-man (he eventually confessed that he had es-caped from Devil's Island), living with anIndian wife and mestizo children; it was onlyby his slightly lighter skin and his heard that Iwas able to identify him. I have heard of otherexamples, and there must be many more.

As can be seen, the cultural influence of theintruder is slight or nonexistent. His biologicalinfluence I cannot saythat is up to the biolo-gists.

The possibility of immigration by sea is sup-ported by the fact that navigation is much easierthan is supposed and much older than is gen-erally accepted. In the Old World, from pre-historic times until the fifteentl, century, boatshugged the coasts, for the fear of the open seawas great and navigation was rudimentary. Butany storm might pull the boat out to sea, andthen the crew had to resign itself to the currentsand the wind. When it is recalled that some ofthe remote Pacific islands were peopled by thetime the Europeans came, the logical conclusionthat man willingly or unwillingly made longjourneys across the oceans cannot be avoided.The most fortunate encountered islands or conti-nents; some learned in time how to get back

again, and others did not.Columbus' diaries, citing encounters with

.., canoes that traveled the Caribbean from islandto island, support the idea that sea journeys arepossible even in small, primitive boats. We alsohave the many incredible transatlantic voyagesof sportsmen (16) and contemporary politicalrefugees who have brought small, crammedboats across the ocean in search of freedom anda new life in America. I do not believe thatBombard (1) was the first to obtain potablewater from fish; this vital technique may well

have been known to the ancients. In preceramictimes they could have stored it in light-weightvessels such as gourds or skins, which whenempty could have been used as floaters.

Once again, therefore, I postulate navigationas a possibility that could have spared the Pa leo-Indian innumerable obstacles on his way andthat furthermore would have permitted migra-tory movements without requiring the existenceof an ice-free corridor east of the Rocky Moun-tains.

Origin and antiquity of man in South America

All recent studies on the origin of man inSouth America agree that migration was chan-neled from north to south across the Isthmus ofPanama. Evidence of this migration is limited,perhaps because there has been very little ex-ploration in this area. So far, no other theoryseems to have been confirmed, riot even that ofMendez Correa (15), who suggests a routethrough the Antarctic from Australia to Tierradel Fuego. As far as 1 know, n) transatlanticroutes have been proposed. However, extraordi-nary similarities have been shown between thestone implements of western Africa and north-eastern South America (5). These parallels aremuch closer than between Pa leo-Indian materialfrom Siberia and from North America.

As to the antiquity of Pa leo-Indian manusing this term for a hunting and gathering cul-ture that coexisted with animals now extinctand is known by its cro,tie c.,koppio9 toois

no accepted chronology yet exists. Wemay estimate that the Pa leo-Indian disappearedabout 7,000 years ago, and very tentatively wemay propose an arrival date in South Americaor Venezuela of 15,000 to 20,000 years ago. Thislatter date is calculated on the basis of finds forwhich the following ages have been obtained:El Jobo complex, 10,000 years; Las Lagunas andEl Camare, more than 16,000 years; and Muaco,14,740 to 16,580 years (21). I do not knowof any earlier dates anywhere else in SouthAmerica. Lanning and Patterson (13) estimatethe Chuqui complex in Chile and the Tortugaand Red Zone complexes in Peru as the mostancient in the Pacific Andean region, both being13,000 to 14,000 years old. For Argentina wehave a date of 7,970 :I: 10t) at Ayampitin-Int; huasi, and for Brazil a date of 7,501 at

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Sambaqui de Maratua (18). Current excavationsin Chile showing man in association with masto-dons and a variety of other animals promise toproduce extremely important documentation(2).

From these and a few other dates that mightbe mentioned, we can make the following ten-tative timetable for Pa leo-Indian man in Amer-ica: North America, 15,000 to 30,000 years (9);northern South America, 10,000 to 20,000 years;western and southern South America, 8,000 to14,000 years. The figure for North Americadeserves a question mark; the experience ofSouth America leads one to believe that furtherstudies will uncover earlier dates (13). Indeed,although it is quite possible that some specialistsmay consider these dates too ancient, I find themnot only logical but overly conservative and Iexpect future studies to at least confirm them.

Principal lithic complexes

Lanning and Patterson (13) have proposed athree-group typology for the South Americanlithic complexes: (1) bifacial industries, (2)burin or graver industries, and (3) chopper in-dustries. An examination of the principal Vene-zuelan complexes shows that the typology ofthat country presents certain characteristics thatare not present in those of Argentina, Chile,Peru, and Ecuador. Earlier this year, when heconsulted our collections in the VenezuelanInstitute for Scientific Research, Dr. Lanningwas able to relate the Camare complex with the"Bifacial Andean Horizon" (large chipped arti-facts, large bifacial stones, absence of projectilepoints). He could not relate the Chuoui, Tor-tuga, Red Zone, or Exacto (Ecuador) complexeswith those of northeastern South America, andhe found some of te Lagunas and El Job°material (plano-convex scrapers, spear points,and other articles) to be quite unlike anythingin the regions he had studied.

To me this circumstance is extremely impor-tant. It permits a working hypothesis as to theexistence of another possible entrance route toSouth America: the chain of Caribbean islandsfrom Florida to northeastern South America,

14

which 1 accept for both Meso-Indian and Neo-Indian times. I may cite herepurely for refer-ence purposes, since I am not sure of theirvalidity for the CaribbeanHester's observations(10) on the rising of the sea level since Paleo-Indian times. Many islands would be intercon-nected, thus making navigation and migrationeasier. The C-14 ages of some Meso-Indian sitessupport the idea of inter-Antillean navigation:Rooi-Rincon, Curacao, 4490-160 years; Mor-dan, Dominican Republic, 4120 ± 160 years;Punta Gorda, Venezuela, 4150 ± 80 years.

As to Paleo-Inclian man in the Caribbean, atthe Mordan site we have found a more ancientlevel of chipped-flint implements, which wehave called Alejandrina (Cruxent and Chanlatte,work in progress). The ypology of the Alejan-drina complex can be r Aated to that of theEl Camare complex, .-.-;.11 large plano-convexknives, scrapers, chisels, and other tools. Thismaterial has not yet been fully studied. Theartifacts are made of excellent-quality flint andare in strict accord with the typology of flintindustries, which is based in part on the natureof the substance. The same is true of the Man-zanillo and El Camare implements, the first ofwhich are of silicified wood and the second ofquartzite. I am one of those who believe that a

single group of artisans trying to manufacturea certain type of instrument with different ma-terials would have to produce different typolo-gies. This must be taken into account in com-paring complexes, for it is easy to make mistakes.There is also the possibility of the fortuitoususe of objects as implements in certain circum-stances. This may be the answer in the case ofTaima-Taima, which is completely atypical;on the other hand, it is just as likely that we callit atypical because this is the first time we haveseen such implements in association with Pleisto-cene fauna.

The presence of Paleo-Indian culture on thestrategic island of Hispaniola raises a series ofproblems. The principal one is how the Ale-jandrina people lived, for no fossil remainsof mastodons, glyptodonts, or megatheres havebeen found. Considering that they were island-

dwellers, we must conclude, if they were greathunters, that if large animals were not to befound on land they may well have been found

at seaperhaps manatee and seals, both ofwhich were abundant in the Caribbean in thosetimes (7 , 23).

Yothing is known of the origin of the Paleo-Indians of the Alejandrina complex, but theyprobably came from the north. Nor is it knownwhether they reached Venezuela, though someslight contact between the Alejandrina complex,or an older one of the same sort, and the ElCamare and Las Lagunas complexes would nothave been impossible. Later groups may alsohave had some influence on the early Meso-Indian or late Paleo-Indian complex of Canaimain Venezuelan Guiana (21), the Rio Claro com-plex in Brazil (4), and the Gran Sabana and

Paragua material.I hope in the near future to be able to clear

up this problem of another route to eastern

South America in Paleo-Indian times. Thiswould extend the validity of the H theory pro-posed by Osgood and Howard (17) as a graphicexplanation of migratory routes in general.

Before concluding, 1 wish to point out thatmany times we fail to take into account a hy-pothesis that should not be ignored in drawingconclusions. I am referring here to the possibilitythat there may have been Paleo-Indian groupswithout a lithic industry. 1 do not understandwhy we always imagine Paleo-Indian man with

a stone implement in his hand; we are evenpresumptuous enough to demand a specific typeof implement, an officially accepted one. We

must not forget that until very recently projec-tile points were the only implements recognized;all others were considered "blanks." For manyyears 1 have been accumulating experience with

an archaeologist's eye in many Indian commu-nities. This in vivo archaeology has given memany answers that would have been hard tocome by from purely academic studies. (Ofcourse, this often puts me in the unfortunate

position of having no erudite citations to make

in support of my arguments.) From this experi-

ence, I do not think we can discard the possi-bility that there were Palto-Indian groups with-out stone implements any more than we canignore the likelihood that they knew how tonavigate.

I also think it a valid working hypothesis thatPaleo-Indians without a lithic culture, which Icall "primary culture groups," could well have

been the ancestors of certain groups of forest

gatherers and primitive agriculturists in SouthAmerica. Lithic culture evolved through a series

of phases before arriving at triangular peduncu-fated points; it is significant that this traditionsurvives to the present day in our llanos andsavannas but that I have not found it in jungleor thickly forested areas.

This could indicate that a diversity of diets

existed from the start or else that it came about

at the end of Paleo-Indian and the beginningof Meso-Indian times, when the great vertebratesdisappeared. Unfortunately, no conclusion canbe reached at present, for we do not knowwhether the jungle-dwellers descended from an-ofaer group of great hunters or from a groupthat entered the New World already carrying a

primary culture. It is also possible that somegroups abandoned the flake industry in adapta-tion to an ecological area that did not allow its

use. Geography is not determining, but it un-doubtedly affects many aspects of the life ofprimitive peoples, who obtain from their habitatthe elements essential to their needs and their

security.In conclusion, I believe that many of the gaps

we observe in Paleo-Indian migration can belogically explained by taking navigation into

account. I do not reject the idea of terrestrialmigrations; I wish only to complement it. In

any case, I am optimistic about the possibilityof solving the problem of the origin and dis-persion of man in South America, because mostgood archaeologists do not regard it as settled.

15

, 21

REFERENCES

1. BOMBARD, A. Naufrage Volontaire. Paris, 1958.2. CASAMIQUELA, J. MONTANE M.- and

R. SANTANA A. Convivencia del hombre con elmastodonte en Chile central. Mus. Nac, Hist. Nat.Noticiario Mensual (Santiago) XI:132, 1967.

3. COMAS, J. Los problemas de la antropologiafisica ante el origen del hombre americana. SIDPaulo, Encontros Intelectuais, 1961.

4. CRUXENT, J. M. Noticia sobre litos de silex delBrasil. Bol. Mus. Cienc Nat. (Caracas) IV, 1958;V, 1959.

5. CRUXENT, J. M. Les Cultures lithiques Pa leo-Indiennes du Venezuela: un curieux phenombse deconvergence typologique es fonctionnelle avec lescultures foresteres centrafricaines. Tervuren Bel-gique. Koninklijk Museum voor Midden-Africa,1960.

6. CRUXENT, J. M., and I. ROUSE. Arqueologiacronológica de Venezuela. 2 vols. Washington,Unión Panamericana, 1961.

7. Enciclopedia Universal Ilustrada Europeo-Americana. Barcelona, Espasa, 1924, Vol. 24, p. 218.

8. CIMPERA, B. P. L'Arn;:rique: Paliolithique etmisnrshique. In Andre Varagnac, Paris, L'Hommeavant Picriture, 1959, pp. 165-187.

9. GRIFFIN, J. B. The origin and dispersion ofAmerican Indians iTI North America. In BiomedicalChallenges Presented by Me American Indian.Washington, Pan American Health Organization,1968, pp. 2-10.

10. HESTER, J. J. Late Pleistocene environmentsand early man in South America. Amer. Naturalist100:914, 1966.

I I. Hui-LIN Li. Mu-Ian-Pi: A case for pre-

16

Columbian transatlantic travel by Arab ships. Har-vard 1. Asiatic Studies 23, 1961.

12. KRIEGER, A. D. Early man in the New World.In J. D. Jennings and E. Norbeck (eds.), PrehistoricMan in the New World. Houston, Texas, Rice Uni-versity Press, 1964, pp. 23-81.

13. LANNING, E. P., and T. C. PATTERSON. Earlyman in South America. Scientif. Amer. 217(5):44-50, 1967.

14. LYNCH, T. F. The nature of the CentralAndean precerarnic. Occasional Pipers Idaho StateUniv. Mus. 21:78-82, 1967.

15. MENDEZ CORREA, A. A. Nouvelle hypothesesur le peuplement primitif de PAmerique du Sud.Anais Fac. Sociologia do Porto XV, 1928.

16. MERRIEN, J. Les Navigateurs Solitaires. Paris,1957.

17. OSGOOD, C., and G. D. HOWARD. An Archeo-logical Survey of Vene.zuda. New Haven, Yale Uni-versity Press. (Publications in Anthropology, 27)

18. PERICOT y GARCIA, L. America indigena.Tomo I. El hombre americano. Los pueblos deAmerica. 2a ed. Barcelona, 1962.

19. REMAN, E. The Norse Discoveries and Ex-plorations in America. Berkeley, University of Cali-fornia Press, 1949.

20. Romou, K. Balbo. of Darien: Discoverer ofthe Pacific. Garden City, New York, Doubleday,1953, p. 94.

21. ROUSE, I., and J. M. CRUXENT. ArqueologiaVenezolana. Caracas, Ed, 1,/e..a., 2962.

22. SAUER, C. 0. Neblina norteiia. Berkeley, 1968.23. SIMPSON, G. G. The principles of classification

and a classification of mammals. Bull. Amer. Mac.Nat. Hise. 85, 1945.

DISCUSSION

William S. Laughlin

I feel a little like an Eskimo shaman comingbefore the College of Cardinals to discuss thedoctrine of the Immaculate Conception. But anEskimo shaman would not hesitate to do this,and so neither will I.

A great deal of ground has been covered veryexpertly by both these scholars, and they haveraised a number of very good problems. I canmake only a few comments and perhaps add oneor two olrervations by way of interpretation.

I would suggest that most or all of the peoplewho entered the New World came by way of theBering land bridge. This, of course, does notexclude other points of entry. But at least theother groups that"Vave come L have left nodistinguishable genetic heritage that can besorted out.

As Professor Griffin pointed out, the Beringland bridge was a large extent, over 1,000 kilom-eters from north to south. This leaves, then, anopportunity for at least two routes across theland bridge and may help to explain some ofthe differentiation between the less MongoloidAmerican Indians and the more Mongoloid Es-kimos and Aleuts of the North.

It is very likely that some of the early peoplelived permanently on the land bridge. Theywere there for a long period of time. They didnot simply run across in order to get to theother side in order to be discovered by peoplewho came later. And for all practical purposesthey were unamwe that they were going to besubmerged. So for a few thousand years theyenjoyed the real estate they held.

Now, those who lived on the coast had, I

17

think, the advantage of a richer ecological zone.They had the marine mammals. They had thefish. And, of course, they had the birds, as wellas those things that grow in the intertidal zone,and, very importantly, invertebrates, mollusks, .1

bccessibe 44 warm's. ech t,Net WteApt ate iiNiciS C35111octopus., and so forth. hts c

I suspect that the ancestors of the Aleuts (ofthe Aleutian Islands) and the Eskimos (of themainland extending over to Greenland) mayhave originated or taken their primary form onthe southern part of the Bering land bridge,and that when the land became submerged theysimply backed up and remained on the coast.Of course, as the waters rose there was morecoastline rather than less, and therefore theyprospered rather than disappeared.

The ancestors of the Paleo-Indians, who morelikely came through the interior, may have neverseen the people on the coast, being separated byseveial hundreds of miles, or have had onlyintermittent contacts with them. They were big-game hunters hunting mammoth, caribou, andpossibly musk-ox. These people may have livedon the Bering land bridge for some time, butwhen the waters rose they had only two options.One was to learn to live under water; the otherwas to go back to Siberia or on to the NewWorld. Obviously, a number of them went onto the New World.

Now, when we look at the early sites, we findvery good documentation for the period between9,000 and 12,000 years ago. There are a greatmany dates that I think can be accepted as beingwell rep!icated. But getting beyond the 12,000-year barrier is difficult.

The most recent piece of evidence is one thatDr. T. Dale Stewart called to my attentionyesterday. Dr. Leakey has rediscovered an olddiscovered skull in Southern California, at La-guna Beach, which has been dated on the boneitselfnot on associated materialsat 17,000years. The skull has not arrived here yet, andwe do not know what it looks like.

In any event, if that date should be substan-tiated, we would be in a position to say thatman had to come prior to the 14,000- or 15,000-year period and must therefore have come before24,000 years ago. This, however, has not yetbeen established.

Now, turning to South America, one thingI should like to mention is the trait complexassociated with the Lag& Santa crania of Brazil.You will recall that these were discovered in thelast century; they are now in the Museum ofZoology in Copenhagen.

Lag& Santa crania are dated around 8760 B.C.

The interesting thing is that although theyappear to be this old, they look like those ofcontemporary Indians, and not only in generalfeatures of morphology but also in discontinuoustraits that may be more similar to single-genetraits, though this is not firmly demonstrated.They have shovel-shaped incisors, which arefound in all New World occupants, both Eskimoand Indian. They have dehiscences of the tym-panic plate. And there are several cases of inter-parietal bones, the separate Inca bone on theposterior of the skull, which reaches a highfrequency in South American Indians.

Taking this example to raise a point, it wouldappear that there has been very little morpho-logical change in American Indians over a periodof 9,000 years.

We can say the sar..e thing for North Ameri-can, though we do not have as good a series asfor Lag 6a Santa. Nevertheless, the amount ofmorphological evolution does not appear to havebeen great.

We can go one step further and point out thatthe Eskimos and Aleuts, who form a singlecoherent population system, demonstrate a simi-larity to Middle Pleistocene man of northern

China, as was originally observed by FranzWeidenreich. This similarity probably indicatessome genetic continuity. If that is ), this againreflects a rather minor amount of external visiblemorphological change and suggests a slow rateof morphological evolution.

One interesting point we must consider thenis the possibility that the morphological diver-gence between peoples within the New Worldand between the inhabitants of the New Worldand the Old may reflect a slow rate of humanevolution, morphologically speaking. Therefore,the fact that some of the earliest physical remainsdo not took like Neanderthal man or likeAustralians does not mean that they have notbeen here for some time.

And there is something else to be emphasizedthat the amount of morphological change doesnot accurately reflect that of other tissue systems.Serological evolution, dental evolution, changesin different tissue systems, are proceeding atdifferent rates. When we look to the past, we arelimited to the skeleton; we cannot assume thatchange in many genetic traits, including behav-ioral traits, has not gone on at perhaps a muchfaster rate.

The other point I should like to make is thefact that the majority of the people comingacross Bering Strait were exposed to a coldfilter. All botanists, glaciologists, geologists, andanthropologists are agreed that, whatever condi-tions were, they were cold. The inhabitantsadapted to the cold for the few or severalthousand years they lived on the Bering landbridge. This may possibly be related to someof the epidemiological and immunological as-pects of contemporary populations. Once theygot south, of course, they could adapt to severalother varieties of zones. But they all had to passthrough a cold filter.

The last point I should like to mention is therate of dispersion and how long it would havetaken to get to the Strait of Magellan. I simplycall your attention to the fact that the Aleutsand Eskimos are spread over a difficult expanseof 8,000 miles, and it took them considerablyless than 8,000 yearspossibly as little as 2,000

18

yearsto ga that way. Therefore, the trip toSouth America may Rot have been as long aswe might otherwise think.

General Discussion

Salzano: Since Dr. Laughlin mentioned theLag Oa Santa material, I want to say a fewwords about the prehistoric remains of BrazilianIndians.

A few years ago a researcher from the Na-tional Museum, Professor Marilia de M. Alvin,did a review of the anthropometric data at handand found a considerable heterogeneity betweenthe different Lagoa Santa sites. We cannot say,therefore, that these people are just one homo-geneous group. She also examined the shell-mound material of different locations and theywere even more heterogeneous.

Moderator: Do you mean to imply that theheterogeneity in the Lagoa Santa material isgreater than might be found in contemporaryIndian populations in Brazil?

Salzano: That is difficult to say, because thematerial available for study is not very extensiveonly about 80-odd individuals. But even inthis small sample the heterogeneity is very great.I am not saying, however, that it is greater thanamong present-day Indians.

Roche: I have a question for Professor Crux-ent. He gives a possible ai;e for man in NorthAmerica of from 15,000 to 30,000 years, inwestern and southern South America of 8,000to 14,000 years, and in northern South Americaof 10,000 to 20,000 years. These ages seem togo from more to less. Does he consider this asone more proof of north-to-south migration?

Cruxent: I do not think the last word has yetbeen said as to ages. We have not been able todate the oldest complexes we have in SouthAmerica, in the alluvial terraces at great alti-tudes, because all the material is on the surfaceand has been exposed to the air. It happens insome places in the States. But I feel that littleby little, here in the States, earlier ages will befound. We keep finding older and older ma-terial in America, and I think that will continue.

Roche: That was not exactly my question.

What I asked is this: You seem to give theimpression that in North America we find olderages than in Mesoamerica, and in turn the agesin Mesoamerica are greater than those in SouthAmerica. Could this be taken as additional evi-dence for a north-to-south migration?

Cruxent: Yes, it seems to confirm the theorythat the migratory current was from north tosou th.

Moderator: Professor Griffin, you have a namefor being a bit of a skeptic in these matters.Would you care to respond at all to Dr. Crux-ent's presentation?

Griffin: The evidence of man in SouthAmerica, both what can be established and whathas been claimed, indicates an antiquity of manin South America greater than that in NorthAmerica, and evidence in which I have someconfidence suggests that we have not found manin North America of the antiquity necessary forhis appearance in South America at the ageclaimed. I think it is possible that we simplyhave not found the evidence in North America.

I should like to comment on one point ofCruxent's paper: If through man's penchant forself-destruction the evidence for our astronautswere completely destroyed, there would be verylittle in the earth's atmosphere to tell the peopleof the future that man had actually gone aroundthe world. Cruxent's "Paleonauts," if I maycoin a phrase, are extremely difficult to trace inthe sea waters. So that while he hinted broadlyat the possibility of man's making voyages fromwestern Europe or western Africa and perhapsacross thc Pacific, my position is that he mayhave done so but I have seen no traces of theboats, or whatever they used, and thus haveno evidence for such an interpretation.

I also wish to comment on the presumed con-tact of Mediterranean, European, African, orrelatively civilized Asiatics with the New World.Such ideas have been current for a long time.They were originally based on the philosophicalposition that it would have been impossible forIndians to achieve high cultures without benefitfrom groups that had achieved reasonably highcultural status in the Old World. But that posi-

19

tion has been abandoned. We no longer needto bring high culture into the New World fromthe Old because now we can clearly documentthe gradual development of the higher civiliza-tions in the New World, both in South Americaand in Mesoamerica.

It is true that a great many contact areas areknown. For example, there are stories of theIrish being present in North America, primarilyaround the hinterland of the Boston area. Phoe-nicians are recognized in eastern Pennsylvaniaaround Lebanon. A major center for pre-Colum-bian Scandinavian influence in North Americais in the area of Minnesota and Wisconsin. Butsome of us are extremely skeptical about theappearance of Roman coins or statues or variousother objects, because they can be reasonablyexplained on the basis of man's pack-rat andsouvenir complex.

And so I admit to somewhat of a skepticalposition on many of these matters that Dr.Cruxent has so delightfully called to our atten-tion.

McDermott: Dr. Griffin, is there any linguisticevidence acceptable to reasonable man, as youput it, on this question of migration from Northto South America?

Griffin: I am told there was tremendous lin-guistic diversity among the American Indiangroups and that none of the New World lan-guage stocks can be traced back to those of Asiawith any degree of certainty. I am also told thatthe linguistic diversity in, for example, theeastern United States could reasonably havetaken place within a period of some 10,000 to12,000 years from a single ancient linguisticstock.

The archaeological evidence we have indicatesto some of us that the original populations ofthe eastern United States were relatively homo-geneous in cultural material and, further, thatcultural extremes can best be explained primarilyas regional developments based on the originalcultural groups.

Water low: Dr. Laughlin suggested that twogroups of people came over by different routesnorthern and southernthrough Alaska, one

being the rather small Eskimo type and theother the North American type. Is there anyevidence that they came from two differentfamilies or groups in central Asia?

Laughlin: I think the answer is no, there isno evidence of two separate groups that can bedisting.,ished today. However, the record innorth China and Japan does suggest that evolu-tion has been proceeding there and that peoplewould differ according to when they sampledthat particular area.

So the fact that the more recent (if indeedthey are more recent) Eskim-)s and Aleuts lookmore like Japanese and Chinese may reflecteither their recency or the fact that they weredrawn up the no-th Pacific riinJapan, theKuriles, Kamchatkaand followed tize coastrather than coming from northern Sibefia.

There is no particular group that could beidentified today, and I think it would be haz-ardous to look for one, since those populationshave been evolving for the same period of timeas those in the New World.

But there is, as Dr. Comas and others havepointed out, a major dichotomy between theAleuts and the Eskimos and the rest of theIndians. This includes several serological factorsas well as growth rates, disease patterns, andother morphological differences.

I would add just one other thing, and thatis that in our views we should take into accountthat Japanese anthropologists have again pointedout that they think the Ainu of Hokkaido, innorthern Japan, are a variant of Mongoloidsand not of archaic whites who were surrounded.The old thesis, originally proposed by ProfessorBirdsell, that there was a group of Australoids,archaic whites, or Ainu-like people living inSiberia is no longer tenable if as much hetero-geneity as that between Ainu and Japanese canbe recognized among Mongoloids.

Griffin: If our archaeological evidence is anygood, then the first migrations seem to have beenfrom the central Siberian area, with culturalcomplexes that date back somewhere around20,000 years or so. These populations seem tohave moved primarily along the northern coastal

20

26

areas of Beringea into the North Americaninterior. The evidence is that the populationsDr. Laughlin has been talking about with hisproto-Eskimo or prehistoric Eskimo of 8,000years ago or more are distinctly different fromthe earliest movers into the New World andhad a cultural complex formulated primarilyon the Pacific side of northern Asia, at a latertime. It was chiefly the first group, moving intothe New World along the northern rim, thatpopulated North America and I think movedinto South America, either on migratory-birdwings, across water by navigation, or ploddingthrough and slowly adapting to various environ-ments.

Roche: I want to make just a brief commentin relation to Dr. McDermott's question. Therehave been studies on linguistics, but there havebeen very few comparative studies on the musicof the Indians. I have been told by the head of

the Institute for Music Study in Berlin that

primitive music shows much less variation andevolution than primitive languages, that originscan be recognized much better through musicthan through language. Practically nothing hasbeen done in this area. For what it is worth, hefeels that the Latin American music he hasheard, particularly the very primitive, such asthat of the Caribbean, has very strong relation-ships with northern Asia, particularly Japan.

Moderator; At this point we have succeededin getting the Indian to the Americas, althoughthere is something less than unanimity as tohow this was accomplished. In the next sectionof the program we propose to look at thephysical and genetic diversity present in the

American Indian. The distinction between

"physical" and "genetic" is of course artificial,since the basis of much physical diversity is

genetic. It is a convenient distinction, however,

and we shall adhere to it today.

2127

BIOLOGICAL SUBDIVISIONS OF THE INDIAN ON THE BASIS OF

PHYSICAL ANTHROPOLOGY

Juan Comas

In accepting the invitation to participate inthis Special Session, I was guided primarily bythe great interest this subject has always hadfor me. I well realize, however, that my knowl-edge of the problem and my information, bothdirect and indirect, leave much to be desired.I present my excuses in advance and ask forleniency on the part of my readers.

For a better understanding of the vah1/4: andscope of the principal biological subdivisions ofthe Indian on the basis of physical anthropology,I believe it necessary to first pose three questionsand go on from there to some provisional con-clusions. The questions are these:

1. Do the American Indians constitute a bio-logically homogeneous population or have they,on the contrary, a certain variability which per,mits thinking in terms of subdivisions?

2. To what cause or causes may the biologicalvariability of the American Indian be attributed?

3. What attempts have been made at a racialtaxonomy of the American Indian?

Let us examine these questions consecutively.

Biological variability of American aborigines asagainst classical conception of "Americanhomotype"

The excellent works of Newman (47) andStewart and Newman (56) make it unnecessaryto devote too much space to this question. Dis-crepancies on this point have a long history.Antonio de Ulloa's statement toward the end ofthe eighteenth century that "If we have seenone American, we may be said to have seen all,

Ak,d't

22

their color and make are so nearly alike," andthe consequent acceptance of the somatic unityof the pre-Columbian population of the NewWorld as a definitive fact, received the supportof such renowned anthropologists as Samuel G.Morton (1842), Timothy Flint (1826), AlesHrdlicka (1912), and Arthur Keith (1948).

The opposite campcomposed of those whorecognized the existence of obvious biologicaldifferences among the Indian groups, describingthem as "races," "varieties," or "sub-species"--in-eluded, among many others, Humboldt (1811),Desmoulins (1826), D'Orbigny (1839), Retzius(1842), Aitken Meigs (1866), Topinard (1878),Deniker (1889), Virchow (1890), Ten Kate(1892), Haddon (1909), Biasutti (1912), Wisier(1922) Dixon (1923), Rivet (1924), Eickstedt(1934), Hooton (1937), Imbelloni (1937-58),Count (1939), Neumann (1952), and Schwi-detzky (1952).1

It is interesting to point out that, while thebelievers in the somatic unity of the Indian re-mained a minority, in -heir forefront was Mor-ton, of whom Stewa t and Newman (56) sayshrewdly:

Indeed, so great was his influence that he was

responsible in large measure for the wide acceptance ofthe generalization embodied in Ul loa's words and forthe conversion of Ulloa's words into an "adage." (p. 22)

Morton's influence lasted for more than half

3 Most of these arc well-known general works andtherefore do not appear in the References. For additionalinformation see J. Comas, Manual of Physical Anthro-pology, (Springfield, 1960), pp. 81-86 and 588-600.

a century, until Hrdlicka arose as the newchampion of the homogeneity of the Amerin-dian. In summarizing his arguments Hrdlickasaid in 1912 (32): "The conclusions are thatthe American natives represent in the main asingle stem or strain of people, one homotype."He reaffirmed this thesis in 1928 (33) in anattempt to refute those who supported the racialplurality of the American Indian:

We find that the various differences presented by theIndians are often more apparent than real; that actualand important differences arc in no case of sufficientweight to permit of any radical dissociation on thatbasis. (p. 481)

This position had the able support of SirArthur Keith (36):

Certainly the American Indian differs in appearancefrom tribe to tribe and from region to region, but un-derneath these local differences there is a fundamentalsimilarity. This, too, is in faveur of descent from asingle, small, ancestral community. (p. 218)

Nevertheless, little by little, the physical varia-bility of the American Indian had shown itselfto be an undeniable fact, leading to differingand even contradictory descriptions and systema-tizations. Laughlin (38) presents the situationvery clearly and objectively:

Much progress has been made since the early days ofanthropology in America when it was assumed that allIndians were essentially alike. The diversity of the NewWorld populations has been well established. The sig-nificance of the diversity in terms of the evolution ordevelopment of types there or of the importation ofpreformed types from the Old World remains to beclarified. (p. v)

Stewart and Newman (56) expressed the sameopinion at the conclusion of their article:

This review of opinions regarding Indian variability hasrevealed the fact that the principle of Indian raitilunity rests almost solely upon the outer appearance ofliving Indians. In so far as the Indians exhibit in com-mon such physical characters as straight, black hair,copper-colored skin, dark brown eyes, high cheek bones,scarity beard and a relatively long trunk, they can besaid to be uniform. . . . That the Indians, on the otherhand, are quite variable within this racial pattern, andespecially when comparisons are made in measurabledimensions, also has been shown. (p. 33)

All this would lead one to think that from1951 on, the theory of the American homotype

23

had been definitely discredited. While the greatmajority of anthropologists are of this opinion,we must not overlook the fact that some dis-tinguished investigators differ. Ashley Montagu(44), for example, has written:

The American Indians exhibit a certain basic homogeneitybut at the same time are evidently characterized by anequally certain diversity of types. Owing to the lack ofthe necessary data it is impossible to say quite howmany diverse types there may be. General impressionsbased on sporadically measured and photographed indi-viduals from various groups provide an insufficient basisupon which to erect a satisfactory account of the Ameri-can Indian. (p. 465)

Some years later the same author does affirm(45) that the Eskimos of the Arctic coast ofNorth America form part of the group of ArcticMongoloids while the other American Indiansconstitute another group composed of "an unde-termined number of ethnic groups of North,Middle, Central and South America."

Coon, in his important volume on humanraces (18) devotes barely two pages to the racialcharacteristics of the American Indians. He says:

The American Indians are more uniform racially thanany other group of people occupying an equally vastarca. In fact, they are more uniform than many peopleswho occupy an arca a tenth as large. All of this indicatesthat a relatively small number of peoples crossed theBering Strait during the last part of the Wisconsinglaciation, and that their descendants gradually filled theuninhabited regions of the New World. They are Mon-goloid in general and despite some of their peculiaritiesin blood groups do not necessarily merit classification asa subspecies of their own. . The American Indiansdiffer from the Asiatic Mongoloids mainly in that theyhave less facial flatness, particularly in the nasal skeleton,and a more variable skin color. There is no valid evidencethat the Indians were derived from more than one sourceor that they came into the New World by a route otherthan the Bering Strait. (p. 152)

In spite of these sporadic casesand quitepossibly there are other adherents of this theoryI believe it can be said that the beginning ofthe second half of the twentieth century coin-cides with an end to the myth of the "Indianhomotype" and an explicit recognition by thegreat majority of anthropologists of the exis-tence of somatic and osteological variability andheterogeneity among the aboriginal groups of

'a7

,45

America. It is then necessary to establish theorigin and the causes of this variability, bearingin mind that it in no way exceeds the limits ofcharacterization of Homo sapiens.

Have we sufficient and adequate information,posterior to 1951, to be able to determine whetherthe differences of physical types among theAmerindians are due to prehistoric immigrationfrom the Old World or to adaptive evolution tothe new habitat? This is what we mwt try toanalyze.

Cause or causes of biological variability ofAmerican Indians

At first glance it seems easy to distinguish twoexplanations for this phenomenon.

First, there is the proposal of those who acceptthe immigration of diverse human types, eachof which represents one of the existing Amerin-dian "races." Stewart and Newman (56) de-scribe it very clearly, attributing it primarily tothose who have been concerned with Americanracial taxonomy:

. . . the classifiers of Indian types operated with astrongly hereditarian bias, out of keeping with the mainstream of biological thought. If explanations were givenfor their dassthcations, they were usually to the effectthat each Indian "race" represented a separate migrationfrom the Old World. . ImpliAy, such explanationsdisavowed the possibility that physical changes couldhave occurred among New World peoples. (p. 29)

However, they themselves indicate that thevarious authors place different degrees of empha-sis on the hereditary aspects of the prehistoricimmigrants, on cross-breeding with each other,and on the environmental influence of the newhabitat to explain the presence and existence ofdistinct Amerindian "races"; and they evaluatethe greater or lesser importance that some of themost conspicuous "polyracialists"for example,Dixon, Griffith Taylor, and Hootonconcede toeach of these factors (p. 30). Even Imbelloni,one of the most devoted defenders of a compli-cated polyracialism, refers to only seven distinctmigratory waves and on the other hand describesand localizes eleven Amerindian "races," whichimplies agreement that in the new habitat newracial types were formed. He even tries (34)

to localize "the sectors and zones where theeffects of mixture and hybridization occurred,"although he rejects every explanation for whathe called the "environmentalist creed."

Second, there is the theory of somatic varia-bility as principally the consequence of environ-mental influences, which Stewart and Newmanexplained as follows:Interpretations of this sort were made largely by Ameri-canists who had no classifications to justify, and ac-cordingly were more willing to admit that anthropometricdeterminations were not always stable in changingenvironments. As a group, these Americanists did notdeny the migrationist postulates of the classifiers, butseemed to believe that hereditarian and environmentalexplanations could be harmoniously blended in overallinterpretations. (p. 31)

But what seems essential to me is a somewhatmore careful analysis of Newman's own view(54), which he expresses thus:The adaptive responses of bodily form to environmentin warm-blooded animals have led, largely in the lastcentury, to the formulation of several ecological rules.

. Extensive testing of these ruks on human materials,however, has not been performed. For this reason, Ihave examined the applicability of two of the best vali-dated of these rulesBergmann's and Allen'sto thebody forms of Ncw Wodd aborigines.2 The principlebehind both rules is that the maximum retention of bodyheat in cold climates occurs when the radiating skinsurface is small relative to body mass. Since this ratiocan bc achieved by larger body size, Bergmann's ruleholds that within a widc-ranging species, the subspeciesin colder climates attain greater size than those inwarmer climates. Allen's rule holds that in addition thecold climate subspecies have reduced extremities andappendages, thus further reducing the body surface. Inwarmer climates, following Bergmann's rule, easier dis-sipation of body heat goes with the low body mass bodysurface ratio achieved by smaller body size (p. 324)

Newman presents with the greatest objectivitsa series of facts, some of which I wish to men-tion because his interpretation of them seems tome in certain cases to be doubtful, erroneous,and even contradictory with respect to the finalcomment.

1. He states (p. 312): "In mammals and birds

2 j. A. Allen, The influence of physical conditions inthe genesis of species, Radical Revicle 1:108-140, 1877.C. Bergmann, Ueber die Verhiiltnisse der Wiirmebko-nomic der Thicre zu ihrer Grösse, Glitiinger Suidien3:595-708, 1847.

30

there are a number of exceptions to these rules:It) to 30 per cent for Bergmann's rule, calculatedonly from subspecies in the most contrastingclimates of the species range (Rensch, 1938:282)." Actually, the percentage of exceptions toBergmann's rule among birds and mammals islarger than this. Rensch (51) mentions "forpalearctic and nearctic birds I calculated 20-30%of exceptions on the average" and "for pale-arctic and nearctic mammals 30-40%."

2. He says (p. 313): "I am aware that incertain parts of the Old World [Bergmann's andAllen's rules] do not seem applicable. Uponsuperficial examination, the rules do not appearoperative in Africa south of the Sahara. Yet, inEurope and the Near and Middle East and inEast Asia and Malaysia, there seem to be north-south body size clines conforming to Bergmann'srule. The explanation of these discrepancies inAfrica and perhaps elsewhere is not yet ap-parent." To admit that Bergmann's rule is notoperative in Africa south of the Sahara indicatesthe impossibility of generalizing such a rule insupport of human variability. Furthermore, itsapplication seems doubtful in Europe, the Nearand Middle East, eastern Asia, and Malaysia.How does one explain, for example, the differ-ences of stature and body proportions in differ-

ent regions of Europe, and among the Veddasand Brahmans of Bengal, the Sikhs of the Pun-jab, the Tapiros and Papuans?

3. In support of his thesis Newman includesn;ne maps showing the distribution in Americ.of stature, sitting height (living), head size(living), cranial module (skeleton), upper facesize (skeleton), morphological facial index (liv-ing), upper facial index (skeleton), and nasalindex (living and skeleton); but he adds (p.315): "The categories used in these maps arearbitrary, and in some areas the data are inade-quate, but probably [italics mine] the mapsrepresent reasonable approaches to the real dis-tributions."

Then he notes that the small stature of theEskimos constitutes an exception to Bergmann'srule but that, as "the Western Eskimo are notinferior in sitting height to the tallest Indians,

their shorter stature, then, is attributable solelyto their short legs. This reduction of extremitylength is in accordance with Allen's rule, andprobably [italics mine] represents an adaptationfostering body-heat retention." As to the easternEskimos, whose stature and sitting height areless than those of the Indians who live furtherto the south, he attempts to explain this bysaying "Possibly [italics mine] the use of heavytailored clothing in combination with factors ofuncertain food supply and periodic undernutri-tion may cancel out the selective adv antage oflarger bodies in colder climates, but his cannotbe demonstrated."

Continuing to note exceptions to the sup-posed applicability of Bergmann's rule to man inAmerica, he mentions groups of small stature"surrounded by taller groups," such as the Yukiof northern California, the Lillouet of southernBritish Columbia, and the Yahgan and Alakalufof the Magellan archipelago. With respect to thelast two groups he further indicates that thesitting height has not been calculated, "but othermeasurements indicate they are not particularlyshortlegged."

Neel and Schull (46) say: "In the simplestterms we may conceive of stature as being thecumulative effect of a number of genes whoseactions are similar and whose effects are addi-tive" (p. 107). "We may surmise, therefore, thatunder the environmental conditions in whichthis study was conducted, the primary cause ofvariation in stature is genetic" (p. 110).

Barnicot (9), referring to geographical varia-tions in stature, says:

There is a great deal of information about stature varia-tion throughout the world, but not infrequently it is

based on samples which are either very small or wereselected in a way which may render them unrepresenta-tive of the general population. . . On the whole thepattern of stature variation throughout the world showsno very striking regularities. Both tall and short peoplesare to be found in most of the major regions. (pp. 203--

204)

And after specifying different cases of geographi-cal distribution of stature, he concludes:

This distribution of stature has been interpreted as anexample of a dine with adaptive significance in relation

25

31

to climate (Bergmann's rule). A substantial negativecorrelation between body-weight and mean annual tem-perature has been demonstrated for various regions ofthe world.

Harrison (27) also writes, in dealing withenvironmental interaction:

Differences in stature are inherited, but they are alsoenvironme.ntally determined, since grrwth is profoundlyaffected by nutritional state, and probably by climaticfactors as well. Further, the nature of the variation pro-duced by both types of factor tend to he the same.(pp. 144-145)

We can see from this how opinions differ withregard to the problem Newman presents.

4. Farther on Newman writes (p. 323): "Ofthe remaining standard dimensions, only [italicsmine} head form and relative head height showdistributional patterns not readily interpreted asadaptive ones. Indeed, the earlier and marginaldistribution of long heads and the apparentlylate arrival of low heads seems best explained bymigrations of people differing in these regards.But since the diagnostic criteria of most racialclassifications of New World aborigines are prin-cipally the body size and proportion traits shownhere to be adaptive, it is most curious that ifexplanations of these classifications are attemptedat all, they are in terms of a separate migrationfrom Asia to account for each race." The "headform and relative head height" are hereditarycharacteristics because head breadth (dominant)and head length (recessive) enter into theirdetermination. The same is true with respect toface height (dominant) and face breadth (re-cessive), broad nose (dominant) and narrownose (recessive)characteristics to which New-man also refers in the course of his argument.

On the other hand, the most discussed racialclassification of the American aborigines (14,47)that of Imbelloni, who uses as his basisthe classifications of Biasutti, Eickstedt, andSchwidetzky takes into account cranial, facial,and nasal indices, all of them hereditary char-acteristics, in addition to stature. Therefore,Newman's statement does not exactly reflectthe real facts.

5. Finally, Newman states (pp. 323-324):"From the foregoing, it seems clear that body

build is influenced by both hereditary and directenvironmental factors." And "without denyingthat the New World was peopled by successivemigrations or infiltrations of physically differingpeoples it is very likely that the American racesof the classifiers are at least partly the productsof adaptive changes that took place in the NewWorld." This, generally speaking, seems accept-able; I have earlier made observations on thismatter, with particular reference to the charac-teristics that are considered hereditary (stature,body proportions, and cranial and facial indices).The problem to be resolved should be to deter-mine preciselyquantitatively and qualitativelythe influence that heredity and environment(in their broadest sense) have exercised on thepresent somatic variability of the Americanaborigines.

However, in his Summary (pp. 324-325)Newman generalizes about the applicability ofBergmann's and Allen's rules for the formationof the Amerindian "races" without regard toall the reservations and exceptions made in thecourse of his article and cited here. And in alater work (49) he reaffirms his opinion: "Allthese data should make it clear why anthropolo-gists have paid serious attention to the applica-tion of the ecological rules to man. If anything,these rules seem to be more closely operative inman than in other species of homeotherms"(p. 104).

This is important, since other anthropologistsnot only accept such a generalization but tendto amplify it; Stewart (55), for example, says:"Thus Marshall Newnan has demonstrated forthe hemisphere at large that many elements ofthe Indian phenotype are primarily adaptive re-sponses to environment and are distributed inaccordance with Bergmann's and Allen's eco-logical rules" (p. 262). And, as expected, hegoes on to state:

When the first Asiatics crossed Bering Strait into Amer-ica they enterid a huge cul-de-sac offering every varietyof environment and no forerunners to mix with. A re-construction of what happened thereafter takes intoaccount that the resulting population at the time ofdiscovery constituted a major isolate that was homoge-neous, both phenotypkally and genotypically. (p. 269;italics mine)

26

I wish, however, to present arguments thatestablish categorically the true scope of this"geographical and climatic determinism." I havealready said above that according to Rensch thepercentage of exceptions among birds and mam-mals to Bergmann's and Allen's rules is veryhigh.

In an interesting paper on the same problem,C. G. Wilber (61) says that "On the basis ofour present knowledge the rules of Bergmannand Allen appear to be of historical or descrip-tive interest only and certainly are not validgeneralizations for animals in the cold" (p. 332).His Summary is as follows:

This brief and rapid survey does not postulate thatclimate is without effect on man. At another time theecological effect of this variable of man will be discussed.This presentation attempted to show in a sketchy fashionthe following:

1) The rules of Bergmann and Allen find little sup-port as causal agents in modern studies of temperatureregulation in homeotherms.

2) The various formal examples often cited in favorof these ecological generalizations do not support thecase of the climatic determinists. One is forced to con-clude that the rules just do not apply causally to animals.

3) In man the ecological forces supposed to be actingare not doing so; Eskimos were not cold, the skinnyaboriginal Australians were.

4) The rules of Bergmann and Allen have no causalrole in the formation of racial diflerences in man. Suchuse of these rules on the part of same anthropologists isa source of misinformation and confusion [italics mine].

5) Some human groups have met the demands ofsevere climate by technological and behavioral adjust-ments; the Eskimos are an example. Others have de-veloped specific heat-conserving functional changes withno gross morphological changes; the Australian aborig-ines are an example.

Gam, on the other hand, concludes as followsa detailed criticism refuting Wilber (22):

I know of no anthropologist so rash as to claim thattemperature and the radiant heat load art exclusive oreven major causes of the differences between geographicalraces, or that the past-century formulations of Bergmannand Allen completely solve the problems of race forma-tion in man. I know of none who adopt the Lamarckianapproach that Dr. Wilber so gleefully demolishes. But,when Wilber asserts that the "rules of Bergmann andAllen have no causal role in the formation of racialdifferences in man," I doubt very much that he intendedsuch a sweeping and untestable counter-generalization.

Other authors confirm a divergence of opin-ions about the applicability and importance ofBergmann's and Allen's rules to the biologicalvariability of the American Indian. Roberts (53),in an important contribution to the subject, says:

The weight/temperature relationships here demon-strated suggest that Bergmann's rule is applicable toman. Clearer definition of "body size" is, however, neces-sary. Defined by reference to stature, although from theseries here considered Bergmann's rule might seem tobe applicable, this suggestion is refuted by more extensivematerial [italics mine]. Defined by weight, it is not onlyapplicable but needs restatement to incorporate, withthe postulated variation in size among subspecies, similarvariation within the subspecies. (p. 551)

Ashley Montagu (44, 45) holds that suchzoological rules "are to some extent also appli-cable to man," but adds:

The application ri Bergmann's and Allen's rules to manhave been seriously and cogently questioned (Wilber),on the ground that the ;nadequate data has been im-properly interpreted, and that in any event man hasnever responded to his environment in a passive manner,but has always done everything within his power tocontrol and shape the environment to his requirements.But while this is undoubtedly true, it should be remem-bered that ecological rules are generalizations to whichexceptions can be found in every group, but that by andlarge they do apply to most populations of a species.The studies of Newman and of Roberts on New andOld World human populations lend strong support tothe view that ccolog :al rules apply to man as well asto other animals.

27

Weiner (58), for his part, states that Berg-mann's and Allen's rules are applicable to animalpopulations in general and continues: "Thathuman body-size and shape tend to follow theserules has been demonstrated in several studies.The mean body-weight of populations in hotregions is demonstrably lower than that in tem-perate and cooler climates" (p. 455). But fartheron in the same work, on examining genetic andnongenetic factors in climatic adjustments, hepoints out:

Twin studies indicate that variations in body-shape, size,fat deposition, growth pattern, skeletal and physiologicalmaturation are all determined by genetic constitution toa larger extent than by purely environmental factors.Certain of the population differences rest undoubtedlyon distinctive genotypes or multifactorial recombinations,e.g. nose-shape, or the ratio of limb length to trunk

length since such characters remain unaffected on changeof environment. (p. 460)

Baker (1), also referring to the racial differ-ences in heat tolerance, says: "These results fur-ther suggested that the differences found werenot a function of transient environmental effectsand may be mostly genetic in origin" (p. 303).Later (2) he arrives at the conclusion that"However, it is not enough to find evidence ofclimatic adaptation. There remains the muchlarger question of how climatic selection wouldoperate on man's genetic structure to producethese adaptations" (p. 4).

In general terms I believe that Dobzhansky(21) best synthesizes the question.

The environment thus instigates, foments, conditions andcircumscribes evolutionary changes; but it does not decideexactly which changes, if any, will occur. (p. 408)

The rules of geographic variation used to be a happyhunting ground for partisans of Lamarckism and selec-tionism, abounding in data intTrpretable as their pre-dilections decreed. Nowadays these disputes may, I hope,be bypassed. The rules attest in any case that the environ-ment is important as an instigator of evolutionarychanges. At the same time, it must be emphasized thatwhat has been observed arc rules indeed, not laws.(p. 412)

Exceptions to the rules do occur, as Rensch, who hascontributed more than anyone else to their study, hasduly stressed. And while these exceptions do not exactlyprove the rules. they arc in some ways as valuable asthe rules themselves. The lesson to be derived fromthem is that, although the environment may guide theevolution of living things, it does not prescribe just whatchange must occur. (p. 413)

Waddington (57) offers an explanation of howthis genetic-environment interaction is effected.

We have, in fact, found evidence for the existence ofa "feedback" between the conditions of the environ-ment and the phenotypic effects of gene mutations. The"feedback" circuit is the simple one as follows: (1) en-vironmental stresses produce developmental modifica-tions; (2) the same stresses produce a natural selectivepressure which tends to accumulate genotypes whichrespond to the stresses with co-ordinated adaptive modi-fications from the unstressed course of development;(3) genes newly arising by mutation will operate in anepigenetic system in which the production of such co-ordinated adaptive modifications has been made easy.(p. 399)

Recently the problems of human adaptability

to ecological and environmental conditions havegreatly interested numerous biologists and physi-cal anthropologists. A human Adaptability Sec-tion is part of the International Biological Pro-gram (1BP), and several international meetingshave been held (Burg Wartenstein, 1964; War-saw, Kyoto, and New Delhi, 1965) to discusssuch subjects as "Human adaptability and itsmethodology," "Human adaptability to environ-mental conditions and physical stress," and aproposed regional study of high-altitude adapta-tion. A detailed presentation of the topics of theHuman Adaptability Section appear in the Guideof the Human Adaptability Proposals;a the re-sults of the meetings have been published (8,41, 63).

In November 1967, 60 scientists from 12 na-tions participated in the Conference on Man atHigh Altitudes, sponsored jointly by the U.S.National Committee for the IBP and the Worldand Pan American Health Organizations. Theyagreed that research on high-altitude peoplescould also be applied profitably to populationsliving at sea level and to their medical problems,and recommended that coordinated studies bemade on "problems of growth, ageing, nutrition,fertility, natural selection and epidemiology."

As for investigations completed or in progressin America on human adaptability to differentconditions of heat, humidity, altitude, and lati-tude, a number of monographs have appearedespecially on peoples of the arctic regions (Eski-mos) and of high altitudes (Quechuas andAymara* Continuing the research program sosuccessfully initiated by Carlos Monge, Hurtado,and other investigators at the Institute of AndeanBiology in Peru in 1928, Paul T. Baker andcollaborator!: are responsible for the most recentstudies on acclimation and adaptability to dif-ferent ecological environments.

Despite these advances, the problem of humanvariability and adaptation to different climaticconditionsthat is, an evaluation of the interde-pendence of nature and nurtureis still unre-solved. Besides Dobzhansky, whose opinion is

Published by the Central Office of the IBP (7, Mary-lebone Road, London, N.W. 1).

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34

quoted above, Neel and Schull (46) had alreadystated:

It is therefore practically impossible when one is dealingwith human populations to crcatc situations which throwa sharply critical light on thc relative importance ofheredity and environment.

Efforts to establish principal biological sub-divisions of Indians

Once the variability of the living aboriginalpopulationsthe presence of different subspe-cific polytypical forms, regardles-s; of origin andcausesis recognized and accepted, all efforts

at a systematization or classification require aprior definition of the concept of race.

This is not the place or time to analyze suchdisputable and controversial themes as the non-existence of human races according to Living-stone (40) and Brace (17), or the "ethnicgroups" of Ashley Montagu (44, 45) as substi-tutes for racial groups, Of the skepticism of Barni-

cot (10) about the possibility of defining thehuman "races" with the necessary precision. Theclassic description of the "human race" based onthe typologist approach is of historical interestonly. Let us stick to the modern populationistview and accept, for our purposes, any of thefundamentally similar definitions of Dobzhansky(20), Laughlin (39), Garn (23), Mayr (43),Bielicki (13), and others. I should like, how-ever, to quote here some considerations pre-sented by Laughlin (39), because of their clarityand conciseness.

Race does not refer to an arbitrarily selected series ofindividuals, even though they may be similar in ap-pearance, i.e., of the same typc. Races may be conti-

nental or local, homogeneous or heterogeneous, large orsmall, ancient or recent, distinctive in appearance ornondistinctive, sharply bounded or imperceptibly boundedand possess a high or low degree of genetic relationshipbetween members. The term race can bc used at dif-

ferent levels or abstraction from a continental race downto a local race or even their tribal subdivisions. Localraces are composed of collections of family lines whichconstitute breeding isolates within thc larger population.No arbitrary standard of magnitude exists for the sizeor number of differences which must exist for a groupto be termed a race. . . . For summary purposes andmajor contrast such high levels of abstraction are suit-able. However, for research purposes it is necessary tocompare the smaller, constituent subdivisions, the local

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35

races or breeding isolates of many authors. . Conse-quently, though the actual number of races in the worldexists apart from observers, the number recognized de-pends..upon the aim of the observers. (p. 90)

The concepts of geographical, local, and micro-races, expounded by Garn first in 1961 and morerecently in 1965, are thus comprehensible. How-ever, before examining these possible biologicalsubdivisions or races of the American Indian, Ithink it advisable to repeat what I said at thebeginningthat certain contemporary anthro-pologists, especially Montagu and Coon, takethe view that the existing variability and bio-logical differences among the diverse groups ofaborigines are not sufficient to justify a racialsubdivision.

Coon (18), however, in referring to a workof Osman Hill on "The Soft Anatomy of aNorth American Indian," says: '`. . . they areMongoloids of a particular kind, just as theywould be Caucasoids of a particular kind hadthe New World been peopled by a small bandof Upper Paleolithic Europeans." Here I wishto point out that the possible presence of Cauca-soid elements of European origin had been spe-cifically noted in 1928 by Cottevieille-Giraudet.4Apparently certain cultural features cited by

Greenman (24) as persisting on the easterncoast of North America tend to confirm thissupposition.

The classicai subdivisions of mankind fromthe serological point of view proposed by Otten-berg, Snyder, Wiener, and principally Boyd (16)mention solely an Amerindian group, to whichthey accord a certain homogeneitythis despitethe fact that Mourant had noted evident sero-logical differences between different populationsof American aborigines.

During the last few years, the multiple investi-gations of Henckel, Layrisse, Lisker, Loria,

Matson, Neel, Robinson, Reynafarje, Salzano,

Sandoval, Sutton, Swanson, Zepeda, and othershave made available greatly increased data on

4 See my own Manual(Springfield, Illinois, 1960,Upper Palaeolithic and the(Current Anthropology, Vol.322).

of Physical Anthropologypp. 633-635) and "TheNov World. Comments"5, No. 4, 1964, pp. 321-

diverse antigens, hemoglobins, transferrins, andhaptoglobins that demonstrate an obvious pheno-

typic and genotypic variability in these aborig-

ines. This confirms the present conception re-garding the evolutionary process of the humanspecies and the formation of races according topopulationist and dynamic criteria.

In this respect, I cite the latest conclusions

of Matson and collaborators (42) on South

America:

Yet as pertaining to the present study, it seems that asensible position of equanimity, based on the availableblood group data, would permit of an hypothesis thatthe American Indians arc not completely Mongoloid,that the present Polynesian populations are a racialmosaic and that migrants from both west and east have

contributed genes to present panmictic potpourri whichis Polynesia. (p. 188)

Since this variability of blood groups observedamong Indian populations does not coincidewith other morphological variations, one is ledto think that Garn's conclusion (23) is correct:

As with classifications based on morphological traits

rather than on the populations themselves, artificial

"serological races" add nothing to human taxonomy.The major use of blood groups in classification is inthe comparison and analysis of natural populations, andin the study of natural selection in contemporary races.(P. 51)

I shall now review in some detail the racialtaxonomy proposed by Garn (23) with referenceto geographical, local, and micro-races, begin-ning with his definitions and continuing withhis subdivision of the aboriginal populations ofAmerica.

1. The concept of geographical race, first usedby Rensch, is defined by Garn as "a geograph-ically-delimited collection of similar races," andhe adds that "the existence of geographical racesis due, of course, to the great geographical bar-riers, chief among them oceans, that formerlylimited the expansion and migration of localraces and protected them from introduction ofdifferent genes" (p. 14). Garn's geographicalrace is equivalent to the concept of continentalraces. On this basis he divides mankind intonine geographical races, only one of whichtheAmerindian--he attributes to the New World(p. 128). This he describes with some morpho-

logically and serologically typical traits. Earlier,however (p. 120), he alludes to the fact that

some anthropologists find the morphological,serological, and biochemical differences betweenMongoloids and American Indians insufficientfor separating them into two geographical racesand join them into a single, polytypic geo-graphical race. I agree with him that there areslight grounds for this racial hypothesis.

2. As for local races, Gan writes: "In con-trast to geographical races which are geographi-cally delimited population collections, local racescorrespond more nearly to the breeding popula-tions themselves. Whether isolated by distante,by geographical barriers or by social prohibitions,local races are totally or largely endogamous, andthe very small amount of gene-flow ordinarily

comes from contiguous and related local races"(p. 16).

3. What Dobzhansky defined as microgeo-graphical races and what Lasker prefers to callbreeding populations are what Garn calls micro-races (p. 18); in these he makes manifest cer-tain differences in the composition of a local

race. He adds: "Micro-races, though not isolatedgeographically or by extensive cultural prohibi-tions, still differ from each other in numerousways."

4. With regard to the value and usefulness of

these concepts, Gam explains (p. 22): "Geo-graphical races, local races and micro-races offeropportunities for very different investigationsin relation to race. One is not more real or morefundamental than the other, but each providestne answer to different questions and the solu-tion to different problems of ongoing evolution

in man."5. In referring specifically to the populations

of the New Worldthat is, the Amerindiangeographical race---Garn mentions a series oflocal races that "in strict contrast with geo-graphical races are true evolutionary units. Aspopulations such local races evolve or have

evolved separately." He recognizes that "withsuch a diversity of local races, it is clearly impos-sible to make a listing of all of them" but saysthat "it is possible to call attention to some local

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36

races that exemplify particular taxonomic, de-scriptive, or evolutionary problems" (p. 140).And before proposing a subdivision of the livingaboriginal populations, he contends: "In pre-Columbian America, there were hundreds ofsuch local races, each with its own language.We still recognize the Penobscot, the Pima, thePapago and so on. Other local races, in theAmericas, as in Europe and Asia, constitute anumber of isolated or semi-isolated populationsas is true for the several Apache and Navahogroups now."

Only after these admonitions does Gam listfive Amerindian groups of local races: NorthAmerican, Central, Circum-Caribbean, SouthAmerican, and Fuegian. His description ofbiological characteristics (pp. 144-146) is quitepoor, and in the case of two of these local raceshe refers exclusively to cultural traits. This inspite of the fact that he qualifies them as "trueevolutionary units."

Incidentally, with reference to the origin ofthese local races Gam takes a firm position(pp. 128-129): "Once, local differentiation inthe Americas was attributed to successive wavesof migrations. Today such diversity is generallyaccepted as the result of natural selection actingon generally small population isolates, some ofwhom may have a respectable antiquity of asmuch as 20,000 years, as shown by radio-carbondating." 5

I have emphasized the concepts on whichGarn bases his racial taxonomy, particularly withreference to the region under discussion, becauseI consider his concepts proper and his principlesvalid. However, I disagree on the subject of thefive local races he proposes, since mere observa-tion of some of the aboriginal populations in-habiting the areas in which he locates themdemonstrates their great biological (especiallysomatic and serologic) heterogeneity.

According to Garn's own definition, I findit difficult to understand how it is possible to

5 Current data indicate that man's antiquity in Americadates back 35,000 to 40,000 years. See Krieger, inprehistoric Man in the New World (J. D. Jennings andE. Norbeck. eds.. University of Chicago Press, 1964,p.

include in a single local race all the aboriginalpopulations of South America, from the Goajiroin the north to the Araucanians in the south(latitude 10° N to 40° S), living at altitudesranging from sea level to 4,000 meters. And thisapplies as well to the North American local race,ranging from the Athabaskan and Algonquianin the north to the Mayas to the south (latitude60° N to 18' N).

Discussion

An appraisal of new techniques for interpret-ing the physical anthropology of the AmericanIndian was on the agenda of the Fourth SummerSeminar in Physical Anthropology, held in NewYork in September 1949. I should like to startby quoting from the report of that discussion(62).

Washburn suggested that much of the confusion preva-lent in the American Indian field today is a result oftoo many' varying techniques being used on the samematerials, each yielding different results and hence some-what different interpretations. He indicated that somere-evaluation of the several morphologic, metric andgenetic techniques was in order if the best results weretoll? obtained from the available data. (p. 33)

This carefully weighed opinion expressed 19years ago still constitutes, to my way of thinking,one of the principal reasons, though not the onlyone, why even now attempts at a racial taxonomyof the American aborigines yield such vague,imprecise, and even contradictory results.

I agree with Baker (4) that the concept ofrace has two uses as a pedagogic device forteaching human variation and as a research toolfor investigating biological variation, and that,as he explicitly recognizes:

Indeed, racial classification systems arc, at best, interimstructures for dealing with genetic and phenotypic dis-tances, and should be replaced by e.uantitative systems.It may be hoped that the comparrtive method will bereplaced by the more accurate m:thod of mechanismanalysis. However, neither of thesc hopes are . tomaterialize in the near future and for decades race islikely to remain a useful scientific concept. As such, itappears that the race concept will remain in humanbiology for many decades even though it will, un-doubtedly, be a constantly changing informational con-struct. (p. 25)

317

I have expressed a similar point of view onvarious occasions, in discussing the usefulnessand importance of anthropometry and ostcome-try in any attempt to determine the variabilitybetween different population groups. I reiteratethis belief and in its support cite the well-docu-mented opinion of Hunt (34).

As remote racial history has ceased to be the chiefexcuse for field anthropometry, microevolutionespe-cially the adaptive value of racial features in differentenvironmentshas become the core of recent studies.Schemes of measurement are being revised in terms ofthe 'hereditability of somatic dimensions and factors ofphysical growth. Work on demography, new techniquesof mapping, models of gene-flow, and racial physiologyis proceeding rapidly. The unraveling of microevolutionis a sufficient challenge to maintain the vitality of anthro-pometry for a long time to come. In particular, it offersmany opportunities for the collaboration of physical andcultural anthropologists. (p. 82)

I have deliberately included in this papermany quotationstoo many, the reader maythinkfrom different workers, so as to presentthe most recent and contradictory opinions onthe topic and thus document as objectively aspossible my own view, contained in the follow-ing provisional conclusions:

1. I consider acceptable the proposal of variousanthropologists for uniting all the aboriginesof the New World under the denominationAmerindian Geographical Race.

2. That biological variations create perceptibledifferences between American Indians in diverseregions of the continent and thus necessitate ataxonomy of local races, in accord with popula-tionist and dynamic criteria, has been fullyproved and substantiated by many investigationsin various fields of human biology.

3. Attempts have been made to explain this

REFE

I. BAKER, P. T. Racial differences in heat toler-ances. Amer. I. Phys. Anthropol. n.s. 16:287-305,

1958.2. BAKER, P. T. Climate, culture and evolution.

Human Biol, 32:3-16, 1960.3. BAKER, P. T. EcoLgical and physiological

adaptation in indigenous South Americans. In P. T.

Baker and J. S. Weiner (eds.), The Biology of

Human Adaptability. Oxford, Oxford UniversityPress, 1966.541 pp.

biological heterogeneity as a consequence of thediverse origin of the immigrating contingentswho peopled the New World some 40,000 yearsago and also as the result of a process of adapta-tion to different environmental and ecologicalconditions. At the present time, this is a pointof controversy among investigators. In all likeli-hood the biological differentiation of the Amer-indian is due to the joint action of the two.However, more data are necessary before it canbe determined which is the more important.

4. The most widespread and best-known sub-divisions of the American Indian in local raceswe owe to Garn. lf, as he says, these "are trueevolutionary units. As populations, such localraces evolve or have evolved separately," thenit is necessary to assemble a series of biologicalcharacteristics that will make it possible to dis-tinguish the local races proposed for America.

5. The Amerindian groups of local races pro-posed by Garn are not precisely defined, and heappears to recognize this himself when he writes(p. 121): "Such differences in taxonomic opinionare both legitimate and salutary. They point outproblem areas that need resolution. Areas ofagreement on the other hand, may reflect prob-lems long settled, or they may reflect a virtuallack of information."

What is absolutely indispensable in the imme-diate future is the organization on a hemisphere-wide basis of intensive, methodical, uniformbiological investigations (somatic, serologic,physiological, psychosomatic, and so on) of thevarious aboriginal populations that permit subse-quent comparative studies and finally the estab-lishing of local races with a clear and indisput-able differential biological base.

RENCES

4. BAKER, P. T. The biological race concept as aresearch tool. Amer. f. Phys. Anthropol. n.s. 27:2126, 1967.

5. BAKER, P. T., E. R. BUSKIRK, E. PICON-

REATEGUI, J. KOLLIAS, and R. B. MAZESS. Regulaci6nde la temperatura corporal en indios quechuasnativos de la altura. Anales del Instituto de BiologiaAndina 5:286-298, 1966.

6. BAKER, P. T., E. R. Busxunt, J. KOLLIAS, andR. B. MAZESS. Temperature regulation at high aid-

32

38

tude: Quechua Indians and U.S. whites during totalbody cold exposure. Human Biol. 39(2) :155-169,1967.

7. BAKER, P. T., and M. A. LITTLE. Bone densitywith age, altitude, sex and race factors in Peruvians.Human Biol. 37(2) :122-136, 1965.

8. BAKER, P. T., and J. S. WEINER (eds.). TheBiology of Human Adaptability. Oxford, OxfordUniversity Press, 1966. 541 pp.

9. BAmicor, N. A. The size and shape of thebody. In G. A. Harrison, J. S. Weiner, J. M. Tannerand N. A. Barnicot. Human Biology. Oxford, 1964,pp. 197-216.

10. BARNICOT, N. A. Le probleme de la race dansl'etat actuel des connaissances scientifiques. Rev.Int. Sciences Sociales , 17 (1) :90-92, 1965.

11. BENOIST, 1. Microraces et isolats. Rev. Mt.Sciences Sociales 17 (1):93-95, 1965.

12. BIELICKI, T. La genetique des populations etla formation des races. Rev. Mt. Sciences Sociales17 (1) :96-98, 1965.

13. BIELtext, T. Typologistes contre population-nistes et theorie genetique. Rev. hit. Sciences Sociales17(1):99-101, 1965.

14. BIRDSELL, J. B. The problem of the earlypeopling of the Americas as viewed from Asia. InW. S. Laughlin (ed.), Papers on the PhysicalAnthropology of the American Indian. New York,Viking Fund, 1951, pp. 1-68a.

15. BOYD, W. C. Blood groups of AmericanIndians. American 1. Phys. Anthropol. 25:215-235,1939.

16. Bovo, W. C. Genetics and the human race.Science 140(3571):1057-1064, 1963.

17. BRACE, C. L. On the race concept, and Com-ments. Current Anthropol. 5(4) :313-320, 1964.

18. COON, C. S. The Living Races of Man. NewYork, Knopf, 1965. 344 pp.

19. DOBZHANSKY, T. Human diversity and adap-tation. Cold Spring Harbor Symp. Quant. Biol. XV:385-400, 1950.

20. DOEZHANSKY, T. Evolution, Genetics, andMan. New York, Wiley, 1957. 398 pp.

21. DOSZHANSKY, T. Evolution and environment.In The Evolution of Life. Chicago, University ofChicago Press, 1960, pp. 403-428.

22. GARN, S. M. A comment on Wilber's "Originof Human Types." Human Biol. 30:337-39, 1958.

23. GARN, S. M. Human Races. 2nd ed. Spring-field, Illinois, Charles C Thomas, 1965. 155 pp.

24. GREENMAN, E. F. The Upper Palaeolithic andthe New World. Current Anthropol. 4(1) :41-91,1963.

25. HAMMEL, H. T. Effect of race on response tocold. Fed. Proc. 22(3), 1963. InYearbook of Physi-cal Anthropology 11:208-213, 1965.

26. HANNA, B. L. The biological relationships

33

39

among Indian groups of the Southwest. Amer.Phys. Anthropol., n.s. 20:499-508, 1962.

27. HARRISON, G. A. Environmental interaction.In 0..A. Harrison, J. S. Weiner, J. M. Tanner, andN. A. Barnicot, Human Biology. Oxford, 1964, pp.144-149.

28, HIERNAUX, J. Le concept de race en anthro-pologic physique. Fl Congres International desSciences Anthropologiques et Ethnologiques 1:471-477. Paris, 1962.

29. HIERNAUX, J. Heredity :;-.nd environment:Their influence on human morphology. A compari-son of two independent lines of study. Amer. 1.Phys. Anthropol. n.s. 21:575-589, 1963.

30. HIERNAUX, J. Applicabilite du concept de racel'espece humaine. Rev. Int. Sciences Sociales 17(1):

117-119, 1965.31. HIERNAUX, J. Problemes de definitions sur la

race. Rev. Int. Sciences Sociales 17(1):120-i 22, 1965.32. HRDLICKA, A. The problems of the unity or

pluta:ity and the probable place of origin of theAmerican aborigines. Amer. Anthropol. 14:11, 1912.

33. HRDLICKA, A. The origin and antiquity of theAmerican Indian. Rev. ed. Smithsonian Report for1923. Washington, 1928, p. 481. (Publication 2778)

34. HUNT, E. E. Anthropometry, genetics andracial history. Amer. Anthropol. 61:64-87, 1959.

35. IMBELLONI, J. Nouveaux apports la classifica-tion de Thomme am&icain. Miscelanea Paul RivetOctogenario Dicata 1:107-136, 1958.

36. KEITH, A. A New Theory of Human Evolu-tion. London, Watts, 1948, p. 218.

37. LASKER, G. W. The Evolution of Man. NewYork, Holt, Rinehart and Winston, 1961. 240 pp.

38. LAUGHLIN, W. S. Introduction. In W. S.Laughlin (ed.), Papers on the Physical Anthro-pology of the American Indian. New York, VikingFund, 1951, pp. v-vii.

39. LAUGHLIN, W. S. Races of mankind: Con-tinental and local. Anthropological Papers of theUniversity of Alaska 8(2) :89-99, 1960.

40. LIVINGSTONE, F. B. On the non-existence ofhuman races. Current Anthropol. 3(3):279-281,1962.

41. MALHOTRA, M. S. (ed.) Human Adaptabilityto Environments and Physical Fitness (Delhi Sym-posium 1965). Madras, India, Defence Institute ofPhysiology and Allied Sciences, 1966.

42. MATSON, G. A., H. E. SUTTON, R. ETCHEVERRY,B. J. SWANSON, and A. ROBINSON. Distribution ofhereditary blood groups among Indians in SouthAmerica, with inferences concerning genetic con-nections between Polynesia and America. Amer. 1.Phys. Anthropol. n.s. 27:157-194, 1967.

43. MAYR, E. Les races dans l'evolution animale.Rev. Mt. Sciences Sociales 17 (1) :126-127, 19,"*.

44. MoNTAou, M. F. A. An Introduction to

Physical Anthropology. 3d ed. Springfield, Illinois,Charles C Thomas, 1960. 771 pp.

45. MONTAGU, M. F. A. The Science of Man.New York, Odyssey, 1964. 158 pp.

46. NEEL, J. V. and W. J. &Hun,. HumanHeredity. Chicago, University of Chicago Press,1958. 361 pp.

47. NEWMAN, M. T. The sequences of Indianphysical types in South America. In W. S. Laughlin(ed.), Papers on the Physical Anthropology of theAmerican Indian. New York, The Viking Fund,1951, pp. 69-97.

48. NEWMAN, M. T. The application of ecologicalrules to the racial anthropology of the aboriginalNew World. Amer. Anthropol. 55:311-327, 1953.

49. NEWMAN, M. T. Adaptation of man to coldclimates. Evolution 10:101-105, 1956.

50. NEWMAN, M. T. Geographic and microgeo-graphic races. Current Anthropol. 4(2) :189-192,1963. Comments 4(2) :192-207, 1963.

51. RENSCH, B. Some problems of geographicalvariation and species formation. Proc. LinneanSociety of London, 150th Session, 4:275-285, 1938.

52. RENSCH, B. The laws of evolution. In TheEvolution of Life. Chicago, University of ChicagoPress, 1960, pp. 95-116.

53. ROBERTS, D. F. Body weight, race and climate.Amer. I. Phys. Anthropol. n.s. 11:533-558, 1953.

54. SALZANO, F. M. The blood groups of SouthAmerican Indians. Amer. 1. Phys. Anthropol. n.s.15 :555-579, 1957.

55. STEWART, T. D. A physical anthropologisesview of the peopling of the New World. South-western J. Anthropol. 16(3) :259-273, 1960.

56. STEWART, T. D., and M. T. NEWMAN. Anhistorical resume of the concept of differences inIndian types. Amer. Anthropol. 53:19-36, 1951.

57. WADDINGTON, C. H. Evolutionary adaptation.In The Evolution of Life. Chicago, University ofChicago Press, 1960, pp. 381-402.

58. WEINER, J. S. Climatic adaptation. In G. A.Harrison, J. S. Weiner, J. M. Tanner, and N. A.Barnicot, Human Biology. Oxford, 1964, 144- 0'0)

59. WEINER, J. S. Acclimatation et differences declimat: !curs effets sur les differences raciales. Rev.Int. Sciences Sociales 17 (1): 159-162, 1965.

60. WIERCINSKI, A. The racial analysis of humanpopulations in relation to their ethnogenesis. Cur-rent Anthropol. 3( 1) :2-46, 1962.

61. WILBER, C. G. Physiological regulations andthe origins of human types. Human Biol. 29:329-336, 1957.

62. Yearbook of Physical Anthropolzgy, 4. NewYork, Viking Fund, 1949, p. 33.

63. YOSHIMURA, H., and J. S. WEINER (eds.)Human Adaptability and its Methodology. Tokyo,Japan Society for the Promotion of Sciences, 1966.

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40

BIOLOGICAL SUBDIVISIONS OF THE INDIAN ON THE BASIS OF

GENETIC TRAITS

Miguel Layrisse

Improved techniques for the identification ofnew traits in the erythrocytes and in chemicalcomponents of the plasma have brought about anew era in the field of population genetics. Sev-

eral of these traits have shown a distribution re-stricted to a single subdivision of mankind,attaining thereby the rank of gene markers;others are common to virtually all populations,although with variable frequencies; still othersare fixed and/or of very low frequency. It is nowpossible to set up a more comprehensive "mo-saic" of gene frequencies in populations, tocomplement the traditional division of mankindbased predominantly on somatological charac-teristics.

Several attempts have been made at classifyingmankind on the basis of genetic traits (2, 3, 30).Originally classifications were made by means ofblood groups; later, other blood traits were alsotaken into consideration. In a recent classificationBoyd ( 3) distinguishes 13 different human racescomprising 7 major groups, one of which is the"American group" of a single racethe "Ameri-can Indian." Boyd sJggests that "it may eventu-ally be possible to distinguish between NorthAmerican and South American Indians serologi-cally. . . ."

Considered as one population, American In-ians in general are characterized by a high fre-

quency of blood groups 0, M, R2, Fyn, Dia, andABH secretor, and by a low frequency or ab-sence of A2, B, Ro, r, Lua, K, Lea, and abnormalhemoglobins (3, 21, 22). These characteristics

differentiate the American Indians so far studiedfrom other subdivisions of mankind. However,intertribal differences suggest that Indian popu-lations do not constitute a homogeneous genepool as is sometimes suggested in the anthropo-logical literature.

Characteristically, Indian populations through-out the Americas have been organized in terri-torial and tribal groups displaying a certainesprit de corps based on a distinctive culturaland linguistic homogeneity. The tribes live orhave lived in a state of semi-isolation, separatedfrom their neighbors by natural and culturalbarriers that have i'..nctioned as more or lesseffective impediments to gene flow. Larger tribesmay be divided into smaller subtribes made upof several villages. These villages are frequentlyquite independent of each other, with a strongtendency to local endogamy. For instance, inthree recently studied villages of the WaraoIndians of the Orinoco Delta, more than 90 percent of the marriages recorded were contractedbetween individuals of the same local group.This high incidence of local endogamy occurredin an almost complete absence of geographicalbarriers to communication. Similarly high de-grees of village autonomy and local endogamywere observed, although under different culturaland environmental conditions, by Salzano, Neel,and Maybury-Lewis (28) among the Xavanteand by Salzano (26) among the Caingang.

Analysis of the peculiar socio-political charac-teristics of the Amerindian is needed so that we

35

41

-1r

may learn how these subdivisions affect the fre-quency of genetic traits. In this connection atten-tion must be drawn to (a) the intertribal and(b) the intratribal distribution of genetic traits.

Intertribal distribution of blood traits

One of the most striking examples of inter-tribal divergence in frequencies of blood traitsis provided by two tribes living in the AmazonTerritory of Venezuela: the Makiritare and theYanomama. The Yanomama occupy an exten-sive area in southern Venezuela and northernBrazil. The Makiritare inhabit adjacent terri-tories, mainly to the north-northeast. There areconsiderable differences in culture between thetwo tribes. The Yanomama are a Pa leo-Indiansociety of bunters and gatherers with a rudi-mentary agriculture (2, 5, 15, 14, 32). The Maki-ritare have what basically can be identified as aneo-Indian culture based on slash-and-burn agri-culture (14). Although there is evidence ofinterbreeding between the Makiritare and theYanomama, the actual gene flow between themcan be considered extremely limited. The com-parisons of blood-group frequencies between theMakiritare and two Yanomama subtribes (Sa-nema and Waica) showed significant differencesin practically all the blood-group systems. S, ofthe MNS system, is high in the Makiritare (63per cent) but only 19 per cent in the Waica and9 per cent in the Sanema. RI, of the Rh system,is about twice as high in both Yanomama sub-tribes as in the Makiritare. The Yanomama sub-tribes showed the lowest frequency of 112 everfound in Indians-6 per cent in the Waica and3 per cent in the Sanema. The frequency of Fyais 83 per cent in the Makiritare and 58 per centin the Waika and Sanema. Dia is 16 per centin the Makiritare, 0 per cent in the Waica, and3 per cent in the Sanema. Since the Sanemalive in close geographical proximity to the north-ern Makiritare, the Diego frequency can pos-sibly be accounted for by intertribal admixture.

This is by no means an isolated occurrence.For example, differencesthough less markedin blood groups have been reported by Matsonand Swanson (17, 18) between Maya and non-

36

42

Maya groups living in Central America; Sal-zano (27) in Brazilian tribes, Matson et al. (19)in Peruvian tribes; and Matson et al. (20) inChilean tribes. COrdova, Lisker, and Loria (7)did not find such divergence in Mexican Indiantribes, but their study was conducted in a largepopulation.

Intratribal distribution of genetic traits

The study of 10 villages of the Yanomamatribe, carried out in 1966, provided excellentinformation on how gene frequencies may varybetween tribal villages in the same area separatedby relatively short distances (2). Five hundredand sixty-eight individuals, 72 per cent of thevillage populations, were examined for 7 blood-group systems, 7 serum protein traits, and 7

erythrocyte enzyme groups. The variation ingene frequencies was greater than in any othertribe examined so far under similar circum-stances. Genes with low frequenciesMS, NS,112, Lpa, and Agawere found to have beenlost in several villages, while genes with highfrequenciesPGM and Sewere fixed in somevillages. Genes with intermediate frequencies,such as R1, Ms, Ns, Fya, and Jka, showed a verywide range of frequencies.

The Warao villages of the Orinoco Deltaprovide another illustration of gene frequencyvariation within the same tribe. Three villageswere studied: Jobure, Sacupana, and Winikina,with populations of 190, 160, and 300 respec-tively (31). Three previous studies of thesetribes had shown a very low M (less than 15per cent) with a relatively high S (40 per cent),traveling mostly with N, which is uncommonin Indians; very high Ri; and negative or verylow frequency of D?. The village of Sacupanawas the eccentric tribe; its frequencies of theMNSs and Diego systems were completely dif-ferent from those found in the other two villagesand from those previously reported. The fre-quency of gene M was 90 per cent and of gene Sonly 13 per cent, and this gene was mostlytraveling with gene M. It was also found thatthese tribes had 3 per cent of D?. The genealogyof the Sacupana village gave a clue to the ex-

planation of this gene distribution. Twenty-oneout of the 48 living members representing thesecond generation come from a polygynousfamily in which the father happens to be MSsand his three sororal wives Ms. All the Diego-positive cases found among the Warao of theSacupana villages came from one family, whichwe were able to trace through three generations.It is interesting to observe that the members ofthis family also carried the transferrin Dem)which is absent in all Warao individuals ex-amined but present at various frequencies inCariban tribes. Since the western and south-eastern Warao territory is surrounded by Cari-ban tribes, it is likely that both Dia and Debigenes were introduced into the Warao popula-tion by Carib in early times.

The three Xavante villages studied by Ger-showitz el al. (9) showed a variation of 1 to15 per cent for the gene SN and of 24 to 39 percent for the gene 112; the other gene frequencieshad comparable results.

Comments

Analysis of the frequency of blood groups andother blood traits has shown that the socio-political unit used in cultural anthropology doesnot always correspond to the biological unit; itappears that the population of each village ratherthan the whole tribe represents, in some cases,an independent gene pool. Therefore, it is notsurprising that independent studies carried outin a tribe may show great divergence in genefrequencies because they are performed in dif-ferent villages. Such possible variations shouldbe kept in mind when it is necessary to decide,in trying to collect information from the litera-ture, whether the sampling is inadequate orreally representative of the population understudy. According to our experience in the studyof two large tribes, the gene frequency obtainedby sampling the less closely related individualsfrom several villages of a tribe fits very well withthe frequency obtained by summing up thegenes counted separately in villages in whichmore than 70 per cent of the population wasexamined. But taking the test results of one local

37

group as representative of the population atlarge would very likely produce a distorted pic-ture of the total gene pool,

Blood tests in Indians are more meaningful ifaccompanied by other anthropologica1 and medi-cal studies. Demographyincluding a history ofthe tribe and formation of the villages, and acareful genealogyprovides valuable informa-tion that could serve for at least a partial under-standing of the variation of the gene pool be-tween villages. The gene pool of a village amongthe Warao, for instance, is the result of thefusion of two, three, or four extended familiesthat have split off from neighboring villages.This pattern is very similar in many respects tothe "fission-fusion" model observed by Neeland Salzano (23) among the Xavantes and byChagnon (5) among the Yanomama. It is notunlikely, therefore, that variants of these pat-terns operate in many tribes.

It is evident that in the formation of the newvillage, as previously described, there are circum-stances that may induce variation of the genefrequency in the following generationsthenumber of individuals from each family whocontribute to the breeding population, sororalmarriage, polygny, and others. Consequently,random genetic drift would seem a likelier ex-planation of the variation of gene frequencies inIndian populations than other genetic forcessuch as selection and gene flow. It is also prob-able that this dispersive process may operatesimilarly in the formation of hybrid populations,explaining, in some cases, gene frequencies equalto or even higher than those observed in theoriginal populations (14,16).

Even though we have considered random ge-netic drift as the most important genetic processoperating in small Indian populations, the In-dians in their habitat must be exposed to selec-tive forces that maintain the polymorphism. Sofar, comprehensive stu dies on mor tali ty, fertility,and diseases in Indians are scarce; however, thenew orientation in the study of Indians, whichincludes such information, will eventually makeit possible to elucidate the role of selection inthe variation of gene frequencies in Indianpopulations.

43

Bearingin mind this variation,

I shouldlike

to discussfinally

the possibilityof a subdivision

of the AmericanIndian populations

that might

reconcilesomewhat

the frequencyofblood traits

with other anthropologicalcharacteristics.

Dr.

Juan Comashas previously

describedhere some

of the attemptsby prominent

Americaniststo

classifyIndians.

However,none of these classifi-

cationsfits the distribution

of blood traits. Gan

(8), for instance,included

all South American

Indiansexcept

the Circum.Caribbean

and Fue.

guianin one homogeneous

population.It is

knownthat in such a large area

there are popu-

lationswith marked

morphological,cultural,

and serologicaldifferences.

Even thoughit is very difficult

to attempta

comprehensivesubdivision

of the aboriginesof

Americaon the basis of genetic

traits, the fol-

lowingtaxonomic

considerationscan be formu-

lated from the informationavailable:

I. It is very likely that the Eskimocan be

distinguishedgenetically

from the other North

AmericanIndians.

They are characterizedby

the presenceof the gene B and absence

of the

geneDil. In frequency

of the other blood traits

they do not differgreatly

from American

Indians.

2. The variousNorth American

tribes are

very difficultto analyze,

partly becauseof heavy

non-Indianadmixture.

They have been classified

in one group characterizedby the presence

of

gene A and a low frequencyof D?; however,

microdifferentiations

are observedin some tribes.

The Blood and Blackfeetof Alberta

show a very

high (60 per cent) frequencyof A, (6), which

distinguishesthis group from

the rest of North

AmericanIndians.

An explorationof the pos-

sible connectionbetween

Navajo,Yaqui,

and

Lacandontribes exhibiting

the presenceof

transferrinBO-1 would be of great interest

(1,

26).

3. It might be possibleto make a first sub-

divisionof the Middle

AmericanIndians:

the

northerngroup including

Totonacsand Mayan

families,and the southern

group of Chibchan

or Hokan affiliations.However,

the only differ-

encefound to exist between

these is thefrequen.

cies of Dia, which tend in generalto be high

(from4 to 18 per cent,

with a mean of 10 per

cent) in the northerngroup,

and low (from

0 to 10 per cent,with a mean

of 3 per c nt) in

the southerngroup.

4. The geographyof the South

American

continentfavors the formation

of micrndifferen-

tiated populations.But in spite of thevariations

in gene frequenciesbetween

subtribesand vil-

lages of the same tribe, it might be possibleto

identifygenetic

peculiaritiesthat characterize

the tribe as a wholewith a common

genetic

heritagedifferent

from that of other tribes or

clustersof tribes.

For example,it would

be

interestingto investigate

the relativelyhigh fre-

quencyof A, among

the AndeanIndians,

first

noticedby Newman

(24), whichis not accom-

paniedby the presence

of other non-Indian

genes; the possibleconnection,

on the basis of

genetictraits, between

the ChileanIndians

and

the Polynesians,as mentioned

by Matsona a/.

(20) in a recent study; and the possibilitythat

the Yanornamaand Warao,

distinguishedby the

absenceof the gene

Dia and by anthropological

traits, could be classified,separately

or together,

as differentfrom the neighboring

tribes.

It is highly probablethat our present

hesita-

tion in subdividingthe American

Indianson the

basis of genetictraits will be overcome

in the

near future with the increaseof gene markers

and the use of mathematicalmodels

in which

all the variablesfound

in a tribe can be com-

puted.

REFERENCES

I. ARENDS,T. and R. LISIKER.

Unpublishedinfor-

mation,1964.

2. ARENDS,T., G. BREWER,

N. CHAGNON,M. L.

CALLANGO,H. GERSHOWITZ,

M. LAYRISSE,J. NEEL,

SHREFFLER,R. TASMAN,

and L. WEITICAMP.Intra-

38

tribal geneticdifferentiation

among the Yanomama

Indiansof southern

Venezuela.Proc. Nat. Acad.Sci.

57:1252-1259,1967,

3. BOYD,W. C. Anthropologic

und Blutgruppen.

KiinischeWochensehrift

37:993,1956.

4. BOYD, W. C. Genetics and the human race.Definition of race on the basis of gene frequenciessupplements definition from morphological char-acters. Science 140:1057-1064, 1963.

5. CHAGNON, N. A. Yanomamo warfare, socialorganization and marriage alliance. Doctoral thesis.Ann Arbor (Michigan), 1966.

6. CHWON, B. and M. LEWIS. The ABO, MNSs, P,Rh, Lutheran, Lewis, Duffy, and Kidd blood groupsand the secretor status of the Blackfoot Indians ofAlberta, Canada. Amer. 1. Phys. Anthropol. 11:369-384, i953.

7. CORDOVA, M. S., R. LISKER, and A. LORIA.Studies on several genetic hematological traits of theMexican populations. XII. Distribution of bloodgroup antigens in twelve Indian tribes. Amer. 1.Phys. Ant hropol. 26:55-66, 1967.

8. GARN, S. M. Human Races. 2nd ed. Springfield,Illinois, Charles C Thomas, 1965. 155 p.

9. GERSHOWITZ, H., P. C. JUNQUEIRA, F. M.SALZANO, and J. V. NEFL. Blood groups and ABM-Le' secretor types in the Somi5es Lopez and SinMarcos Xavantes. Amer. f . Human Genetics 19:502,1967.

10. GREENBERG, J. In J. H. Steward, and L. C.Faron, (eds.), Native People of South America.New York, McGraw-Hill, 1959, p. 22.

11. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.Blood group antigen tests of the Waica Indians ofVenezuela. Southwestern I. Anthropol. 18:87-93,1962.

12, LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.The blood groups of northern continental Caribs.Human Biol. 35:140-166, 1963.

13. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.Blood group antigen studies of four Chibchantribes. Amer. Anthropol. 65:36-55, 1963.

14. LAYRISSE, M., and J. WILBERT. Indian Societiesof Venezuela: Their Blood Types. Caracas, Sucre,1966, p. 72.

15. LAYRISSE, M., C. PEDREIRA, and J. WILBERT.Blood groups in Rankokamekra. To be published-

16. LISKER, R., A. LORIA, and M. S. CORDOVA.Studies on several genetic hematological traits of theMexican population. VIII. Hemoglobin S, glucose-6-phosphate dehydrogenase deficiency and other char-acteristics in a malarial region. Amer. j. HumanGenetics 17:179-187, 1964.

17. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Maya and non-Maya Indians in Mexico. Amer /. Phys. Anthropol.17:49-74, 1959.

39

18. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among AmericanIndians in Middle America: Lacandon and otherMaya. Amer. J. Phys. Anthropol. 63:1292-1322, 1961.

19. MATSON, G. A., H. E. SUTTON, J. SWANSON,and A. ROBINSON. Distribution of hereditary bloodgroups among Indians in South America. Am. 1.Phys. Anthropol. 24:325, 1966.

20. MATSON, G. A., H. E. SUTTON, R. ETCHEVERRY,J. SWANSON, and A. RomsoN. Distribution ofhereditary blood groups among Indians in SouthAmerica. Am. 1. Phys. Anthropol. 27:157-194, 1967.

21. MOURANT, A. E. The Distribution of theHuman Blood Groups. Oxford, Blackwell, 1954, p.136.

22. NEEL, J. V., and F. M. SALZANO. A prospectusfor genetic studies on the American Indian. ColdSpring Harbor Symp. Quant. Biol. 29:85-98, 1964.

23. NEEL, J. V., and F. M. SALZANO. Furtherstudies on the Xavante Indians. X. Some hypotheses-generalizations resulting from these studies. Amer.1. Human Genetics 19:554, 1967.

24. NEWMAN, M. T. A trial formulation present-ing evidence from physical anthropology for migra-tion from Mexico to South America. In R. H.Thompson (ed.), Migration of the New WorldCulture History. Tucson, University of Arizona,1958. (Social Science Bulletin 27)

25. PARKER, W. C., and A. G. BEARN. Haptoglobinand transferrin gene frequencies in a Navajo popu-lation. A new transferrin variation. Science 134:106-108, 1961.

26. SALZANO, F. M. Studies on the CaingangIndians. I. Demography. Human Biol. 33:110-130,1961.

27. SALZANO, F. M. Blood groups of Indians fromSanta Catarina, Brazil. Amer. J. Phys. Anthropol.22:91-106, 1964.

28. SALZANO, F. M., J. V. NEEL, and D. MAYBURY-LEWIS. Further studies on the Xavante Indians.I. Demographic data on two additional villages:Genetic structure of the tribe. Amer. I. HumanGenetics 19:463-489, 1967.

29. SUTTON, H. E. In E. Giblett, The plasmatransferrin. Progress in Med. Genetics 2:34, 1962.

30, WIENER, A. S. Blood grouping tests in anthro-pology. Amer. J. Phys. Anthropol. 6:236, 1948.

31. WILBERT, J., and M. LAYRISSE. The WaranIndians. In preparation.

32. ZERRIES, 0. Waika. Die KulturgeschiechtlicheStellung der Waika-lndianer des oberen Orinoco imRahmen der tieilkerkunde Sudamerikas. Munchen,1964.

45

DISCUSSION

Moderator: Dr. Comas' paper emphasized thevariability existing in the American Indian onthe basis of morphological characteristics. Dr.Layrisse has now emphasized the variability onthe basis of genetic traits, but has also directedour attention towards an aspect of the Indipnthat is increasingly occupying the thinking ofthose of us who work with the Indian: thatwithin a relatively undisturbed tribe, there is agreat deal of genetic variability from one partof the tribal distribution to the next. The geneti-cist has tended in the past often to think of atribe as a kind of homogeneous beanbag, butit now becomes clear that this is not the caseand that there may be very significant differencesbetween, say, one part of the Yanomama terri-tory and another.

The discussion of these two papers will beopened by Dr. Arends.

Tulin Arends

The physical variability of the AmericanIndian was recognized even by the conquista-dors. In 1530, Federman described a tribe ofdwarff in western Venezuela "not taller thanfive to six handbreadth" and found the Guay-queri in the eastern part of the country to beit people as black as coal."' Anthropometricstudies have accumulated a great many data onstature, cranial and cephalic indexes, body pro-portions, and so forth, which multiply thesedifferences. If to the somatic characteristics areadded .he many inherited biochemical andhematological variations known today the di-versity of the American Indian becomes infinite.

1 Federman, N. Historia indiana. Trans!. J. Fricde.Madrid, Aro, 1

As Dr. Comas pointed out, to determine whichof these characteristics stems from nurture andwhich from nature makes the problem morecomplex.

However, if we accept that the original popu-lation of America derived from a small groupof hunters-and-gatherers from eastern Siberiawho crossed the Bering Strait during the latterpart of the Wisconsin glaciation and whosedescendants gradually became masters of anuninhabited continent, we can understand bet-ter the great influence of environmental factorsupon the 'American Indian. There is still thequestion of contact with other racial groupsduring the pre-Columbian era, especially withCaucasoids of European origin as mentioned byDr. Comas.

The great progress made lately in the study ofblood groups, serum protein groups, and enzymepolymorphism nullifies the idea expressed someyears ago: "Type one Indian and you have typedthem all; so much are they alike in their bloodgroups."2 The view that serology has not addedanything new to human taxonomy2 is also nolonger tenable. On the contrary, we who workin this field believe that the amount of informa-tion already accumulated wit', play an importantrole in the reinterpretation of the AmericanIndian taxonomy and is laying thc foundationsfor a future molecular anthropology. Boyd hassaid: "The genetic method has, in short, madecontributions to anthropology that morphologicmethods could hardly have made, and is pro-

40

2 Stewart, T. D. A physical anthropologist's view of:he ). of the New World. Southwest. 1, Anthropol.16. )9 1960.

..: S. M.: Human Races. 2na ed. Springfield,.;harles C Thomas, 1965.

46

viding a new and fundamental basis for thestudy of race."4

Important factors in the study of the Americanpopulations

To establish biological subdivisions of theAmerican Indians based on the study of theirgenetic chiracteristics, the best-known methods

populatioa genetics should be used, withspecial emphasis on the following points:

1. It is advisable to study as many genetktraits as possible, in order to avoid biased inter-pretations and rule out gene drift, especiallywhen dealing with small populations subjectedto epidemics, wars, displacements, and otherevents that might have modified the frequencyof some traits.

2. Indian villages should be studied inten-sively from a historical and genealogical pointof view, for the purpose of evaluating the so-called "founder effect" or pursuing a foreigngene introduced through a nonapparent ad-mixture.

3. The "fission-fusion" phenomenon, whichaccording to Neel et al.,5, 6 is not infrequent in

4 Boyd, W. C.: Genetics and thc human race. Science140:1057-1064,1963.

5 Ned, J. V. F. M. Salzano, P. C. Junqueira, F. Keitter,and D. Maybury-Lewis. Studies or thc Xavante Indiansof the Brazilian Mato Grosso. Am. 1. Human Genet.16:52-140,1964.

Neel, J. V., and F. M. Salzano. Further tudies on

TABLE I. Characteristics common to American Indians

the dynamics of indian populations, could ex-plain some odd findings in the prevalence ofgenetic traits.

Common characteristics in the American Indian

From a genetic standpoint, most of the Ameri-can Indians share certain characteristics thatdifferentiate them from other racial groups(Table 1), as Dr. Layrisse has already men-tioned. We may say that the authen SouthAmerican Indians are all of group 0; usuallylack r and R° rne complexes of the Rh system;are negative for the main factor of Kell, Lewis,and Lutheran blood group systems; have onlyHb-A; and are not deficient in glucose-6-phos-phate dehydrogenase. 8 It could be added thatthey are equally negative for, or have a very lowfrequency of, the atypical pseudocholinesterasegene Eia.9) 10

the Xavante Indians. X. Some hypothesis-generalizationsresulting from these studies. Am. 1. Hum. Genet. 19:554-575,1967.

Mourant, A. E. The Distribution of the HumanBlood Groups. Oxford, Blackwell, 1954.

s Arends, T. Haetroglobinopathies, thalassaemia andg1ucose-6-phosphate hhydrogenase deficiency in LatinAmerica and the West Indies. New Zealand Med. 1.65;831-844,1966.

Gutschc, B. B., E. M. Scott, R. C. Wright. Hereditarydeficiency of pseudocholinesterase in Eskimos, Nature215:322-323,1967.

10 Motulsky, A. G. and A. Morrow. Atypical cholines-terase gene Eia: rarity in Negroes and most Orientals.Science 159:202-203,1968. Le lima n1)- A bsenee

Arcwas, T 0.4 .1Vvies,31\Jorizurv44 tipt-tx.fr, Pt4000nSr at

ca.c.y WI i Ikea 1)-c 4 h ia se) Sotkiit AVM riCab'4tiN4rNe-A. AtIN0 Ob-Ct_ ict67.

GENETIC SYSTEM

CHARACTERISTICS

COMmON TO ALL

SUBJECTS EXCEPTIONS

ABO

Rh

Kell

Lewis

Lutheran

Hemoglobin

Group 0

r and R° absent

kk

Le(a)Lu (a)Flb-A

G-6PD Absence of deficients

Navajo, Pueblo, Blood, Shoshone,Blackfoot (U.S.A.)

Apache, Pawnee (U.S.A.); Tarasco, Chontal(Mexico); Itza Maya (British Honduras)

Dieguerio (U.S.A.); Brazilian (Brazil)

Nahua, Chiapas (Mexico); Oyana, Arawak(French Guiana)

Ciana, Carib (Dutch Guiana)

41

Where published reports give different char-acteristics from those in Table I, the reason ismainly the small size of the sample studied (insome cases fewer than 50 individuals) or ad-mixture with other racial groups. Nevertheless,there are some tribes for which the results alsodisagree although they are unmixed and a largeenough sample was examined. These popula-tions deserve to be thoroughly studied for agood explanation of this exception, and tiliscould be the so-called heterc of AmericanIndians. (The same may be sd., of the figuresin Table 2.)

Quantitative differences in the genetic systemsof the American Indian

In certain genetic characteristics the AmericanIndian is distinguished only by a quantitativefrequency widely different from that of otherracial groups (Tab It 2). The interpretation hereis really difficult b,:cause different samples fromthe same population have sometimes given dif-ferent results. For example, when the hapto-globin system of two Makiiitare samples wasstudied," results for Hp' as dissimilar as 0.610and 0.342 were found. These results depend

11 Arends, T. Los grupos s6ricos humanos determina-Hes por métodos electroforéticos: su distribuci6n en SurAm&ica. Acta Cient. renez. SuppL 3:162-178, 1967.

greatly upon the condition of the sample ob-tained. In addition to the exceptions mentionedby Dr. Layrisse, there are tribes that have givenfrequencies different from those mentioned eventhough the sample was larger than 100. Again,here are many populations that could be veryusefully studied with the available genetic, bio-chemical, and hematological battery of tests.

Differential characteristics of some Indian tribes

Finally, there are some genetic markers thatidentify certain tribes (Table 3). The antigenDi(a+ ) of the Diego system, for instance, is

a Mongoloid characteristic. The same may besaid of the transferrin Doit. The absence of thosemarkers in many tribes could be an indicationof gene drift, fission-fusion, or founder effect.Furthermore, the transferrin system has anothervariant (Tf-B11_1) that distinguishes the Northand Central American from the South AmericanIndians.12

Human alloalbuminemia, or the presence ofalbumins will electrophoretic miglation differ-ent from the no-mal, expressed by either one

ia Arends, T.. G. Brewer, N. Chagnon, M. L. Gal-lango, H. Gerashowitz, M. Layrisse, J. Ned, D. Shreffler,R. Tashian, and L. Wietkamp. Intratribal genetic differ-entianon among the Yanomama Indians of SouthernVentzuela. Proc. Nat. Acad. Sci. 571252-1259, 1967.

TABLE 2. Quantitative differences in some genetic systems of American

GENETIC SYSTEM

MNSs

CHARACTERISTIC

Gene M '5 0.7

Rh Gene complex R2 > 0.35

Duffy

ABH Secretor

Haptoglobin

Gammaglobulin

Inv

Gc

Gene Fyn 5: 0.6

Gene Se

Gene Hp' 0.5

Gene Gni° ,= 1.0

Phenotype Inv(a+) 5: 0.6

Gene Ge1 > 0.65

Indians

EXCEPTIONS

Jicague (Honduras)

Seneca, Pima (U.S.A.); "league (Honduras); Miskito,Sumo (Nicaragua); Mayal Mazatel (Mexico); Ticuna(Peru): Quechua (Ecuador); Xavante (Similes Lopes,Brazil); Waica (Venezuela)

Guavmi (Panama); Jicaque (Honduras); Mazatel(Mexico); Xavante (Brazil)

Xavpnte (Brazil)

Yupa (Venezuela); North Athabascan, Tlingit,Navajo (U,S.A.)

Xavante (Brazil)

Xavante (Brazil)

42

48

TABLE 3. Genetic markers in some Indian tribes

GENETIC SYSTEM CHARACTERISTIC

Diego

Transferrin

Albumin

TRIBES IN WHICH IT HAS BEEN FOUND

Di(a+)

Tf

Tf

Naskapi

Mexico

Maku

Warao

North American, Central American, South American

Navajo (U.S.A.); Yaqui, Cora, Chinantec, Lacandon.Tzotzil, Zapotec (Mexico) Quidie (Guatemala)

Irapa, Macoita, Paraujano, 111,64 Shaparu, Monk),Piarea, Warao, Guahibo, Guayqueri (Venezuela);Paez (Colombia); Quechua (Peru)

Naskapi, Montagnais (Canada); Sioux, Athabascan(U.S.A.)

Zapotec (Mexico)

Maku (Brazil)

\Vara() (Venezuela)

(homozygous form) or two components (het-erozygous form), is a system that could be veryuseful in the American Indian taxonomy. Thissystem, which at present is the subject of inten-sive study, has made it evident that certaintribes in Canada and the United States have analbumin variant faster than normal (albuminNaskapi). In Mexico a tribe was found to havean albumin slower than normal (albuminMexico). In Brazil a faster variant (albuminMaku) and in' Venezuela a slow variant (al-bumin Warao) different from those previouslymentioned were found.

Summary

I. Some characteristics are shared by all theIndians of the American hemisphere. Popula-tions that seem to be an exception should beinvestigated by the best serologic, immunologic,electrophoretic, and chromatographic methodsat hand in order that characteristics reported in

the past, when modern methods and reagentswere not available, may be rechecked.

2. The differentiation of populations by fre-quency gradients of genetic traits should be thesubject of careful studies, about their formation,cultural level, and kinship organization. Sincethese populations have been under physical,pathologic, and war pressures, it will always bevery difficult to evaluate how much these agentshave influenced the distribution of the inheritedvariations.

3. Some genetic markersfor example, Di(a+) group of the Diego system, transferrinDem and B01, and albumin Naskapi, Mexico,Maku, and Waraohave been found in onlysome Indian tribes. The characterization of eachof them and their differentiation from othertraits of the same system should be determinedby the best biochemical and physico-chemicalmethods available.

4. The finding of some genetic traits (trans-ferrin Dchl, Diego group Di(a+ )) amongtribes is positive proof of present or remote rela-tionship. Their absence in other tribes could beexplained by gene drift, founder effect, or fision-fu s ion.

5. The more genetic systems are discovered,the more urgent it is for them to be studied inAmerican Indianr before these populations dis-appear through cultural and economic pressures

or through epidmic, endemic, or sporadicpathological processes.

Ruben Lisker

The data presented today by Dr. Layrisseclearly show that present-day Amerindian popu-lations do not have a homogeneous geneticconstitution. However, the task of subdividingthem on the basis of genetic traits is not aneasy one, especially if to taxonomy is added aninterest in interpreting or understanding the

reason tor the differences encountered. A gen-

43

49

era! cause of this difficulty is that the Amer-indians as a group have characteristic genefrequencies for many traits that do not allowfurther subclassification. A good example wouldbe blood group 0 and the Rh-negative pheno-type. A reasonably "pure" Indian populationshould have close to 100 per cent of group 0individuals and no Rh-negative subjects; devia-tion from ti,is pattern would be generallyinterpreted as the result of non-Indian admix-ture.

Even so, some g..netic traits do show enoughvariability in apparemly unmixed Indian groupsthat attempts at taxoucmy are possible. Thedifficulty hereand I should like to stress thispointis what the classification means. I feelsure that this considerati3n explains, at least inpart, Dr. Layrisse's understandable hesitation insubdividing Amerindians.

I want to consider briefly some examples ofthe difficulties I have mentioned. The Diegoantigen appeared to be an excellerrt marker ofIndian groups, especially suitaFte for taxononii-cal purposes since it is not present in other ethnicgroups (except some Mongoloids) and showsenough intertribal variability to allow for sub-divisions.1 However, it soon became apparentthat the correlation of its distribution witheither geographical or cultural critena was nottoo good,2 and furthermore, although its ab-sence in Negroes and Caucasians is accepted,some hybrid populations in which they certainlycontribute to the gene pool have higher Diegofrequencies than the original Indian popula-tions.2. 4. 5 This is clearly seen in Ta lie 1; seven

1 Layrisse, M., arid J. Wilbert. El antigen° dd sistemasanguinco Diego. Caracas, Sucre.

2 Comas, J. Significado de. la presencia del antigenoDiego entre lo.s Amerindios. Anal. Antropol. (Mexico)2:89, 1965.

2 List:el-, R., A. Loria anti M. S. Cordova. Studies onseveral genetic hematological traits of the M:xican popu-lation. VIII. Hemoglobin S. glucose-6-phoiphate dehy-drogenase deficiency, and other characteristIcs in a ma-larial region. Am. 1. Hum. Genet. 17:179, I 965.

4 Rodriguez, H., E. Rodriguez, A. Loria, and R. Lisker:Studies on several genetic hematological traits of theMexican population. V. Distribution of blood group anti-

/

44

50

TAI1LE 1. Frequency of Diego antigen in 18 Indiantribes and 9 coastal mestizo groups of Mexico

GROUP

PHENOTYPE

RANGE (%)FREQUENCY

(70)

Indiansa5 tribes9 tribes3 tribes

2-812-1920-24

1 tribe 40

MestizosWeSt Coa.tit

Ometepec 28.2

Cuaiin'cuilana 26.3

San Pedro M. 23.4

Pochutia 31.3

East CoastSaladcro 4.1Veracruz 32.8Paraiso 32 AEl Carmen 38.6Tamiahua x .5

More than 50 individuals studied in ail but twotribes.

b Mare than 90 individuals studied in each location.

out of the iiine hybrid groups studied on thecoasts of Mexico have higher Diego frequenciesthan most of the pure Indian tribes. Beforelearning the meaning of this phenomenon, onewould hesitate to use this marker to subdivideAmerindians. Incidentally, I would say thatalthough these populations show less variabilitythan those Dr. Layrisse has studied, there is stillno pattern to Diego frequency because individ-uals with the same linguistic affiliation showvery marked differences in frequency.

An additional difficulty stems from the factthat in the study of Indian tribes with somedegree of non-Indian admixture, the variationin the gene frequencies of 'ome of the traitsdoes not follow the expected trend The follow-ing examples will clarify this statement. In theinvestigation of Mexican Indian groups, four

gens in Nahuas, Yaquis, Tarahumaras, Tarascos andMixtecos. linm. Biol. 35:359, 1963.

.5 Cordova, M. S., R. Lisker and A. Loria: Studies onseveral genetic hematological traits of the Mexican popu-lation. Xli. Distribution of blood group antigens intwelve Indian tribes. Am. 1. Phys. Anthropol. 2655,1967.

had evidence of Negro admixture, as judged bythe presence in them of a few individuals withthe sickle-cell trait and/or red cell glucose-6-phosphate dehydrogenase (G-6-PD) deficiency.°These groups would be expected to have higherfrequencies of the M gene and the cDe chromo-some and lower of the Fya gene than the othertribes. As can be seen in Table 2, neither ofthese expectations was confirmed.5 It would bealso logical to expect the Hpl gene frequenciesof the Indian tribes with evidence of Negroadmixture to be higher than in the I-est. Table2 shows that this is not the case, and that infact the Cora have the lowest Hpi gene fre-quency in our material.'

The recently described polymorphism of thealbumin locus seemed to have taxonomicalvalue, since in all the initial reports it followedan orderly geographical distribution.° Albumin-,-ariants are rare in all groups so far studiedCACt pt the Amerindians, and it appeared that afa,l- variant known as albumin Naskapi 9 wasprevalent only in Eskimos, Canadian Indians,and northern North American Indians, while

6 Lisker, R., C. Zárate, and A. Loria. Studies on severalgenetic hematological zrait., M Hcar2 . IX. Aho.-:7-rnal

hemoglobins and erytlm,(N 0,1!..-ose-6-phcmpi,:irt t!ehy-

drogenase deficiency in sevv...! trib:..-, Blood27:324, 1966.

7 Lisker, R., G. Zaratc, and E. Rodrigu,.;'..several genetic hematological traits of the Mexican t+,,7,!-lation. XIV. Serum polymorphisms in several India,tribes. Am. I. Phys. Anthropol. 27:27, 1967.

8 Melartin, L. Albumin polymorphism in man. Studieson albumin variants in North American native popula-tions. Acta Path. Microbiol. Stand. Suppl. 191, 1967.

9 Mdartin, L., and B. Blumberg. Albumin Naskapi, anew variant of serum albumin. Science 153:1664, 1966.

the slow variant known as albumin Mexico 10was present in southern North American In-dians and in some Mexican Indian groups andmestizos. The only information from SouthAmerica relates to two groups of Peruvian In-dians, another from Brazil, and a fourth fromBrazil and Venezuela (the Yanomama), whereno variants were found except in the lastgroup.n This pattern has already at least threeexceptionst the Huasteco in northeast Mexicoand the Chol in southeast Mexico have a fastvariant that has electrophoretic mobility similarto the Naskapi type and may be the same, andthe variant recently encountered in the Yano-mama is fast bu different from the Naskapi.

It is also interesting to remark that whereasthe presence of albumin variants in Eskimosmight lead to an attempt to group them to-gether witil other Indian groups, it is evident,as stated by Dr. Layrisse, that the only Ameri-can aboriginal population that clearly deviatesfrom the rest of the Amerindians in the distribu-tion of several genetic traits is the Eskimos.

It seems to me that, regardless of the rathererratic distribution of some traits in the Amer-indians, and despite the fact that the precisereason for this is unknown, it is important tocolitinue the characterization of the genetic con-

iolou of the Arnerindians, quite apart fromthe ciu.tstion whether or not it can be used atthis 1,oint for meaningful st,bclassification.

Mciartio. 1 , 81,:.-nherg, and R. Lisker. AlbuminMexico: -a iE alarr 3 i5:

288, 1967.11 Weitkamp, L., J. Chagnon, I. Saave, F. Salzano,

and J. Gall. Serum albumin variants in American andNew Guinea indigenes. Clin. Res. 16:298, 1968.

TABLE 2. Comparative frequencies of genes M, Fya, Hp1, and chromosome cDe+cde in groups having some caseswith Hb.S and bor 0-6-PD deficiency with other tribes investigated for these markers

GROUP

NO. CASES

NO. Hb.S G-6PD

GENES CHROMOSOME

Fya cDe cdeHp1GENE

Huastcco 235 o 3 0.51

Nahua 141 o 4 0.77 0.64 0.04 0.44Chontal 101 2 2 0.69 0.67 0.11 0.57Cora 96 1 0 0.76 0.99 0.06 0.40Others (range) 0.65 0.79 0.50 1.00 0.03 0.12 0.44 0.65

45

51

offer at least two important reasons: one, thatthis will provide the geneticist of tomorrow witha good baseline for understanding populationdynamics in the future; the other, that longi-tudinal study of the correlation between thegenotype and the biological development of apopulation, for which at least some Indiangroups are quite adequate, might significantlycontribute to our understanding of the reasonsfor the variability observed today.

General DiscussionBier: I would like to know whether the

albumin variants are antigenically identical.Lisker: When I say there are two iticrikital

albuminsI am only saying that they have the same

eleetrophoretic mobilky. Nobody has done anamino acid sequence, so that is all we know.Whether or not it is the same mutation is un-known.

Bier: Before doing the sequence, wouldn't itbe easier to make an Ouchterlony plate to seewhether or not they have common determi-nants?

Lisker: It has been done, and no differenceshave been found.

Salzano: I think that the studies on Vene-zuelan Indians in different stages of culturalevolution, and a!so the researches of Dr. Liskerin Mexico, are very important since a patternappeared among the Brazilian groups that canbe tested. Three stages can be visualized. Thefirst would be that of the hunting-gatheringtribes, who have a kind of fission fusion model.That is, the pattern is one of exchange betweengroups carried out mainly by more or less largesubgroups of the tribes. In what I would callthe second stage, the groups would rely moreon agriculture hut woukl not yet have a criticalsize. These vs-uuld conform inore to what SewallWright calls the island model: -that is, theircopulations would be small and separated bylarge distances. A prier', more variation wouldperhaps be expected in the second groups than

in the first. The third stage would he thatreached by tribal groups in Mexico. The geneticstructure would also be different then; it wouldbe more likely to be the one that Sewall Wrightcalls the isolation-by-distance model. This meansthat the genetic diffeeentiation of these groupswould follow a different pattern from the othertwo, with less variability. In a general way, Ibelieve the genetic and demographic data aresubstantiating this. But, of course, in order tobe stoi: we need more data on different groups,in different ecological situations.

I do not thir,k that genetic data per se wouldbe very important for the differentiation of

Amerindians unless they were correlated withthis kind of data. For 'instance, the selectionacting on groups in the second stage is probablyquite different from that acting on the othertwo. This was clearly indicated by Dr. Dubosin his book Man Adapting. The nutrition ofthese groups would become somewhat morelimited; they would rely on just a few cropsthat can provide enough .calories but make foran unbalanced diet. I could give many othersuch examples to show that the situation be-tween groups in these three stages is quitedifferent and that if data from populations atthese different cultural stages are mixed, a

meaningful picture is probably impossible.Waterlow: Dr. Neel, is it really proved that

all these thingsalbumin variants, haptoglobinvariants, red-cell variantsare genetically de-termined or is that an assumpdon?

Moderator: I believe the speakers could takecare of this point better than I could, but verybriefly the answer is yes, it is proved. However,I should qualify this a bit. The genetic basiscannot be determined from a simple populationsurvey Family studies are required. And inevery instance in which a variant has beendescribed today, there have been svidies thatshow it is tranyrt;tted accordi3-3- !.o del;: !-

laws within family linf:c. thi... kirrjevidence is necessary befort p K ot

variant with any assurance.

THE AMERICAN INDIAN IN THE INTERNATIONAL

BIOLOGICAL PROGRAM

James V. Neel

Administrative background

As is a matter of common knowledge, in 1960

the International Council of Scientific Unions(1CSU) took the initiative in the promulgationof an International Biological Proram As e.inally eovisioned b\ obrctives of this

program wt re the world 'dt ( oi-

ganic production on the land, in fresh 'voters,and in the seas, and the potentialmes and usesof new as well as existing natural resources; and12) human adaptability to changing conditions.

A Planning Committee appointed by ICSU inturn established a number of :Aibcommittees toconsider various aspects of the program and toelaborate a more extended protocol. These van-

subcumm combined their efforts intoa stries of sogw:.tions ind recommendations,which the Pianning C.:Ayanitte,.: coordinated andsubmitted to It:.;U in Novemix; I963. ICSU,after approving these sligg:.:ions ;IAC.I recom-

mendations, then called ti,,ori the vAdOliS cuun-tries having representation in it through nationo,J

societies to formulate national programs. Theiimetable for IBP, several times revised, consist.of a "planning phase," which officially termi-

nated in mid-1967, and an "operational phase,"

to continue until mid-1972.

It has been clearly understood from the outset

that the various national committees were in no

way bound by this international formulationitwas designed merely to provide convenientguidelines. Thus far ten countries in North,Central, and South America have established

committees to formulate national programs, and

four other countries may do so soon. It will bethe purpose of this presentation to attfmipt topoint out the manner in which wriPt\ f-f types

of studies of the Americat within

the framework of tne ITU'section concenicd with human adaptalAity. Infact, the Indian provides the Americas with aunique resource in IBP-oriented studies and atthe same time presents interdigitating medical

and humane challenges that are worthy of theconsideration of this Organization.

At all the various kvels of consideration ofhuman adaptability, it has been clear there are

two interrelated components: the genetic, which

sets the limit of the organism's ability to re-spond, and the physiological, which determines

the range of response available to the organism,

given its genetic set. At one extreme in the spec-

trum of interests that can be brought to bear on

human adaptability is environmental physiology,

and at the other is population geneticsand in

isveen there is room for many aspects ofmodern medicine and anthropology.

Prom the earliest considerations of most of

the various committees and subcommittees con .

cerned with human adaptability, it has h.:erapparent that the surviving primitive pope,"a-

dons afford an opportunity to study physiologi-

cal and genetic adaptations potentia:ly quite

different from those of highly civilizr.1. gri ups.Parenthetically, although our cultwal oricritation is such that we tend to view man:, of tliese

surviving primitive groups as representing ex-tremes of adaptability, the fact is !.1:at they haw

3

lived under their conditions far longer than weunder ours. Viewed from their vantage point,we are the ones pressing for new limits of adap-tability, and it is only an article of faith that wewill adapt to our man-made environment assuccessfully as they have done to theirs. We mustnote in passing that some of the adaptations ofthese groups are complex and ingenious, arthat the term primitive as commonly tificcisomething of a misnomer, amounting to dpriliterate with a relatively simple technology."

In late 1962 the World Health Organizationconvened in Gene\ a Scientific Group on Re-search :i l'oi ilation Genetics of PrimitiveGroups. its purpose was to consider studies ofpopulations of unusual genetic interest, with par-ticular reference to the surviving hunting andfood-gathering groups of the world, to adviseon the most suitable populations for suchstudies, and to draw up appropriate researchdesigns. The pertinence of this to IBP-relateddevelopments is obvious. In the preliminary in-ventory of these societies published in the reportof the Scientific Group, various South Americantribes figure prominently (26). This report, inci-dentally, was updated in the summer of 1967and a revised version has just been issued asWHO Technical Report 387.

A recurrent consideration in the consultationsof both IBP-related and WHO-related groupshas been the rate at which these primitive groupsare disappearing. It can be said without exag-geration that ours is probably the last generationprivileged to study such groups in a relativelypristine state. If there are important scientificlessons to be learnedand the WHO documentwould seem to develop that case adequatelythen there is an urgency to this problem notshared by many other areas of research.

The dimensions of Indian-oriented studies

These are days in which those of us who areconcerned with human biology view our speciesas beset by a growing number of pressing prob-lems of our own making: the population in-crease, trace chemicals in foodstuffs, air pollu-tion, water pollution, the so-called stress diseases,cultural alienation, to mention only a few. Each

of these problems has reached such a magnitudeas to call for concerted action on a hithertounknown scale. But I submit that behind theseimmediate problems lurks a far larger issue.Now that man so largely controls both the en-vironment and his reproduction, is there any

ng-range objective more important than thatu.h,l..rstand the genetic potentialities of the

and the species, the manner in whichthis potential interacts with an environment thatis increasingly man-made, and the rate of geneticchange in response to a changing environment?You will recognize that I have only restatedin a different context the need to understandthe genetic aspects of human adaptability. TheAmerkan Indian offers prime research materialfor this objective. The principal lines of attackcan be conveniently summarized under threeheadings (see 12).

1. Population structure and natural selectionin primitive man. One of the basic tenets ofbiology is of course a belief in the role of naturalselection in shaping each species to its ecologicalniche. As biologists we believe that natural selec-tion has guided human evolution and will con-tinue to guide the evolution necessary for a suc-cessful genetic adjustment to a changing world.It is clear that modern man evolved under cir-cumstances approximating the conditions foundin primitive cultures. Otherwise stated, there isno evidence that the developments of the pastfew thousand years have yet resulted in any verysignificant modifications of man's genetic po-tential. It follows that one way of understandingthe genetic impact of our chunging environmentis from the baseline supplied by detailed knowl-edge of primitive man in his primitive ecosys-

tem. The simple fact is that at present we knowvirtually nothing about how selection works inman. What few insights we have are largelybased on the results of artificial selection withexperimental animals and deal with traits, suchas extremes of egg production or milk yield,considerably more important to us than to theanimal species involved.

What the geneticist terms "population struc-ture" places limits on the effectiveness of natural

48

54

or artificial selection. Thus, hand in hand withefforts to understand selective pressures must goefforts to understand the genetic structure ofpopulations. To the geneticist, this means pat-terns of mating, fertility, and survival; amountof inbreeding; migration patterns; mutationrates; and so on. Although some data on thesesubjects are to be found in the voluminous an-thropological literature, in the main what isavailable simply lacks the precision and depthnecessary to the precise statistical treatments of

the geneticist.Even with all the facilities of modern science

and the conveniences of our culture, such com-prehensive studies remain extremely difficult incivilized countries. How much more difficultare they, then, in the remote primitive popula-tionsproblems of logistics and communicationbeing what they are. Even so, from our ownexperience of the past several years and that ofseveral other groups with kindred interests, itis clear that a variety of types of data relevantto population structure can be collected.

In1962, aided by a grant from this Organiza-tion, Dr. Francisco Salzano of the University ofRio Grande do Sul, Brazil, and I, with severalcollaborators, undertook a pilot study on theXavante of the Brazilian Mato Grosso (13).These and further studies on the Xavante, in1963 and 1964, raised a number of rather basicquestions for population genetics (14), but itwas felt that the Xavante were neither a largeenough group nor sufficiently undisturbed for acritical approach to these questions. Accordingly,after a careful consideration of the possibilities,a second study was undertaken, concerned withthe Yanomama Indians of Venezuela and Braziland involving as principal colleaguesin addi-tion to Dr. SalzanoDrs. Miguel Layrisse andTulio Arends of the Venezuelan Institute forScientific Research (IVIC) and Drs. William J.Schull and Napoleon Chagnon of the Universityof Michigan. We have now been in the field onthree different occasions. The composition of theteam varies from year to year, hut ideally it

includes an ethnologist, a linguist, a physicalanthropologist, a geneticist, and several physi-

49

cians. Although the precise nature of the datacollected depends upon local circumstances, un-der optimal conditions we assemble as completedemographic and genealogical data as possible;conduct physical, dental, and anthropologicalexaminations; and obtain blood, urine, saliva,and stool specimens for a variety of genetic andother determinations. The effort to understandbetter man's interaction with his environmentcarries far beyond the identification of genetictraitswe are fortunate to have the collaborationof such groups as the Communicable DiseaseCenter of the U.S. Public Health Service, theVirus Institute at IVIC, and many specializedlaboratories at the University of Michigan.

This is not the time for a detailed review ofthe findings on either the Xavante or the Yano-mama, which in any event must be regarded aspreliminary. Not at all surprisingly, both thepopulation structure of these people and thebiological pressures on them are qualitativelyand quantitativly different from those of civi-lized groups. These are populations in whichinfertility is rare, practically all women con-tributing to the next generation; in which effec-tive fertility seems intermediate, and infant andchildhood mortality also intermediate; and inwhich the variance of male reproductive indicesis significantly greater than of female (15). Asurprising amount of genetic microdifferentia-tion between villages has been encountered (1),originating, we believe, in the fission-fusion pat-tern that dominates village proliferation andresults when a new village comes into being ina very non-random sampling of the tribal genepool. We reason from this that if new tribesoriginate in general as new villages do, thenchance may have played a greater role in muchmeasurable human genetic variation than here-tofore seemed likely. The roles of traumatic,infectious, and nutritional disease in determin-ing survival are far different than in the nextstep on the cultural ladderthat is, in relativelydensely populated agricultural societies.

We do not pretend to understand as yet thefull genetic implications of all that we see. Onereason for our lack of understanding is that a

55

substantial portion of the mathematical theoryof population genetics is currently being re-worked. A second reason is that the data are socomplex that precise mathematical formula-tions do not appear imminent, and we are beingforced to involved computer simulation pro-grams to explore the genetic consequences ofthe differences between these societies and ourown. However, even at this stage it is very clearthat it will be possible to define objectives andtest hypotheses in a way that will justify theeffort expended.

I mentioned above that a substantial portionof the mathematical theory of population ge-netics is being rt worked. One of the most pro-vocative developments in the biomedicine of thepast twenty years has been the realization of theextent of man's concealed genetic variability, asrevealed by modern biochemical techniques.Many of the newly recognized variant typesoccur in populations in such frequencies that wespeak of the underlying systems as genetic pu!:,-morphisms. The maintenance of such poly-morphisms is thought to require selective pres-sures of one kind or another; not only is thenature of these forces unknown, however, butunder the previous formulations the mortalityand fertility structure of our population scarcelyseems adequate to accommodate the necessaryselection, and new formulations are being con-sidered (7, 9, 25). Understanding how all thisvariability is maintained is one of the greatchallenges to the human biologist (see discus-sions in 8 and 16). Now, the genetic polymor-phisms are well represented in all the primitivepopulations studied to date. This is where theycame into being. Accordingly, it seems self-

evident that, despite the inherent difficulties, wemust make every effort to conduct studies indepth of population structure and the relation-ship at this cultural level between the poly-morphisms and specific biological attributes.

There is an urgent scientific need for similarstudies, while the opportunity exists, on as manyas possible of the other unaccultUrated groups ofIndians. None of the surviving primitive Indiancommunities can safely be labeled "typical"

, 50

each may be unusual in one or several respects.Only from the perspective of numerous studiesin depth can we begin with any assurance tofactor out the significant common denominatorsthat have guided human evolution. Alreadyparallel studies are in progress on such groups asthe Cayapti of Brazil by Salzano and colleaguesand the Kashinawa of Peru and Brazil by Johns-ton and colleagues, as well as in other parts ofthe world, and more are to be hoped for.

2. The rate of human evolution, i.e., geneticdiversification. Despite the many unansweredquestions discussed earlier in this session byProfessors Griffin, Cruxent, and Laughlin, thedate and place of arrival of the Indi=th in theAmericas is more accurately known than thecorresponding information for any other majorsubdivision of mankind. In view of what can bededuced concerning population density in north-ern Europe 20,000 years ago, we may surmisethat the total number of immigrants across theBering Bridge, whether they came in one or inseveral discrete waves, was not large. The ge-netic characteristics of this original group willof course be forever conjectural, but let us as-sume that the tribal population(s) concernedhad the rangt. of variability we see in such agroup as the Yanomama. (I am assuming inthis discussion that the contribution to the genepool of individuals reaching the Americas otherthan by the Bering Bridge is negligible.) Oncehere, extension throughout the Americas seemsto have been rapid. In this extension, the diver-sity of habitats explored and occupied representsmost of the extremes of the habitable portions ofthe earth. If we make the assumption of areasonably homogeneous beginning, then thediversity of types of Indians at the time of therediscovery of this continent five centuries agoconstitutes an unusual opportunty to measurethe rate of human evolution.

Much of the early thinking on this topic drewon morphological characteristics, and these, asProfessor Comas has just demonstrated, stillremain valid and pertinent. However, in recentyears the newly discovered polymorphisms men-tioned earlier have provided a powerful battery

of objective indicators of genetic distance. Dr.Layrisse has just provided us with an overviewof how great the range is with regard to avariety of specific systems. In theory, for anygiven genetic system the position of each Indianpopulation with respect to all the others can bedefined by a point in a space that has one lessdimension than there are alleles in the system,the precise position in this space being deter-mined by the frequency of each allele. Furtherin theory, when many different genetic systemsare considered simultaneously, the position ofeach population vis-a-vis the others can be plot-ted in a space that now has as many dimensionsas there are genetic systems. Previously, the com-putations when a considerable number of sys-tems was involved were as laborious as thisdescription sounds (6, 22). But the advent of themodern computers has dramatically altered thesituation, and now a number of groups are de-veloping computer-based measurements of popu-lation distance (see 3).

Although considerable progress has been made,there is still a great deal to be done in the wayof characterizing the genetic attributes of therelatively pure Indian groups, as a basis for

exploring the evolutionary problem discussedabove. Incidentally, the HA/IBP/IUBS empha-sized the need for continuing efforts at the

genetic characterization of all the human strains,so that this type of investigation of the Indianfits readily into a larger framework. The pub-lished data on the Indian are widely scattered,no survey having been attempted since those ofMourant (10, 11) and Salzano (18). Dr. Rich-ard Post, Dr. William Schull, and I have nowcompleted a compilation of all publications priorto November 1967 that deal with the prim- ipalgenetic polymorphisms known to occur in theIndian.1 The rate of discovery of new poly-morphisms being what it is, any such compila-tion is soon dated, but for the specialist it atleast provides a nidus for updating. The 271papers on which the tabulation is based attestto the strong interest in this subject. Since thedata on unmixed Indian groups have in

' Sec Appendix of this volume.

most

contexts far greater interest than the data onmixed, an effort has been made to recognizethree levels of miscegenation: (1) essentially

none; (2) known, but probably accounting for

less than 5 per cent of the gene pool; and (3)greater than 5 per cent. The tabulation containsdata on the following polymorphic systems(these being the ones on which there seemedenough data to warrant a tabulation): ABO,Rh, MN, Kidd, Duffy, Diego, P, Lewis, hapto-globins, transferrins, and Gm. Gene frequencieshave been computed for each study with com-puter programs written in Fortran and available

on request.In closing this section, let me agree with those

who feel there has already been quite enoughof surveying populations for gene frequencies inthe vague hope that someday the informationwill be valuable (see discussion in 2). In thecase of the Indian, however, such surveys bearon a clearly defined problem on which consider-able progress may be expected in the near future.

1 The response of genetic systems to a rapidlychanging environment. As I mentioned earlier,we recognize that our species is all over theworld subjected to a rapidly changing environ-ment. Unfortunately, only in the last few yearshave biology and medicine found themselves ina position to begin to document with any pre-cision what biological adjustments really takeplace. We have probably lost forever the oppor-tunity to study what occurred in Caucasianpopulations. We are about to lose the opportu-nity to document what happens in Negro andMongoloid (including Indian) populations.

The transition of surviving primitive Negroor Indian groups will be telescoped into a farshorter time period than was true for Caucasiangroups. Thus, some Indian groups will be called

upon to move from the Stone Age to the AtomicAge in a few hundred years, whereas the transi-tion for most Caucasian groups took thousands.It seems reascliable to argue that here is anopportunity to study changes in population

structure and adjustments to new stresses thatwe must not lose.

As for the previous two sections, so here the

5157

intellectual challenge is to convert an easilyenunciated but somewhat diffuse series of prob-lems into speciiic issues susceptible of precisestudy. A number of exact studies of populationstructure in transitional groups have alreadybeen completed or are in progress, notably thoseof Salzano and colleagues on the Caingang fBrazil (19, 20), of Layriss and colleagues onthe Warao of Venezuela, of Covarrubias andcolleagues on the Pewenche of Chile, and ofCann and colleagues on certain Quiche speakersof Guatamala. There are also studies in theUnited States on groups in a more advancedstage of the transition, namely by Spuhler andcolleagues on the Navajo (21) and Hackenbergon the Papago (5).

Also in progress are studies of specific medicalissues that arise in transitional groups, as thelatter poi tion of this session will attest. Thework of Roche and colleagues in particular willillustrate just how rapid and subtle may be thechanges introduced by minimal acculturation. Ifgenetic factors are important in the suscepti-bility to the thyroid hyperplasia and diabetesmellitus now so common in certain Indiangroups, then, because of the recency, frequency,and intensity of the phenomena. these groupsmay be unusually iavorable material for thestudy of these genetic factors.

Some unpublished studies of Drs. WarrenEveland, William Oliver, and myself may helppoint to some of the nuances of this transition.Six E. coli strains were isolated by Dr. Evelandfrom each of 77 Yanomama stools, each stoolfrom a different subject. An effort is in progressto type each of the resulting 462 strains, usingsome 140 different typing sera. Thus far ap-proximately 44 per cent of the strains fail totype out. By contrast, experience indicates thatonly a very small fraction of E. coil strains iso-lated in the United States would fail to type.What remains to be determined is whether thisis a unique finding in a long-isolated populationor whether similar studies en other such groupswill reveal the same pattern, with the inferenceof a predictable shift in the intestinal flora withacculturation.

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58

Some moral issues

It has seemoi appropriate, in a presentationto an audience of scientists, to stress researchopportunities. But as in the 1960's we increas-ingly recognize the issues created by scientificinquiry divorced from ethical and humanitarianconsiderations, it also seems appropriate to con-sider briefly what these st:zdies, and especiallythe type mentioned in the last section, mightmean to the Indian. We have no accurate cen-sus of the relatively pure Indians left in theAmericas, or of the persons of mixed but "sub-stantial" Indian ancestry. Estimates of the orderof 16,000,000 (17, 20, 24) have been made forthe former, while the latter come to easily sev-eral times that figure. We are talking about largenumbers of people.

Who among us can read the history of therelations between the early settlers of his countryand the Indians without deep shame for thebarbarism heaped upon a people who weredriven to defend the land they occupied? Theworld is watching my country as it agonizeso.er the Negro problemit might equally wellbe watching the Americas for signs of a belatedmoral resurgence with respect to the Indians.How satisfied are any of us with the officialprograms of our governments for the health,economic advancement, and education of theIndians? How can we translate the results ofour sciti,tific investigations into concrete act;onprograms, programs that must be carefully re-lated to other government measures? It is adubious favor to lower infant mortality amongthe Indians without parallel economic measuresto ensure food for the extra mouths. Nor doesit seem likely that Indians' accident-proneness(see references in 23), so easy to attribute un-critically to their heritage of violence and lackof familiarity with our gadgets, will yield toeducation until the frustrations that contributeto accident-proneness are relieved.

In a world that seems to be groping for per-spective, the Indian provides a reference pointfrom which to view the fantastic distupt'---,that modern men, intrinsically still little different in all essential biological attributes from

Indians, havc brought about. There are those

who wul take umbrage at my characterization

of us representatives of Western culture as "in-

trinsically still . . Indians." I am aware of theso-called intelligence tests that purport to show

the inferior intellectual qcalities of the American

Indian, ;ust as I am aware of similar results with

the American Negro. These results can be andhave been used as an excuse for less-then-equal

schoolin. But in both instances it is a matter of

a culturally deprived and alienated group--per-haps also subjected to early nutritional defi-

ciencies, whose role in impaked intellectual per-

formance we are just beginning to recognize-being judged by tests designed by and standard-

ized on a very different group (see also 4). Bythese remarks I do not mean to dismiss the

possibility of intellectual differeuces betweenethnic groups, but only to insist that to date the

data are grossly inadequate and we who callourselves scientists must adhere to the null

hypothesis, the more so since its various alterna-

tive ,. can be so conveniently misused by those

who would evade their social responsibilities.

Be this last digression as it may, each time I

return from the field there is a period of cultureshock as I realize how greatly in a short period

of time we have contrived to disrupt our eco-

system, and how profound is our ignorance ofthe long-range results of this disruption. Now

in this time of greatly intensified concern overthese problems, studies in depth of the Indian,

within or without the framework of IBP, will

surey contr:bute not only to his well-being but

also to our own pe;spective and, eventually, the

necessary adjustments toward which we areevolving.

REFERENCES

1. ARENDS, T., G. BREWER, N. CHAGNON, M.

GALLANGO, H. GERSHOWITZ, M. LAYRISSE, J. NEEL,

D. SHREFFLER, R. TASH IA N, and L. WE ITKAMP.

Intratribal genetic differentiation among the Yano-

mama Indians of Southern Venezuela. Proc. Nat.Acad. Sci. 57:1252-1259, 1967.

2. BEARN, 'k. G., 13. H. BOWMAN, and F. D.KITCI-HN. Genetic and biochemical considerations of

the serum group-specific component, Cold SpringHarbor Symp. Quant. Biol. 29:435-442, 1964.

3. CAVALLI-SFORZA, L. L., and A. W. F. EDWARDS.

Analysis of human evolution. In S. J. Geerts (ed.),Genetics Today, vol. 3. Oxford, Pergamon Press,1965, pp. 923-932.

4. FiscHER, J. L. Letter to the editor. Perspectives

in Biol. & Med. 11:325-328, 1968.5. HACKEN BERG, R. A. An anthropological study of

demographic transition. Milbank Memorial FundQuart. 44:470-493, 1966.

6. HANNA, B. L. The biological relationshipsamong Indian groups of the Southwest. Amer. J.Phys. Anth..op. 20:499-508, 1962.

7. KING, J. L. Continuously distributed factorsaffecting fitness. Genetics 55:183-492, 1967,

8. LEWONTIN, R. C. Population genetics. Ann.

Rev. Genetics 1:37-70, 1967.9. MILKMAN, R. D. Heterosis as a major cause of

heterozygosity in nature. Genet:es 55:493-495, 1967.10. MOURANT, A. E. The Distribution of the Hu-

man Blood Groups. Springfield, Illinois, Charles CThomas, 1954, 438 pp.

11. MOURA NT, A. E., and A. C. Konic. The ABOBlood Group:: Comprehrnsive Tables and Maps ofWorld Distribution. Springfield, Illinois, Charles C

Thomas, 1958. 276 pp. (Royal AnthropologicalInstitute Occasional Publication 13)

12. NEEL, J. V., and F. M. SALZANO. A prospectusfor genetic studies of the American Indian. ColdSpring Harbor Symp. Quant. Biol. 27:85-98, 1964.

13. NEEL, J. V., F. M. SALZANO, P. C. JUNQUE IRA,

F. KEITER, and D. MA Y BUR Y-LEWIS. &tidies on theXavante Indians of the Brazilian Mato Grosso.Amer. I. Hum. Genet. 16:52-140, 1964.

14. NEEL, J. V., and F. M. SALZA NO. Furtherstudies on the Xavante Indians. X. Some hypoth-

eses-generalizations resulting from these studies

Amer. I. Hum. Genet. 19:554-575, 1967.

15. NEEL, J. V., and N. A. CHAGNON. The demog-raphy of two tribes of primitive, relatively un-acculturated American Indians. Proc. Nat. Acad.

Sci. A:680-689, 1968.16. NEEL, J. V., and W. J. Salm.. On some

trends in vnderstanding the genetics of man. Per-

spectives in Biol. & Med. 11:565-602, 1968.17. ROSE NBLAT, A. La poblai:ion indlgena de

America. Buenos Aires, Institución Espaiola, 1945.

18. SALZANO, F. M. The blood groups of SouthAmerican Indians. Amer. J. Phys. Anthrop. 15:555-

579, 1957.19. SALZA NO, F. M. Studies on the Caingang

Irodians. I. Demography. Human Biol. 23:110-130,1961.

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59

20. SALZANO, F. M. Some genetic aspects of thedemography of American Indians. In J. Sutter (ed.),Human Displacements, Entretiens de Monaco enSciences Humaines, Premiere Session. Monaco, Im-primerie Nationale de Monaco, 1962.

21. SPUHLER, J. N., and C. KLUCKHOHN. In-breeding coefficients of the Ramah Navaho popula-tion. Human Biol. 25:295-317, 1953.

22. SANGHVI, L. D. Comparison of genetical andmorphological method for a study of biologicaldifference. Amer. I. Phys. Anihrop. 11:385-404,1953.

23. SCHMITT, N., L. W. HOLE, and W. S. BARCLAY.

54

Accidental deaths among British Columbia Indians.Canad. Med. Assoc. J. 94:228, 1966.

24. STEWARD, J. H., and L. C. FARON. NativePeoples of South America. New York, McGraw-Hill, 1959.

25. SVED, J. A., T. E. REED, and W. F. BODMER.The number of balanced polymorphisms that canbe maintained in a natural population. Genetics 55:469-481, 1967.

26. World Health Organization. Research onPopulation Genetics of Primitive Groups. Gen ev a,World Health Organization, 1964. 26 pp. (Techni-cal Report Series, 279)

DISCUSSION

Dubos: Before we open the general discussion.Dr. Neel, I should like to ask you to take overagain the problem raised by Dr. Water lo v. awhile ago. He asked about the evidence for thegenetic character of some of the differences inblood groups and you answered. But I shouldlike to ask if you could outline for us what kindof genetic evidence you can hope to obtain withregard to those adaptive processes of ,Jhich youhave spoken, especially with regard to the prob-lems of suscep:ibility to disease, which will bediscussed this afternoon. In other words, howpossIle ;s it in practice to obtain the kind ofinformation that would determine whether thechange is genetic or simply phenotypic?

Moderator: I am afraid that an answer to thatquestion might anticipate a good deal of ourdiscussion for this afternoon. ft is relativelysimple to obtain evidence for the genetic natureof the kinds of traits that Dr. Layrisse, Dr.Arends, and Dr. Lisker have presented. It is

clearly mucA more difficult to obtain evichncefor the genetic basis of such attributes as diseaseresistance.

We shall hear from Dr. Nutels this afternoonaly ut some of the medical problems ai Indiangroups in transition. We have recently had theexperience of being in the middle of a measlesepidemic in a virgin population of Indians. Itwas a very instructive and sobering experience.But one of :he strong impressions we cameaway withand Dr. Centerwali will presentsome of the datais that there may have beena great deal of uncritical thinking in the pastabout the constitutional susceptibility of theIndian to this, that, and the other disease. Wefeel that the secondary epidemiological charac-teristics of populations living at this level may

determine the hign mortality to a much greaterextent thnn any innate susceptibility.

Now, how to pin down that kinJ of impres-sion? It is very difficult. One practical approachis simply to provide the Indian, when he firstencounter:: tuberculosis or meLsIes or pertussis,with the same kind of medical care and nutritionthat corresponding Caucasian pepulations aregiven and see what the difference is.

As you know, Dr. Dubos, there is a consider-able literature, basal largely on stAies in twins,on disease susceptibilities in man. The.-e is alsoa large literature of studies in experimentalanimals, the results of which are sometimestransferred to man. This literature leaves muchto be desired; there is a need for precise investi-gations, as with standardized challenges undercontrolled conditions.

Waterlow: What is worrying me, Dr. Nedand I am very ignorant of this subjectis thatthe markers you are studying may in a sense beof no physiological importance, just as the colorof one's iris might be said to be of no importancephysiologically.

I am assuming that the variety of polymorphicproteins, the isoe7.zymes such as the phospha-tases, dehydrogenases, and so on, are alsogenetically detcrmined. I do not know whetherthis is proved yet. Such proteins are likely onphysiological grounds to be more important inrelation to adaptability. What I am not clearabout is how far your program of the kind ofthings you study is complete in itself. It ratherlooks as if geneticists had their own list ofproteins that they call markers, whereas webiochemists are thinking of rather differenttypes of proteins.

Moderator: Dr. Waterlow, you have asked a

55

very perceptive question, on which, again, wecould spend a great deal of time. Probably themost important development in human geneticsin the past decade has been the realization ofthe tremendous amount of genetically deter-mined biochemical diversity in our species. 1,

for one, think that one of the outstanding chal-lenges in human genetics is to understand thesignificance of this diversity. What is it all therefor? It is so great that we are having difficultyin seeing how it can all be maintained at onceby selective pressures. The problem is to sort outwhich oi these polymorphisins are like vestigialorgans and which are meaningful to the species.

Now, to come more directly to how we getat this. It is quite clear that those polymorph-isms arose in primitive man. And we feel thatmany dues to their function may come fromprimitive man. One of the things we attempt todo in our field work is collect all our data infamily relationships. We can then analyze familymaterial to see whether cercain polymorphismsare associated with increased fertility or withdecreased infant mortality. This is a long, slowbusiness. T'arallel studies on civilized populationsare also needei. The numbers necessary to estab-lish a significant associaton are tremendous.And, in fact, we almost have to think in ahigher order of magnitude than our past studieswhen we try to come to grips with these issues.

To sum up, althongh we are interested inthese traits as "markers," for which purpose we

need not understand their physiological signifi-cance, we are also just as interested in under-standing what they do.

Dubos: Do you see any possibility of deter-mining whether adaptation to high altitude is agenetically determined or a purely phenotypicadaptation? I think this is relevant to our dis-cussion last year.

Moderator: There is a great deal of interestnow in adaptation to high altitude, not only inthe Andes but also in the Himalayas and otherparts of the world. And there is, as you know,a running debate on how much of the adapta-tion we seefor example, the barrel chest of theAndean Indianis genetic and how much is

simply physiological adjustment to life at highaltitudes.

Now, one of the better opportunities to getat a question like that exists in Ethiopia. In thehighlands and lowlands of Ethiopia are groupswho on the basis of the genetic r ,arkers wehave been discussing appear to be very similar.And yet one group lives at a very considerablealtitude and one group not far above sea level.There is thus an experiment of nature, as itwere, in which a group has been subdivided andthe resultiug subgroups placed in &verse en-vironments.

The situation does not seem to be quite sosimple in the Americas. We have not yet foundthe "control" for Andean man. Once there aresuch controls it is possible to investigate whetherthey are physically more similar to high-altitudetry.ri than other Indian groupsthat is, whetherthere has been self-selection of groups able tolive at high altitudes. There is also the hope offinding marital exchanges between the high-and low-altitude groups.

Dubos: Would you elaborate on the state-ments that were made last year about the ana-tomica' differences in the heart between manborn at a high altitude and man born at ouraltitude?

Moderator: I would prefer that those whomade the statements were here to elaborate onthem. As I recall it, what we were shown wasevidence that changes appear very early on inthe heart and lungs, But I did not see anyconvincing eidence that these early changeswere genetic in nature. As far as I am concerned,it is a wide-open question whether this is

genetic or an environmental adaptation.Griffin: I have a suggestion on the general

problem Dr. Neel is working on. There was asomewhat comparable dispersal, by a quite dif-ferent group, into Australia at about the sametime, according to radiocarbon dates. Studies ofthe Australian aborigines, which were a muchless diversified and much smaller population,might be important with regard to evolutionamong "isolated" human groups.

Moderator: Yes, I agree that the Auitralian

56

aborigine does represent the group most neatlycomparable to the Indian. However, the disrup-tion and decimation of the Australian aborigineis even further along than that of the AmericanIndian. It is extremely difficult now to findgroups of any size that have not been seriouslydisturbed by being displaced into very unfavor-able country or in which there has not been aforced amalomation of previously separate

groups.Cohen: Following up Dr. Water low's and Dr.

Neel's remarks, I would like to ask Dr. Neelwhether geneticists\ are being prepared for thefact that, at least in molecular biological or bio-chemical terms, the concept of the regulation ofreadouts at the translational level as well as atthe transcriptional level is beginning to emerge.What brings this to mind is your allusion to theprimitive Indians' often being relieved of theburden of contamination carried by our popula-tion. They are living with quite different intes-tinal flora, parasites, and perhaps even types ofnatural foodstuffs to which our population isnot exposed, but I do not know whether in facttheir environment can necessarily be spoken ofac less contaminated. The primitive populationwould be less contam:nated by synthetic andnon-natural factors; relative to our own situa-tion, however, it may be more contaminated.This comes to affect the whole question ofseparation of genetic potential because of thepossibility that transcription may be regulatedat the level of translation. There may be allkinds of factors in terms of the phenotypicresult that could emerge by very subtle devices.I am wondering whether even the familial teststhat the geneticists traditionally use would getaround this problem.

Moderator: I would remind you that thegeneticist has had quite a hand in molecularbiology.

Obviously, there is at present no answer toyour question about differences in transcription,qualitative or quantitative, at that cultural levelas compared with our own. I think all of uswho have done field work have emerged witha feeling that here in a very different world

and it is a very different worid, the world ofprimitive manyou nevertheless quickly recog-nize all the familiar types of our own culture.You do not have to be very long in an Indianvillage before you get the same feeling for thestrong men and the weak men and the operatorsand so on that you encounter in our own cul-ture.

So I would say that at least part of the tran-scription is probably much the same at all cul-tural levels. Whetho-, on the other hand, thereare sabtle differences in the genetic readout,who can say?

McDermott: ig the lines of Dr. Dubos'question, Dr. Neel, arc the people who areconducting the studies of Ifswer-animal behaviordso making ths.se batteries of observations onthe various genetic markers? I was thinking,for example, that the question of adaptability tohigh and low altitude might conceivably beapproached from that standnoint. Is there workin this field, attempting to relate these genetictraits to the behavioral pattern of the animal?

Moderator: We know more about man'sgenetic constitution than about that of any othermammal at the present time. However, whatmight be called the comparative polymorph-ology of the primates is under very ac ive investi-gation. A great deal of effort is now going intoexploring the extent to which the higher pri-mates have polymorphisms comparable to thoseof man. It is too early !or any generalizations,but it is a fact that some polymorphisms en-countered in man are found in the higher pri-mates. On the other hand, the primates showpolymorphisms that are not found in man. Nopattern has yet emerged. I assume that in duetime it will be possible to try again to make thekinds of associations you refer to. But, again, Icome hack to the problem of numbers. It is

going to be very difficult to get large numberson any of the higher primates. It is much easierwith man.

Dubos: There can be no doubt that Dr. Neelhas not only touched on but developed for usthe foremost problems of man's adapting tothe new conditions he is creating. All sorts of

57

63

statements are continuously being made, such"Modern man has become adapted to crowding"or ". . . cannot become adapted to crowding";"Modern man has become adapted to pollution"or ". . . cannot adapt to pollution." And, infact, these problems, which are so crucial to thewhole development or survival of our civiliza-tion, have not as ytt been formulated in suffi-ciently clear terms for us to determine whetherwe are dealing only with genetic adaptability,only with phenotypic characteristics, or whetherwe are simply playing on the polymorphic rich-ness of the human race.

The problem is so large and so important that

58

we obviously are not going to solve it here. ButI hope at least that Dr. Neel will conclude witha general statement on this issue.

Moderator: I merely want to agree that weare not going to solve the problem this morningand w agree with one other thing Dr. Duboshas impliedthat there are grkat difficulties ;r1clear formulations in this field. How do we setup specific questions to which we can get whatwould be called scientifically hard answers? Ithink we are in accord ;hat this is an importantarea. And I think we are in accord -sith respectto the methodology: we have a long way to gL.

SURVEY OF THE UNACCULTURATED INDIANS OF CENTRAL AND

SOUTH AMERICA'

Francisco M. Salzano

Acculturation and biological change

Before trying to make the survey mentionedin the tide it is important to indicate the prob-lems that arise when an attempt is made todefine a specific group as "acculturated" or

"unacculturated." The term acculturation is

generally employed by American anthropolo-gists, while their British colleagues prefer theword culture contact and the Cuban scholarF. Ortiz the term transculturation, which em-phasizes the reciprocal character of most contactsituations. Though much criticized and modi-fied, the most widely med definition is that ofRcdfield, Lindon, and Herskovits (19): "Accul-turation comprehends those phenomena whichresult when groups of individua's having dif-ferent cultures come into cot; tinhous first-handcontact, with subsequent changes in the originalcultural patterns of either or both groups."

A number of basic problems exist in the inter-pretation and analysis of these situations; theyare reviewed by, among others, Beals (1) andOliveira (16). For instance, we have sometimesconflicting views of culturaliqs and sociologists,and in some specific cases the intrinsic nature ofthe process and its consequences are difficult toidentify. A new dimension, which so far as Iam aware has not been properly analy2ed in this

I Research supported in part by the Rockefeller Foun-dation, Consdho NaCior,;11 de Pestwisas, Conselho dePesquisas da Universidade Federal do Rio Grande do

Sul, U.S. Public Health Service. and Wenner-GrenFoundation for Anthropological Research.

context, is that related to the biological changesthat occur and sometimes are decisive for thedirection and speed of acculturative modifica-tions.

Ribeiro (20) recognizes for Brazilian Indiansthree stages on the road to acculturation. Thefirst would be represented by the isolated tribesthose living in regions not yet occupied by theBrazilian society and having only accidental andrare contacts with our civilization. Some simplyavoid such contacts, while those living nearpioneer settlements may have suffered violenceand be frankly hostile to "foreign" people. In

either case, they can obtain all they need fromthe region wherc they live and from their work;they are therefore able to maintain completecultural autonomy. The second stage would be

that of populations having intermittent contactswith civilization. They live in regions already

reached by the expanding frontiers of the na-tional society; though they maintain a certaincultural autonomy, they already have needs that

can only be satisfied through economic relationswith civilized people. The third stage is repre-sented by groups in permanent contact with

more numerous and more differentiated mem-

bers of the civilization. They have lost theircultural autonomy to a large degree, being en-tirely dependent on others for the supply of

many tools and products. They still preserve

some of their traditional customs, but alreadyshow profound changes due to ecologic, eco-nomic, and cultural pressures.

59

65-.4 )

What concomitant modifications occur in thebiology of these groups? Only very limitedstart has been made on quantifying the observa-dons made in groups at these three stages, andmuch more is needed to obtain a complete pic-ture (12, 13). One important point that shouldbe emphasized is the speed of these changes.Probably the first characteristics to be affectedare the epidemiological ones, and here manygroups that show all the other traits typical ofuntouched populations may present patterns re-sembling those of groups at other stages ofacculturation. A typical example is provided bythe Txukahamae, a Cayap6 group of centralBrazil (14). They have a completely autono-mous life and in every instance are representa-tive of an isolated population, but they alreadyhave a high inci'lence of tuberculin reactors.Since the Amerindian populations apparentlyhad no contact with tubercle bacilli in pre-

Columbian times, the question arises. Fromwhat groups did they get the infection? Theircontacts with neo-Brazilians are recent and in-termittent, and it is reasonable to suppose thatthe source of infection was the Gorotire, anotherCayapb group from whom they separated at thebeginning ot this century but with whom theystill have frequent interchange. The diffusion ofthis Pathological agent in some ways parallelsthe cAusion of cultural traits. The speed ofthese epidemiological changes is such that it is

improbable that the study of present groups, nomatter how untouched, would give us exactduplicates of past populations. But investigationof the biological and nonbiological factors thatinfluence the genetic and physiological adapta-tion of these groups to new diseases and infec-tious agents has intrinsic interest and can eluci-date important problems of human biology.

Source of the data and their limitation

In the next section I shall try to present asurvey of the relatively unacculturated Indiansof Central and South America. Since I havefirst-hand contact only with Brazilian Indians,information concerning other countries has hadto be limited to printed material and the per-

sonal communications of many colleagues. Therapidity of change in these poputations and alsothe discovery of new groups indicate that sucha list should be considered as merely an approxi-mation of the situation in the several areas stir-veyed. Moreover, the publications examinedsometimes do not give basic details about thedegree of acculturation of the group in question.Even with these reservations, the list may per-haps serve to give a rough idea of the opportuni-ties that still exist for the study of populationsat this cultural level. In all cases the figures con-cerning the country's total and its Indian popu-lations were checked in the must recent officialpublications. The references indicated are thoseexamined in addition to these sources. Onlyrelatively recent estimates were included; forreviews concerning the older ones, see Rosenblat(21) and Steward (23).

The survey

CENTRAL AMERICA

Political subdivisions: Bahamas, Belize, Bermuda.Costa Rica. Cuba. Dominican Republic, El Salvador.Guadeloupe (and depLndencics), Gu:uemala, Haiti, Hon-duras. Martinique, Mexico, Netherlands Antilles, Nica-ragua, Panama, Puerto hico, Virgin Islands, Wcst Indies.

Total population: 77 million.Countries with significant number of Indians: Belize.

Costa Rica, El Salvador. Guatemala, Honduras, Mexico.Nicaragua, Panama.

Indian population: 8,000,000 (10 per cent of thearea's total population).

Unacculturated Indians: Perhaps 1,000,000 (1.3 percent of total population).

BELIZE

Total population: 100,000.Indian population: 8,000-10,000.Information about the Indians: Mainly Maya and

Chekchi, who came from Mexico and Guatemala.Unacculturated Indians: Probably none.Reference: 9.

COSTA RICA

Total population: 1,500,000.Indian population: 7,200.Information about the Indians: Most important grcups

appear to be Bribri (about 3,500), living in TalamancaRange in south, and Boruca (about 1,000) in southweston the Pacific side. Remaining Indians belong to groups

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66

of Chorotegamangue (Nicova Peninsula) and Guatuso(northern and western bordeis).

Unacculturated Indians: Probably none.Refermices: 9, 24.

El. SALVADOR

Total population: 3,000,000.Indian population: 100,000.Information about the Indians: Most important group

is Pipil (about 80,000) of Nahuatl origin, concentratedin various towns in Sonsonatc Department. Also smallergroups of Nahua and Cakchiquel distributed over severaldepart men ts.

Unacculturated Indians: Probably none.References: 9, 24.

GUATEMALA

Total population: 4,438,000 (1965).Indian population: 2,500,000.Information about the Indians: Main groups in center

and west: Maya, Cakchiquel, Tzutujil, Uspanteca, Achi.West: Mam, Aguacateca, jacaltec, Kanjobal, Chuj, Ixil.North: Kcehki, Pocomchi, Pocomam, Lacand6n, Mopan.East: Chortf, Lacand6n Chol, Chontal. Southeast: Xinca.

Unacculturated Indians: Some groups living in in-accessible places could provide information on thc influ-ence of a non-European culture on genetic and othertraits.

References: 9, 18.

HONDURAS

Total popula'i,?n: 2,400,000.Indian population: 110,000.Information ab ,1 the 'ndians: Main groups in west:

Chorotega, Miquirano, Guajiro. On coast: Moreno. Other:Opatoro, Jicaque, Paya, Zambo, Miskito, Sumu. ThcMiskito nave mixed with Negro groups.

Unacculturated Indians: Probably none.References: 9, 18, 24.

MEXICO

Total population: 40,913,000 (1965).Indian population: Estimates vary widely. A conserva-

tive number would be 5,000,000.Information about the Indians: Main groups in north:

Kikapti, Tcpchuano, Nahuatl, Panic, Huastec, Otomi.Northern Pacific: Cora. Huichol, Yaqui, Seri, Papago.Center: Mazahua, Matlatzinca, Tarasco, Mazatec, Mixtec,Popoloco, Totonac. Zoque, some of previous groups.Southern Pacific: Chol, Tzeltal Tzotzil, Tojolabal, Maya,Lacand6n, Amuzgo, Tlapancc, Chatirio, Chinantec, Cho-cho, Chontal, Huave, Mixe, Triche, Zapotec.

Unacculturated Indians: LacandOn (only about 200).Some groups living in inaccessible places could provideinformation on influence of a non-European culture ongenetic and other traits.

References: 4. 9. 18, 25.

NICARAGUA

Total population; 1 ,631.,000 ( 966) .

Indian population: 80,000.Information about the Indians. Most important groups

arc Miskito (with a krge component of Negro mixture),Sumu, Rama, and Ulva,

Unacculturated Indiars: Stor,:2 (24) mentions the Ulvatribe bettk e.,,r) the Mico and Siquia rivers, and the Sumu(3,000-4,00) in 1948).

References: 9, IS. 22, 24,

PANAMA

Total population: 1,31-.A60.Indian population: 65,000-100. 000.Liformation about the Indians: Main tribes are Guaytni

(about 36,000), Cuna (some 22,000), and Choc6 (6,000).Two other small groups are Bocota (2(10) and Teribe(400), Guaymi are found in Chiriqui, Bocas del Toro,and Veraguas provinces; Cuna mainly in San Bias Pri.v-ince, both mainland and some islands: Chou; in Dari&IProvince.

Unacadturated Indians: Some Choc6 groups of Pan-amanian-Colombian border (:).

Reference's: 9. 24, 26,

SOUTH AMERICA

Political subdivision: Argentina, Bolivia, Brazil, Chile,Cokmbia, Ecuador, French Guiana, Guyana, Paraguay,Peru, Surinam, Uruguay, Venezuela.

Total population: 175 nUllion.Countries with significant number of Indians: All

except Uruguay.Indian population: 10 million (6 per cent of the area's

total population)Unaccultw.ated Indians: Perhaps 980,000 (0.6 per cent

of the total population).

ARGENTINA

Total population: 22,254,102 (1965).Indian population: 130,000.Information about the Indians: Main groups in Chaco

region: Mataeo, Chulupi, Chorote, Chiriguano, Pilag(totaling about 30,000). Andean region: Quechua andColla (some 18,000). South: Araucanian. Other regions:Caingui, Mocobi, Toba.

Unacculturated Indians: Perhaps some Chaco groups.References: 8, 9.

BOLIVIA

Total population: 3,800,000.Indian population: 2,450,000.Information about the Indians: Main groups in Andean

region: Quechua (about 1.500,000) and Aymara (850,-000). Northeastern region: The forest-dwelling popula-tions (approximately 87,000) are divided into about 63tribes belonging to 15 linguistic families. Sonic of them

arc as follows: Beni Depanment: Sirion6, Baurc, lora,Chacobo, Tacana, Chimane, Movima, Yan, Sirineire,Cayubaba, Itoma; Department f Santa Cruz: Guarayo,Borosese, Chamacoco, Zainuco, Lengua, Tapieti, Otuqui,Guatose, Yuracare; Pando Department: Ara( na, Toro-norna, Pacaguara, Machicanga; Department of La Paz:Chama. Chimane, Guarayo, Leco. Soutilcastern region(Bolivian Chaco): Tarija Department; Chiriguano,Mataco, Toba, Chulupi, Guaycuru, Chanese (about14,500); Quiluisaca Department: Chorote, Chiriguano(some 3,800); Cochabamba Department: Sirion6. Yura-care (2,000). General total for the region: approximately50,000 Indians.

Unaccultw-ated Indians: Almost all forest-dwellers.References: 9, 28.

BRAZIL

Total population: 90,193,000.Indian population: 100,600.Information about the Indians Tribes or groups classi-

fied by Ribeiro (20) and others as isolated or in inter-mittent contact (excluding those with fewer than 50individuals): Agavotokueng, Apalai (100-250). Araras,Asurini (250-500), Atruahi, Baraw5na, Boca Negra,Canoeiros, Cayabi (250-500), Diore (500-1,000),Gaviiks (1,500-2,000), Guaji (100-250), Ipewi, Javai(250-500). Kabixi, Kalapalo (100-250), Kamayuri(100-250), Katawiin, Kren-Akoro (2,500-3,000),Kuben-Kran-Kegn (250-500) Kuben-Kragnotire (400),Kuikuro (100-250), Makii, Mandawgka, Maopityan,Makir; tare or Mayongong (500-1,000), Mehiniku(50-100), Mentuktire (560-1,000), 1udjetirc (50-100), Nahuktui (50-100), Nambicuara (500-1,000),Pakainovas (500-1,000), Parakanin (250-500), Pari-

kot6, Pianokot6, (250-500), Purubori (50-100),Sikiâna, Tapaytina, Tine.) (2,000-3,000),

Txicio, Txukahamae (200), Urubus-Kaapork500-1,000), Waimiri, Waiwai (100-250), Wauri (100-250), Xavante (2,000-3,000), Xikrin (250-500), Ya-baina, Yanomama (2,000). For location, sec references11. ind 19. The former presents many othcr names, butit is not always clear whether tribes or tribal subdivis.onsare meant.

Unacculturated Indians: Pertaps about 40,000.References: 11, 20.

GIME

Total population: 8,567,000 (1965).Indian populatior. 130,000.Information aboia the Indians: Main groups in North-

ern region: Quechua and Aymara. Southern region:Araucanian (Mapuchcs).

Unacculturated Probably none.References: 9.

COLOMBIA

Total population: 11,787,000.Indian popdatio-,: 300,000.Information about the Indians: Main groups in Cauca

region: Guambiano, Pgez, Guanaco, Yanacona, Coc.)-

nuco (approximately 80,000). Narifio: Quillacinga.Kwaiker, Inga, Kamsi (about 60,000). Gn..;i-a: Guajiro(50,000). Magdalena: Kogi, Ika, Chimila, Yu,o (15,000).Antioquia: Cuna (2,000).

Unacculturated Indians: Perhaps 100,000.References: 2, 9.

IR

Tovi? population: 5,084,000.India:i population: 2,000,000.Information about the Indians: Main groups in coastal

region and cast: Colorado, Jivaro (13,000), Yumbo,Auca. Sic:ra: Quechua groups: Quindivana, Saguatoa,Salasate, Poat), Ilumane, Peguche, Quinchuqui, Quilotoa,Zunibagua, Pilaloe, Siquisilie, Puruhay, Caiiaris, Sara-guro.

Unacculturated Indians: Perhaps 25 ),006 (50,000 inthe juggle).

References: 9. 15, 17, 2".

FRRNCII GUIANA

Total population: 36,000.Indian popdation: 1,200.Information about the Indians: In coastal region:

Galibi (600), Arawak (100), Palikour (100). In interior:Wayapi (130), Mereyo (60), Waiyana (200).

Unacculturated Indians: About 900 (Galibi, Palikour,Waiyana).

Pejo ences: 3.

GUYANA

Total pop;ilation: 647,000.Indian population: 27,840.Information abdut the Indians: Main groups in coastal

region: Arawak Carib, Warrau, Akawaio (about 10,000).In interior: Carib, Akawaio, Patamona, Arckuna, Makusi.Wapisiana, Waiwai.

Unaccuiturated Indians: Perhaps 2,000.References: 3, Iniorroillon note n Arte4d9.T4(1111.efft et) V. a 'Spew.

PARAGUAY

Total population: 2,030,000.Indian population: 37,570.Inform.:tion about the Indians: They speak languages

of 6 linguistic families and live in i7 locations. Maingroups: Chiripi, Mbia, Tabiterii, Guayaki, Guarayti,Chiriguano. Tapicti, Maki (about 600), Chulupi (morethan 10,000), Chorote (approximately 100), Lengua(5,000), Sanapana (3,400), Guana (400), Angaitc (400),Toba (1,400), Chamacoco, Morotoco.

Unacvulturated Indians: Perhaps 10,000.References: 9; data supplied by Department of Indian

Affairs.

PERU

Total population: 11,800.000.Indian population: 4,800,000.Informatior about the Indians: Main groups in North-

Aguz,runa, Jivare, Huambisa, Andoa, Shapra,

Curaraye, Chayhuita, Jebero. Northeast: Bora, Ocayna,

Orejon, Pano, Yagua, Mayoruna, Charna, Huitoto,

Ticuna, Cocoma, Capanahua, Cashibo, Shipibo. Center:Campa, Amuesha, Amahuaca, Marinahua, Cashinaua.

Southeast: Sirinayri, Machigiienga, Piro, Mashco, Hua-

rayo. Carneiro (5) also mentions following tribes frommontaiia: Yaminahua, Remo, Marobo and Iiiapari.

Unacculturated Indians: Perhaps 450,000.References: 5. 9, 27, 28.

SURINAM

Total population: 360,000.Indian population: 4,500.Information about the Indians: Main groups in coastal

region: Galibi (2,400), Arawai: (1,500). In interior:

Waiyana (2(A)), Trio or Tiri6 (00).Unacculturated Indians: Perhaps 2,000.Reference: 3.

VENEZU ELA

7 otal population: 8,880.000.Ihdian population: 62.700.Information about the Indians: Layrisse and wilhert

(9) list the following: Guajiro (8,429). Paraujano

(1,348). \Alp (2,057), Bari (1,000), Yaruro (1,427),Guahillo (5.397), Piaroa (1,886). Panarc (412), Yaba-rana (64), Makiritarc (1,200), Piapoco (99), Curipaco(212), Puinave (240), Bare (645), Yanomama (20,000),Sap6 (100), Pemon (2.700), Warao (11,700), Carilia

(2,776), unknown (1,000).Unacculturaoed Indians: Perhaps 30,000.References: 6, 7, 10, 29, 30.

Discussion

As was mentioned preyiously the estimatesobtained present at least two types of error. One

has to do with the identification of the accultura-

tion process per se; the other is the proper place-

ment of the group studied into "acculturated"or "unacculturated" categories. Because of thelack of detailed studies in most of the tribessurveyed here, and of reviews placing them inthe appropriate category, the numbers obtainedhave a very relative value. They should beviewed as indicating orders of magnitude only.

With these reservations in mind it is now pos-sible to examine the numbers arrived at. Thepopulation of Centi al America was estimated at77 million and the number of unacculturatedIndians at about one million (1.3 per cent). InSouth America the proportion is even lower:for a total of 175 million I calculate approxi-mately 980,000 (0.6 per cent). But the fact thatwe may still have about two million largely"untouched" Indians points to the magnitudeof the task, if we want to obtain truly compara-tive data in a number of populations living indifferent ecosystems. As a matter of fact, wesimply do not have experienced persons to un-dertake the study of even, say, 10 per cent of thisnumber in the immediate future.

With acculturation changes occurring so

quickly, we iiced to work fast to establish on afirm basis the biological and nonbiological forcesacting at this cultural level and determining .hefate of these populations. This information is

basic to our understanding of human evolution,but it is also important in relation to practicalproblems. The acculturation process is generallypainful and distressing. In fact, a large propor-tion of the groups affected by it si:nply disappearphysically. Data on populations living at dif-ferent cultural levels can provide clues to aneasier and more humane way toward techno-logical advance.

REFERENCES

1. BEALS, R. Acculturation. In A. L. Kroeher(ed.), Anthropology Today. Chicago, University of

Chicago Press, 1953, pp. 621-641.2. BURGOS GUEVARA, H., and G. PESANTEZ REINos.,

Plan nacional indigenista de Colombia: 1966-1969.

America lndigena 27:751-781, 1967.

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3. BuTT, A. J. The Guianas. Bull. Intern. Comm.Urgent Anthrop. Ethnol. Res. 7:69-90, 1965.

4. CAMARA, P. Rescate etnogra'fico nacional enMaico. Bull, Intern. Comm. Urgent Anthrop.Ethnol. Res. 7:99-104, 1965.

5. CARNEIRO, R. L. Little-known tribes of the

69

Peruvian Montana, Bull. intern. Comm. UrgentAnthrop. Ethnol. Res. 5:80-85, 1962.

6. ComsION INDIGENISTA NACIONAL (VENEZUELA).Nuestro Indio. Caracas, Ministerio de Justicia, 1960.26 pp.

7. COMISION DIGE NISTA NACIONAL. Informe dela ComisitSn Indigenista Nacional 'del Ministerio deJusticia de Venezuela, correspondiente al -nio de1964. America Indigena 25:131-145, 1965.

8. Focx, N. Utgent ethnographical tasks in theArgentire Chaco. Bull. Intern. Comm. UrgentAnthrop. Ethnol. Res. 5:162-166, 1962.

9. Guia de la población indigena de America.Indigenista 21 :170-266, 1961.

10. LAYRISSF., M., and J. WILBERT. Indian societiesof Venezuela. Their blood group types. Caracas,Instituto Caribe de Antropologia y Sociologia,Fundación La Salle de Ciencias Naturales, 1966.318 pp. (Monograph 13)

1 I MA LCHER, J. M. G. indios. Crau de integracilona comunidade nacional. Grupc 'lnguistico. Locali-za0o. Rio de Janeiro, Conselho Nacional deProteciio aos Indios, 1964. 266 pp. (Nova sArie,Publicaciio 1)

12. NEEL, J. V., and F. M. SALZANO. A prospectusfor genetic studies on the Americau Indian. In P. T.Baker and J. S. Weiner (eds.), The Biology ofHuman Adaptability. Oxford, Clarendon Press, 1966,pp. 245-274.

13. NEEL, J. V., and F. M. SAL1ANO. Furtherstudies on the Xavante Indians. X. Some hypotheses-generalizations resulting from these studies. Amer.I. Hum. Genet. 19:554-574, 1967.

14. NUTELS, N., M. AYRES, and F. M. SALZANO.Tuberculin reactions, X-ray and bacteriological stud-ies in the Cayapó Indians of Brazil. Tubercle 48:195-200, 1967.

15. OBE REM, U. 1962. Dringende ethnologischeForsehungsaufgaben in Ost Ekuador. Bull. intern.Comm. Urgent Anthrop. Ethnol. Res. 5:75-79, 1962.

16. OLIVEIRA, R. C. DE. 0 Indio e o mundo dosbrancos. Sk Paulo, Difusk Europela do Livro,1964. 144 pp.

17. ORBE, G. R. Destribalización de indigenas ciEcuador. In Homenaje a Juan Comas en su 65

aniversario, I. Wxico, D. F., Libros oe Mexico,1965, pp. 79-134.

18. PEP ICOT Y GARCIA, L. America In digena. TomoI. El hombre americaro. Los pueblos de Amer;ca.2nd ed. BarTelona, Salvat. 1962. 1182 pp.

19. REDFIELD, R., R LINTON, and M. J. HERSKO-vas. Memorandum on the study of acculturation.Amer. Anthrop. 38:149-152, 1936.

20. RIBEIRO, D. Culturas e linguas indigenas doBrasil. Educa4o e Ciencias Sociais (Rio de Janeiro)2:5-102, 1957.

21. ROSENBLAT, A. La población indigent: deAmerica. Buenos Aires, Institución Cultural Es-panola, 1945, 296 pp.

22, STEWARD, J. H. (ed.) Handbook of SouthAmerican Inthans. Bull Bur, Amer. Ethnol. 143 (5volumes, 1946-1950).

23. FrEWARD, J. H. The native population ofSouth America. Handbook of South AmericanIndians 5:655-668, 1949.

24. STONE, D. Urgent tasks of research concerningthe cultnres and languages of Central AmericanIndian tribes. Bull. intern. Comm. Urgent Anthrop.Ethnol. Res. 5:65-69, 1962.

25. SWANTON, J. R. The :ndian tribes of NorthAmerica. Bull. Bur. Amer. Ethnol. 145:1-726, 1952.

26. TORRES DE ARAUZ, R. Los grupos humanos dePananmi. In Homtnal? a luan Comas en su 65aniversario, I. Mexico, D. F., Libros de Mexico,1965, pp. 135-142.

27. VILLA Ropts, A. Departamento de Investiga-clones Antropológicas del Institut(' indigenistaInteramericano. Programa de actividades, julio de1965 a junio de 1966. Anuayio lndigenista 25:87-98, 1965.

28. VILLA RojAs, A. Informe de labores del De-partamento de Investigaciones Antropológicas, 1965-1966. Anuario Indigenista 26:7-95, 1966.

29. WILBERT, J. Dringliche Forschungsaufgabenin Venezuela. Bull. Intern. Comm. Urgent Anthrop.Ethnol. Res. 5:86-96, 1962.

30. ZERRIES, 0. Die völkerkundliche Fol.schungs-situation in Südost-Venezuela. Bull. Intern. Comm.Urgent Anthrop. Ethnol. Res. 5:97-111, 1962.

Achi (Gua)Ag tvotokueng (Br)Aguacate (Gun)Aguaruna (Pc)Akawaio (Gui)Amahuaca (Pc)Amuesha (Pe)Amuzgo (M)Andoa (Pc)Angaize (Par)Apalai (Br)Araana (Bo)Araras (Br)Araucanian (A)Araucanian (Mapuche) (Ch)Arawak (Fr G, Guy, S)Arckuna (Gui)Asurini (Br)Atruahi (Br)Auca (E)Aytw.ra (Bo, Ch)

Baraw:ma (Br)Bare (V)Bari (V)Baure (Bo)Boca Ncgra (Br)Bocota (Pan)Bora (Pc)13orosese (Bo)

Boruca (CR)Bribri (CR)

Cainguii (A)Cakchiqud (ES, Gua)Campa (Pc)Caiiaris (E)Canociros (Br)Capanahua (Pc)Carib (Guy)Carifia (V)Cashibo (Pc)Cashinaua (Pe)Cayabi (Br)Cayubaba (Bo)Chacobo (Bo)

Country abbreviations

A = ArgentinaBe = BelizeBo = BoliviaBr = BrazilCh = Chile

Appendix

ALPHABETICAL LIST OF TRIBES CITED 1

as follows:

Chama (13o, Pc)Chamacoco (Bo, Par)Chanese (13o)Chatitio (M)Chayhuita (Pe)Chekchi (Be)Chimane (Bo)Chimila (Co)Chinantec (M)Chiriguano (A, Bo, Par)Chiripa (Par)Chocho (M)Choc6 (Pan)Choi (M)Chontal (Gua, M)Chorotc (A, Bo, Par)Cnorotega (H)Chorotegamangue (CR)Chorti (Gua)Chulupi (A, Bo, Par)Chuj (Gua)Cocoma (Pc)Coconuco (Co)Culla (A)Colorado (E)Cora (M)Cuna (Pan. Co)Curarayc Pe)Curipaco (V)

Diore (Br)

Galibi (Fr G, S)Gaviiies (Br)Guahibo (V)Guaja (Br)Guajiro (H, Co, V)Guamhiano (Co)Guana (Par)Guanaco (Co)Guarayo (Bo)Guarayti (Par)Guatose (Bo)Guatuso (CR)Guayaki (Par)Guaycuru (Bo)Guaymi (Pan)

Co = ColombiaCR = Costa RicaE = EcuadorES = El SalvadorFr G = French Guiana

65

fluambisa (Pe)Huarayo (Pc)Huastec (M)Huave (M)Huichol (M)Huitoto (Pe)

Ika (Co)Ilumane (E)1fiapari (Pc)lnga (Co)Ipewi (13r)Itoma (13o)lxil (Gun)

Jacaltec (Gua)Javai (Br)jcbcro (Pc)Jicaque H)Jivaro (E. Pc)lora (Bo)

Kabixi (Br)Kalapalo (Br)Kamayura (Br)Ka 1115A (Co)

Kanjobal (Gun)Katawi:in (Br)Kechki (Gua)Kikaptic (M)Kogi (Cc)Kren-Akoro (Br)Kuben-Kragnotire (Br)Kuben-Kran-Kegn (Br)Kuikuro (Br)Kwaik, r (Co)

LacandOn (Gua, M)Lacand6n Choi (Gua)Leco (13o)Lengua (Bo. Par)

Machicanga (Bo)Machigiienga (Pe)Maka (Par)Makiritare (V, Br)

Gua = GuatemalaGuy = GuyanaH = HondurasM = MáxicoN = Nicaragua

Pan = PanamaPar = ParaguayPe = PeruS = SurinamV = Venezuela

Mak6 (Br)Makusi (Guy)Mam (Gua)MandawAka (Br)Maopityan (Br)Marinahua (Pe)Marobo (Pe)Mashco (Pc)Mataco (A, Bo)Matlatzinca (M)Maya (Be, M, Gua)Mayongon#7 (Br)Mayoruna (Pc)Mazahua (M)Mazatec (M)Mbia (Par)Mehináku (Br)Mentuktire (Br)Mereyo (Fr G)Miquirano (H)Miskito (11, N)Mixé (M)Mixrc (M)Mocob: (A)Mop lin (Gua)Moreno (H)Morotoco (Par)Movima (Bo)Mudjet;re (Br)

Nahua (ES)Nahuaktui (Br)Nahuatl (ES, M)Natnbicuara (Br)

Ocayna (Pc)Opatoro (H)Orejon (Pe)Otomi (M)Otuqui (13o)

Pacaguara (Bo)Piez (Co)Pakaánovas (Br)Palikour (Fr G)Pame (M)Panare (V)Pano (Pe)Papago (M)Parakanln (Br)ParLujano (V)Parikot6 (Br)

Patamona (Guy)Paya (H)Peguche (E)Pemon (V)Pianokot6 (Br)PiapoLo (V)Piaroa (V)Pilagi (A)Pi lapoe (E)Pipil (ES)Piro (Pe)Poato (E)Pocomam (Gua)Pocomchi (Gua)Popoloco (M)Puinave (V)Puruborii (Br)Puruhay (E)

Quechua (A, Bo, Ch, E)Quillacinga (Co)Quilotoa (E)Quinchuqui (E)Quindivana (E)

Rama (N)Remo (TA)

Saguatoa (E)Sa:asate (E)Saluma (Br)Sanapana (Par)Sape (V)Saraguro (E)Seri (M)Shapra (Pe)Shipibo (Pc)Sikina (Br)Siquisilie (E)Sirinayri (Pe)Sirineire (Bo)Sidon() (Bo)Sumu (H, N)

Tabitirii (Par)Tacana (Bo)Tapaytina (Br)Tarieti (Bo, Par)Tarasco (M)Tepehuano (M)Teribt (Pan)Ticuna (Pc)

Tiri6 (Br)Tlaponeco (M)Toba (A, Bo, Par)Tojolabal (M)Toronoma (Bo)Totonaco (M)Triche (M)Trio (or Tiri6) (S)Trumiii (Br)Txiciio (Br)Txukahamac (Br)Tzeltal (M)Tzotzil (M)Tzutujil (Gua)

Ulva (N)Urubus-Kaapor (Br)Uspanteca (Gua)

Waimirf (Br)Waiwai (Br, Guy)Waiyana (Fr G, S)Wapisiana (Guy)Warao (V)Warrau (Guy)Wauri (Br)Wayapi (Fr G)

Xavante (Br)Xikrin (Br)Xinca (Gua)

Yaba:na (13r)Yabarana (V)Yagua (Pc)Yaminahua (Pc)Yanacona (Co)Yanomam6 (Br, V)Yaqui (M)Yari (Bo)Yarero (V)Yuko (Co)Yumbo (E)Yupa (V)Yuracare (Bo)

Zarnbo (14)ZatiluCo ( 3o)Zapotcc (M)Zoque (M)Zumbagua (E)

DISCUSSION

Moderator: Dr. Salzano, I wonder whetherthere is perhaps a decimal point misplaced. Youestimate that there are 1,000,000 unacculturatedIndians in Central America and 980,000 in allof South America. But when I go through yourtreatment of Central America country by coun-try, I simply do not f!nd those numbers. Wherea;.e these 1,000,000 concentrated?

SaIzano: As I said, these are very preliminaryestimates. They make allowance for the verylarge groups in Guatamala and Mexico onwhich we do not know enough for mr: to set aspecific figure. But I am sure that there shouldbe some groups there that are sufficiently un-acculturated to be worth studying.

Cohen: How reliable is the tuberculin test inthis population that you referred to in the caseDf central Brazil? Are you sure the 1.ndiansdo not have histoplasmosis or some other condi-tion that would cross-react and you wouldappear to be getting a tuberculin that mayunrelated to the exposure to the disease?

SaIzano: Dr. Nutels will probably speak aboutthat. But what I can say is that there are notonly problems in relation to the nonspecificreaction but o problems of reading and the

proper injection of the solution. We have justpublished a paper on these questions in Tubercle.

Moderator: To be a little more specific, we doknow there is a high frequency of positive skinresponse to histoplasmin among many of theIndian groups of the interior, in the absence ofany tuberculin reaction. So I do not think thatin this particular instance cross-reactivity is aproblem.

Cohen: I was using that only as an example.Unless one knows what the spectrum of sensi-tivity of a population is to a test that has beendeveloped for a different population, one hassome questions about the significance.

Hilleboe: I had the same question on thissmall point, ano I wondered about two things.First, was anything done to see how muchtuberculosis was really present in the groupwith positive tuberculin tests, and whether ornot there was positive sputum? Second, in thcgroup from which it was thought :.hat theinfection might have come, what was knownabout the amount of tuberculosis caused bymycobacterium tuberculosis and not atypicalstrains?

Moderator: That is just about to be discussedby Dr. Nutels.

67

73

MEDICAL PROBLEMS OF NEWLY CONTACTED INDIAN GROUPS

Noel Nutels

Before entering on the topic of this paper,I should like to present a few questions on themeaning of "newly contacted Indian groups":To what period of time should this classificationbe objectively applied? Might not a group classi-fied as newly contacted have had direct or in-direct contacts previously ignored? How do wedefine a tribe that has had one and only onerapid contactfor example, eighty years ago?How would we classify groups of Indians who,living in isolation in their own primitive en-vironment, have had rare, intermittent, and briefcontacts during the past sixty years? I shall notattempt to answer these questions. My aim inthis paper is simply to mention facts and reporton my personal experience, not to interpret them.

In considering the deficiencies of such a studyit is necessary to take into account the difficultiesthat prevail in this enormous and primitiveregion, lacking in means of transportation andcommunication, where a diyersed and almostevtinct population still live as in the Stone Age.

According to various authors cited by Wag ley(20), the native population of Brazil at the timeof the discovery is estimated at 1,500.000. Nowa-days this population, scattered over the nationalterritory, is reduced to approximately 80,000Indians living in tribal conditions. Among thecauses of this decline, infectious diseasesattimes used deliberately as a means of extermina-tion by so-called civilized menhave perhapsbeen the most efficient (13). Many are thedocumented instances of extermination of theindigenous copulation through grippe, measles,

68

smallpox, venereal diseases, malaria, and otherdiseases (15).

In 1946, the Brazilian Government createdthe Xingu National Park in an area of 22,000square kilometers in the upper basin of theXingu River, one of the largest tributaries of theAmazon, at an altitude of 820 feet (see Fig-ure 1). This region in the geographical heartof the country was considered by zoologists,botanists, anthropologists, and other specialiststo be representative of primeval Brazil from thestandpoint of flora, fauna, and human condi-tions. The present population is approximately1,000 Indians distributed among the KamaiurA,Kalapalo, Kuikuro, Wauri, Iawalapiti, Aueti,Trumai, Juruna. Aupatse, Nahukwi, Matipuhy,Kajabi (since 1952), Suii (since 1960), Txu-karram5i (since 1962), and Tchicão tribes (5) .

Table 1 shows the age distribution in the groupsthat have been examined.

These fifteen tribes are autonomous. Somegroups now dispersed are to be found amongthem. There are others, not yet contacted, livingin or around the Park. The tribes belong mainlyto four linguistic groups: Tupian, Cariban,Arawakan, and Tapuyan. There is also an iso-lated linguistic group, the Trumai.

Access to the Park is almost exclusively by air,for there are no roads and river transport ispoor. Only military and other government planesmay land on the Park airstrips, and special per-mission is needed by all strangers wishing toenter. Communications within the Park arelimited by the fact that it has only one airplane,a few canoes, and a radio station.

Since its inception the Park has been directedby Orlando Villas BOas, who is famous for hispractical knowledge of the Brazilian backlands.Assisted by his brother Claudio, also well knownin this field, he keeps a very close watch on the

FIGURE 1. Location and distribution oftribes in Xingu National Park, Brazil.Inset shows location of tribes

relations between the Indians of the area andthe visitors, mainly anthropologists, ethnologists,psychologists, physicians, dentists, nurses, andothers who do research in the Park or assist theIndians in various ways.

TABLE I. Population of Xingu National Park, Brazil, in July 1967, by age group

TRIBE NO. MEMBERS

AGE GROUPS

0-4 5-9 10-14 15-19 20-29 30 AND

OVER

Kamaiuni 89 16 11 '1 9 18 24

Kajabi 152 32 21 15 13 35 36

Kalapalo 68 14 14 5 11 13 11

Juruna 49 10 8 4 6 11 10

Meinaco 35 5 6 2 8 5 9

Suiti 67 11 7 11 6 18 14

lawalapiti 34 2 8 3 3 6 12

Trumai 22 5 3 2 3 4 5

Aucti 40 9 8 6 3 14

Kuikuro 118 20 19 10 8 38 23

WaurA 62 17 14 1 7 15 8

Txukarram5i 170 36 21 19 16 33 45

Tchicio 53 9 4 5 9 22 4

Total 959 186 144 94 99 221 215

69

Is

The first known contact between this area andso-called Western civilization occurred in 1884,when the first Karl von den Steinen expeditionpassed through (18). Three years later Von denSteinen came again. Expeditions since then in-clude those of H. Meyer, in 1896; Max Schmidt,in 1900; the Rondon Commission, directed byLieutenant Ramiro Noronha, in 1920; PercyFawcett, also in 1920; Heinrich Hintermann,in 1924; the Ro. don Commission, this time di-rected by Captain Vicente Vasconcelos, also in1924; Percy Fawcett again, in 1925 (his sec-ond expedition, during which he disappeared);G. M. Doyott, in 1923; Vincent M. Petrullo, in1931; and the National Service for the Protectionof Indians, in 1940 (1).

In 189E: Kari E. Ranke, a German physicianand demographer who had participated in theMeyer expedition, reported on the diseases hehad observed (12). His account is still relevant,and I feel it is worth quoting in full:

The diseases observed in 10 Indian villages amongapproximately 800 to 1000 Indians arc the foilowinj:many healed fractures and one old haunch luxation but,according to the anamnesis, not congenital; one case ofclubfoot, congenital; a very frequent skin disease, de-

scribed as "Tinca imbriata,- from the Malayan Archi-pelago and the Southern sea; numerous furuncles, mostof them in the glutcal region; two cases of ithocy; onecase of apparently parasitical tumor in the liver. whichhad as a consequence an ascites, not very developed; akind of rheumatic disease of the joints; numerous casesof malaria and malarial "cachexia" in children under 10years old; and a fairly mild enteritis among newborninfants. The occurrence of Ieucomas and staphylomaswas extretaely frequent in the Xingu area. Among theBakairi from Kulisehu, none had been spared.

With ihe help of a Bakair: from Paranatinga, thefamous Antonio, who up to now has accompanied allexpeditions to the Xingu arca, I learned the history oftheir existence. Once, after the second expedition to theXingu arca, the Bakairi from Kulisehu went to Parana-tinga and from there proceeded to Rosario. They werewekomed, and, although they had no knowledge of theBrazilian language, they were immediately baptized andafter a few days' stay they went back carrying a heavyload of gifts.

One of the tribesmen acquired an ophthalmic blen-norrhagia in Rosario, which spread after his return tothe Bakairi village on the Kulisehu and became a terri-ble epidemic. All the inhabitants were affected; somedied, othcrs survived with the loss of an eye or withleucomas. The numerous cases of conjunctivitis that I

70

.4

myself saw were all of a benign nature, so I think thatthe gonococcus has vanished from the Xingu area. Itseems rather peculiar that I found no sign of it, not evencongenital, and that it had not spread throughout theIndians or affected their sexual organs.

Leprosy, syphilis, and tuberculosis are totally non-existent in the Xingu area. The nonexistence of tuber-c-losis is of the greatest significance, since whereverIndians come into direct contact with whitc men, terribledevastation results.

It may 'also be that measles, scarlet fever, and small-pox are likewise unknown in the Xingu area, althoughwe a re not m) sure about their nonexistence at timeof our visit as we are in the case of the previouslymentioned diseases. Only in the case of smallpox canwe assure its nonexistence, because we found no onedisplaying smallpox scars.

In 1946 the white man took firm hold of theregion, though not in large numbers. Beforeentering the area that later be-ame the XinguNational Park, they were all given a medicalexamination. Between 1947 and 1950, in mycapacity as a doctor in the Roncador-Xinguexpedition, I imposed a sort of moral and sani-tary quarantine on every person entering theregion. Thus we were able to prevent venerealdiseases and to piotect the Indian women hornthe "civilized" men who would have competedwith the native males.

At the time of their first contact with tht. Ron-cador-Xingu expedition of 1946, about 25 Kala-palo Indians died in an outbreak of grippe (5).Another outbreak was recorded in 1950 in thesame tribe and also in the Karr ayuni tribe,killing 12 persons this time. In June 1954 thcrewas an epidemic of measles in the upper Xingu(7). Neither from the recollections of the eldersnor from the unditions of any of the tribes werewe able to gather information about it. EveryIndian who came in contact with the Roncador-Xingu expedition at that time was struck bythat outbreak. Of the 654 patients, 114 died.Among those who received medical care, thedeath rate was 9.6 per cent; among those whocould not be treated in time, it reached 26.8per cent.

Following is a list, on which I shall makeno comment, of the diseases observed by usand other doctors who have been in the area:endemic malaria (Anopheles darlingi, Plasrno-

chum vivax and P. falciparum); Tinea imbrt-cata; gastroenteritis; a purulent lung abscess ofunknown etiology; furunculosis; childhood um-bilical hernia; arthritis deformans; helminthia-sis; pemphigus foliaceus; gallstones; Blastomy-cosis cheloidiana (Paracoccidioides Loboi) (3);warts; polymorphous acne; pediculosis; Pityria-sis alba; gravidic striation; Pulex penetrans;conjunctivitis; pigmentary and cellular nevi (6);leucoma; pinguecula; pterygium; pupillary seclu-sion; melanic pigmentation of the conjunctiva;chalazion; cataract; ocular hypotension; talipes;malarial hematological disturbances (17); de-formation of the auricular pinna due to a fight-ing game called huca-huca; atrophy of the lowerlimbs due to the ritual custom of prolonged con-striction in infancy; scapulo-humeral luxation;tegumentory leishmaniasiF (4); reversible pa-ralysis of the lower limbs due to ritual ingestionof rnucund (Dolichos pruriens and/or Dolichosurens); toxoplasmosis, recently discovered (2);filariasis (2); and various arboviruses, recentlydiscovered (2).

Since I believe that the purpose of my par-ticipation in this meeting is to tell about mypersonal experience in deali.ig with groups ofrecently contacted Indians, I shall concentrateon tuberculosis, which is the inain field of myobservations. Beginning in 1952, at first withX-ray and sometimes with old tuberculin (Von

Pirquet modified: cutipuncture) and since 1960with purified tuberculin (PPD-Rt 23-1 UT), Ihave investigated tuberculosis not only in thePark but also in other hiclian villages, boththose contacted long ago and those that havejust been contacted (Table 2).

In 1952 the Kajabi Indians came to the Parkfrom the Teles Pires River, in the valley of theTapajcis River, bringing with them Blastorny-cosis cheloidiana (Jorge LObo's disease) (3).This group had already been in contact withwhite men in its origilial area.

In 1960 the Villas BOas brothers establishedcontact with the SuiA tribe. This small groupof approximately 80 Indians had had onlysporadic encounters, over a three-day period,with the first Von den Steinen expedition in1834. At that time Von den Steinen estimatedtheir number at 150. No other encounter wasrecorded, even by Von den Steinen himself onhis second expedition in 1887 (19). The pres-ence of the Sui6 group on the upper ParanajubaRiver was known because of their periodicattacks on other tribes, for which they weregreaty feared. A few days after the Villas Mascontact had been established, we were able toinclude 42 members of the tribe in our tuber-culin survey (PPD-Rt 23-1 UT). Though atthat time we did not have much suitable equip-ment and had had little experience with PPD,

TABLE 2. Reactions to tuberculin test (PPD-Rt23-1 UT) in ndian tribes ot Xingu National Park. Brazil. July 1960

TRIBE

NO.

TESTED

TESTS READ

TOTAL

0-4 NiNt 5-9 SIM 10 MM

NO. NO. NO.

Karnaiurti 76 76 74 97.4 2 2.6Kajabi 63 63 60 95.2 1 1.6 2 3.2Kalapalo 51 51 51 100.0Juruna 45 45 45 100.0Meinaco 38 38 36 94.7 2 5.3Suia 42 42 34 81.0 1 2.4 7 16.6lawalapiti 37 37 37 100.0Trumai 17 17 17 100.0Aucti 15 15 15 100.0Kuikure, 3 3 3 100.0Wauri 2 2 1 50.0 I 50.0

Total 389 389 373 95.9 5 1.3 11 2.8

71

77

we found eight positive rea-.:tions-one weakand seven strong-among this population, foran infection rate of 19 per cent. We also, onthat occasion, gave the PPD test-again for thefirst time-to the other tribes of the upperXingu, finding infection rates of 3.2 per centamong the Kajabi and 5.3 per cent among theMeinako. The former, as I have said, had hadcontact with civilized men before settling in thePark. The Meinako reactors, furthermore, hadspent a few months in the city of São Paulo (8).The other tribes were to-ind to be nonallergic.Subsequent research with X-rays revealed casesof lung shadows among the Sui6, and in 1967,for the first time, we were able to obtain fromthem a positive sputum by BK. In spite of allthe natural difficulties, we were able to take aculture of bacilli in a Su la solution to the Cen-tral Tuberculosis Laboratory in the State ofGuanabara, where they are being studied byProfessor Milton Fontes Magark and his staff( Tables 3, 4, and 5).

In 1965, 180 Indians of the Txukarram5itribe, fleeing the pressure of so-called pioneerfronts (in this case a group of garimpeirns,prospectors of precious stones and metal), soughtrefuge in the Park. These Indians, who belongto the Kayapó (Tapuyan) group, settled in aplace called Porori, on the left bank of theXingu River. When observed in 1962, this tribehad shown a low rate of tuberculin infection(Table 6). In 1966, after the Txukarraniii hadalready settled in the Park, we classified 158 ofthem in our thoracotuberculin file and examinedtheir sputa (Table 7) (10). Three persons re-

TABLE 3. Reactions to tuberculin test (PPD-Rt23-1 UT)among Suii Indians of Xingu National P.irk, Brazil,June 1960

AGE NO.

TESTS READ

0-4 5-9 10

MM MM MM

GROUP TESTED NO. NO. 510 NO. %

Adults 21 17 80.9 - 4 19.1Children 21 17 80.9 1 4.8 3 14.3

Total 42 34 80.9 1 2.4 7 16.7

TABLE 4. Reactions to tuberculin test (PPD-Rt23-1 UT)by age group among Suizi Indians of Xingu NationalPark, Brazil, August 1966

TESTS READ

AGE

GROUP

NO.

TESTF.D

0-4NiNt

5-9MM

10

MM

NO. 7-0 NO. NO. Je

0-4 8 8 100.0 -5-9 10 9 90.0 - 1 10.0

10-14 13 11 84.6 2 15.415-19 5 4 KO - 1 20.020-29 22 17 77.3 1 4.5 4 18.2

30 andover 13 7 53.8 - 6 46.2

Total 71 56 78.9 1 1.4 14 19.7

vealed BK in their sputa. Moreover, we dis-covered other strongly positive cases presentingradiologic forms of the type that do not usuallyreveal BK in direct sputum analysis, such as,for example, two ganglionary forms. All weretreated with INH, PAS, and SM (Table 8).

In 1967 there came to the knowledge of thePark administrators the fact that a tribe of com-pletely isolated Indians-the Tchikk-were be-ing pressed by anothei group of prospectors.These Indians used to live on the banks of thejatobá River, a subtributary of the Xingu. Thefew contacts they are known to have had con-sisted of attacks against other tribes living inthe Park, from whom they attempted to take

TABLE 5. Reactions to tuberculin test (PPD-Rt23-1 UT)by age group among Suii Indians of Xingu NationalPark, Brazil, July 1967

TESTS READ

AGE

GROUP

NO.

TESTED

0-4Nti4

5-9NiNt

10

sukt

NO. 7.0 NO. NO. 470

0-4 11 11 100.0 ^5-9 7 4 57.1 3 42.9

10-14 11 8 72.7 3 27.315-19 6 4 66.7 2 33.320-29 18 14 77.8 4 22.239 and

Over 14 6 42.9 - - 8 57.1

Total 67 47 70.1 - - 20 29.9

72

8

TABLE 6. Reactions to tuberculin test (PPD-Rt23-1 UT)among Txukarramiii Indians of Xingu National Park,

Brazil. 1962

AGE

TESTs READ

NO.

0-4 5-9 10Nt.Nt

GROUP TEST ED NO. % NO. NO. (70

Adul ts 19 17 89.4 1 5.3 1 5.3

Children 20 20 100.0 - -Total 39 37 94.8 1 2.6 1 2.6

women and utensils. In order to prevent indis-

criminate and undisciplined contact with mem-bers of our civilization, the administrators wereable to resettle the whole 54-member tribewithin the boundaries of the Park. We werethen able to give these newcomers the tuberculintest at the moment of their arrival, with negativeresults.

In 967 we repeated the research among theTxukarrarniii and verified, this time, an absenceof bacilli in the direct sputum analysis and theradiological regression of lung shadows in spiteof an increase in the general rate of infection.This result was perhaps due to better equipmentand technique employed in the test (Table 9).

We were surprised at both the clinico-radio-logical and the epidemiological aspects of tuber-culosis in populations so primitive as the Suia'and the Txukarramai. It was to be expected,once the disease was found among them, that

TABLE 7. Reutions to tuberculin test (PPD-Rt23-1 UT)by age group among Txukarramii Indians of XinguNational Park, Brazil, August 1966.

TESTS READ

AGE

GROUP

NO.

T EST ED

0-4MM

5-9ikiNt

10

MM +NO. NO. /0 NO.

0-4 36 31 86.1 1 2.8 4 11.1

5-9 25 19 76.0 2 8.0 4 16.0

10-14 15 10 66.7 2 13.3 3 20.015-19 16 14 87.5 - 2 12.5

20-29 28 18 64.3 1 3.6 9 32.1

30 + 38 23 60.5 5 13.2 10 26.3

Total 158 115 72.8 11 7.0 32 20.2

TABLE 8, Findings of tubreculin tests, X-rays, andbacilloscopy in Txukarram5i tribe of Xingu NationalPark, Brazil, August 1966

PULMONARY

SHADOWS

TUBERCULIN TESTS

TOTAL

0-4MM

5-9M M

10

MM

MinimumModerate

- -- 1

2(16)1

.-,Advanced 1* 1 1* 3

Pulmonary Ganglion 1 1 2 4

Pleural - - - -Total 2 2 6 10

No. X-rayed 105 11 32 148

Percentile ofpulmonary shadows 1.9 18.2 18.7 6.7

*Positive sputum.

an epidemic would have occurred that wouldhave presented differ .it foi ms such as the so-called infant form in adults and the rapidlyevolving acute and miliqry forms, similar tothose found among the Senegalese soldiers takento France during the First World War (16).Such dramatic epidemics among primitive peo-ples are often described in medical literature.Nevertheless, we were able to verify that amongthe SuiA and Txukarram5i the forms were thesame as those that often occur among civilizedwhite people, whose natural and acquired re-sistance gives them means to thwart the evolu-tion of the disease. The X-rays presented here(Figure 2) leave no doubt, in my view, that

TABLE 9. Reactions to tuberculin test (PPD-Rt23-1 UT)by age group among Txukarram5i Indians of XinguNational Park, Brazil, July 1967

TESTS READ

AGE

GROUP

NO.

TESTED

0-4mid

5-9MM

10

MM

NO. (70 NO. % NO.

0-4 34 32 94.0 1 3.0 1 3.0

5-9 20 13 65.0 1 5.0 6 30.0

10-14 19 13 68.4 1 5.3 5 26.3

15-19 16 12 75.0 - 4 25.0

20-29 33 16 48.5 1 3.0 16 48.5

30 + 44 26 59.1 2 4.5 16 36.4

Total 166 112 67.5 6 3.6 48 28,9

tuberculosis among these Indians, in its clinical,radiological, and even epidemiological aspects,can be equated with that of peoples with a longexperience with BK.

Had these tribes at one time undergone a so-called epidemic period of tuberculosis like otherpeoples? This question is not easy to answer.Is it possible that the BK responsible for thedisease among them is less virulent than thatresponsible for the disease among whites? Thishypothesis may be answered by the result ofProfessor Magarao's research mentioned above.

In any case, we believe that the Park is anappropriate environment for planned and con-trolled scientific research on the response ofprimitive populations to the introduction oftuberculosis and other infectious or noninfec-tious diseases by white invaders.

I consider it useful to conclude with Table 10,which shows the rate of tuberculosis infection

TABLE 10. Reactions to tuberculin test (PPD-Rt23-1UT) by age group among three tribes of Mato GrossoState, Brazil, September-October 1965

TESTS READ

0-4 5-9 10

AGE

GROUP

NO.

TESTED

MM MM MM

NO. % NO. % NO.

0-7 584 559 95.7 4 0.7 21 3.68-14 634 537 F4.7 37 5.8 60 9.5

15-49 746 525 70.4 71 9.5 150 20.150+ 145 98 67.6 19 13.1 28 19.3

Total 2,109 1,719 81.5 131 6.2 259 12.3

among the Terena (11), Kayua, and KadiweuIndians living in the southern part of MatoGrosso State, who have been in close contactwith white civilization for at least a hunderdyears (9).

REFERENCES

1. BALDUS) H. Bibliografia Critica da EtnologiaBrasileira. São Paulo, Comissão do IV Centethio daCidade de S5o Paulo, Serviço de ComemoraciksCulturais, 1954.

2. BARuzzi, R. G. Determination de l'Etat deSante d'un Groupe d'indiens lsoles et des MesttresProphylatiques Necessaires a leur Preservation, Par-que Nacional do XingU, Brésil. Memoire présentel'Institut de Medicine Tropicale "Prince Leopold".Anvers (Belgique), 1967.

3. BARUZZI, R. G., C. D'ANDRETTA JR., S. CAR-VALHAL, 0. L. RAMOS, and P. L. PONTES. Ocorrenciade blastornicose queloideana entre indios Caiabi.Rev. Into. Med. Trop. são Paulo 9(3) :135-142.

4. CARNERI, I., N. NUTELS, and J. A. MIRANDA.Epidemia de leishmaniose tegumentar entre osindios Waurli do Parque Nacional do Xing6. Rev.Inst. Med. Trop. São Paulo 5(6) :271-272, 1963.

5. GALvAo, E. Cultura c sistema de parentesco dastribos do Alto Xing6. Antropologia (Rio de Janeiro)No. 14, 1953.

6. MATTOS, R. B. Acuidade visual para longe efrequencia de discrornatopsia em indios brasileiros.Descricão de alguns aspectos oftalmológicos emindios examinados. Tese apresentada para o concursode docencia-livre da cadeira de clinica oftalmologicada Escola Pau lista de Medicina. São Paulo, 1958.

7. MOTA, J. L. DA. A epidemia de sarampo noXingt;. Condensação do relat6rio em 10 de outubro

de 1954 apresentado ao Diretor do S.P.I. (pp. 131-141). Rio de Janeiro, Servico de Proteção aos Indios,1955.

8. NUTELS, N., and L. V. DUARTZ. SUSA-1960:Cadastro tuberculinico na Area indigena. Separatada Rev. SNT 5(1 9):259-270. Rio de Janeiro, !961.

9. NUTELS, N., J. A. NUNES DE MIRANDA) EJGEL,

I. YAMASAKI, and A. FRAGA HAUTEQUEST. A tividadesdo SUSA em 18 aldeiamentos indigenas do Sul doMato Grosso. Rev. SNT 11(41), 1967.

10. NUTELS, N., M. AYRES, and F. M. SALZANO.Tuberculin reactions, X-ray and bacteriologicalKudies in the Cayap6 Indians of Brazil. Tubercle48(3), 1967.

I I. OLIVEIRA, R. C. DE. 0 processo de assimilacaodos Terina. Rio de Janeiro, Museu Nacional, 1960.

12. RANKE, K. E. Beobachtungen Ober Bevolke-rungsstand und Bevölkerunsbewegung bei IndianernCentra1-Brasiliens. Correspondenz-Blatt der Deut-schen Gesellschaft far Anthropologic', Ethnologicund Urgeschichte XXIX (11), 1898.

13. RISEIRO, D. Convivio c contarninacio. Efeitosdissociativos da depopulação prot ocada por epi-demias ern grupos indigenas. Sepa dt cologia(São Paulo) XVIH(1), 1956,

14. RIREIRO, D. Linguas e culth ,c doBrasil. Separata de Educagto e Ldric. aais.Rio de janeiro, Centro Brasileiro de PescwisasEducacionais, 1957.

15. RIBEIRO, D. Politica indigenista brasileira. Riode Janeiro, Ministerio da Agricultura, Servico deInformacties Agricolas, 1962.

16. RICH, A. R. Patogenia de la tuberculosis% Ver-sion castellana por el Dr. 0. C. Croxatto. BuenosAires, Alfa, 1946, p. 651.

17. SILVA, M. P. DA. C'ontribuição para o estudo dosangue perifdrico e d i medula 6ssea em indios doAlto-Xingti. Tese de doc8ncia-1ivre de hemato1ogiaapresentada ao Departamento de Medicina. SoPaulo, 1966.

76

18. STEINEN, K. VON DEN. 0 Brasil Central.fraduck de Catarina Baratz Cannabrava. Ri3 deJaneiro, Companhia Edit6ra Nacional, 1942. (Origi-nal edition Leipzig, Brockhaus, 1886)

19. STEINEN, K. VON DEN. Entre os aborigenes doBrasil Central. Tradu0o de Egon Schaden. Sepa-rata renumerada da Revista do Arquivo 1:XXXIVLVIII. Sfio Paulo, Departamento de Culiura, 1940.

20. WAGLEY, C. Races and Classes in Rural Brazil.Paris, UNESCO, 1952, p. 123.

DISCUSSION

Willard R. Centerwall: A Recent Experience with Measles in a "Virgin-Soil"Population'

I have elected to use the time allotted for thepresentation of recent experiences we have hadon the effect of both measles and measles vaccinein a "virgin-soil" population of South America.

In January of this year a team of seven scien-tists, representing the United States and Vene-zuela, made an expedition into the YanomamaIndian territory. The map shows the approxi-mate location of the territory, which covers anarea extending from the Equator to 5 degrees

N' ift

751 t-NoynAreimINT or MfANC.5LIVN TH4- y44,0Abtivo rihwIropy

or n Otqn, ,v,hyRk

IgNC11, VI4N,g5- APAR, *AkOM1M0 60,6,04my-,m,1110.31A7,69*-MfAiLIS fwfwOOtcea wrcYA40.4.0 001,ihry vmooga ,,r 4.'14

Ne''

61'

north latitude, deep within the tropical rainforest of the Orinoco-Amazon River basin ofVenezuela and Brazil. The expedition wasoriented toward the collection of ethnographic,genetic, medical, dental, demographic, and epi-demiological data. Three members of the teamale present here today: Dr. James Neel, theexpedition leader, who needs no introduction;Dr. Napoleon Chagnon, the anthropologistwhose work, study, and life among these In-dians since 1964 2 was so essential to our mis-sion; and myself, a pediatrician with interest inand some experience with the diseases andnutritional disorders of the tropics. This was thethird such expedition led by Dr. Neel into thisgeneral region, the first having taken place in1966 on the Venezuelan side and the second in1967 on the Brazilian side. The present expedi-tion was in essence a cooperative venture of theUniversity of Michigan and the VenezuelanInstitute for Scientific Research, and in particu-lar Drs. Layrisse and Tulio Arends of the

Institute. Both are present at this session also;thus, if what I say in the next few minutesgenerates questions, there are several resourcesavailable for possible answers.

There are believed to be about 10,000 Yano-mama Indians living in more than 100 villages

scattered throughout the region. They are veryprimitive forest-dwellers who practice a slash-

I Investigations supported in part by U.S. AtomicEnergy Commission Grant AT ( 11-1)-1552.

2 Chagnon, N. A. Yanomamo Warfare, Social Organi-zation and Marriage Alliances, Ph.D. thesis, The Univer-sity of Michigan (1966).

77

82

and-burn agriculture along with hunting andgathering. Although some mission stations havebeen established along the Upper Orinoco andits tributaries since early in the past decade, themajority of these Indians are as yet uncontactedand unaffected by the outside world.

The typical Yanomama village is a circularstockade, with families living in hammocksunder the shelter of the enclosure. In generalthe people are healthy and handsome, well pro-portioned and strong but almost pigmoid instature. Their cheerful, friendly countenancesbely the aggressiveness and hostility for whichthey are sometimes known.

Because measles antibody studies in 1966 and1967 demonstrated that this was a virgin-soiltribe and because measles was known to havepenetrated into the nearby regions, practicallysurrounding the Yanomama territory by 1967(see map), we brought along with us into SouthAmerica 2,000 doses of donated Edmonston-strain attenuated live measles vaccine, plusgamma globulin.3 Half of these doses wediverted to the mission stations on the Brazilianside, where measles was beginning to penetratethe region, and the rem inder went with us. Wehad intended to var.-,late and to advise themissionaries on the ,,rocedure toward the endof our scientific studies. We did not anticipateencountering mt:asies during our two-to-three-month expedition. It was thus a fortuitous occur-rence that our an ival into the region was almostsimultaneous with the introduction of measles(we believe for perhaps the first time) into thisterritory.

A party of Brazilian workers had, the weekbefore, come across from the Rio Negro regionin Brazil to the south. They were at the Ocamomission, at the junction of the Orinoco andOcamo rivers, when a 14-year-old boy amongthem became sick with a high prostrating fever.He was seen shortly after the onset by Dr.Marcel Roche, Direc, - of the Venezuelan Insti-tute for Scientific Research, who happened to

3 Wc arc most grateful to Parke, Davis and Co.,Phillips Roxane Laboratories, and Lederle Laboratoriesfor their donation of the vaccine.

78

be at the mission in connection with a studyon thyr Did physiology.

The boy never developed the characteristicmorbilliform rash, so the differential diagnosisfrom any of a variety of "jungle fevers" wasuncertain; nevertheless, 31 Indians and 9 Bra-zilians at the mission were vaccinated at oncewith no gamma globulin coverage. It turned outthat the boy indeed did have measles and thatvisitors to the mission meanwhile had returnedto their own villages carrying the virus in itsincubating form with them. Thus started a full-scale epidemic, which, by the time our last teammember had left the field three months later,had spread up and down river along a hundredmiles of waterways and tributaries and adjacentinland regions involving no fewer than 15villages.

Within a few weeks we had exhausted ourvaccine supply. Observations on these Yano-mama Indians of the effect of the wild measlesand of the measles vaccine with and withoutthe concomitant gamma globulin form thebasis of this report. Since it was neither con-ceived nor designed as a scientific study in itseifand since our data-collection responsibilitit!s didnot permit a prolonged stay in any oneour observations are of necessity disjointed andfragmentary, but still, we believe, of sufficientinterest and value to warrant presentation.

Most of the Indians and also the severalBrazilians we observed became very ill and pros-trate with their measles. In several Indian vil-lages where documentation was possible by di-rect examination, from 24 to 43 per cent ofthe victims had frank bronchopneumonia, withonset usually during the acute attack and some-times during the recovery phase. This seemedto respond well to antibiotic therapy. We wereunable to evaluate the possibly adverse effect ofa respiratory flu-like epidemic, which had imme-diately preceded and sometimes co-existed withthe measles epidemic. The complication of otitismedia appeared to be practically nonexistent.

We were particularly impressed with thedevastating effect of measles in its near-totalinvolvement of the Indian community. When

83

parents and children were simultaneously in-volved, there was a drastic breakdown of boththe will and the means for necessary nursingcare. We have even seen several instances wherethree generations of Indians were simultane-ously ill with measles.

The reaction of those not already prostratedin a fatalistic depression was usually one ofpanic. Sometimes the well members of thevillage even abandoned the sick, and normalcommunity structure and function were lost.Village fragments often fled to other villagesfor haven, thus increasing the spread of thedisease.

In three villages with approximately 170 casesof measles there were 29 deaths, a rate of 17.1per cent. Most of these were due to associatedpneumonia, complicated by dehydration. Thisdespite some measure of applied, though lessthan optimum, nursing care. In a fourth village,the authors were present for two days at thepeak period of measles reaction involving nearly40 Indians, a majority of them extremelyVigorous and dramatic treatment included fliidadministration, cooling measures, aspirin, andlong-acting antibiotics. No deaths occurred dur-ing our stay, but we did hear later that subse-quently two Indians died (approximately 4 percent mortality).

These and other observations supported ourfeeling that difference-, in medical and nursingcare play the major role in the measles-mortalityrate among the Indians. In this connection, itshould be recalled that the mortality frommeasles among Caucasians in the United Statesonly half a century ago was in excess of 3 percent; it has steadily dropped to a present-daylow of less than 0.1 per cent. Nearly two thirdsof this reduction occurred in the period beforethe advent of modern chemotherapy and anti-biotics.' Other evidence that the death rate inhighly susceptible groups can be substantiallyreduced by eleinentary organization and medicalcare emerges from a 1954 study on a measlesepidemic among the Eskimos of the Canadian

4 Langmuir, A. D. Medical importance Of measles.Atn. 1. Dis. Child. 103:224-226, 1962.

79

84

Arctic 5; in the first of two outbreaks the deathrate was 7 per cent, whereas in the second, withbetter organization and provision of medicalcare, it was only 2 per cert.

The Jse of measles vaccine permitted us tosee some of its effects on the Indians. In villageswhere we could observe and measum the effectsat their height, we found no real complicationsbut considerable reaction, especially in terms offebrile response. That this response was asso-ciated with the production of protective measiesantibodies was borne out clinically. To ourknowledge, no persons vaccinated prior to theexposure to measles later developed the disease.This protective value of the vaccine showed upin peculiar ways, as for example in the case ofan unvaccinated mother who Ezcame very iiiwith measles while her previously vaccinatedand healthy youngver was playing about andpestering her for attention she could not give.This is just the reverse of the situation com-monly seen in civilized societies.

Searching the literature for reports of reac-tions of other peoples to similar vaccine bothwith and without concomitant use of gammaglobulin, we observed that these Indians in gen-eral seem to react with a greater febrile responsethan has been reported in North American Cau-casians," Europeans,' Icelanders," Africans"' °and Micronesians.'" Again, however, as with

Pert, H. F. W., and F. P. Nagler. Measles in theCanadian Arctic, 1952. Canad. I. Pub, Health 45:146.156. 1954.

" Krugtnan. S., J. P. Giles, A. M. Jacobs. and H. Fried-man. Studies with live attenuated measles vi,us vaccine.Am. 1. Dis. Child. 103:353-363, 1962.

T Cockburn, W. C., J. Pecenka. and T. Sundaresan.WHO-supported comparative studies of attenuated livemeasles virus vaccines, Bull. Wld. Hlth. Org. 34:223231, 1966.

" Gudnadotter, M.. and F. L. Black. Response of adultsin Iceland to live attenuated measles vaccine. Bull. Wld.Hlth. Org. 30:753-762, 1964.

Mey'r, H. M.. Jr., D. D. Hostetler, Jr., B. C. Bern-heim, N. G. Rogers. P. Lambin, A. Chassary, and J. E.Smadel. Response of Volta children to live atten hatedmeasles virus vaccine. Bull. Wld. Hlth. Org. 30:760-781.1964.

Brown, P.. M. Basnight, and D. C. Gajdusck. Re-sponse to live attenuated measles vaccine in susceptibleisland populations in Micronesia. Am. 1, Epidem. 82:115-122, 1965.

the wild measles, we are unable to define accu-rately the role of concurrent respiratory infec-tions in enhancing the reaction to the vaccine.

Summing up, although the evidence for ge-netic influences in mammalian resistance to awide variety of diseases is of course incontro-vertible, the present data nevertheless suggestthat given a comparable previous disease experi-ence (other than measles), similar care when ill,and a less resigned attitude toward the prospectof death, the death rate from measles in a pre-viously unexposed Indian population would notbe much greater than in a group of "virgin-soil"civilized Caucasians whose ancestors had beenrepeatedly exposed to the experience of measles.There is thus, in our opinion, only very limitedevidence for a greater innate susceptibility ofthe Indian to this disease. It seems likely thata re-evaluation is in order with respect to theprimary susceptibility of the Indian to certainother diseases of civilization, such as pertussis,smallpox, and tuberculosis.

General Discussion

Moderator: As I am sure you gathered fromthat capsule presentation, there were some prob-lems in conducting our-elves like calm and de-tached observers in the midst of a measles epi-demic. And when it was all over, we realizedthat in many respects we had failed to documentthis experience adequately.

Dr. Nutels in his presentation gave data onhow the mortality rate in an Indian group canbe lowered by even what I think he would agreeis less than adequate medical care. Certainlythis was our experiencethat the mortality ratefor Brazil and Venezuela in this epidemic wouldrun under 10 per cent, which is a half to a thirdof what is often reported. It is very difficult tosay how much lower this rate would go if thesewere Indians given the kind of care that aCaucasian would receive today in Europe or inthe United States, but we believe it would dropdown to a few per cent.

The other side of the coin, of course, is

revealed by Caucasian populations that aftercenturies of exposure to measles have somehow

80

be7ome "virgln-soir populations and have thenexperienced an epidemic of measles. The classicexample is the epidemic Dr. Peter Panum re-ported from the Faroe Islands. A Danish popu-lation had been free of measles for some 65years and then was stricken much as an Indianvillage is stricken.

I was most impressed by Dr. Nutels' remarksabout tuberculosis and what I took to be hisquestioning attitude toward how differently theIndian reacts to it. Now, quite aside from itstheoretical interest, this seems to me a matter ofgreat practical importance. If we believe thatthe Indian is more susceptible to tuberculosisor measles or pertussis, we are apt to be satisfiedwith less than optimal clinical results in themanagement of those diseases. But if we thinkhe is no more susceptible than we are, then wewill not settle for anything less than the best.This is perhaps an important point that has beenlost sight of in the past.

McDermott: I think both of these presenta-tions represent very fine contributions to ouraccumulating knowledge on this subject. Inprevious meetings of this committee, several ofusamong them Dr. Neel and Iexpressed thebelief that evidence that a genetic predispositionplayed a significant part in measles and tubercu-losis should be very sharply challenged. Indeed,we did not believe it.

It seems to me the evidence in both thesestudies is in that direction. As Dr. Nutels said,it is conceivable that the strain of mycobacteriaeither may not have been tuberculosis or maybe attenuated, but I do not think that is verylikely. The evidence he presented makes itperfectly credible that these people did indeedhave tuberculosis infection and disease. Ourchallenge to notions of genetic predispositionarises from our greater knowledge nowadays ofhow these two particular infections, measles andtuberculosis, are spread. Both can be spread(though this is not necessarily the only way) bywhat is known as the airborne route. When thisis possible a whole constellation of circumstanceshaving to do with the culture, and f n particularthe material culture and way of living, then

obtains: So far as measles is concerned, we ilustremember first of all that it may be a verysevere disease in any adult. Adults with measlesare just as sick as the adults Dr. Centerwall wasdescribing.

Secondly, the incidence of complications ofmeaslesand the complications are what peopledie ofcan be very high, depending upon theage at which the infection is acquired. Seventy-five per cent of the post-measles complications inNew Delhi, for example, where they have largenumbers, occur under the age of 18 months. Inthe particular circumstance of primitive societieswith high sustained fertility, a high proportionof the population exposed is extremely young.

As for tuberculosis, I think the evidence iseven clearer, because work over decades hasproved the need to distinguish between tubercu-losis infection and tuberculosis disease. It is onlysince the infection has become less prevalentthat we have been focusing on it and hence havenumbers on which to base greater understanding.

Tuberculosis infection can be spread andprobably usually is spread by the airborne route.This means several things. One is thr.,t the infec-tious agentin this case the tubercle bacillican be suspended in the air and in an enclosedspace will remain in that air whether a humanis there or not; anyone entering the room couldacquire the infection. How long the air will staypoisoned is net known, but it is an appriableintervala matter of an hour or two. And theactual event of infection takes place presumablyin a flash. This is relevant to contacts with pre-viously unexposed populations.

In any case, the evidence now is quite con-vincing that given the proper physical circum-stances for the transfer of tubercle bacilli fromone person to another, circumstances such as arefrequently seen in unventilated huts in aboriginalor primitive societies, there is no inherent im-

81

munity against infection with tubercle bacilli.By this I mean that practically all members ofa group exposed under the proper circumstances,irrespective of their diet or way of life or levelof civilization or anything else, will becomeinfected. We know of course that infection leadsto disease in only a minority of those infected;the exact percentage is not known. If we had,let us say, 10 per cent diseased in a society thatwas virtually 100 per cent infected, we mightsimply think that 10 per cent is an awful lot oftuberculosis and hence that this group of people,this race, is especially predisposed to it, whereasin point of fact they may have no more tubercu-lous disease per infection than any other group.It is simply that the particular circumstances oftheir society allow infection to be more prevalent.

Now with both tuberculosis and meerles, andcertainly with measles in infancy, there is ofcourse an additional factor: nutrition. Malnutri-tion and lack of high-quality protein are char-acteristically present in the so-called unaccul-turated societies. What I am really saying is thatour knowledge of the pathogenesis of both in-fections now gives us perfectly credible alterna-tive explanations for what has been seen withoutits being necessary to invoke the idea of a sig-nificant hereditary predisposition.

Behar: How was the nutritional status of thechildren in that population determined?

Centerwall: By simple inspection and physicalexamination. The nutritional status of the 2.hil-dren was remarkably good as a whole. Therewere a few areas in which there was active

malaria, and some of the children were sick withthat. But in general they were fine. There wasno evidence of the protein deficiency seen inIndia and other tropical areas of the world.

Moderator: The next part of our program isdevoted to some special medical problems af-fecting Indian populations.

THE PROBLEM OF GALLBLADDER DISEASE AMONG PIMA INDIANS

Thomas A. Burch, Leonard J. Comess, and Peter H. Bennett'

Introduction

The etiology of gallbladder disease is uncer-tain, though the problem has excited consider-able speculation and controversy. Diet (11),female hormones (10), obesity (16), and dia-betes (13) have all been said to be associatedwith cholelithiasis. In addition, differences in thefrequency of gallbladder disease among variousracial groups have been noted. On the basis ofautopsy data Caucasians have been reported tohave a higher frequency of gallstones thanNegroes (6), and several studies based on hos-pital admission rates have suggested that Ameri-can Indians have a still higher prevalence of gall-bladder disease (9, 12, 15). A recent epidemio-

Presented by Dr. Burch.

TABLE I. Prevalence ot documented gallbladder disease

logic study (5) has confirmed the higher preva-lence of "clinical gallbladder disease" amongPima Indians than was established by identicalcriteria among the predominantly Caucasiancommunity of Framingham, Massachusetts (7)(Table I).

The purpose of this paper is to report pre-liminary data on a partly completed epidemio-logic study of gallbladder disease based on chole-cystography in a population sample of PimaIndians, a Uto-Aztecan tribe living in the des,...rt.of the southwestern United States.

Methods and materialsSample selection

Since 1963, the Clinical Field Studies Unit ofthe National Institute of Arthritis and Metabolic

in Framingham community and among Pima Indians

AGE AT

ENTRY

INTO

STUDY

(YEARS)

FRAMINGHAM GROUP

NO.

AT RISK

WITH DISEASE

PIMA INDIANS

NO.WITH DISEASE

NO. AT RISK NO.

Males30-39 832 1 0.1 51 1 2.040-49 779 7 0.9 45 1 2.250-62 725 23 3.2 57 7 12.3 n

Total 2,336 31 1.3 153 9 5.9 n

Females30-39 1,037 24 2.3 45 16 35.6 n40-49 963 58 6.0 51 20 39.250-62 873 88 10.1 62 21 33.8

Total 2,873 179 5.9 158 57 36.0 n

n p < 0.01.

82

Diseases has been performing prospective studiesof the natural history of arthritis (2) and dia-betes mellitus (14) among Pima Indians livingon the Gila River Indian Reservation in Arizona(see Figure 1).

A house-to-house census of the Gila RiverReservation was compiled, using aerial surveyphotographs to ensure that all houses werevisited. Attempts are made to examine eachreservation Indian aged fifteen years and overevery two years. This biennial examination in-cludes a 75-gram oral glucose tolerance test; ahistory and physical examination pertaining pri-marily to diabetes and arthritis; radiographs ofthe chest, cervical spine, hands, feet, pelvis,thigh, and calf; a 12-lead electrocardiogram;photographs of both optic fundi; a bio-thesi-ometer examination (quantitative test of vibra-tory sensation in both great toes and index fin-gers); a urinalysis; and determinations of serumcholesterol, creatinine, uric acid, hematocrit, andrheumatoid factor by sheep-c:ell agglutinationand bentonite flocculation titers. In addition, theblood of each subject examined has been typedfor several blood groups.

A sample of 600 Pima Indians was selectedwith random numbers for a study of gallbladderdisease. This sample consisted of 50 males and50 females in each of the six decades between15 and 74 years of age. Since the gallbladderstudy was started on 1 February 1967, 258 ofthe 600 members of the sample have attendedthe Unit for their comprehensive biennial ex-amination. The subjects were selected accordingto their age at the time of the census (as of 1January 1966), but in the present analyses theyhave been grouped according to their age at thetime of the examination for gallbladder disease.

Cholecystogram procedure

Eight Telepaque 2 tablets were ingested on theevening prior to examination and the respondentwas instructed to take nothing thereafter bymouth except water until the cholecystogramhad been completed. Prior to the examination,

2 lopanoic acid manufactured by Winthrop Labora-tories. New York.

each respondent verified that he or she had fol-lowed the instructions. No attempt was madeto cleanse the bowel with laxatives prior to thecholecystography.

Initially two radiographs, a 14" x 17" PAscout film of the abdomen and a 10" x 12'oblique film of the right upper quadrant, weretaken on each respondent. If the gallbladder wasidentified on either of these views, a 10" x 12"upright PA and a 10" x 12" right lateral decubi-tus view of the right upper quadrant were ob-tained. After this, most respondents were givena fatty meal consisty of 30 cc. of Cholestim 3gallbladder stimulant and either the upright orthe decubitus film was repeated.

Respondents in whom no gallbladder couldbe identified on the scout and oblique films wereconsidered to have a nonvisualizing gallbladder,and an attempt was made to perform a repeatcholecystogram on them four to six weeks later.

Clinical gallbladder disease at surgery or bycholecystography had been documented previ-ously in 60 of the 258 members of the samplewho have attended the NIAMD Clinic since thebeginning of the gallbladder study. An oralcholecystogram has been performed on an addi-tional 132 of these respondents. The present re-port analyzes the findings on this subsample of192 Pima Indians.

Of the remaining 66 respondents, 61 did nothave a radiologic examination-8 because of acontraindication to the procedure, 43 becausework or school made it impossible for them toreturn at the specified time, and 10 because theyrefused cholecystography. Five respondents wereexcluded because of the poor technical qualityof their radiographs.

Criteria for Gallbladder Disease

The diagnosis of previously documented gall-bladder disease was based on either a hospitalrecord of gallbladder surgery, the patient's his-tory of having had gallbladder surgery, or ahospital record of an abnormal cholecystogram(stones or a nonvisualizing gallbladder).

" Distributed by Gencral Electric X-Ray Department,Milwaukee.

83

1431

L.*SALT LAKE CITY

UNITED PUEBLOS

ALEinuat

M E X

Hi

I C

FIGURE 1. Indian reservations of southwestern United States. Gila River Reservation is a lower left.

84

The cholecystograms performed at the Clini-cal Field Studies Unit Clinic were analyzed forthe patient's clinical record by a radiologist ofthe Division of Indian Health. All radiographswere reanalyzed by one of us (L. J. C.) prior tothis report without knowledge of the age or sexof the respondents. A disagreement in interpre-tation was noted in only eight instances; thesecases were carefully re-evaluated (by L. j. C.)without reference to the previous readings andthe new interpretation was used.

Results

Prevalence of gallbladder disease

Table 2 shows that gallbladder disease wasextraordinarily prevalent in both male and fe-male Pima Indians. In males the disease fre-quency increased with age, with 66.7 per centof those aged 65 years and over affected; infemales the prevalence of disease was strikinglyhigh after the age of 24 and reached a remark-able 92.6 per cent in those 65 and over.

As Table 3 indicates, 6 of the 21 Pima maleswith disease had previously been diagnosed bycholecystectomy or an abnormal hospital gall-

TABU 2. Prevalence of gallbladder disease in PimaIndians

AGE

NO.

EXAMINED

WITH GALLBLADDER

DISEASE

NO.

Males15-2425-3435-44

5

69

0.0

0.0

11.1

45-54 10 4 40.0

55-64 11 6 54.5

65 and over 15 10 66.7

Total 56 21 37.

Females15-24 11 9.1

25-34 18 13 72.2

35-44 33 22 66.7

45-54 28 19 67.9

55-64 19 12 63.2

65 and over 27 25 92.6

Total 136 92 67.6

TABLE 3. Diagnosis of gallbladder disease in sample

METHOD OF DOCVMENTATION MALES FEMALES TOTAL

Total examined to date 56 136 192

Normal cholecystogram atCFSU Clinic 35 44 79

Number with gallbla&kr disease 21 92 113

Cholecystectomy 5 41 46

Abnormal cholecystogram athospital 1 13 14

Gallstones 2 2

Two nonvisualizations 7 7

One nonvisualization 4 5

Abnormal cholecystogram atCFSU Clinic 15 38 53

Gallstones 3 14 17

Two nonvisualizations 7 9 16

One nonvisualization 5 15 20

bladder radiograph. Thus, 15 (30.0 per cent) of50 Pima males without known gallbladder dis-ease had abnormal cholecystogram. Of 92 af-fected females, 54 were previously known; thus,abnormal radiographs were demonstrated in 38(46.3 per cent) of the 82 Pima females withoutpreviously diagnosed disease.

In 5 males and 15 females who were examinedat the Clinical Field Studies Unit Clinic, thediagnosis of gallbladder disease was based ononly a single nonvisualization. However, whencholecystograms were repeated on these 20 cases,17 (85.0 per cent) had either second nonvisuali-zations or gallstones on the repeat radiographs.

85

Morbzdity from gallbladder disease

In Table 4 the clinical importance of gall-bladder disease among Pima Indians is shown.Among males, "silent" gallstones were relativelyfrequent: only 6 (28.6 per cent) of the 21 af-fected males related "gallbladder symptoms" 4or had a history of such symptoms noted in theirmedical records. Among the females, however,gallbladder disease resulted in considerable mor-bidity: 39 (42.4 per cent) of the 92 affectedfemales had had fu previous cholecystectomy andan additional 25 (27.2 per cent) had had gall-

4 Defined as an affirmative answer to the question"Have you ever had pain in your stomach or vomitedafter eating certain kinds of food?"

00

TABLE 4. Morbidity from gallbladder disease in Pima Indians

MALES FEMALES TOTAL

NO. NO. NO.

Total examined 56 100.0 136 100.0 192 100.0

With gallbladder disease 21 37.5 92 67.6 113 58.9

Postprandial abdominal pain or nausea 6 10.7 64 47.1 70 36.5

Cholecystectomy 5 A.9 39 28.7 44 22.9

Abn. cholecystogram (hospital) 1 1.8 13 9,6 14 7.3

Abn, cholecystogram (CFSU) 0 0.0 12 8.8 12 6.3

No postprandial distress 15 26.8 28 20.6 43 22.4

With no gallbladder disease 35 62.5 44 32.4 79 41.1

Postprandial abdominal pain or nausea 5 8.9 7 5.1 12 6.3

No postprandial distress 29 51.8 33 24.3 62 32.3

No information 1 1.8 4 2.9 5 2.6

bladder symptoms but still retained their gall-bladders. Thus, 64 (69.6 per cent) of the 92affected females in this sample were having orhad had clinical manifestations of gallbladderpathology at the time of the examination. Theactual magnitude of gallbladder disease as aclinical problem among Pima women is bestillustrated by the fact that 64 (47.1 per cent) ofthe 136 females in this sample had symptomaticgallbladder disease.

Discussion

These data, though as yet incomplete, indicatethat the gallbladder was an extremely frequentsite of pathology among Pima Indian females.Gallbladder disease was responsible for numer-ous hospitalizations, which often culminated ina major surgical procedure with its attendantmorbidity and slight mortality. Unfortunately,we have no data on complications that may havecompounded the morbidity from gallbladderdisease in the members of this sample.

Gallbladder disease was less common amongPima males than among the females. Fewermales admitted to symptoms and fewer had hadsurgery. The earlier onset of gallbladder diseaseand the more frequent occurrence of biliarysymptoms in females may perhaps be due to theeffects of female hormones (10) on gallbladderphysiology.

An analysis of other factors possibly cont ')ut-ing to gallbladder disease in the Pima-5u( as

diet, pregnancy, obesity, diabetes, and serumcholesterol-will be reported when a higher pro-portion of this sample has been examined.

A review of the medical records of 575 mem-bers of the sample for evidence of documentedgallbladder disease and possible associated con-ditions has previously been reported (5). Inthat study gallbladder disease was found to berelated to increased parity but not to diabetes,body weight, or serum cholesterol except thatin older Pima males ther.; was an associationwith diabetes. These data must be interpretedcautiously, since the present study indicates thatnearly a third of the Pima males and nearlyhalf of the Pima females without documentedclinical gallbladder disease actually had gall-

bladder pathology.In order to advance the study of cholelithiasis

and to further explore the problem of gallstonesin Indians, it would be desirable to supplementthe epidemiologic studies currently being per-formed among the Pima with selected biochemi-cal and physiological investigations.

Fundamental to the concept of gallstone for-mation is the chemistry of the hepatic and gall-bladder bile at the time stones are first beingformed. In mice it has been possible to alter bilecomposition and to produce gallstones by feed-ing "lithogenic diets" (3). The biochemistry ofhuman hepatic bile and the significance of thechanges found in pathologic bile have recentlybeen reviewed (I). Since other groups of Ameri- ;

86

" 1

can Indians appear to have a high rrevalence ofthe disease, it is possible that the bile of Ameri-can Indians, perhaps as a rault of geneticallydetermined factors, differs fundamentally in itscomposition from that found in other racialgroups. To investigate this possibility, specimensof bile from Indians both with and without gall-bk dder disease should be analyzed. These couldbe obtained from the gallbladder at the time oflaparotomy for some unrelated condition andat the time of cholecystectomy. Bile obtained atautopsy would be suitable for study only if it

could be determined that its composition in thepost mortem state was similar to bile examinedbefore death, and particularly if the informationcould be supplemented with pertinent ante mor-tem data. An analysis of the constituents of gall-bladder bile and their relation to age and sex inthis gallstone-prone population, together with acomparison of bile from Indians w;th that ofother racial grups, might add significantly toknowledge concerning the biochemical factorspredisposing to cholelithiasis

The Pima Indians have low levels of serumcholesterol (5), even though their diet seems tobe high in saturated fats (8). It is possible thatan unusually efficient mechanism for clearingserum cholesterol may be present, which mightbe mediated through exaggerated biliary excre-tion of cholesterol. Studies of the intake andabsorption of dietary fats and of the synthesisand excretion of cholesterol might give :1_11es tothe etiology of gallbladder disease in ;.his ;.!roup.

It has been reported that peptic ulcers are rarearr^ng southwestern Indians (9). This observa-tion may be relevant to the excess of gallstonesamong Indians, since a recent study found gas-tric secretion to be diminished in the majority ofpatients with cholelithiasis (4). Further studiesrelating gastric secretion to gallbladder functionin Pima Indians appear to be indicated.

Summary

A preliminary report of a survey based onoral cholecystograms on a population of PimaIndians from Arizona has been made. The prev-alence of gallbladder disease among those ex-amined to date was significantly higher than hadpreviously been reported, with 2 1 (37.5 per cent)of 56 males and 92 (67.6 per cent) of 136 fe-males affected. Clinical symptoms attributableto gallbladder disease were found among 10.7per cent of the 56 males and 47.1 per cent of the136 females. Nearly a third of the males andnearly half of the females without previouslyknown disease had abnormal cholecystograms.

Further biochemical and physiologic studiesto supplement the current epidemiologic investi-gations are suggested.

Acknowledgments

We wish to thank the Tribal Council of the Gila RiverIndian Community and the Division of Indian Health ofthe United States Public Health Service for their encour-agement and assistance. Special thanks are duc to Drs.W. J. Held and Jon E. Gustafson, the radiologists at thcPhoenix lidian Hospital who read the cholecystograms.

REFERENCES

1. BOUCHER, I. A. D., and J. W. FRESTON. Theetiology of gallstones (hypothesis). Lancet i:340-344,1968.

2. BumiN, J. J., T. A. 13tAcx, and W. M. O'BRIEN.Influence of genetic and environmental factors onoccurrence of rheumatoid arthritis and rheumatoidfactor in American Indians. Bull. Rheum. Dig. 15:349-350, 1964.

3. CALDWELL, F. T., K. LEVITSKY, and B. ROSEN-BERG. Dietary production and dissolution of choles-terol anstones in the mouse. Amer. I. Physiol.209:473-478, 1965.

4. CAPPER, W. M., T. J. BUTLER, J. 0. KILBY, andM. J. GinsoN. Gallstones, gastric secretion, and flalti-lent dyspepsia. Lancet, 1:41 3-415, 1967.

87

5. COMM, L. J., P. H. BENNETT, and T. A.BURCH. Clinical gallbladder disease in Pima Indians.Its high prevalence in contrast to Framingham,Massachusetts. New Eng. I. Med. 277:894-898, 1967.

6. CUNNINGHAM, J. A., and F. E. HARDENBERGH.Comparative incidence of :holelithiasis in the Negroand White races. A study of 6185 autopsies. Arch.Intern. Med. 97:68-72, 1956.

7. FRIEDMAN, G. D., W. B. KANNEL, and T. R.DAWBER. The epidemiology of gallbladder disease.Observations in the Framingham Study. I. ChronicDig. 19:273-292, 1966.

8. HESSE, F. G. Dietary study of Pima Indians.Amer. I. Cfin. Nutr. 7:532-537, 1959.

9. HESSE, F. G. Incidence of chokcystitis and

92

other diseases among Pima Indians of southernArizona. IRMA 170:1789-1790, 1959.

10. IMAMOGLU, K., S. L. WANGENSTEEN, H. D.Roo; P. A. SALMON, W, 0. GROFEN, and 0. H.WANGENSTEEN, Production of gallstones by pro-longed administration of progesterone and estradiolin rabbits. Surg.Forum 10:246-249, 1959.

11. KAMEDA, H. Gallstone disease in Japan. Areport of 812 cases. Gastroenterology 46:109-114,1964.

12. LAM, R. C. Gallbladde diseases among Ameri-can Indians. /. Lancet 74:305-309, 1954.

13. LIEBER, M. M. Incidence of gallstones andtheir correlation with other disease. Ann. Stag.135:394-405, 1952.

14. MILLER, M., T. A. BURCH, P. H. BENNETT,and A. G. STEINBERG. Prevalence of diabetes mellitusin American Indians. Results of glucose tolerancetests. in Pima Indians of Arizona. Diabetes 14:439,1965.

15. SIEVERS, M. L. and J. R. MARQUIS. South-western American Indians' burden. Biliary disease.MMA 182:570-572, 1962.

16. VAN DER LINDEN, W. Some biological traitsin female gallstone disease patients. A study of bodybuild, parity and serum cholesterol level with a

discussion of some problems of selection in observa-tional hospital data. Acta Chit. Scand. 269, Supple-ment 1, 1961.

HYPERGLYCEMIA IN PIMA INDIANS: A PRELIMINARY

APPRAISAL OF ITS SIGNIFICANCE

Max Miller, Peter H. Bennett, and Thomas A. Burch'

There have been several reports in recentyears indicating that certain groups of NorthAmerican Indians have a high prevalence ofdiabetes mellitus (5, 14). It has also been sug-gested that the frequency and types of theassociated clinical manifestations and complica-tions differ in the American Indian from thoseobserved in the Caucasian and the Negro (12).This report will examine the frequency of hyper-glycemia and related variables in a NorthAmerican Indian tribe, the Pima Indians ofArizona.

Methods

Thc Pima Indians have resided for at leastseveral centuries in the region of the Gila Riverin south-antral Arizona, which is typical of thehot, dry Sonoran desert of the southwesternUnited States. The Pima were traditionally anagricultural group, and they 3r their forebears,with the aid of irrigation water from the GilaRiver, have farmed its valley for about twothousand years (4). The majority of them nowreside on the Gila River Indian Reservation, tothe south and east of Phoenix, Arizona.

The inhabitants of the reservation reside intwo main regions, one of which receives its

medical care from the U.S. Public HealthService Indian Hospital in Phoenix and theother from the PHS Indian Hospital in Sacaton,Arizona. The latter region contains severalvillages that form an independent natural popu-

I Presented by Dr. Miller.

lation group, geographically isolated from theother. Some 3,300 Indians aged 5 years and overreside in this community; of these 3,041 claim tobe half- to full-blooded Pima.

Between 1 March 1965 and 1967, 1881 of thesePima Indians received a modified glucose toler-ance test at the National Institutes of HealthClinic at the Sacaton PHS Indian Hospital. Anoral 75-gram glucose equivalent carbohydrateload 2 (6) was given to each subject who at-tended the examination center regardless of thetime of the previous meal. Two hours latervenous blood was drawn into a tube containingsodium fluoride and another specimen wasplaced in a plain glass tube. Glucose concentra-tion was measured on the AutoAnalyzer, usingthe modified Hoffman method,8 in plasma ob-tained from the fluoride tube. Serum creatininewas determined on the additional serum sample.

Before drinking the carbohydrate load eachsubject was asked to void, and two hours later aurine sample was collected, which was testedfor protein and glucose with dipsticks.4 When-ever protein wa F. found in a concentration ofapproximately 30mg/100m1 or more ( >1+ ),quantitative determination of the urinary pro-tein concentration in a sample of the urine wasmade together with determination of the urinary

89

2 Glucola, Ames Company, Elkhart, Indiana, orDexcola, Custom Laboratories, Baltimore, Maryland.

Technicon AutoAnalyzer Method File N-20, Tech-nicon Instruments Corporation, Chauncey, New York,1965.

4 Labstix, Ames Company, Elkhart, Indiana.

94

creatinine concentration. Among those aged 15years and over a subsample was e,;amined morethoroughly and retinal photographs, electrocar-diograms, and radiographs of the soft tissues ofthe left calf (lateral view) and thigh (AP view)were taken!'

A prospective study of the outcome of thepregnancies among the Pima women living inthe same community was initiated in October1965. The modified glucose tolerance test wasperformed on these women one to three daysafter parturition, and data on the course ofpregnancy and the characteristics of the off-spring were collected. In addition, a retrospec-tive study was made of all previous pregnancies

5 The subsample consisted initially of a one-in-twosample of those aged 30 years and over but was ex-tended, after examination of the first 1,100 persons, toinclude all those examined aged 15 years and over.Though this is not a truly random sample, we believethat it is unlikely to be significantly biased in relationto any findings associated with plasma glucose levels.

and their outcome among the Pima womenaged 25 to 44 years on 1 January 1966 (/).

Autopsy data were collected on members ofthe Pima Indian population who have died sinceour initial survey in 1963, and death certificateshave been collected systematically since 1964.

Results

Table 1 shows the number of Pima subjectsin the sample with hyperglycemia by age andsex and the number with previously diagnoseddiabetes who have received specific hypogly-cemic therapy in the course of routine medicalcare. The prevalence of previously treated dia-betes was highest in the males aged 65 to 74(26.2 per cent) and in the 55-to-64-year-oldfemales (40.8 per cent).

If "diabetes" is arbitrarily defined as a venousplasma glucose level of 160mg/10Orn1 or moretwo hours after a 75-gram glucose equivalentload, the majority of cases of the disease were

TABLE 1. Carbohydrate intolerance among Pima (4/8-8/8) Indians of the Gila River Reservation aged 5 yearsand over, 1965-1967

AGE GROUP

BY SEX

NO.

EXAMINED

NO. WITH

KNOWN PREVIOUSLY

TREATED DIABETES

NO. WITH

TWO-HOUR

GLUCOSE LEVELS

>160 MGNO. WITH

"DIABETES''

% WITH"DIABETES'.

Males

5-14 238 0 0 0.015-24 146 0 4 2.725-34 86 0 15 15 17.435-44 91 10 20 30 33.045-54 70 13 17 30 42.955-64 74 16 15 31 41.965-74 61 16 12 28 45.975 and over 38 4 12 16 42.1

TOTAL 804 59 95 154 19.2

Females5-14 284 0 7 7 2.5

15-24 230 1 11 12 5.225-34 149 9 21 30 20.135-44 150 23 50 73 48.745-54 93 25 34 59 63.455-64 93 38 26 64 68.865-74 55 16 15 31 56.475 and over 23 3 9 12 52.2

TOTAL 1077 115 173 288 26.7

90

undiagnosed at the time of the modified glucosetolerance test. The combined prevalence of pre-viously and newly diagnosed "diabett:- reacheda maximum of 45.9 per cent in the males aged65 to 74 years and 68.8 per cent in the femalesaged 55 to 64. In all age groups, especially thoseof 35 years and over, the prevalence of "dia-betes" in the females exceeded the rate in themales, the differences being significant in eachdecade between 35 and 64 years. Thus, bothmale and female Pima Indians had an extra-ordinary frequency of "diabetes"higher thanthat reported in any other population studied.Table 2 and Figure 1 show the distribution ofthe two-hour plasma glucose results on all PimaIndians examined regardless of whether theyhad previously diagnosed diabetes, provided theydid not have concurrently treated diabetesi.e.,had not taken specific hypoglycemic medicationwithin the period in which the two-hour glucosedetermination could have been directly influ-enced.° Such a determination was made on 1,776of the subjects. The age- and sex-specific cumula-tive frequency distributions of the plasma glu-cose values indicated that there was a relativelysteep rise in the cumulative frequency distribu-tion in the lower range of the glucose valLes inall age groups. There was not, however, a uni-form increase in each successive age group atall percentile levels. Below the median (fiftiethpercentile level) in both sexes the increases wererelatively small, but the upper percentile glucosevalues were much higher in the older age groupsof both sexes than in the younger subjects. Thissuggests that, as age increased, the proportionof subjects with hyperglycemia increased mark-edly.

From this the inference was drawn that theplasma glucose levels in all except the youngestgroups of each sex were not homogeneous butconsisted of two or more components. Furtheranalysis indicated that in each sex and in alldecades from 25 to '74 years the frequency distri-bution of the logarithms of the two-hour glucose

° For patients taking tolbutamide or phenformin thisperiod was 24 hours; for patients taking insulin orchlorpropamide or other oral agents or combinations oforal agents, 48 hours.

CUMULATIVE PERCENTAGE DISTRISUTION OF TWO HOURPOST LOAD VENOUS GLUCOSE LEVELS IN PIMA INDIANS

*ISLES

-worammaw....voinzammimi100 SOO SOO 800 500 800 700PLASMA SLUG Olt ittel00

FIGURE I. Age- and sex-specific :umblatiyc per-centage distributions of two-hoarplasma glucose kvds in Pima Indians

values had a bimodal distribution. Using aniterative maximum likelihood procedure, thesedistributions were dissected mathematically andeach of the observed distributions in those aged25 to 74 yearsfor example, that shown inFigure 2 for males aged 55 to 74proved to bea statistically satisfactory fit for two overlappinglog10 normal (Gaussian) distribution curves. Inthose below 25 years, however, only a unimodaldistribution was found, as is shown in Figure 3for males aged 15 to 24, which was a satisfactoryfit for a single logio normal distribution (13).Hence the heterogeneity inferred from thecumulative percentage distribution in the oldergroups appeared to result from the presence of

91

20 MALES 55-74

5

SO ibotASMA

200

GLUCOSI 1.1/100

FIGURE 2. Frequency distribution of two-hour post-load venous plasma glucose levels (logarithmic scale) inPima Indian males aged 55-74 years

66

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. Cum

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00

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Pt ASMA G UC OSI Ing /190 PRI/

FIGURE 3. Frequency distribution of two-hour post-load venous plasma glucose levels (logarithmic scale) inPima Indian males aged 15-24 years

two components, one characterized by a muchhigher mean plasma glucose level than the other.

The parameters of the distributions were suchthat bimodality was apparent only because theproportion of subjects who contributed to thehigher curve was relatively high.

In order to determine whether the subjects inthe two distributions consisted of those with andwithout diabetes mellitus in the clinical sense,the relationship of other parameters of thisdisease to glucose tolerance levels was examined.

Diabetic retinopathy

"Diabetic retinopathy" is allegedly one of themost specific signs of diabetes mellitus. Its fre-quency was assessed in the Pima Indians by theevaluation of retinal photographs for the pres-ence of microaneurisms, preretinal and vitreoushemorrhages, exudates, and neovascularization.Table 3 shows the frequency of diabetic retinop-athy in all subjects aged 15 years and over whohad one or more satisfactory retinal photo-graphs.

No definite evidence of diabetic retinopathywas observed in male or female Pima Indiansunder 35. In those above this age, it was foundonly in those with the h:gher plasma glucoselevels. In those with two-hour plasma glucoselevels of 200mg/100m1 and over, retinopathywas approximately twice as frequent as in thosewith levels between 160 and 199mg/l00m1.

Among those with diabetes concurrently undertreatment, retinopathy was observed in 20.0 percent of the males and in 19.6 per cent of thefemales.

Proteinuria

Other evidence that hyperglycemia among thePima Indians was associated with vascular com-plications was investigat 1 by examination forevidence of renal disease. Table 4 shows therelationship of proteinuria ( >1 +) to the two-hour post-load plasma glucose level. The fre-quency of proteinuria among both males andfemales increased with age and plasma glucoselevel. Within each age group there was a gradi-ent of increasing frequency of proteinuria withincreasing severity of hyperglycemia. This rela-tionship was similar in males and females, aswas the over-all frequency of proteinuria in bothsexes and in every age group of each sex.

In 105 of the 128 subjects with proteinuria itwas possible to make more quantitative esti-mates of proteinuria by determining albuminand creatinine concentrations in the two-hoururine samples. Since the daily excretion ofcreatinine in the urine is relatively constant(H), the albumin/creatinine (A/C) ratio willyield an approximate estimate of the 24-hoururinary excretion of protein. Thus, an A/C ratioof 1 or more indicates that one or more grams ofprotein are excreted daily.

Markedly elevated A/C ratios ( >1.0) werefound more frequently in those who had two-hour post-load glucose levels in excess of 200mg/100m1 and in the concurrently treated diabeticsthan in subjects with lower values (Table 5).Thus, among those with high glucose values,proteinuria was both more frequent in any de-gree and also much more severe.

The nephrotic syndrome associated with se-vere intercapillary glomerulosclerosis is recog-nized as one of the important complications ofthe renal disease of diabetes mellitus. The essen-tial feature of this syndrome is the occurrenceof excessive proteinuria, usually exceeding 3grams a day. It is noteworthy that of those withplasma glucose values of 200mg/100m1 andover, 11 of the 39 with proteinuria on whom the

93,

TABLE 3. Diabetic retinopathy and two-hour post-load plasma glucose levels in Pima (4/8-8/8) Indians examined1965-1967

PLASMA GLUCOSE LEVEL (MG/lOOML)AGE GROUP WITH CONCURRENTLY

BY SEX 0-100 101-159 160-199 200+ TREATED DIABETES TOTAL

Males15-34 years

No. examined 43 43 0 8 1 95

No. affected 0 0 0 0 0 0

Per cent 0.0 0.0 0.0 0.0 0.0 0.0

35-54 yearsNo. examined 26 35 9 27 9 106


Per cent 0.0 0.0 0.0 14.8 22.2 5.7

55 and overNo. examined 15 41 11 19 10 96

No. affected 0 0 1 3 2* 6

Per cer t 0.0 0.0 9.1 15.8 20.0 6.3

TotalNo. examined t-; 4 119 20 54 20 297


Per cent 0.0 0.0 5.0 12.9 20.0 4.0

Females



Per cent 0.0 0.0 0.0 0.0 0.0 0.0

35-54No. examined 13 67 27 45 23 175


Per cent 0.0 0.0 0.0 8.9 13.0 4.0



Per cent 0.0 0.0 16.7 20.0 30.0 14.9

TotalNo. examined 58 167 39 87 46 397

No. affected 0 0 1 10 9 20

Per Lent 0.0 0.0 2.6 11.5 19.6 5.3

a Includes one male who at the time of the retinal photographs had a plasma glucose of 156 mg/100 ml while noton medication. He had, however, lost weight and had carcinoma stomach with metastases, and in 1961) had a

fasting blood glucose of 165 mg/100

4.1C 9

z

TABLE 4. Proteinuria and two-hour post-load plasma1965-1967 (> 1+ on dipsticks 4)

glucose levels in Pima (4/8-8/8) Indians examined

AGE GROUP

BY SEX

PLASMA GLUCOSE LEVEL (M0/100ML)WITH CONCURRENTLY

TREATED DIABETES TOTAL0-100 101-159 160-199 200+

Males15-34 years

No. examined 108 90 5 13 0 216No. affected 6 5 0 1 0 12

Per cent 5.6 5.6 0.0 7.7 0.0 5.6



Per cent 5.1 10.2 20.0 11.1 40.0 11.7


No. affected 2 6 3 10 6 27

Per cent 9.1 8.6 17.6 28.6 35.3 16.8


No. affected 10 17 5 15 10 57

Pcr cent 5.9 7.8 15.6 17.9 37.0 10.7

Females15-34 years

No. examined Irv/ 176 16 17 6 324


Per ccnt 3.7 4.0 12.5 29.4 0.0 5.6


No. affected 0 4 2 10 5 21

Per cent 0.0 4.7 5.6 15.7 17.2 8.9


No. affected 2 2 0 15 13 32

Per cent 25.0 3.9 0.0 31.8 32.5 20.3


No. affected 6 13 4 30 18 71

Per ccnt 4.4 4.2 6.5 24.0 24.0 10.0

fuo

TABLE 5. Albumin/creatinine ratios in subjects with > 1+ proteinuria

PLASMA GLUCOSE LEVEL (MG/lOOML)WITH CONCURRENTLY


MalesNo. examined 5 17 4 13 9 48

A/C> 1.0 0 2 2 9 7 20

Per cent 0.0 11.7 50.0 692 77.8 41.7

FemalesNo. examined 5 10 2 26 14 57

A/C> 1.0 2 2 0 14 11 29

Per cent 40.0 20.0 0.0 53.8 78.6 50.9


A/C> 1.0 2 4 2 23 18 49

Per cent 20.0 14.8 33.3 58.9 78.3 46.7

A/C ratios were determined had values of 3.0and over, as did 11 of the 23 with concurrentlytreated diabetes. A/C ratios of this magnitudewere not encountered in subjects with two-hourglucose levels of less than 200mg/100m1 exceptin one 32-year-old male who was known to havehad acute glomulonephritis nine years pre-

viously.

Serum creatinine levels

In order to determine the frequ,:ncy ofsubjects with significant reductions in renalfunction, serum creatinine levels were examined.Elevated levels were defined for this :....pose as15mg/100m1 and over in males, and 1.3mg/100m1 and over in females. Such levels werefound mainly among subjects with two-hourplasma glucose levels of 200mg/100m1 and overand among those with concurrently treated dia-betes (Table 6). They occurred predominantlyamong the older subjects in the same groups inwhich marked proteinuria was found.

The records of four male subjects with plasmaglucose levels of 101 to 200mg/100m1 who hadelevated serum creatinine levels were examinedto determine possible reasons for these. Two hadhistories of hypertension and congestive heartfailure, and another had received renal dialysisfollowing trauma and shock. The fourth, witha glucose value of 160-199mg/100m1, was aknown diabetic t. f many years' duration. He had

previously had several blood glucose values inexcess of 250mg/100m1 and had received insulinand tolbutamide for many years. Prior to testinghe had lost at least 26 pounds in weight, and hedied 23 days after examination.

Thus, evidence was found that hyperglycemiaamong the Pima Indians was strongly associatedwith proteinuria and impairment of renal func-tion, especially among the older subjects of bothsexes.

Vascular calcification

Evidence of disease of the peripheral vascula-ture was evaluated in soft-tissue radiographs ofthe thigh (femoral artery) and the calf (tibialarteries), since vascular calcification has beenshown to be more frequent among diabeticsthan among nondiabetics (3) and to developconcomitantly with increasing duration of dia-betes among the younger subjects with diabetes(1 5) . Tables 7 and 8 show the frequency ofcalcification in these vessels. In both sites calci-fication was found more frequently in the malesthan in the females, was age-related, and wasencountered more frequently in the tibial arte-ries than in the femoral artery. The calcificationobserved was mainly medial in type; the intimaltype was rarely seen and never occurred alone.

Calcification in the femoral artery and in thetibial arteries was not found in any Pima Indiansbelow the age of 35 years. In the older groups

WI

TABLE 6. Elevated serum creatinine and two-hour post-load plasma glucose levels in Pima (4/8-8/8)Indians examined 1965-1967 (Males > 13 mg/100 ml : Females 1.3 mg/100 ml)

PLASMA GLUCOSE LEVEL (MG/100ML)AGE GROUP WITH CONCURRENTLY

BY SF.X 0-100 101-159 160-199 200+ TREATED DIABETES TOTAL

Males15-34 years

No. examined 84 61 2 8 0 155No. affected 0 0 0 0 0 0Per cent 0.0 0.0 0.0 0.0 0.0 0.0

35-54 yearsNo. examined 27 49 9 30 10 125No. affected 0 2* 0 0 2 4Per cent 0.0 4.1 0.0 0.0 20.0 3.2

35 r nd overNo. examined 19 64 17 26 16 142No. affected 0 1* 1' 2 1 5Per cent 0.0 1.6 5.9 7.7 63 3.5

TotalNo. examined 130 174 28 64 26 422No. affected 0 3 1 2 3 9Per cent 0.0 1.7 3.6 3.1 11.5 2.1

Females15-34 years


Per cent 0.0 0.0 0.0 9.1 0.0 0.6

35-54 yearsNo. examined 14 67 26 52 26 185No. affected 0 0 0 0 2 2Per cent 0.0 0.0 0,0 0.0 7.7 1.1

55 and overNo. examined 6 48 6 41 34 135No. affected 0 0 0 5 4 9Per cent 0.0 0.0 0.0 12.2 11.8 6.7

TotalNo, examined 82 199 38 104 62 485No. affected 0 0 0 6 6 12Per cent 0.0 0.0 0.0 5,8 9.7 2.5

4 See text.

97.

102

TABLE 7. Medial calcification of the femoral artery and two-hour post-load plasma glucose levels in Pima(4/8-8/8) Indians examined 1965-1967

PLASMA GLUCOSE LEVEL (MG/IOOML)AGE GROUP WITH CONCURRENTLY

BY SEX 0-100 101-159 160-199 200+ TREATED DIABETES TOTAL

Males15-34 years

No. examined 59 49 3 7 0 118


Per cent 0.0 0.0 0.0 0.0 0.0 0.0



Per cent 0.0 0.0 20.0 7.1 11.1 3.9


No. affected 5 17 5 7 8 42

Per cent 29.4 28.8 35.7 26.9 53.3 32.1


No. affected 5 17 6 9 9 46

Per cent 5.1 11.6 27.3 14.8 37.5 13.1

Females15-34 years

No. examined 39 68 10 11 3 131


Per cent 0.0 0.0 0.0 0.0 0.0 0.0



Per cent 0.0 0.0 0.0 4.1 0.0 1.2



Per cent 0.0 4.8 0.0 19.4 17.6 12.1



Per cent 0.0 1.2 0.0 9.4 10.2 4.1

1C3

TABLE 8. Medial cakification in the tibial arteries and two-hour post-load plasma glucose levels in Pima(4/8-8/8) Indians examined 1965-1967

PLASMA GLUCOSE LEVEL (MG/100ML)AGE GROUP

BY SEX

WITH CONCURRENTLY


Males15-34 years

No. examined 58 47 3 7 0 115


Per cent 0.0 0.0 0.0 0.0 0.0 0.0



Per cent 0.0 5.3 20.0 21.4 22.2 10.9


No. affected 4 24 5 11 8 52Per cent 25.0 42.9 35.7 42.3 57.1 41.3


Females15-34 years


Per cent 0.0 0.0 0.0 0.0 0.0 0.0

35-54 yearsNo. examined 12 58 21 49 23 163No. affected 0 0 3 2 0 2

Per cent 0.0 0.0 0.0 4.1 0.0 1.2

55 and overNo. examined 5 42 7 34 32 120No. affected 0 3 2 10 7 22Per cent 0.0 7.1 28.6 29.4 21.9 18.3


fb4

both sites wete affected more frequently, but notexclusively, in subjects with the higher two-hourplasma glucose values and with concurrentlytreated diabetes. In the majority of subjects withfemoral artery involvement, the tibial arterieswere also affected.

Hyperglycemia and pregnancy

Diabetes mellitus is well recognized as havingcharacteristic effects on pregnancy and its out-come. In order to determine whether similareffects were found in the Pima Indians a reviewwas made of the past pregnancies of femalesaged 25 to 44 years on 1 January 1966 who badreceived a moditied glucose tolerance test andhad borne at least one child. On the basis ofthis recent test and clinical history, the femaleswere divided into three groups: those with two-hour post-load venous plasma glucose levels ofless than 140mg/100m1, those with either clini-cal diabetes requiring hypoglycemic treatmentor plasma glucose values of 160mg/100m1 orover, and those who had intermediate plasmaglucose levels. The last group were consideredto be in a "gray zone" and were not analyzed.Pregnancies among the second group were di-vided into those that occurred before the clinicaldiagnosis of diabetes ("prediabetic") and thosethat occurred after the diagnosis ("diabetic").The results appear in Table 9. Among thePima females studied, 47 (3.8 per cent) of the

1,253 pregnancies were considered "diabetic,"as against a frequency in the Cleveland, Ohio,metropolitan area of 0.28 per cent (8). The fre-quency of "diabetic" pregnancy was thereforesome 10 to 15 times greater among the PimaIndians than among the women of Cleveland.

The frequency of offspring weighing ninepounds or more at birth was significantly higherin the Pima "diabetic" group than in the "nor-moglycemic" mothers. The frequency of con-genital anomalies and the perinatal mortalityrate were also significantly higher among the"diabetic" group. The perinatal mortality ratein the latter was 25.5 per cent, which is in thesame range as that reported in other populations(10).

A prospective study of the current pregnanciesof Pima women was started in 1965. The modi-fied glucose tolerance test was performed on themother generally two to three days postpartum,but irt a few instances it was done on the firstday. Table 10 shows the relationship of theinfant birth weight to the two-hour post-loadplasma venous glucose level among such women.While the number with high postpartum glu-cose values was small, there was a highly sig-nificant relationship between birth weight andmaternal postpartum glucose level, an associationcor,sistent with that noted in the retrospectivestudy.

TABLE 9. Outcome of pregnancy among 215 Pima females (retrospective study)

OUTCOME 'NORMOGLYCEMIe' '.PREDIABETIC" "DIABETIC" TOTAL

Birth weightNo. of offspring>9 pounds at birth

Per cent

Zongenital anomaliesNo. of offspringWith congenital anomalies

571

376.5

78531

2292611.4

37513

3815

42.9

47

9

838789.3

1207

53

Per cent 3.9 3.5 19.1 4.4

Perinatal mortalilyNo. of births 815 391 47 1253

No. of deaths 10 12 12 34

Per cent 1.2 3.1 25.5 2.7

" Includes stillbirths and neonatal deaths occurring in first 28 days of life.

100

JAZ

TABLE 10. Infant birth weight and maternal postpartum two-hour post-load plasma glucose levels inPima (4/8-8/8) Indians examined Oct. 1965Dec. 1967

OFFSPRING

WEIGHINGMATERNAL

PLASMA

GLUC6SE

(MG/ HOMONO. OF

PREGNANCIES

>4000 GRAMS

AT BIRTH

NO.

0 63 17 0 0.064 80 49 2 4.181-100 90 5 5.6

101-126 76 5 6.6127-159160-199

33 9

2}33.3

27.3

200+ 3 1

Total 274 24 8.8

Mortality

Death certificates have been collected on thePima Indians of the Gila River Indian Reserva-tion since 1964, and autopsy data were obtainedon persons who have died since 1963. About halfof those who died received post mortem exami-nations. Over a four-year period there were 53male and 49 female deaths among persons aged15 years and over who had available glucoseestimations or whose diabetic status was known,excluding those due to accidents or violence(Table 11).

For comparative purposes the subjects wereclassified as "diabetic" on the basis of a clinicalhistory of diabetes and/or high glucose values.Age-standardized death rates for subjects with"diabetes" in both sexes we e found to be higherthan those of the "nondiabetics," although the

TABLE 11. Four-year mortality, excluding accidentaland violent death (1964-1967) in Pima Indians aged15 years and over

MALES FEMALES

Total no. deathsNo. with diabetesAge-standardized rates/

100 personsDiabeticsNondiabetics

5327

7.8

49

34

9.84.4

diagnosis was sometimes based upon less-than-ideal criteria. The rate was approximately twiceas high in the females and at least 40 per centhigher in the males with "diabetes." The find-ings indicate that mortality rates among Pimasubjects with hyperglycemia were substantiallyhigher than among those with "normal" plasmaglucose levels.

Post-mortem study

Of the Pima Indians who died since ourinitial study in 1963, autopsy data were availableon 34 subjects with "diabetes" and on 19 with-out. Evidence of nodular intercapillary glomu-lerosclerosis was reported in six of the "dia-betics" and in none of the others. Seven of the34 diabetics had myocardial infarcts, comparedto 2 of the 19 "nondiabetics." Tuberculosis wasfeund in 7 "diabetics" and in only 1 "nondia-betic." Pyelonephritis, howover, was reported asfrequently among the "nondiabetics" as the"diabetics." Amputations had been performedon 2, and mucormycosis was present in 1 ofthose with "diabetes."

Discussion

The data plc ented show that hyperglycemiais extremely frequent among the Pima Indians.As complete glucose tolerance tests were not per-formed routinely and as only a single venousglucose determination made two hours after a75-gram glucose equi lt load was availableon all subjects, the ust... ;teria for the diagno-sis of diabetes mellitus cob not be applied.

In order that comparisons might be made withother studies, however, the frequency of subjectswho had received specific treatment for diabeteswas determined, as was the frequency of subjectswho had two-hour venous plasma glucose levelsof 160mg/10Gml and over. It was felt that thislevel, which corresponds to a whole-blood sugarof approximately 140mg/100m1, was suitable forcomparison with several studies in which some-what ,irrai;ar testing methods were used. It wasfound that known diabetes and hyperglycemia,as so defined, occurred more frequently amongthe Pima Indians than in any other populationthus far studied. Unusually high frequencies of

101

106

diabetes have been found among the CheiokeeIndians of North Carolina, but the prevalenceobserved in the Pima Indians was even greater(14). It was also very much greatcr than hadbeen found among Alaskan Eskimos (9) andwas 10 to 15 times greater than the rate believedto be representative of the United States as awhole (7).

To determine whether hyperglycemia in PimaIndians was associated with the chronic vascularcomplications that are characteristic of diabetesin other populations, analyses were made todiscover the frequency of diabetic retinopathy,renal disease, and vascular calcification amongPima subjects aged 15 years and over as a func-tion of their plasma glucose level or previouslyknown diabetes. Retinopathy, as shown on fun-dus photographs, and impaired renal function,as indicated by elevated serum creatinine levelsor heavy proteinuria (A/C ratio >3.0), werefount.. exclusively among those with two-hourglucose levels in excess of 200mg/100m1 or withconcurrently treated diabetes, except in rareindividuals in whom the findings were clearlyexplained on another basis. Proteinuria of alldegrees was more frequent among those withhigh glucose levels or treated diabetes and,when present, was moderately severe (A/C ratio>1.0) four times as frequently as in those withglucose levels below 200mg/100m1.

Since retinopathy and nephropathy are consid-ered highly specific findings in diabetes mellitus,their frequent occurrence in Pima Indians withelevated two-hour plasma glucose levels impliesthat the hyperglycemia in this population was amanifestation of the diabetic syndrome as recog-nized elsewhere. This conclusion was strength-ened by the reports of cases of nodular inter-capillary glomerulosclerosis at autopsy amongsuch subjects.

On the other hand, disease of the larger vessels,as shown by the presence of vascular calcificationin the lower limbs, occurred among older sub-jects over the Whole range of glucose levels butwas again more frequent among those of thesame age and sex with glucose levels in the upperrange or with concurrently treated diabetes.Standard twelve-lead electrocardiograms have

also been performed on the same subjects, andthe findings will be reported separately. Postmortem studies, however, have already indicatedthat myocardial infarction occurred twice as fre-quently among the "diabetics" in the autopsyseries.

Over a four-year period the age-standardizedmortality rate amorig Pima Indian subjects onwhom glucose determination had been made,either in the course of routine medical care orfor research purposes, was shown to be greateramong those of each sex with the higher glucoselevels than among those with lower levels. Thisfinding was consistent with the increased mor-tality from diabetes mellitus reported in Jos linClinic patients, which is mainly related to thechronic vascular complications (2). Theughsimilar processes appear to be responsible forthe excessive Pima mortality, the number ofdeaths is so far too small for deducing the rela-tive importance of the various types of vascularcomplications. Serial studies of renal functionand electrocardiograms as well as systematicautopsy, whenever possible, will make possiblesuch a definition in the future.

The frequency of "diabetic" pregnancy amongthe Pima Indians was in accordance with thatwhich might be predicted from the over-allprevalence of hyperglycemia. The demonstrationof significantly increased perinatal mortality,high infant birth weight, and high frequencyof congenital anomalies resulting from thesepregnancies further implies that hyperglycemiain Pima Indians has the same pathologic signifi-cance as diabetes mellitus among Caucasians andNegroes (8, 10).

As the classic symptoms of diabetes mellitusare related mainly to the individual levels ofhyperglycemia and are ameliorated by the spe-cific hypoglycemic medications, the substatrialproportion of subjects who had received suchtreatment may reflect the past frequency of thecharacteristic symptoms of diabett's mellitusamong the Pirna Indians. While only 40 per centof the subjects with glucose values of 160mg/100m1 and over had received such therapy, theyincluded 60 per cent of the females and 50 percent of the males aged 55 to 64 years with such

102

167

levels. This observation suggests that substantialnumbers of the younger persons with hyper-glycemia will become symptomatic in the future.

Before the systematic study of the PimaIndian community was begun, diabetes mellituswas locally recognized as an important healthproblem but the true frequency of hypergly-cemia and of the vascular manifestations wereunknown. Although some other southwesternIndian tribes are recognized as having a highfrequency of the disease, others are said to havea low prevalence. The significance of this varia-tion, if it were confirmed and if the reasons forthe differences could be identified, would be animportant contribution to our understanding ofthe etiology of diabetes mellitus.

A definition of the geography of the disease inthe southwestern American Indian seems to beneeded as a matter of some urgency, since theseemerging groups are likely to be subjected toradical and rapid change. Some may lose theiridentity; others may adopt ways widely differ-ent from those of their forebears. The study of

differing tribes with high and low prevalencesof diabetes at present could contribute to ourknowledge of the etiology, especially if identicalmethods of evaluation could be used in severalof the groups. Such investigations could beenhanced by parallel study of groups of thesame race in Central and South America. Asthese groups are subjected to change and as theirlife expectation is increased, it is possible thatothers may go the same way: in them diabetesmellitus may emerge as a major chronic diseaseproblem, as it is today among the Pima Indians.

Acknowledgments

We gratefully acknowledge the help and assistance ofmany persons who have contributed to this studyinparticular, Dr. E. I. Ballintine for his evaluations of theretinal photographs, Dr, F. A. Rose for the soft-tissueradiographic readings, and Miss P. E. Sperling for themajority of the labo-atory determinations. We alsothank the Division of Indian Health, the Tribal Council,and members of the Gila River Indian community,whose collaboration and cooperation made this studypossible.

REFERENCES

1. Com Ess, L. J., P. H. BENNETT, T. A. BuRcH, andM. MILLER. Congenital anomalies and diabetes inthe Pima Indians of Arizona. To be published.

2. ENTMACHER, P. S., H. F. RooT, and H. H.MARKS. Longevity of diabetic patients in recent years.Diabetes 13:373-377, 1964.

3. FERRIER, T. M. Radio logically demonstrablearterial calcification in diabetes mellitus. Aust. Ann.Med. 13:222-228, 1964.

4. HAtmv, E. W. The Hohokam, first masters ofthe American desert. Nat. Geographic 131:670-701,1967.

5. JoHNsoN, J. E., and C. W. Mc Nun. Diabetesmellitus in an American Indian population isolate.Texas Rep. Biol. Med. 22:110-125, 1964.

6, KENT, G. T., and J. R. LEONARDs. Mass screen-ing for diabetes in a metropolitan area using fingerblood glucose after a carbohydrate load. Diabetes14:295-299, 1965.

7. MCDONALD, G. W., and G. F. FISHER. Diabetesprevalence in the i..Tnited States. Public Health Rep.82:334-338, 1967,

8. MILLER, M. Diabetic pregnancy and foetalsurvival in a large metropolitan area. In B. S. Liebe!and G. A. Wrenshall (eds.), On the Nature andTreatment of Diabetes. Amsterdam, Excerpta MedicaFoundation, 1965, pp. 714-717.

9. MOURATOFF, G. J., N. V. CARROLL, and E. M.SCOTT. Diabetes mellitus in Eskim3s. IAMA 199:961-966, 1967.

10. PEDERSEN, J. Perinatal mortality in babies ofdiabetic mothers. In B. S. Liebel and G. A. Wren-shall (eds.), On the Nature and Treatment oDiabetes. Amsterdam, Excerpta Medica Foundation,1965, pp. 722-726.

11. PETERS, J. P., and D. D. VANSLYKE, Quantita-tive Clinical Chemistry; Interpretations. Baltimore,Williams & Wilkins, 1946, p. 908.

12. RIMOIN, D. L., Genetics of diabetes mellitus.Diabetes 16:346-351, 1967.

13. RUSHFORTH, N. B., P. H. BENNETT, A. G.STEINBERG, T. A. BURCH, and M. MILLER. Studiesof plasma glucose measurements in the Pima Indiansof Arizona. I. Application of a composite of twoGaussian distributions as a model for plasma glu-cose distributions. In preparation.

14. STEIN, J. H., K. M. WEST, 7. M. ROBEY, D. F.TIRADOR, and G. W. MCDONALD. The high preva-lence of abnormal glucose tolerance in the Chero-kee Indians of North Carolina. Arch. Intern. Med.116:842-845, 1965.

15. WHITE, P. Natural course and prognosis ofjuvenile diabetes. Diabetes 5:445-450, 1956.

MALARIA IN THE AMERICAN INDIAN

George G. Gig lion

Malaria prevails, or has prevailed up to re-cently, over very wide areas of the WesternHemisphere, lying betv een latitudes 50 N and40' S and from the shores of the Atlantic Oceanto those of the Pacific. The American Indianranges from Canyda to Patagonia, and somethirteen species of American anopheles mos-quitoes have been linked with malaria transmis-sion, seven species being vectors of major publichealth importance in one country or another.The range of ecological and epidemiologicalvariation is therefore practically unlimited, andit would be quite impossible to submit a concise,comprehensive account of malaria in the Ameri-can Indian, even if adequate information on thesubject were available. Unfortunately, publisheddata are conspicuously absent from the literature,and none of the principal malaria eradicationservices have been able to supply information onthis special malariological problem.

During the great upsurge of antimalarialactivities over the last twenty years, emphasiswas placed on vector destruction and chemo-therapy, not on epidemiology. Excessive hopeswere founded on the new insecticides with long-lasting residual effect, and on the powerful anti-malarial drugs developed during the war and inthe early postwar period. Malaria eradicationcampaigns were launched widely and wagedwith little or no attempt to establish base-linedata on the local epidemiology of the disease.

For obvious economical, political, and logisti-cal reasons, efforts in the sparsely inhabitedcountries of the American tropics were concen-trated on the more populous areas, no distinction

being made in respect to the different ethnicgroups that might be present. Given the magni-tude of the task, the remote, scattered. and eco-nomically unimportant Irdian communitieswereto a great extentmissed, overlooked, orignored.

The present discussion will be restricted to theIndians of Guyana, who are estimated to num-ber 32,000, widely scattered over the least accessi-ble parts of the country. At the present day, ninetribes are represented: the Warau of the coastallowlands, mostly in the North-West District,adjoining the delta of the Orinoco; the Arawak,of the lowland forests of the near interior; theWapishana (Arawak stock), of the South Ru-pununi Savannah; the Carib, formerly verynumerous and widely distributed, but now re-duced to very small numbers, mainly on theupper Barama and Barima rivers in the North-West District; the Akawai, of the upper Berbice,Demerara, Cuyuni, and Mazaruni rivers; thePatamona, of the southern portion of the Paka-raima Plateau; the Arekunz, of the upperCuyuni and Mazaruni mountains and savan-nahs; the Makusi, of the North RupuliuniSavannah; and the Wai-Wai, of the Essequiboheadwaters. The last five tribes are of Caribstock.

Some of these tribes extend beyond the politi-cal frontiers into Venezuela and Brazil. Gen-eralizations about malaria are not permissible,and my observations refer specifically to Guyana;it may be noted, however, that few environ-ments pi esent greater stability and u! ;ormitythan the equatorial rain forest, which covers

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109

most of the Guianas and Amazonia, whereAnopheles darlingi, the most efficient malariacarrier in the Western Hemisphere, is the pre-vailing, and often the only, vector. It is in thisvast region that the majority of American In-dians live still fully exposed to the ravages ofuncontrolled and untreated malaria.

The study of racial differences in .r..spect tothe epidemiology of malaria and the clinical andimmunological reactions induced by the malariaparasites presents many difficulties; for validconclusions studies must be based on observa-tions made under identical conditions of en-vironment and exposure. Such situations arerare, and this is probably the reason why studieson this aspect of malariology are few and theconclusions drawn somewhat tentative andguarded.

The Negroes of West and Central Africa haveevolved, throughout the ages, in continued con-frontation with malaria; they have acquiredpractically total immunity to Plasmodium vivaxand a high degree of tolerance to P. falciparum.Tolerance to the latter species implies no im-munity to the parasite, but a high degree oftolerance to the effects of parasitization. Rai-chenow (10), in 1929, working among theHausa of the Cameroons, reached the conclusionthat toxin resistance was inherited but parasiteresistance was acquired by continued exposureand reached its peak in early adulthood; there-after, the parasite rate and the degree of para-sitization remained low and more or less stable,Others in Africa have reached similar conclu-sions.

Holoendemic malaria is regarded as thehighest expression of malaria endemicity: thespleen rate in children 2 to 12 years old is con-stantly above 75 per cent; the spleen rate and thesize of the average enlarged spleen fall progres-sively with age, becoming low or negligible inthe adult population. Mortality may be high inyoung children, but the adults enjoy goodhealth so far as malaria is concerned. Ho lo-endemic malaria is typical of Africa but has alsobeen recordcd in other rather restricted situa-tions, as, for instance, among the aboriginals of

northeastern India and in New Guinea. In theWestern Hemisphere, however intense malariatransmission may be, so far as I know it hasbeen recorded only among the Bush Negroes ofSurinamdescendants of runaway slaves whohave lived, for many generations, isolated inthe Guyana forest, where other races, equallyexposed, suffer severely and never acquire thehigh degree of adult tolerance to malaria infec-tion that is characteristic of holoendemic ma-laria. This suggests that race may be a factorconnected with holoendemicity.

Among the Bush Negroes, Swellengrebel andVan der Kuyp (12) found a very high P. falci-parurn rate in both children and idults; themortality at all ag t. was low, howeve-, and theywere not much incommoded by the infection.Thus, in a village on the upper Surinam River,P. falciparum accounted for 75 per cent of theinfections in children, and for 73 per cent inadults. The actual parasite rate averaged 70.5per cent in children and 37 per cent in adults,yet during the twelve-year period from 1927 to1939, the population of the village increased by30 pet- cent, from 698 to 901, with an averagearcual death rate of 21, a birth rate of 39 per10J0 inhabitants, and infant mortality of 113

per 1000 birth ! Creole Negroes from theSurinam coastland, living in similar surround-ings, showed the same or even higher infectionrates and iff,-.red severely.

The Amerindians of Surinarn, living underthe same conditions as the Bush Negroes,showed little evidence of tolerance to the infec-tion. On the Wayombo River, in September1939, 172 Indians were examined; P. falciparumaccounted for 50 per cent of the infections inchildren (106 examined) and 61 per cent inadults (64 examined), and the spleen rates were82 and 83 per cent respectively. Swellengrebeland Van der Kuyp found that

The adult spleen rate and the average size of thc en-larged adult spleen (2.2 Schaffner units), surpassinganything we encountered in Bush Negroes, arc evidenceof the lack of tolerance of these people to malaria para-sites. We may add that a high spleen rate and a largesize tyf the swollen spleen arc peculiar of Indian malaria,as distinct from the push Negro and Creole malaria onemeets everywhere in Surinam. . . Besides a strong

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' 140

spknic reaction to the presence of malaria parasites intheir blood, the Indians give evidence of their lack oftolerance by sickness and death. . . The importanceof Indians as carriers of malarial infection does not,like the Bush Negroes, consist in a tolerance to theparasite (manifesting itself by a moderate splenic reac-tion and a low morbidity and mortality), but ir theirseminomadic life which enables them to carry rr dignantmalaria infection from the Bush to the Savannan,

American Negroes, descendants of slaves

brought from Africa between the sixteenth andthe nineteenth centuries, who have lived forgenerations under conditions of more or lessmoderate malaria endemicity, still enjoy someof the immunity built up by their ancestors. TheNorth American Negro presents considerableresistance to provoked infection with P. vivax(1), and West Indian Negroes throughout theCaribbean, though equally susceptible to infec-tion, on the average suffer much less and presentlower spleen rates and smaller average enlargedspleens than other races living in the sameenvironment (2).

In Guyana, people of six races have beenliving for many generations in the same generalenvironment and often under the same condi-tions of exposure to malaria infection.' TheEuropeans (mainly of Portuguese descent) andthe Chinese constitute small minorities and livemostly in Georgetown. The rural population ofthe coastlands comprises large numbers of

Negroes and East Indians, and ideal conditionsexist for comparative racial studies of all kinds.Up to 1946, when large-scale DDT sprayingoperations were introduced, malaria used to bestable and hyperendemic throughout the coast,from the Berbice Estuary to the PomeroonRiver (7). Systematic surveys of schoolchildrenwere conducted between 1937 and 1946, separaterecords being kept for the two main races. Theparasite rate showed no significant racial varia-tion; splenic reaction in the Negroes was, how-ever, decidedly and consistently more moderate,and decreased rapidly with age so that spleens of

1 According to the last census,. the population ofGuyana in 1960 totakd 560,406, comprising East Indians,267,840; Negroes, 183,980; Mixed. 67,189; Amerindians,25,450; Chinese, 4,074; Europeans, 3.218; and Others,8,655.

considerable size were found rarely in the olderchildren and even less frequently in adults.

Among East Indians, on the contrary, theincidence and degree of splenic enlargement wasmuch higher and was hardly affected by age.Clinical experience in sugar-estate hospitalsshowed that the majority of adults went throughlife afflicted by largeoften very largespleensand failed to come to terms with the infection;they suffered frequent attacks of fever, andanemia of some degree was practically uni-versal. Mortality directly due to malaria washighest in children, but the tolerance establishedin adults by life-long exposure to infection wasboth low and unstable; at all ages, malaria andits sequelae continued to be major causes ofdeath.

The 239,000 immigrants who came to Guyanafrom India between 1838 and 1917 originatedmainly in Bengal, I3ibar, Orissa, the CentralProvinces, and Madras, where malaria is mostly,though not exclusively, hypoendemic or meso-endemic, and seasonal in its occurrence. Thisexplains the lack of any inherited resistance tomalaria and the severe reaction these immigrantssuffered when they were transferred to thehyperendemic Guyana coastland.

Further inland, along the tidal course of theBerbice, Demerara, and other rivers, the autoch-thonous population is formed by Amerindiansof the Aiawak and Akawai tribes and by per-sons of mixed race, usually with Amerindian,European, and Negro blood in very variableproportion. There are few permanently settledNegroes, but a considerable fluctuating popula-tion of this race, mainly adult males, is employedin the mining and timber industries. At the timewhen malaria was hyperendemic in these dis-tricts, the Negroes came not only from the in-tensely malarial coast but also, and in high

proportion, from the more mildly malarialLeeward and Windward Islands and frommalaria-free Barbados. Whatever their origin,their reaction to malaria infection followed thesame pattern: they contracted the infection soonafter arrival, suffered an attack or two of fever,

106

and after that enjoyed normal health and rarelyreturned for treatment.

In contrast, the mixed population born andbred in the area suffered severely and continu-ously, all ages being affected; mortality andmorbidity were certainly graver in children, butthe tolerance acquired by the adults was poorand very unstable. The Amerindians reacted inthe same way as the mixed population, but evenmore severely; the largest spleens recorded,reaching the pubis and partly filling the pelvis,were seen in adults of this race.

Blackwater fever was not common in Guyana,in spite of the very high incidence of P. fda-parum; it appeared at long intervals, duringperiods of malaria exacerbation, and tended torecur in some localities, with clustering of casesin certain neighborhoods, homes, and families.On the Demerara River between 1923 and 1931,53 cases were recorded, mainly in 1926-1927,with the following racial incidence (4):

Race

NegroesEast IndiansAmerindiansMixed races

Incidence of Blackwater Fever

Per 1000inhabitants

2.67

24.0011.7921.83

Per 1000patients treated

19

191

84

189

Nephrosis and chronic nephritis associated withP. malariae infection were frequent on theDemerara River. The racial incidence per 1000patients during eight years was 20.4 in Negroes;48.8 in East Indians; 33.6 in Amerindians; and35.6 in mestizos. Children and young personsare more liable to blackwater and nephrosisthan adults; thus the low incidence of thesesyndromes in Negroes might be due, to someextent, to the preponderance of adult males inthis ethnic group. Ten years' experience on theDemerara River, in conclusion, showed that theArawak and Akawai Indians of the arca suf-fered severely from malaria and its complicationsand, like the East Indians of the coastlands,acquired only a very relative degree of toleranceto the infection, suffering from its effects atall ages.

In the far interior the population is widely

scattered and can be estimated at 45,000 (1967),of whom approximately half are Amerindiansbelonging to the Wapishana, Macusi, Patamona,Aka ',Rai, Arakuna, and Carib tribes. On theRupununi Savannahs and the Pakaraima Pla-teau, the inhabitants are almost exclusivelyIndians. Among them, malaria surveys havebeen few and irregular, and no systematic, long-term observations have been made; the same canbe said of other medical studies. Prior to theintroduction of control measures, malaria oc-curred throughout the year but transmissiontended to be much more seasonal than on thecoast, being related either to the May-Augustrains or to the floods of the larger rivers. Amongthe Indians of the lowland forest, spleen ratesranged from 40 to 60 per cent.

In some of the less accessible areas, the intro-duction of malaria appeared to be recent andpossibly related to increased traffic with thecoastlands. Thus, the savannahs of the Ru-pt., uni, which were difficult to reach before theadvent of the airplane, were reported to behealthy up to 1930; the only Indians who suf-fered were those who had visited the coast,traveling down the Essequibo River or drivingcattle through the Berbice trail. By 1938 (5),the infection had spread all over the savannahs,and more than 30 per cent of the children hadenlarged spleens, the rates increasing with age.By 1943 (6), fears were entertained that theMakusi of the North Savannah were dying out.During a malariortelTAsurvey of this area, 424Indians of all ages were examined; 68 per centhad either enlarged spleens, parasites, or both,and 46 per cent of the adults had large spleens,which in 20 per cent of cases extended belowthe transverse umbilical line. In the settlementssituated nearest to the forest, 80 per cent of theinhabitants showed evidence of malaria. Thelack of old people was very striking; only twowere seen, who appeared to be about 60 yearsof age. This was reported to be a recent develop-ment; it was said that before malaria appearedon the savannah, in 1930, old and very oldpeople were numerous. (One rancher who cameto the area in 1922 had known two Mahwut

107

ancients who remembered quite well the Britishmilitary expedition to Pirara in 1843.) Duringthis 1943 survey, many settlements in the Indianreservation along the northern Kanuku Moun-tain foothills were found deserted and some ofthe houses burned, as is customary after thedeath of an inmate.

This high susceptibility cf the Guyana Indiansto malaria is without doz.i.lit one of the majorcauses of their decline over the past 150 years.Smallpox, measles, yellow fever, influenza,whooping cough, and tuberculosis have all beencontributing factors, sometimes causing disas-trous epidemics; none of these diseases, however,was as constant in its onslaught as malaria.

The early Dutch colonists sought the allianceof the Indiansparticularly the Caribs, then a

very numerous and warlike triberelying onthem for the procurement of Indian slavescaptured in raids on villages and Spanish mis-sion settlements on the upper Cuyuni andOrinoco. Later, during the long years whenAfrican slaves were brought to the colony, boththe Dutch and the British planters relied onIndian help in subduing slave rebellions and inthe capture of fugitives. From 1778 to the endof slavery, annual official receptions were heldin honor of the Indian chiefs. At the end of theeighteenth century, the Amerindian populationappears to have been numerous and flourishing.The figures that have been given, however, areunreliable and differ widely; 50,000 would ap-pear to be a reasonable guess. With the abolitionof slavery, the Indians ceased to be of any inter-est to the colonists, and were left to themselvesand neglected. Their numbers dwindled rapidly,and the Caribs, the most rowerful and fearedtribe, practically vanished; only a few survive atthe present day on the upper Barama andBarima rivers. In 1848, after proper surveys, it

was established that the Guyana Amerindiansaggregated approximately 15,000, of whom only7,000 were still in the aboriginal or semi-aborigi-nal state (3).

Systematic malaria-control operations wereinaugurated in the interior in 1947; thougheradication has not as yet been achieved, the

incidence of the disease has been drasticallyreduced. The rapid increase that has followedin all the tribes is a clear indication of thedisastrous effect of malaria on this populationgroup over the pa years; in 1968, their numberis estimated at 32,000.

This high susceptibility and reactivity of theAmerindian to malaria is without doubt relat,c1to the recent introduction of the infection in theWestern Hemisphere. It is generally acceptedthat malaria, as well as many other diseases,came to America with the discoverers, the con-quistadors, and the hundreds of thousands ofslaves brought from West Africa. In the Ameri-cas the new arrivals found, wherever theylanded, native anopheles capable of acquiringand transmitting the disease; given the pro-longed infectivity of malaria subjects, the lackof curative medicines at the time, and the widediffusion of anopheles, it is not surprising thatserious early outbreaks occurred among theinvaders and that the infection spread rapidlyto the highly receptive Indians.

In spite of tradition, it appears that even thePeruvian Indians were ignorant of the propertiesof cinchona bark. Richard Spruce, the botanist,spent fifteen years, from 1849 to 1864, on theAmazon, and in the cinchona forests on theslopes of Chimborazo in the Ecuadorean Andes(//). It was he who was responsible for thecollection and shipment of seeds and youngplants from which the cinchona plantations ofIndia and Ceylon eventually originated. Hefound that the cascardleros (Indians employedin the collection of cinchona bark) not only werecompletely ignorant of its medicinal propertiesbut regarded his explanations with skepticismand suspicion, for they were convinced that thebark was used for the extraction of a valuablebrown dye.

In equatorial America, altitude, in the Andeancordillera, has probably been the only barrier tothe spread of malaria to even the most remoteand isolated Indian communities. The Wai-WaiIndians are an entirely primitive tribe that hasits main settlements in Brazil on the MapueiraRiver, which flows, through the Trombetas, to

108

the Amazon, some 400 miles to the south. A fewused to visit the headwaters of the Essequibo inGuyana. Their nearest neighbors are the Wapi-shana of the South Rupununi Savannah, some70 miles to the northwest, through high rainforest. Cassava graters and feather ornamentshave been traditional items of trade betweenthese two tribes, but contacts are maintained byonly a few individuals. For the last 15 years, amission has been established at Kanashen, onthe upper Essequibo, and it has attracted con-siderable numbers of Wai-Wai from across theborder. In 1966 a group of 80 paid their firstvisit to the mission, after a journey of severalweeks; of these, 14 were found infected withmalaria, P. falciparurn, P. vivax, and P. rnalariaeall being identified.

So far I have dealt with the incidence ofmalaria and its effects on the American Indian.The Indian's way of life, however, also hasimportant bearings on malaria epidemiology andeven more so on the practical development ofantimalaria operations.

Indian villages are small, with widely spacedhouses. The larger buildings usually accommo-date several families, each having its fireplaceand allotted space. Completely isolated housesar.: frequent. The large villages to be found inthe more civilized areas are due to missionaryinfluence. The houses are made of materials thatare easily procurable on site: round wood poles,bush ropes, palm leaves for roof thatching, barkand split palm trunks for walls and floors, andso forth. By community effort even the largerhouses can be erected in the course of a fewdays, and a serviceable shelter may be put upin a matter of hours. This makes it easy for theIndians to move from one site to another forsecurity, for better hunting or fishing, and,probably, for the purpose of escaping disease.As has been mentioned, houses in which adeath has taken place are frequently abandonedand burned down. This instability of settlementshas been recorded by most observers, and it isreasonable to expect that such a practice mayhelp in the avoidance of malaria, which in theforest is eminently a place disease, prevailing in

localities where conditions for abundant A.darlingi production exist.

The more permanent type of house consti-tutes the Indian's operational base, but, with hisentire family, he spends a large part of hisexistence elsewhereworking on his farm,usually situated at a very considerable distance;on hunting or fishing expeditions; attendingsprees; or just visiting his neighbors. In the morecivilized areas, he may seek temporary employ-mentas a guide, a porter, or a boathand, bleed-ing balata (wild rubber), collecting Brazil nuts,and so onand when so engaged he is usuallyaccompanied by his family. When away fromtheir permanent home, the Indians camp undertemporary shelters, ranging from a few largepalm leaves stuck into the ground to an openpalm-thatched shed.

This great and continuous mobility of theIndian is without doubt a factor favoring thewide and rapid diffusion of malaria infection.In 1947 a sharp outbreak occurred among thePatamona Indians on the Potaro-Ireng water-shed, on the Pakaraima Plateau, a mountainous,mainly forested region at an elevation of 1,000to 2,000 feet above sea level (7). Infected personswere discovered scattered widely over some 500square miles; all of them, however, had workedat, or had visited recently, a diamond placer,and this was the only locality where transmis-sion was actually occurring; a creek had beendammed and many gravel pits sunk in thevalley bottom, and in these A. darlingi foundideal conditions for continued production. Themigration of 80 Wai-Wai, of whom 14 weremalaria parasite carriers, has already been men-tioned.

These characteristics of the Indian way of lifeintroduce serious difficulties in practical malariacontrol and may frustrate even the most efficienteradication program. In the sparsely inhabitedinterior, A. darlingi, in adaptation to the en-vironment, is by no means as anthropophylicand endophylic as it is on the coast; it is widelydistributed as a silvatic mosquito, and malariatransmission takes place not in villages andhouses but at camping sites, on the farms, and

109

114

3*.

4.

P. vIvax. RESIDUAL FOCI

1111:* AND LINES Of SPREAD

++1-P. faklpxium. RESIDUAL FOCUS

oa + Of SILVATIC IRANSMISSION

MALARIA ERADICATED

90% OF POPULATION

B It A ZIL

*. 10.

FIGURE I. Map of Guyana. showing residual Plasmodium vivax foci that survived1961-1965 chloroquinized-salt campaign; lines of spread of infection by wandering Amer-indians; small focus of P. falciparum in south, persisting among wild-rubber bleeders; andpoint of intrusion of primitive Wai-Wai Indians from Brazil. Elsewhere medicated salt and/orDDT house spraying have eradicated malaria or greatly reduced its incidence (see text).

In south, the campaign failed, following the introduction of a chloroquine-tolerant P. ft:hi-parurn strain from Brazil in 1962. DDT house spraying on both sides of the border hasinterrupted transmission on the permanently inhabited Rupununi Savannahs, but a smallfocus of P. falciparum, transmitted by silvatic A. darlingi, persists among Amerindian balata-bleeders who camp, with. their families, in the otherwise uninhabited Rewa-Kwitaro forest,from May to November. In all, 3,500 persons are involved, with an annual average of only24 cases.

In the extreme south, the point of intrusion of primitive Wai-Wai Indians is indicated.

110

115

in the forest. The main villages can be sprayedwith insecticides without excessive difficulty, butthe existence of remote, isolated houses is veryfrequently unknown, and the systematic spray-ing of temporary shelters is not only impossiblebut futile, since they offer next to nothing in theway of sptayable surfaces. Under such condi-tions '.1-,'cticida1 methods can reduce, but noteradic nalaria, and their application is diffi-cult and expensive. Systematic spraying ofhammocks with DDT solution or emulsion is auseful practice, for the Indian always traveiswith his hammock and the insecticide residueresists occasional washing.

Mass chemotherapy, through systematic, per:-odic distribution of antimalarial drugs, is obvi-ously impracticable, owing to the terrain, thewidely scattered population, and its elusiveness.Even when a case of malaria has actually beendiscovered, treating it is a difficult matter; radi-cal treatment of P. falciparum infection needsat least three days, and for P. vivax 14 days arerequired. Pinning down an Indian for regulardaily dosage is no easy matter, and he usuallyfades into the forest in mid-treatment.

In Guyana, malaria, and its carrier A. dar-lingi, were eradicated from the coastlands andthe more accessible and populated inland areas(93 per cent of the population) exclusively byDDT house spraying (7). In the far interior theresults were by no means satisfactory, and nia-laria control only was established. This partialfailure of DDT was due to the wide scatteringof the population over an impervious terrain, itsinstability and mobility, and, above all, the

silvatic adaptation of A. darlingi (8).From January 1961 to December 1965 an

attempt was made to eradicate these residualfoci of malaria in the interior by means ofchloroquinized salt (9); in order to assess fullythe value of this new technique, DDT housespra}qng was suspended. This campaigr coveredan area of 42,000 square miles and a populationof 48,500, mainly Amerindians. The campaignwas conducted under strict administrative andscientific control; specific legislation was enactedmaking the use of chloroquinized salt compul-

sory in proclaimed areas and regulating its

shipping, transportation, and sale in the interior.Epidemiological evaluauon preceded, accom-

panied, and followed the campaign. In the areasin which chloroquinized salt was used, con-tinued DDT operations, from 1947 to 1960, hadgreatly reduced the frequency of the disease; thereservoir of infection within the population wastherefore relatively small.

In the North-West District and in the Paka-raima sectors, aggregating an area of 35,000square miles and a 1964 population of 39,550,malaria disappeared within six months (theparasite rate in 1960 had been 8.3 per cent);thereafter, only four sporadic, cryptic cases ofP. vivax infection were recorded up to April1965, when the campaign was closed down.

Early in 1966, ten months after the cessationof all antimalaria measures in the area, a smallfocus of P. vivax infection was discoveredamong the Caribs of the upper Barama Rivera very inaccessible locality that could receive

chloroquinized salt only irregularly and prob-ably in insufficient quantity, as no shops or othernormal means of salt distribution exist. TheseIndians, traveling down the Barama, spread theinfection to the Waini and Moruca rivers and,crossing overland, caused an outbreak at the

manganese mines on the upper Barima andKaituma rivers (see arrows at top of map)From there the infection spread rapidly to thylower course of these streams and to the Aruka.

In June and July the outbreak reached its

peak, with 372 widely scattered cases. During1966 a total of 643 cases were recorded on atotal of 20,811 slides examined, out of a popula-tion of 16,850; P. vivax was the only parasiteinvolved. The ontbreak has been controlled byDDT house spraying and the reissue of chloro-quinized salt, these techniques being used in

combination for the first time. Only 15 caseswere recorded in 1967 (9,116 slides examined)and only 3 from December 1967 to J, 1968.

An identical incident occurred among the4 vv.0 ndians of the Wenamu and upperCt\ .1 along the Venezuelan border, the firstcases ixing discovered in April 1966, one year

4

after the cessation of antimalaria operations.This again is a very inaccessible area, with asmall population of Akawai Indians who canobtain salt and other supplies more easily fromVenezuela than from the Guyana side; P. vivaxwas responsible for all cases discovered. Indianscrossing overland from the Wenamu to theKamerang, an affluent of the Mazaruni, spread..he infection to the upper Mazaruni and it3

tributaries, a sparsely inhabited arca with anestimated population of 3,000 Indians anddiamond miners. During 1966, 280 cases werediscovered in this sector. Many infected personsreached the coastlands, but were intercepted bysystematic examination of plane passengers fromthe interior. DDT house spraying and chloro-qv inized salt (issued free to Indians) havebrought the situation under control, thoughprogress has been slow, owing to the verydifficult terrain.

It is important to note that both these re-crudescences were due exclusively to P. vivax;the 1961-1965 medicated-salt campaign, even inremote and poorly supplied areas, appears tohave achieved the eradication of both P. falci.parum and P. malariae, which before the intro-duction of chloroquinized salt accounted for 57and 15 per cent, respectively, of the infections.

Among the 10,000 Makusi and WapishanaIndians who inhabit the savannahs of the Ru-pununi, close to the Brazilian border, chloro-quinized salt failed, after a favorable startduring 1961, owing to the introduction of a

chloroqu:nc-tolerant P. falciparum strain fromthe neighboring Rio Branco Tcf-ritory (9). Thisnew strain spread rapidly over the whole area,even where chloroquinized-salt coverage wasadequate. DDT house spraying, interruptedsince 1960, was reintroduced in 1962, and assoon as systematic spraying operations wereestablished by the Brazilians across the border,beginning in January 1965, malaria transmissionon the savannahs was interrupted. Si !vatic A.darlingi still persists in the surrounding forest,however, and occasional cases of P. falciparummalaria continue to occur, but exclusively amongIndians engaged in bleeding balata, who camp

in the ferest during the rainy season, from Aprilto November. Among 700 bleeders and theirdependents (estimated at 2,800), 24 cases werediscovered in 1966 and 22 in 1967.

For the 1968 season it is proposed to issue toall bleeders, along with the other rations theyreceive, 20 pounds of salt medicated with chloro-quine (0.43 per cent chloroquine base) andpyrimethamine (0.043 per cent), and, in addi.tion, to give to every indi :dual who can be"caught" before leaving for the forest a two-daytreatrient with a combination of Fanasil (Sul-furthomidine) and pyrimethamine. The resultof this new approach will not be known till theend of the year.

These various developments in the course ofthe Guyana campaign illustrate clearly thepeculiar difficulties encountered in malaria con-trol and eradication operations among the Amer-indians. As I have .said, in the early planning ofthe many campaigns that have been undertakenof late years throughout tropical America, littleimportance was attached to the specific problemof malaria in the Amerindian, priority beinggiven to the larger, more accessible communities,which were economically more important andpolitically more voca.. Today, with eradicationor, more frequently, control established overwide areas, the problem of malaria among theIndians assumes a new dimension, for it is

evident that eradication will remain a dreamuntil means have been discovered to extendcontrol to even the most remote of Indiansettlements. I have shown how rapidly andwidely malaria can be broadcast from extremelylimited foci, by wandering or migrating Indians.

Of the preventive techniques known at pres-ent, medicated salt appears to be the mostpromising, since it can find its own way farbeyond the reach of organized public healthagencies. We do not yet possess, however, theideal drug for this purpose. Those in use today,among other shortcomings, fail to act on certainparasite strains and may thus bring about theemergence and favor the diffusion of drug-tolerant or drug-resistant infections, introducingtherapeutic problems which may be serious.

112

417

I have shown how, in Guyana, chloroquinizedialt was completely succesul against all formscf native malaria parasite, only failing whereand when a chloroquine-tolerant strain was in-troduced from Brazil. Our campaign, it thouldbe emphasized, was inaugurated at a stage whenthe reservoir of infection had beim greatly de-pleted by DDT spraying. Under such conditions,the probabilities of the presence of recistantstrains were much redur- "ith the drugs atpresent available, we benn- , at medicated saltshould not be used under conditions of highendemicity.

Indians still in the aboriginal stage of civiliza-tion are not acquainted with commercial saltand manufacture salt substitutes by washingcertain soils or fr3m the ash of certain palms.Natural deposits of salt are not likely to occurthroughout the vast equatorial rain forest. Onthe other hand, civilized and semicivilized In-dians take to the use of commercial salt veryreadily, as in it they find not only a means forseasoning their food but a valuable preservative

fo i. the fish and game on which they subsist andwhich tend to abound in certain seasons and notin others; the traditional method of preservationemployed is smoking. The entirely primitiveWai-Wai Indians, for instance, who reachKanashen Mission from the depth of theBrazilian virgin forest, take to the use of saltwith great readiness as soon as it is madeavailable.

Obviously, spreading the use of salt to themore remote tribes will take years, and thesame can be said for eradicating malaria whereprimitive Indians exist; at the present stage ofmala.lological knowledge and antimalaria tech-nique, it appears likely that treatment and pre-vention may be extended more eas;ly to theprimitive and semiprimitive Indians throughthe established chailnels of intertri:3al bartertrade, in a bag of salt, than through a spray gunor a bottle of tablets. For this purpose, however,

more effective drugs for salt medication have

to be found.

REFERENCES

I. BOYD, M. F., and W. K. STRATMAN THOMAS.Studies on benign terian malaria. 4. On the re-fractoriness of .7.-,1cgioes to inoculation with P. vivax.Amer. Hyg. 18:485-489, 1933.

2. CLARK, H. C. A comparison of the spleen andparasite rates as measures of malaria incidence inthe races of the mainland of Central America. InMedical Department, United Fruit Company, Seven-teenth Annual Report, 1928, pp. 77-83.

3. COMMISSIONER OF THE INTERIOR. (1948) TheAmerindian problem. In Development Report.Georgetown, Government of British Guiana, 1948,pp. 10-22. (Mimeo.)

4. Giamota, G. Malarial Nephritis. Epidemiologi-cal Notes on Malaria, Blackwater Fever, Albuminu-ria and Nephritis in the Interior of British Guiana,Based on Seven Years Continual Observation. Lon-don, Churchill, 1930. 164 pp.

5. Giouou, G. Notes on health conditions in theSouth Rupununi Savannah. Appendix to Report ofthe British Guiana Commission to the President'sCommission on Political Refugees. Georgetown,1939, pp. 56-59. (Legislative Council Paper No. 12/1939)

6. Gtomou, G. Malaria Survey of the NorthRupununi Savannah. Georgetown, 1939, pp. 1-14.(Legislat. Council Paper No. 3/1944)

7. CIGLIOLL G. Malaria, Filariasis and YellowFever in British Guiana: Control by ResidualD.D.T. Methods. Georgetown, Medical Depart-ment, 1948. 226 pp.

8. thomou, G. Fifteen years experience in malariaeradication in British Guiana. Maintenance policiesand residual problems. Riv. Parassit. xx(4) :280-288,1959.

9. GIGLIOLL G., F. J. RUTTEN, and S. RAMJATTAN.Interruption of malaria transmission by chloro-quinised salt in Guyana. Bull. Wld. Hlth. Org. 36:283-301, 1967.

10. RAtcriENow, E. Zur frar - der Malaria-resisten,bei Negren. Behefte Z. Arch. f. Schiff; u. TropenHyg. 3358-64, 1929.

11. SPRUCE. R. Notes of a Botanist on the Ama-zon and in the Andes, II, ed. by A. R. Wallace.London, Macmillan, 1908, pp. 271-272.

12. SWELLENGREBEL, N. H., and E. VAN DER KUYP.Health of White Settlers in Surinam. Amsterdam,Colonial Institute, 1940, pp. 92-97.

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'118

FOOD AND NUTRITION OF THE MAYA BEFORE THE CONQUESTAND AT THE PRESENT TIME'

Moisés Béhor

". . . and grinding then the yellow and the white carsof corn, the goddess hmucané prepared nine beverages,and from this food came strength and stoutness and withit they created the muscle and vigor of man. . . ."

"Their flesh was made from yellow and from white corn;from ground and kneaded corn were moulded the armsand legs of man. Only damp, ground corn went into theflesh of our fathers. . ."

A great civilization developed in MiddleAmerico on thc basis of corn. The above quota-tions from the Topol Vuh, the sacred book ofthe ancient Quiche Maya, emphasize the im-portance ascribed to this staple grain by theMayan populations. Nevertheless, our presentknowledge of nutritica has demonstrated thatcorn, if not properly supplemented (16), is

nutritionally very poor as a staple. As in most ofthe cereal grains, its protein concentration islow; in addition, corn proteins have a very lowbiological value. They are deficient in at leasttwo of the essential amino acids: lysine andtryptophane (5). Furthermore, the deficiency oftryptophane in corn, plus a low concentrationand/or availability of niacin, favor the develop-ment of pellagra in those whose diet is basedon it (10).

Tt must therefore be asked how an importantcivilization like the Mayan could develop withsuch a great dependence on corn as its staplefood; and why the present-day descendants ofthe Mayas have serious nutritional problems,also because of their dependence on corn.

1 Research supported by Contract PH43-65-640, National Institute of Child Health and Human Develop-ment (NICHD), Bethesda, Maryland, U.S.A.

In this paper I shall try to review our unfortunately small store of information on the clietir)practices and nutritional status of the Ma)arpopulations before the Spanish conquest of tai:region. I shall examine the same conditions irtheir direct descendants, the Guatemalan Indians of today, and attempt to determine thtmain changes that have come to pass. It is m)hope that, in so doing, some general principle!applicable not only to this particular groupAmerican Indians but to others as yell wilemerge. This seems to me more useft.:, thanpurely descriptive paper on the nutritional problems now afflicting the American Indian groups

Dietary practices and nutritional status of thepre-Columbian Mayan Indians

Corn, prepared in many different ways, waseaten at every meal, every day, as the most irnportant .:ood. In addition, the Mayas cultivatedanu consumed beans, vegetables, fruits, rootstubers, cacao, and spices (15). Animal products.mainly meat and to a much lesser extent eggs.were apparently not a .-egular item in theirsdietary; they were consumed sporadically andon special occasions, and were obtained mainlytby hunting. Very significant in this regard isthe existence, in a Mayan dialect of the Guate-imalan highlands, of a spcial word, tcibex, fori"to eat meat," as distinct from the general word;lobex meaning "to eat" (14). Only the groupsliving on the coasts consumed fish. Milk was notiused at all.

Our present knowledge of nutrition indicates;

that, with such a diet, it is difficult to satisfy therequirements for at least three important nutri-mts: protein, calcium, and niacin. The defi-ziency of calcium and niacin was corrected bythe way in which corn was processed. For the?reparation of tortillas and other corn products,the grain was first soaked overnight in halewater a-od then cooked in the same water (thepurpose was to remove the husk). The resultwas a product very rich in calcium, for whichthe Mayas had no other adequate dietarysources. This method also yielded a higher con-centration of tryptophane in relation to theother amino acids, and more available niacin(13), thus preventing pellagra. We can onlyspeculate on how this practice was adopted, butit is now evident that it was indispensable fortheir survival.

We are still left with the problem of how theysatisfied their nutritional requirements for pro-tein. As I have said, the main drawback of cornproteins is that they are deficient in some essen-tial amino acids, particularly lysine and trypto-phane. However, an amount of 39 grams of cornprotein a day, which satisfies the average proteinrequirement in an adult male weighing 65kilograms (17), does contain the neededamounts of all essential amino acids (12). Thisamount of protein is provided by about 370 gof corn, which is not an unreasonable quantityfor a man to consume per dayin iact, Guate-malan Indians now consume around 500. Inspite of the low biological value and low con-centration of proteins in corn, it is thereforepossible for aduits to satisfy their protein needswith tliis grain as the main staple, if they con-sutne enough of it.

But the situation i, completely different forsmall children, who have relatively higher pro-tein requirements and in whom the need foressential amino acids is also greater. A two-year-old child, for instance, would need about 18 gof protein a day to satisfy his nitrogen require-ments if the protein has an ideal composition,with a biological value of 100 per cent; in otherwords, if it is fully utilized (17). With corn asthe source, the child would need 3G g of protein,

because the biological value of corn protein isabout 50 per cent (4). This means that hewould have to consume about 450 g of corn aday, or about 800 g of tortillas, to satisfy hisprotein needs. Not only is this physically im-possible but, in addition, the child would bereceiving many more calories than he needs.

Of course, the Mayas did consume other foodsbesides corn. From what we know, the otherimportant items in the regular daily diet weiebeans, fruits and vegetables, and roots andtubers. Beans are a more concentrated source ofprotein, but the remaining food items, althoughthey contribute other needed nutrients, reducethe over-all concentration of protein in the diet.The situation would again be one in whichadults can satisfy their nutritional needs butsmall children cannot.

I have mentioned that the Mayas did not con-sume milk, and that other animal products(meat aPcl eggs) were only eaten irregularly.It is also very unlikely that they fed meat toinfants and small children, for they had notdeveloped thz requit..:d processing facilities.There was only one solution, and they applieditprolooged lactation. The information nowavailable indicates, in fact, that Mayan mothersbreast-fed their children for at least three yearsand frequently even longer (15, p. 44).

Our present knowledge indicates that breastmilk can satisfy all the nutritional requirementsof a baby up to approximately six months of age.It is probable that from about that age Mayanmothers started to give their children what therest of the family ate but continued to feed thembreast milk as an indispensable protein supple-ment. By the time they were completely weaned,after the age of three, they were able to eatenough of the family food to satisfy their nutri-tional requirements without the use of anyspecial product, such as milk in the case ofWestern civilization, It is also probable thatduring this transitional period, from about sixmonths to three or four years of age, they didnot grow to their full genetic potential. Thiscould be the main reason for the small size ofthe adults, which is well dormmented. This

115

reduction in body size, a consequence of en-vironmental conditions and particularly of nutri-ent availability, can also, I believe, be considereda mechanism of adaptation to those environ-mental conditions. In fact, with reduction inbody size resulting in a similar reduction innutrient requirements, titt. Mayas were betterable to meet these requirements with the avail-able foods.

Unfortunately, we have no information onthe health conditions of children in those popu-lations. Data on infant and early childhoodmortality could be particularly illustrati- Theinformation available indicates that, in general,the children were healthy. De Landa (15) says:

They grew wonderfully handsome and fat during thefirst two years. Later, their skin waxed dark with con-tinuous bathing by mothers and many suns; they werenonetheless bonny and mischievous throughout child-hood. never ceasing to w,,nder about carrying bows andarrows and frolicking among themselves and thus theygrew until they began to adopt the ways of the youthsand to acquire a more exalted self.concept, and to leavebehind the things of childhood.

We cannot say the same about the majority ofpiTschool children of Mayan descent today; theyare usually apathetic. and very ofter sick.

Another is'aponont dedu&on that can bemade from the wtion lace we,ri;rwconcerns birth spacing. th' pro:aablyhad at least three years betwcin 0;1,1

the next. To what extent prolonged l. tati:;ncontributed to this situation we still do Lotknow. However, it was definitely very con-venient, because only in this way could themothers breast-feed their children as required.Accurate information on the nutritional condi-tion of pre-Columbian Mayan adults is alsononexistent, but all known facts indicate that,although small, they were in general strong andhealthy. We can thus conclude that, in terms ofnutrition, they did not have serious problemsand were well adapted to their environmentalcircumstances and degree of cultural and tech-nological development. They did, however,undergo acute crises, and there is information onthe famines they suffered when natural disasters(droughts or locust invasions) interfered withtheir corn crops.

Dietary practices and nutritional condition ofthe Guatemalan Indians of today

The dietary practices of the Guatemalan In-dians of our time have not changed very muchfrom those of their pre-Columbian ancestors.The changes that have occurred, however, havegradually brought about a deterioration in theirdiet and have upset the balance under whichthey lived.

Corn, processed in the same way, is still themain staple. It provides up to 80 per cent of thecalories and 70 per cent of the proteins in thediet of the adult population (9). Beans, vege-tables, and fruits complement the basic diet (8).These products, however, now have a marketvalue for which the more affluent non-Indit ngroups in the population are better able to com-pete. This is even more true of animal products.Wild animals have practically disappeared, andhunting is no longer an important means ofobtaining precious foods. Domestic animals arenow the only important source of animal prod-ucts, and the market for them is very competi-tive. The majority of the Indian families raisesome animals in their homes, mainly poulti yand pigs. But these are more a source of badlyneeded cash than of food. They and their prod-ucts are consumed only on very rare occasions;cl-kost of the time, !!'),Pv are sold. The meat mostfrequently ,2onsuined is beef, which has to be

trorn i:he market and therefore is onelor hidi rash is needed.

Not eini); La-ce indianl, ;1'w their oldsources of food in the wild forests, but also theamount of land available to them for cultivationhas been drastically reduced. Before the Conquest, they had all the land they needed toproduce their corn. Although the method ofcultivation they used cannot be considered veryefficient today, its relative inadequacy was com-pensated for by the availability of sufficient landfor a rotation system. They did not need toproduce cash crops, which now compete withfood crops for the best lands.

Under present-day circumstances, the Indiansare frequently forced to buy even their corn,which they had always produced before. Owing

116

:o their poverty, this greater dependence on themarket to satisfy food needs has caused theirdiet to deteriorate. Another change in the adultliet is the introduction of coffee, which hasreplaced the more nutritious corn and chocolatebeverages they used to drink, Distilled alcoholicbeverages have also become part of their con-sumption habits, with deleterious effects fromthe nutritional and even more from the eco-nomic standpoint.

Changes in dietary practices concerning smallchildren are even more important, and thesehave been mainly the effect of cultural influ-ences. In the first place, the period of weaninghas been shortened. In pure Guatemalan In-dians, prolonged lactation is still essential tochildren's survival. Complete weaning in thesepopulations now takes place between the ages ofabout two and two and a half years; this time,already shorter than it used to be before theConquest, is being progressively reduced as theprocess of integration into the ladino or Westernculture advances (11). This situation is very

dangerous and has caused acute nutritionalproblems, since the populations adopting earlierweaning are not as a rule prepared culturallyand economically to feed their children properlyduring the critical post-weaning period. Theirgeneral ignorance in matters of hygiene, and thelack of the most elementary physical facilities intheir homes, renders the use of milk very dan-gerous. Most of them, in any case, cannot afford

to feed milk to their children.The ,itu Ition is further aggravated by the

introduction, by foreign civilizations, of refinedproducts with a much lower nutritive value thanthe foods they replace. This is particularly trueand deleterious for the child during the post-weaning period. A v, example of this problem isthe pure starch preparations made from corn ormanioc that are otten used nowadays in gruelsfor small children, instead of the more nutritieuswhole-corn gruels of old.

The Guatemalan Indians of today thus seemto be in a less favorable balance with their en-vironment than their ancestors were, and theirdietary practices have deteriorated. Food intake

at the present time is barely adequate for adultsand frequently inadequate for children. As aresult, environmental stresses, particularly theheavy burden of frequent infections in earlychildhood, have caused poor nutritional condi-tions for the general population, with frequentand F. cvere cases of nutritional deficiencies foundparticularly in early childhood. Briefly, the nu-tritional peoblems now affecting the GuatemalanIndians art ;.,ks follows:

The most important by far is protein-caloriemalnutrition (19). As has been indicated, it isthe result of the synergistic effect of an insuffi-cient and inadequate dietary intake and fre-quent infectious episodes, particularly diarrhealprocesses and the common diseases of childhood(3). This condition contributes very significantlyto the high mortality rates in infancy and earlychildhood (2). It causes a relatively high preva-lence of severe cases of protein-calorie malnu-trition (kwashiorkor and marasmus) (/), whichare usually fatal if not properly treated in ahospital. Even more important from the publichealth standpoint are the chronic, subclinicalforms of malnutrition, which usually go unrec-ognized. These affect a large majority of thepopulation, both children and adults (18). Theconsequences of this condition are not yet clear,but there is information suggesting that it mayinterfere significantly with mental developmentin children (6) and with work performance inadults (20). If these observations are confirmedand studies are now under way to test thehypothesisit is easy to understand the tremen-cous importance of the problem in terms of thegeneral well-being of these populations and oftt-eir participation in the social and economicdevelopment of their societies and countries.

Among the other nutritional problems may bementioned vitamin A deficiency, primarily theresult of diets in which the sources of t.1,15 vita-min are vegetable prodects with iowactivity consumed in insufficient amounts (8).This deficiency rewIts in problems as serious askeratomalacia, which ends ;n te tal blindness

during early childhood. Riboflavin deficiency isamong the most prevalent of the vitamin defi-

117

w

ciencies (8). It is closely interrelated with pro-tein deficiency, since the adequate dietarysources of the two are frequently the same.Mucosal and cutaneous lesions characteristic ofthis deficiency are frequently seen. Its possiblegeneral effects are not clearly understood.

Nutritional anemias are also highly prevalent;the deficiencies of iron and folic acid are thefactors most frequently responsible, but againprotein malnutrition contributes to their devel-opment (21). Anemias may also be importantin restricting work capacity. Endemic goiterused to be highly prevalent in Guatemala, butfortunately it has now been controlled by meansof salt iodization (7).

The nutritional problems herein summarizeddo -1t3t affic t. the hidian pouPil,,on r. Guate-mala viittifn7 or i.ieterentiaily. They are asso-uiated wit:0 !w,A, cur. ,ioial inomic levelsand poor sanitary conditions. There are non-Indian populations 1,1 .,Lilar conditions, butpractically all the Indian populations fall intothis category. Their difficulty is one of properintegration into and adaptation to new ecologi-cal and cultural conditions and social structure.

In my opinion, the situation described inrelation to the Mayan Indians, and the changestbat have come to pass, are applicable to a lesser

-..1.can:r extent to other Indian groups nowwith Western civilization in the

kmcricali cotintries. On the other hand,many intl;an groups ;Ail: 13ving in isolation fromWestern Cure and from the present LatinAmerican societics have less serioLs m.tritionalproblems; some of them seem to be liNiug underexcellent conditions in this respeu. e groupsare still very dependent on hunting and Usliingto satisfy their food needs, and still follow the"primitive" practice of raising their children at

the mother's breast for as Icni; as Fo,sible. Theydo not have at their disposal the 'benefits" olcivilization, such as the practice of bottle feedingand very inadequate weaning foods. We mustconsider the situation of these groups of prirni.tive Indians as they become incorporated intoour societies, with the hope that we will findmeans to prevent or minimize the nutritionaldeterioration to which they may be exposed inthe process of integration.

Summary

An analysis of the dietary patfrr ,:. f3nd thenutritional conditi.,-1 of Mayrn populatiotIs.before the ihe ,tindicates tLy. a:tL .or,A coist :11e:

r,ain stapk kr both pnpul-auon groups, thepre-Columbian Mayas were probably betteradapted to ecological conditions. The availabilityof game, greater availability of land for cultiva-tion, the absence of competitive markets, pro-longed lactation of infants, and the lack ofindustrialized products were among the factorsthat brought about a better diet for the Indiansat that time. The sociocultural and economicchanges that have taken place since the Con-quest have worsened the diet of the presentIndians and resulted in serious nutritional prob-lems, among which protein deficiencyparticu-larly in small childrenis the most important.This experience should be considered both intr, mg to solve the nutritional problems of thisahd other American Indian gro..ips now livingwith pui.,Intions of Western culture and in pre-venting similar changes that could occur as thestill primitive and isolated Indian groups areincorporated into modern Latin American cul-ture.

REFERENCES

1. Au Tiirr, M., and M. BEHAR. Sindrome poli-carencial in/anti! (kwashiorkor) and its preventionin Central America. Rome, Italy, Food and Agri-culture Organization of the United Nations, 1954.(FAO Nutritional Studies, 13)

2. BEHAR, M., W. ASCOLI, and N. S. SCRIMSHAW.An investigation into the causes of death in children

in four rural communities in Git9tcipall. Bull. Wld.Hlth. Org. 19:1093-1102, 195e.

3. BEHAR, M., and N. S. SCRIMSHAW. Epidemi-ology of protein ii.alnutrition. In Iago Caldston(ed)., Human Nuto,i Historic Scientific.New York, International Universities Press, 1960,pp. 257-273. (Institute of Social and Historical

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123

Medicine, The New York Academy of Medicine,Monograph III)

4. BLOCK, R. J., and H. H. MITCHELL. The corre-lation of the amino-acid composition of proteinswith their nutritive value. Nutrition Abstr. Rev.16:249-278, 1946-1947.

5. BRESSANI, R., N. S. SCRIMSHAW, M. BEHAR. d

F. VITERI. Supplementation of cereal prot":amino acids. 11. Effect of amino acid sth:ple:1tion of corn-masa at intermediate -levels o roteinintake on the nitrogen retention of young children.1. Nutrition 66:501-513, 1958.

6. CRAVIOTO, J. Application of newer knowledgeof nutrition 1-.1 physical and mental growth and(I. )1. t Am. 1. Pub. Health 53 :1803-1809,11,1;3.

7. DE LEON, J. R., and 0. G. RETANA. La erradi-caciOn del bocio endémico en Guatemala; informefinal. Nutrición Bromatol. Toxicol. 5:43-54, 1966.

8. FLORES, M., B. GARCIA, Z. FLORES, and M. Y.LARA. Annual patterns of family and children'sdiet in three Guatemalan Indian communities. Brit.1. Nutrition 18:281-293, 1964.

9. FLORES, M., and E. REH. Estudios de htibitosdieteticos en poblaciones de Guatemala. I. Magda-lena Milpas Altas. Bol. Ofic. San. Pan. Sup. 2, 90-128, 1955.

10. GowsmITH, G. A., G IEBE NS, W. G. UNGLAUB,

and 0. NEAL MILLER. Studies of niacin requirementin man. III. Comparative effects of diets containinglime-treated and untreated corn in the productionof experimental pellagra. Am. 1. Clin. Nutrition 4:151-160, 1956.

11. GoNzAuz, M. L. SOLIEN DE. Breast-feeding,weaning and acculturation. J. Pediat. 62:577-581,1963.

12. HEGSTED, D. M. Variation in requirements of

nutrients-Amino acids. Fed. Proc. 22:1424-1430,1963.

13. KODICEK, E., R. BRAUDE, S. K. KON, and K. G.MITcHELL. The availability to pigs of nicotinic acidin tortilla baked from maize treated with lime-water. Brit. J. Nutrition 13:363-384, 1959.

14. LA FARGE, 0. The Religion of a Cuehumatan.'rd;an Town. Chicago, University of Chicago Press,1947, p. 37.

15. LANDA, FRAY DIEGO DE. Relación de las cosasde Yucatan (compuesto por el alio 1560). 8a. ed.Mexico, Editorial Porrua, 1959, pp. 36, 37. (Biblio-teca Porrua, 13)

16. ORGANIZACION DE LAS NACIONES UNIDAS PARA

LA AGRICULTURA Y LA ALIMENTACION. El maiz enlu alimentaeión. Estudio sobre su valor nutritivo.Roma, FAO, 1954. (Estudios sobre NutriciOn, 9)

17. Protein requirements. Report of a Joint FAO/WHO Expert Group. Published jointly by FAO andWHO. Rome, Food and Agriculture Organizationof the United Nations, 1965. (FAO NutritionMeeting Report Series, 37; WHO Tech. ReportSeries, 301)

18. SCRIMSHAW, N. S., and M. BinAR. Malnutri-tion in underdeveloped countries. New England J.Med. 272:137-144, 193-198, 1965.

19. SCRIMSHAW, N. S., and M. BEHAR. Proteinmalnutrition in young children. Science 133:2039-2047, 1961.

20. ToRt3N, B., F. VITERI, F. SARANTIA, and M.FLORES. Body composition in Guatemalan adults ofdifferent nutriture. Fed. Proc. 27:679, Abt. 2605,1968.

21. VITERI, F., J. ALvARAno, D. G. LUTHRINGER,and R. P. Wool), H. Hematological changes in pro-tein-calorie malnutrition. Vitamins & Hormones.26, 1968. In press.

"9124

IODINE DEFICIENCY WITHOUT GOITER IN ISOLATED YANOMAMAINDIANS: PRELIMINARY NOTE

René Rivière, Dominique Comer, Monte& Colonomos, Jean Desenne, andMarcel Roche'

Roche et al. (10) showed that, in a region ofendemic goiter, subjects without as well as thosewith goiter had an elevated thyroid radioactiveiodine uptake. A similar finding was reportedin New Guinea by Cboufoer, Van Rhijn, Kas-senaar, and Querido (1). In an isolated primi-tive Venezuelan Indian community, Roche (9)demonstrated a generally elevated thyroid up-take without goiter; and this was again de-scribed in the eastern region of the CongoRepublic by Delange, Thilly, and Ermans (3).

In the present preliminary note, further quan-titative aspects of thyroid metabolism in a

Yanomama group from the upper Orinocoregion are presented.

Material and methods

The area chosen for study lies roughly be-tween the Ocamo and Mavaca rivers on theOrinoco (Figure I), in the extreme south ofVenezuela. It is reached by plane to La Esrne-raldaan old mission site visited by Humboldt(7) in 1800and upstream from there by fastriver boat in about four hours. Two expeditionswere carried out.

During a preliminary one in February 1962,thyroid iodine uptake was determined on 41Yanomarna Indians living in Bisaasiteri, at theconfluence of the Orinoco and the Mavaca. Allthe subjects studied were ad- quately nourished,in good health, and with thyroids that were

I Presented by Dr. Roche,

72 ?0FIGURE 1. Area selected for study of thyroid metabolismin Yanomarna Indians (see page 77 for map of Vene-zuda)

either not palpable or barely palpable. ACatholic and a Protestant mission were estab-lished at the site, but the Indians still lived inwide-open thatch huts, ate their own food, andwent completely naked.

Another expedition was carried out in Janu-ary, February, and March 1968 to Bisaasiteriand to the neighboring Ocamo River (Tyowci-teri). The living conditions of the Indians hadchanged, although they remained very primi-tive. They no longer lived in the characteristii:

120

123

huts, but rather in closed dwellings; they occa-sionally received food and medicines from themissions. A third group, from Macorimateri onthe Manaviche river, was also contacted thistime; this group, unlike the first two, was stillculturally isolated in all respects.

On the second expedition, 56 adult subjects-44 male and 12 femalewere studied. Theydiffered from those studied on the first expedi-tion. They were in apparently good clinicalnutritional state, of short stature (males 1.57 mand 52 kg, females 1.44 m and 45 kg, on theaverage) and without any clinical evidence ofthyroid dysfunction. In 45 of them the thyroidwas not palpable; in 10 it was palpable butestimated to be of normal size. In one subject(a male) there was a small diffuse goiter, esti-mated to weigh around 50 g.

Twenty-four-hour thyroid uptake was deter-mined after the oral or intravenous administra-tion of 5 to 30 c of "'I, in the manner recom-mended by the Intei national Atomic EnergyAgency (12). A figure on the uptake of the firstgroup has been published (6). Kinetic studiesare being continued after the oral administrationof 100 fic of laq and will be reported later, aswill the effect of TSH and of methimazole andother measurements.

Radioactivity was measured on the site of thestudy; the various iodinated fractions of plasmawere separated on ion exchange resins and mea-sured separately. Measurements of urinary '271and creatinine were performed on single urinarysamples because of the practical impossibility ofobtaining reliable 24-hour samples.

The blood, urine, and river drinking watersamples were refrigerated around 40 C whenindicated and sent by plane to the central labora-tory in Caracas. Stable iodine was measured byactivation analysis in the Nuclear ChemistryDepartment of the Venezuelan Institute for

Scientific Research and at the Service HospitalierFrederic Jo liot in France (2). The iodine/creatinine ratio was measured to give an idea ofthe daily urinary iodine excretion. The average24-hour creatinine excretion was assumed to be1.6 g for mcn and 1.0 g for women (5, 8).

Results

Figure 2 shows the thyroid iodine uptake inBisaasiteri in 1962 (left) and the uptake in thecombined populations of Bisaasiteri, Tyoweiteri,and Macorimateri in 1968. Table 1 shows data oniodine metabolism. The iodine content of riverwater was 3.2 pg/liter (average of six samples).

Discussion

As Figure 2 shows, the thyroid iodine uptakeis higher in all the subjects studied in 1962. In1968, although many uptakes are still high, thistime five individuals have uptakes below 40 percent. It is presumed that the lowered uptakes aredue to the introduction of foreign food andmedications; none of the uptakes in the moreisolated group were low, and the average in thatgroup was higher than in the other two (Table1).

The urinary iodine/creatinine ratios (Table1) are low compared to normal values (5). Thetotal 24-hour iodine excretion can only be indi-rectly evaluated. The values obtained are ap-proximations, since urinary excretion of iodineis not uniform throughout the day and since24-hour urinary creatinine is not an accuratelyfixed value. As a matter of fact, creatinine excre-tion is related to muscle mass and in these short,

thin Indians is likely to be less than is takenhere as normal (4.) In a group of Makiritare In.

121

0-

5

1968

10 20 30

Thyroid Uptake i',44

70 100

FIGURE 2. Frequency distribution of iodine131 thyroiduptake of Yanamama Indians

126

TABLE 1. Iodine metabolism in isolated Venezuelan Indians (average, standard deviation, range, and number ofsubjects)

SITE

24-nouRTHYROID 1311

LIPTAK E

( OF DOSE)

127I0DINE (AO /CREATIN1NE (g)

RATIO

PLASMA

THYROXINEI 271

(jig/ l 00 cc)URINARY 127I

(Aig/DAY)

- ---MAXIMUM 1 25I

PLASMA

THYROXIN

(70/LITER)

Bisaasiteri

Tyoweiteri

Macorimateri

64.3±-7.4

36.0-81.3(26)

61.1

48.6-70.0(10)

74.1

32.9-93.0(12)

29.1

10.0-104.0(35)

19.1

30.0-70.0(10)

4.42

(22)

5.07

2.6- 7.4(12)

42.6±-7.8

15.0-166.0(35)

30.5

±-6.416.0-48.0

(10)

0.445±.0.107

0.194-1.100(18)

0.679

0.207-1.450(10)

dians, at the Ventuari River, Roche, Perinetti,and Barbeito (Li) found a 24-hour iodine excre-tion of 21.2 p.g/day with a mode between 10 and20 pg. Iodine in the drinking water was low inthe Orinoco, although not as low as in theVentuari, where, by a different method, 0.2 to0.6 lig of iodine was found.

Plasma thyroid 127I was normal in both ofthe groups studied, which is in accord with theobservatioil that these subjects are clinicallyeuthyroid.

The high thyroid iodine uptake and the lowurinary 19 excretion are comparable to thosefound in a goitrous Andean region of Venezuela(Riviere, Camuzzini, Comar, and Roche, to bepublished) and indicate that these goiter-freeIndians are indeed iodine-deficient. It again ap-

pears evident that goiter may fail to occur eventhough, as is likely in this case, iodine deficiencyhas been present through many generations.What other factor or factors are needed remainsin question.

Summary

A study of iodine metabolism was carried outin 48 Indians from the Yanomama tribe livingnear the confluence of the Orinoco and Mavacarivers in Venezuela. Elevated thyroid iodine up-take, low urinary iodine/creatinirie ratio, normalplasma thyronine, and apparently normal clinicalthyroid status were demonstrated, in the absenceof goiter. It is suggested that iodine lack is anecessary condition for the formation of endemicgoiter.

REFERENCES

1. CHOUFOER, J. C., M. VAN RHIJN, A. A. M.KASSENAAR, and A. QUERIDO. Endemic goiter inwestern New Guinea: iodine metabolism in goitnousand nongoitrous subjects. I. Clin. Endocrinol. andMetab. 23:1203-1217,1963.

2. COMAR, D., R. RIVIERE, and C. KELLERSHOHN.L'analyse par activation et ses applications auxsciences biologiques. In Troi.iietne Congres Interna-tional de Biologie de Saclay. Paris, Presses Univer-sitaires de France, 1964, pp. 307-336.

3. DELANGE, F., C. THILLY, and A. M. ERMANS.Iodine deficiency, a primitive condition in thedevelopment of endemic goiter. I. Clin. Endocrinol.and Metab. 28:114-116, 1968.

4. DE VENANZI, F., M. ROCHE, and A. GERARDLCaptación de yodo radiactivo (1131 ) por sujetoseutiroideos de nuestro medic), y algunas considera-clones sobre aplicaciOn al diagnOstico de las enfer-medades tiroideas. Acta Med. Venez. 3:114-118,

1955.

5. DWORIlsi, H. J., J. P. CHANDLER, and W. H.BEIERWALTES. Estimation of fecal and urinary excre-tion of iodine, J. Clin. Endocrinol. and Metab. 25:149-151, 1965.

6. GAEDE, K. Algunos eswdios recientes sobre elbocio endemico. Acta Cientifica Venez. Supp. 1:58-74, 1963.

7. HUMBOLDT, A. DE. Voyage aux regions equi-noxiales du Nouveau Continent. Paris, LibrairieGrecque-Latine-Allemande, 1816.

8. JOLIN, T., and F. ESCOBAR DEL REY. Evaluationof iodine/creatiaine ratios of casual samples asindices of daily urinary iodine output during fieldstudies. J. Clin. Endocrinol. and Metab. 25:540-54',1965.

9. ROCHE, M. Elevated thyroidal P31 uptake in

the absence of goiter in isolated Venezuelan Indians.J. Clin. Endocrinol. ind Metal,. 19:1440-1145, 1959.

10. ROCHE, M., F. DE VENANZI, J. VERA, E. COLI.,M. SPINETTI-BERTI, J. MENDEZ MARTINEZ, A. GER-ARD!, and J. FORERO. Endemic goiter in Venezuela,studied with P31. I. cli,i. Endocrinol. and Metab.17:99-110, 1957.

11. ROCHE, Y., H. PERINETTI, and A. BARBEITO.Urinary excre,.ion of stable iodine in a small groupof isolated Venezuelan Indians. f. Clin. Endocrinol.21:1009-1012, 1961.

12. The Calibration and Standardization of Thy-roid Radioiodine +Uptake Measurements. Vienna,International Atomic Energy Agency, November28-30, 1960.

STUDY OF ENDEMIC GOITER IN THE AMERICAN INDIAN'

José Bane lotto and Edmundo Covarrabias2

The existence of endemic goiter in Americacan be traced back to pre-Columbian times (5,4i), although the opposite view can be sustained(14, 15). Endemic goiter areas have been

demonstrated during the last decades in practi-cally every couutry in the Americas. From thereview published by Kelly and Snedden in 1960(21), it can be estimated that at least 20 percent of the population is affected by goiter.From epidemiological surveys comprising in

some cases huge samples, it can be inferred thatall races are affected. Unfortunately, there is noprecision about racial distribution in most ofthe studies; present-day American Indians aremixed in different degrees and have been in-cluded in variable proportions. Those Indianswho live in prinlitive conditions and are pre-sumably less mixed have been the subjects ofonly a few specific goiter surveys (35, 46).

Iodine deficiency in the populations of en-demic goiter areas in America, as judged byurinary excretion, has been found in prac,icallyevery case where it has been looked for (2. 17,

18, 19, 24, 26, 36, 4!). This is not surpris.ng,since except for the nitrate deposits in northcmChile (2d) iodine is not abundant ib the surfaciof this hemisphere as it is in the rest of theworld. Wherever the diet has been supple-mented with iodine, the incidence of endemicgoiter has been greatly reduced; well-docu-

I Work supported by Comisi6n de Ayuda a la Investi-gaci(in Cientifica. Facuity of Medicine, University of

Chile, Contvact 64/4, and Comisión Nacional de Investi-gad6n Cientifica y Tecnol6gica, Project 41.

2Presented by Dr. Barzelatto.

mented examples are those of the United Statcs(22), MLxico (40), Guatemala (39), Colombia(6), and Argentina (33). Iodine prophylaxisprograms are being increased in number andeffectiveness in America and will soon influencegoiter epidemiology, at least among Indiansmore closely integrated with the surroundingsoc iety.

The idea that endemic goiter reflects only theadaptation of man to iodine deficiency can nolonger be sustained. As n other parts of thewczld, it is contradicted ir America by suchexamples as the finding of groups of Indianswithout goiter who were iodine-deficient (37)

and the persisting development of endemicgoiter in children born in areas where effectiveiodine prophylaxis was under way (13). Naturalgoitrogens occurring in food have been suspectedof playing a role in the pathogenesis of someendemic goiter (a 23. 32, 34). An example inour continent is the pilion or nut of the Arauca-

nia araucana, a pine tree abundant in south-central Chile (42).

Contrasting with the situation in sporadicgoiter, genetic mechanisms have not been welldocumented in the pathogenesis of endemicgoiter. Enzymatic detects have not been demon-:grated in its etiology. A concentration of en-demic goiter cases within families has beenreported in America (16, 25) and elsewhere (7,27). A positive association of nodular goiterwith the distribution of nontasters of phenyl-thiocarbarnide (PTC) I as been reported in ageneral mixed population in Brazil (28). How-ever, the search for this assccidtion among

124

4;9

American Indians is rendered difficult by thesmall proportion of nontasters usually foundamong them, as was the case in a study of thePewenche (10).

Another aspect to be considered is the prob-lem of endemic goiter variability. The anatomicand physiological characteristics of goiter mayvary in a single individual during his rietime;other levels of variation are to be defined amongthe members of a given community and amongdifferent populations. These three types of vari-ability make it a hard task to compare resultsof different authors, especizlly because there isstill no general agreement on definitions. Somemethodological limitations should also be bornein mind, such subjective differences when notall individuals are examined by the same per-son. Even if these are overcome, difficulties inclassification persist, such as estimating the sizeof a goiter in the presence of retrosternal exten-sion and the error induced by missing goitersthat have become totally retrostemal.

The impact of endemic goiter in public healthis another matter of debate. Severe endemicgoiter is associated with endemic cretinism,deaf-mutism and neur)logical defects, but themechanisms involved are not clearly understood.There are also no adequate studies of mortalityand fertility differentials in comparable popula-tions with and without endemic goiter, or inindividuals within an endemic goiter area. Inboth cases fruitful information may be obtainedfrom looking into relations with endemic goitervariability.

Comparative studies among different groupsof American Indians could provide an excellentopportunity to study the pathogenesis of en-demic goiter. They presumably have very differ-enz genetic endowment, and also are influencedby different environments. The interplay of allthese factors in the genesis of endemic goiter isprobably unique in each population; hencestudies in depth of endemic goiter in certaincommunities may be scientifically rewarding,besides providing the basis for rational pro-phylaxis programs.

,

Endemic goiter in Pedregoso

In accordance with the foregoing line otthought, we have been involved for the last fiveyears in a study of endemic goiter on a PewencheIndian reservation in Chile. Some of our find-ings will provide a good basis for discussion ofthese ideas.

Pedregoso is a geographically isolated Andeanvalley at an altitude of 1310 meters, with acold climate. According to a 1965 census, 592Pewenches live there, by relatively primitiveagriculture and some cattle raising. Pinon is astandard item in their diet. The availablegenetic data show that these Indians L....e less

mixed than other groups of the Araucaniancomplex to which they belong (8, 10, 29, 30, 38)and constitute a highly inbred population in

which a quarter of the marriages are con-sanguineous (10).

Endemic goiter in Pedregoso was found tohave a prevalence of 66.8 per cent in a samplecomprising 81 per cent of the total population(the remaining 19 per cent, mainly youngpeople, were not examined in our house-to-house survey because for one reason or anotherthey were away from home). The distributionaccording to sex and age is shown in Table I,which also gives the frequencies of clinicallynodular and large goiters (including those esti-mated to weigh 60 grams or more and all thosewith retrosternal extensions). As in most otherstudies, women were found more frequentlygoitrous at all ages than men. The fact that thefrequency does not diminish after puberty andthe finding of nodular goiters in the first decadesof life are indications of the severity of theendemic. On the other hand, huge goiters weree.;ceptional and only one cretin and no deaf-mutes were found.

The first problem to be considered is whetherthe increases in size and in nodularity with ageare independent effects. Nodularity inereaseswith age in both sexes, appearing earlier amongwomen (Table 2). Large goiters are more fre-quently nodular than small ones with advancein age, but some individuals have small nodviargoiters in the first decades. It is obvious from

125

TABLE I. Goiter in Pedregoso

MEN WOMEN

AGE

(YEARS)

EXAMINED GOITROUS EXAMINED GOITROUS

%LARGEGOITROUS N NODULAR LARGE N GOITROUS NODULAR

0-9 63 25.4 16 0.0 6.2 71 39.4 28 3.6 0.0

10-19 55 72.7 40 2.5 2.5 55 72.7 40 15.0 15_0

20-29 37 62.2 23 26.1 21.7 44 95.5 42 23.8 45.2

30-39 28 67.9 19 47.4 42.1 33 100 0 33 54.6 30.3

40-49 16 75.0 12 66.7 50.0 17 94.1 16 81.2 68.8

50 and over 29 76.9 22 68.2 63.6 18 96.4 27 77.8 81.5

Total 228 57.9 132 29.5 2(.3 248 75.0 186 37.1 36.6

these data that if th2 influence of other etiolog:-cal factors upon endemic goiter variability is tobe studied, sex, age, size, and nodularity shaildbe considered separately. A number 2e factsreinforce this conclusion: (I) The greater sever-ity of goiter among women, as judged here bygreater frequency, larger size, and more nodu-

larity, and also by the earlier appearance of thesecharacteristics, is due to poorly understoodmechanisms related to sex. (2) Men frequentlyremain away from Pedregoso for long periodsworking in nearby towns or farms, whilewomen and children tend to stay on the reser-vation. (3) Since most of the goiters becomenodular with age, nodularity among youngerirdividuals may have a different meaning fromthat seen in most older subjects. (4) Estimat2sof size among older individuals are liable togreav-.1 error, because c retrosternal extension,

TAItl_,E 2. Nodularity and goiter size in Pedregoso

which may have been ignored when diagnosingsmall goiters, particularly if nodular.

The data should therefore be analyzed bothby sex and by age group. in each et' these cat..:-gories, five subgroups have to he studied: with-out goiter and with small diffuse, large diffuse,small nodular, and large nodular goiter-. Sincethe size of the population aqd the distribution ofgoiter in Pedregoso do not generally allow suchanalysis, more inclusive groups are necessary. Inthe first decade of life it is only important tocompare subjects with and without goiter, ignor-ing their sex. The second decade is a transitionalgroup, in which large and nodular goiters arestill infrequent and cannot be considered apart.Among the ar'ailts there are relatively adequatenumbers of all groups except that of womenwithout goiter. Finally, among older individualsthe meaning of thzse group: becomes less pre-

MEN WOMEN

AGE

(YEARS)

SMALL .JOITERS LARGE GOITERS SMALL GOITERS LARGE GOITERS

% NODULAR % NODULAR % NODULAR N NODULAR

0-9 15 0.0 1 0.0 28 3.6 0 0,0

10-19 39 2.6 1 0.0 34 14.7 6 16.7

20-29 18 22.2 5 40.0 23 13.0 19 36.8

30-39 11 36.4 8 62.5 23 39.1 10 90.0

40-49 6 50:0 83.3 5 80.0 11 81.8

50 and over 8 25.0 14 92.8 5 40.0 22 81.8

Total 97 14.4 35 71.4 118 21.2 68 64.7

126

13t

cise, except for small diffuse goiters, which arcless subject to errors in classification.

Let us first consider the effect of pregnancyupon goiter variabilicy in Pedregoso. In eachdecade, women with either large or nodulargoiters have had a greater average number ofpregnancies (Table 3)which would suggestthat gestation increases goiter size and nodu-larity if this interpretation were not challengedby the fact that the same tendencies are ob-served among men. Men and women under 30years of age were not included in Table 3,although they showed these same iendcncies.The differences are significant only for menwith large as against those with small goiters inthe older group ("t"(3,)=2.337; p<0.05). Itshould be added that men without goiter aver-age a slightly higher number of descendantsthen goitrous men in these two age groups.

Inbreeding also seems to affect goiter inPedregoso --(Table 4). The prevalence of goiteramong children under 10 yeafs whose parentsare consanguineous is significrmtly lower thanamong children of parents who were born inPedregoso but in whom consanguinity was notdetected (x( 1)2( Yates) = 4.275; p<0.05) or chil-dren of parents born on daerent reservations(x, )2( yti.$) = 4.275; p<0.05). The oppositetrend seen among persons over 20 years of ageis not significant. Inbred adults show a consist-ent and significant tendency to have fewer nodu-lar goiters (x(r)a(Tate.)=6.264; p<0.025) than

TABLE 3. Fertility and goiter in Pedregoso (total off-spring, abortions excluded)

GOITER

30-39 YEARS 40 YEARS OR OVER

N X se se

WomenDiffuse 11 4.73 0.406 7 7.43 0.922Nodular 15 5.73 0.547 31 8.29 0,605Small 18 4.89 0.427 9 7.33 ).414Large 8 6.25 0.620 29 8.38 0.531

MenDiffuse 9 4.88 0.389 11 7.55 0.790Nodular 6 6.00 0.775 22 9.59 0.973Small 5.00 0.408 13 7.00 1.104Large 6 5.83 0.792 20 10.20 0.841

127

those whose parents were born in differentreservations. Other comparisons show no signifi-cant differences. To sum up, it can be said thatinbred -people in Pedregoso develop goiters at alater age and that the r goiters are somewhatless prone to develop nodules.

PTC-tasting ability was determined, with theHarris and kalmus technique, in 255 persons inPedregoso. Since only 4.3 per cent were non-tasters, this characteristic could not be properlyrelated to goiter. Nevertheless, a comparisonmade among tasters showed that both men andwomen with nodular goiters in the third andfourth decades of life had significantly lowermean threshold values than those with diffusegoiters (9).

Height was also correlated with goiter (Table5), and it was shown that taller subjects of bothsexes had larger goiters, in the third and fourth..iecade. An analysis of variance combining allthese groups showed that this relation is signifi-cant at the .05 level (F{,,loe)--7-4.04). Nongoi-trous men of the same age are in general tallerthan goitrous ones, but this difference is notsignificant even when the comparison is madeonly with males with small goiters ("t",,," =1.857).

Nutritional surveys made in Pedregoso re-vealed two relevant facts: first, the existence ofiodine deficiency as judged by an average dailyurinary excretion of 33.2 micrograms (2); andsecond, the fact that all year round the peopleconsumed pifion (1), which has been demon-strated to be goitrogenic in rats (42). Goiter isapparently influenced by these two factors.Subjects with large or nodular goiters havelower mean urinary iodide excretions than thosewith small or diffuse goiters (Table 6). Thesedifferences are better demonstrated by the per-centage of subjects in each group excreting 50micrograms or more. With this approach, sta-tistical significance at the .05 level is reachedwhen large goiters are compared with small(X(1)2(Yates)= 4.162); nongoitrous subjects donot differ significantly from those with diffuseand small goiters. On the other hand, there is adirect relation between mean piiion ingestionand thyroid size (Table 7), nongoitrous subjects

132

TABLE 4. Inbrce&ng and goiter in Pedregoso (men and women)

AGE GROUP INERELDING

EXAMINED GOITROUS

% GOITROUS % NODULAR % LARGE

0-9 a 35 14.3 5 0.0 0

72 38.9 28 3.6 3.6

27 40.8 11 0.0 0

10-19 18 61.1 11 18.2 9.1

56 80.4 45 4.4 11.1

35 65.7 23 13.0 4.3

20-29 a 8 87.5 7 0.0 14.3

53 84.9 45 24.4 40.0

19 63.2 12 33.3 33.3

30-39 a 5 100.0 5 40.0 20.0

42 88.1 37 54.0 35.1

14 71.4 10 50.0 40.0

40 and over a 4 100.0 4 50.0 50.0

43 86.0 r 70.3 73.0

33 87.9 29 82.8 65.5

°Parents born in Pedregoso; consanguinity detected.b Parents born in Pedregoso, consanguinity not detected.e Parents born on different reservations.

showing the lowest consumption. Since thevalues observed differ widely, it is preferable tostudy in this case the proportion of subjectseating greater amounts, say 100 or more gramsdaily; again the same trend is seen, the differencebeing significant when subjects with large thy-roids are compared with the rest (NX(1)2( 'Yates) =

4.061; p <0.025). Diffuse and iiodular goiters donot differ by this approach.

Kinetic studies of iodine metabolism per-formed in Pedregoso (3, 4) are summarized inFigure 1, the most striking findings being (1)

comparable and slightly-abovf.-normal figuresfor net iodine intake by the thyroid and periph-eral consumption of thyroid hormones; (2) aconsiderable "iodine kak," since the total out-put of iodint by the thyroid is five to ten timesthc amount incorporated into thyroid hor-

mones; and (3) the abnormal presence the

blood of increased amounts of endogenouslylabeled triiodothyronine (T3), iodinated poly-peptides (NBEI), and iodotyrosines. Thesefacts, plus increased radioiodine uptake andPBP25 levels, express an accelerated turnove- of

TABLE 5. Height (centimeters) anc. ,.ademic goiter in Pedregoso

AGE

(YEARS)

NONGOITROUS

GOITROUS

DIFFUSE NODULAR SMALL LARGE

se se se S, N 3c" se

Men20-29 14 162.1 1.85 17 159.8 1.22 6 160.0 2.81 18 159.4 1,41 5 161.5 1.00

30-39 9 164.2 2.41 9 160.8 1.18 8 163.1 1.47 11 160.7 1.02 6 164.2 1.67

40 an I over 10 159.5 1.10 11 159.8 1.37 20 159.0 1.48 13 159.0 1.04 18 159.4 1.15

Women20-29 2 150.0 2.50 32 150.2 0.90 10 150.5 1.86 23 148.4 1.07 19 152.5 1.01

30-39 - 15 150.8 1.54 17 149.0 1.12 22 149.3 1.02 10 151.0 1.07

40 and over 2 150.0 2.50 9 151.9 1.76 30 149.8 0.86 9 150.3 1.88 30 150.3 0.85

128

TABLE 6. Urinary iodide and goiter in Pcdregoso TABLE 7. Piiion ingestion and goiter in Peciregoso(micrograms per day) (grams per day)

S2

50 Aeg oR

MORE (%) N X 52100 G OR

MORE (%)

Nongoitrous 12 36.6 388.99 25.0 Nongoitrous 22 16.0 1604.67 4.5Goitrous Goitrous

Diffuse 30 38.1 545.13 26.7 Diffuse 43 61,6 3315.72 18.6Nodular 37 31.2 324.20 13.5 Nodular 50 75.7 13665.77 16.0Small 32 38.5 560.13 31.2 Small 41 57.5 2921.71 9.8Large 35 30.4 288.24 8.6 Large 52 78.4 13462.44 23.1

radioiodine by the gland and considerable ineffi-ciency in handling iodine in terms of the per-centage used for the synthesis of thyroid har-mones. Some of these findings have been foundin other instances of endemic goiter in America(31, 41) and elsewhere (12).

How should radioiodine studies be correlatedto goiter variation? The PB1125 reflects the sp.tedof the thyroid in incorporating radioiodine intocirculating iodinated compounds, and Table 8

shows that nodular goiters have significantlyhigher values for this parameter, as is also truefor NBEI125. In a previous publication (4) wehave shown that nodular goiters have the widestrange of values of thyroidal iodine pool, com-prising both the smallest and the largest figuresobserved. This finding may explain why PBP2avalues have the greatest variance among nodulargoiter, small pools determining the high valuesobserved. In support of this view, the thyroidal

Thyroid iodine pool a 11 mg.

r 97,6ugioy j + TYROSINE MIT- DIT

13 - T4

FIGURE I. Iodine metabolism in Pedregoso

NBEI

102 ,ug/doy

MIT-DIT

T3 14 1- +TYROSINE

Thyroid cltput a 512 - 833 - 974 iug/doy

129

134

TAB1E 8. P8112;1 and NBEI12 in Pedregoso (%/dose/liter)

pm 125 NBEI 125

N .7c 52 71-Z52

Nongoitrous 10 0.17 0.0135 7 0.012 0.04176

Gpitrous'9Diffuse 30 0.18 0.0204 19 0.012 0.04823

Nodular 34 0.50 0.1874 29 0.028 0.038736

Small 30 0.31 0.1147 23 0.022 0.017575

Large 34 0.39 0.1529 25 0.022 0.035058

F for nodularity 13.709 a 8.005 b

F for size 2.323 0.097

a p < 0.001.b p < 0.010.

iodine pool among 21 subjects in Pedregoso,calculated by the Riggs isotopic .,..quilibrium

method (4), shows a significant inverse rela-tionship with the PBP25 values observed inthese subjects (r=0.472; p<0.025). A similarcorrelation has been observed in euthyroid pa-tients in Scotland (45). Furthermore, smalliodine pools could also explain high NBEP25values, since this parameter shows a significantpositive correlation with P131125 (r =0.50; p<

0.001).Endogenously labeled triiodothyronine is chro-

matographically present in the same proportionamong all goitrous subjects and absent in thenongoitrous (Table 9), although the differenceis not significant (x(n2,1-1,tes)=2.549). On the

other hand, endogenously labeled iodotyrosineswere present in a significantly higher percentageof the Indians with nodular goiters than of

those with diffuse goiters (x1( )2( yates)=5.71 ;

TABLE 9. Endogenously labeled triiodothyronine andiodotyrosines in Pedrcgoso

,r' 31ODOTYROSIN ES

NO. NO.

Nongoitrous 8 0.0 14 21.4

GoitrousDiffuse 11 36.4 28 10.7

Nodular 25 36.0 34 41.2

Small 14 35.7 26 19.2

Large 22 36.4 36 33.3

p<0.01), while there is no significant differencebetween subjects with small and large goiters.Nongoitrous persons have labeled iodotyrosinesin a smaller proportion than goitrous ones,particularly in comparison to those with nodulargoiters. Subjects with labeled iodotyrosines havesignificantly higher PBP25 values ("t"(40)=2.31; p<0.05); this is not true for those withlabeled triiodothyronine. The demonstration ofiodotyrosines can be directly ascribed to smallthyroid iodine pools, as is suggested by the factthat six subjects in whom they were present hadan average pool of 1.97 mg±0.327, while fiveothers in whom they were not demonstrated hadan average value of 6.22 mg± 1.757 ("t"{4,=2.37; p<0.05).

130

Discussion

Multiple causes are involved in the etiologyand pathogenesis of endemic goiter, many ofwhich still require proper identification andevaluation. Iodine deficiency is usually the pre-dominant etiological factor; other environmentalinfluences are probably also present and, wherethere is adequate iodine, would sometimessuffice to explain endemic goiter. Natural goitro-gens are the best.known example. Genetic fac-tors have not been shown to influence the preva-lence of endemic goiter, although the possibilityof their playing some role cannot be discarded.

The participation of all these factors shouldbe studied in relation not only to the occurrencebut also to the variability of goiter. Such studiesare seldom made, presumably because of thedifficulties in definition and methodology thathave been mentioned. It is upon variation thatgenetic factors have been demonstrated, as ex-emplified by the association of PTC-tastingability with nodular goiter. Weak environmentaletiological factors may also be better studiedwith this approach, when a predominant causelike iodine deficiency is present.

In Pedregoso we have looked into goiter varia-tion with three different elements in mind:presence, size, and nodularity of goiter. Theseobviously interact in some measure, but each ischaracterized in our data by a particular con-

stellation of statistically significant factors. Nodu-larity is related to the two clearly defined geneticaspects studied so farinbreeding and PTC-tasting abilityand to some radioiodine parame-ters. Inbred people develop fewer nodular goi-ters; Indians with nodular goiters have lowerthresholds for tasting PTC; and radioiodinestudies shuv high 1313I125 and NBEI125 valuesand a greater proportion of endogenously la-beled iodotyrosines in subjects with nodulargoiters. All these rahoiodine findings can belinked to the predominance of small thyroidaliodine pools among those with nodular goiters.Large goiters, on the othcr hand, are associatedwith the two best-defined environmental factorsstudied by us: the subjects eat less iodine andmore piiion. Size is also positively associatedwith two complex factorsheight and fertility.Presence, unlike the other two elements, hasbeen cot nected significantly only with inbreed-ing and during the first decade. it is noticeablehere that eally appearance of goiter, like nodu-larity, is negatively influenced by inbreeding.Sex and age, as such, are involved with all threeelements, but we feel that their relevance shouldbe sought mainly through interaction types ofeffects.

In view of the complexity and number offactors to be considered acting together, it would

seem necessary to apply to all these data a multi-variate analysis through which the proper valuecould be attached both to main factors and tothe many kinds of interactions present. Thismight not be possible, however, for two mainreas xis: the small size (34 our sample, especiallysince the subsamples in which parameters wep:recorded did not always comprise the same indi-viduals, and the fact that the categories of goitercontain different types of error in a nonrandomway and have different meanings. For example,relationships with age are difficult to study be-cause small diffuse goiters at an early age maydevelop into large and/or nodular goiters. Ourinterpretation of the Pedregoso data requires usto extend these studies to other similar Pewenchecommunities, but even then comparisons withentirely different situations using similar typesof analysis would be necessary to determine thebearing of such findings on the general problemf,f endemic goiter. Is endemic goiter the adapta-tion of man to iodine deficiency? Our data leadus to suggest that subjects with certain types ofgoiter are better adapted than others. The factthat Indians with large goiters are taller andhave more children might bc in line with suchan interpretation, even if we are unable to in-terpret the mechanisms involved.

REFERENCES

I. ARTEAGA, A., J. BARZELATTO, E. COVARRUBIAS,

A. VALIENTE, E. ROSALES, C. MICHEL!, and C.TORRES. Nutr. Bromatol Toxicol. 4:125, 1965.

2. BARZELATTO, J., C. BECQUERS, C. STEVENSON,E. COVARRUBIAS, A. GIANETTI, E. BOBADILLA, A.PARDO, H. DONOR), and A. ATRIA. Acta Endocr.54:577, 1967.

3. BARZELATTO, J., C. BECQUERS, C. STEVENSON,A. GIANETTI, E. BOBADILLA, and A. PARDO. MinervaNucleare 9:259, 1965.

4. BECQUERS, C., J. BARZELATTO, C. STEVENSON,A. GIANETTI, A. PARDO, E. BOBADILLA, and M. DEVISSCHER. Acta En doer. 54:591, 1967.

5. Bolumvi, S. F., and N. S. SCRIMSHAW. 13o1.Ofic. Sanit. Panamer, Suplemento 3:157, 1959.

6. CALLEJAS, L., J. GOMEz, R. ALMANZAR, andA. UCROS-CUELLAR. Rev. Soc. Colomb. Endocr. 4:55, 1966.

7. CAMPOS, P. C., B. S. BALTASAR, N. GRABATO,

131

L. T. MOYA, and A. 0. CLEMENTE. In Radioisotopesin Tropical Medicine, Vienna, IAEA, 1962, p. 151.

8. COVARRUBIAS, E. BiolOgica (Chile), FaL. XXX-VII:62, 1965.

9. COVARRUBIAS, E., and J. BARZELATTO. ThirdMeeting PAHO Study Group on Endemic Goiter,Puebla, Mexico, 1968. To be published.

10. COVARRUBIAS, E., J. BARZELATTO, C. STEVENSON,

E. BoBADILLA, A. PARDO, and C. BECQUERS. Nature205:1036, 1965.

11. EKpEctu, 0. L., A. DIMITRIADOU, and R. T.FRASER. In C. Cassano and M. Andreoli (eds.),C'urrent Topics in Thyroid Research. New York,Academic Press, 1965, p. 866.

12. ERMANs, A. M., J. E. DUMONT, and P. A.BASTENIE. 1. Clin. Endocr. 23:550, 1963.

13. GAYTAN, E. Personal communication.14. GREENWALD, I. Texas Rep. Biol. Med. 17467,

1959.

*136

15. GRE ENWALD, I. Texas Rep. Biol. Med. 15:874,1957.

16. GREENWALD, I. In G. B. Astwood (ed.), Clini-cal Endocrinology, I. New York, Grune & Stratton,1960, p. 123.

17. FIERRo, R., L. DE G ROOT, M. PAREDES, andW. PERAFIEL. Rev. Ecuator. Wed. Cienc. Biol. 5:15, 1967.

18. FoLus, R. H., JR. Bol. Ofic. Sanit. Panamer.60:28, 1966.

19. Fouls, R. H. Am. J. Clin.Nutr. 14:253, 1964.20. iodine Facts, I (217). London, Iodine Educa-

tional Bureau, 1940-1946.21. KELLY, F. C., and W. W. SN EDDE N. Bull. Wld.

Hlth. Org. 44:27, 1960.22. KIMBALL, 0. P. Arch. Int. Med. 107:290, 1961.23. KRuslus, F. E., and P. PELTOI.A. Acta Endocr.

53:342, 1966.24. LOBO, L. C. G., J. FRIDMAN, D. ROSENTHAL,

R. ULYSSEA , and S. FRANCO. J. Endocr. 22:1182, 1962.

25. LOBO, L. C. G., A. QUELCESALGADO, D. ROSENTHAL, A. FREIRE-MAIA, and M. A. RE BELLO. VIPan American Congress of Endocrinology. ExcerptaMedica, Internat. Congress Series 99, 1965.

26. MA ISTERRE NA, J. A., E. TOVA R, A. CANCIand 0. SERRANO. J. Clin. Endocr. 24:166, 1964.

27.. MALAMOS, B., K. MIRAS, P. KOSTAMIS, J.

MANTZOS, A. C. KRALIOS, G. RworouLos, N. ZE REFOS, and D. A. KOUTRAS. In C. Cassano and M.Andreoli (eds.), Current Topics in Thyroid Re-search, New York, Academic Press, 1965, p. 851.

28. MORTON, N. E. Cold Spring Harbor Symp.Quant. Biol. 29:69, 1964.

29. NAGEL, R., d R. ETCHEVERR Y. Nature 197:187, 1963.

30. NAGEL, R., R. ETCHEVERRY, C. GUZMA N, A.HILLE, J. BARZELATTO, and E. COVARRUBIAS. Rev.Med. Chile 90:616, 1962.

31. PAR RA4IM ENEZ, N., P. RODhIGUEZGARC IA, M.ROCHE, and K. GAEDE. J. Clin. Endocr. 22:754, 1962.

32. PELTO L A, P. In C. Cassano and M. Andreoli(eds.), Current Topics in Thyroid Research. NewYork, Academic Press, 1965, p. 872.

33. PERINETTI, H. et al. In Advances in ThyroidResearch. London, Pergamon Press, 1961, p. 283.

34. PoDovn, J., and P. LANGER. Naturally Occur-ring Goitrogens and Thyroid Function. Bratislava,Slovak Academy of Sciences, 1964.

35. ROCH E. M. J. Clin. Endocr. Metab. 19:1440,1959.

.3('. ROCHE, M., F. DE VENANZI, J. VE RA, E. COLL,M. SPINETTI.BE RTI, J. MENDEZFARTINES, A. GERARD,and J. FORE RO. J. Clin. Endocr. 17:99, 1957.

37. ROCHE, M., H. PERI NETTI, and A. BARBE ITO.1. Clin. Endocr. 21:1009, 1961.

38. ROTHHAMMER, F., R. BLANCO, E. COVARRU-BIAS, and M. DIXON. Ztschr. f Morph. v Anthrop.In press.

39. SCRIMSHAW, N. S. Public Health Rep. 75:731,1960.

40. STACPOOLE, H. H. Bull. Wld. HIth. Org. 9:283, 1953.

41. STANBURY, J. B., G. L. BROWNELL, D. S. R IGGS,H. PERINETTI. J. I TOIZ, and E. B. DEL CASTILLO.Endemic Goiter: The Adaptation of Man to IodineDeficiency. Cambridge, Massachusetts, Harvard Uni-versity Press, 1954.

42. TELLEZ, M., A. GIAN ETTI, E. COVARRUBIAS,

and J. BA 11 ZELATTO. Proc. Third Meeting PAHOStudy Group on Endemic Goiter, Puebla, Mexico,1968. To be publishcd.

43. UCROS CUELLAR, A. Unidia 7, Suplemento 1:1,1960.

44. WAHNER, H. W., E. GAYTAN, and P. CORREA.I. Clin. Endocr. 26:279, 1966.

45. WAY N E. E. J., D. A. KourRns, and W. D.ALEXANDER. Clinical Aspects of Iodine Metabolism.Philadelphia, F. A. Davis, 1964, p. 48.

46. WEINSTEIN, E. D., J. V. NEEL, and F. M.SALZA N O. Amer. J. Hum. Genet. 19:532, 1967.

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1:37

DISCUSSION

J. D. Niswander

The speakers today have each considered onespecial diease problem of the Indian. I shouldlike to Jiscuss three of these in relation to oneanother. I will discuss diabetes mellitus, gall-bladder disease, and nutrition in the context ofthe over-all variability in frequency of diabetesamong various Indian tribes in the United States.

Specific studies have reported an unusuallytrequency of diabetes among several North

Amei ican triheswith the studies being con-ducted among the Pima, reported by Dr. Miller,being the foremost example. There are, how-ever, very few data on the question of juzt howprevalent diabetes is throughout the variousAmerican Indian groups or whether it is moreor less uniquely confined to particular tribes.Certairly such a hypothesis as that put forwar:'by Dr. Neelthat diabetes may represent theeffects of changing dietary patterns on genomespreviously adapted tt-, a "feast or famine" situa-tionwould . uggest that a high frequency ofdiabetes might be expected among populationswho have been both recently and rapidly trans-formed from this primitive pattern to a moresedentary and overfed condition.

The only source of information that I amaware of on this subject, although the data areless than :deal, is the records of the U.S. PublicHealth Service, Division of Indian Health Hos-pitals. Accordingly, I have obtained tabulationsof discharge diagnoses fiorn these hospitals forthe four-yea priod 1963-1967. This representsapproximately 250,000 discharges. I have tabu-latrd the proportion of discharges from eachhospital in which the primary cr.agnosis was

diabetes mellitus. The rank order for the hos-pitals changes very little if, instead of the totalnumber of discharges, the total beneficiary popu-lation of each hospital is used as the denomi-nator. I believe there is enough uniformity be-tween Public Health Service Indian Hospitalsto make these data reasonably adequate for relative frequency comparisons, although one cer-tainly would not want to attribute a great dealof precision to them.

The map shows the location of the variousPublic Health Service Hospitals throughout theUnited States and their grouping into sevenadministrative areas. The eighth area (Portland)delivers servicP through contract with local fa-cilities and not directly through Public HealthService Hospitals.

The mean frequency for the 46 Indian hos-pitals is 2.2 per cent. This compares with figuresof 1 to 1.5 per cent for similar data for severalsurveys of general non-Indian hospitals through-out the United States representing over 26,000,-000 hospital admissions.

The table groups the hospitals by the relativefrequency of admission for diabetes and indi-cates the major tribes served by each. As can beseen, the range expressed by the mean frequencyof 2,2 per cent is very wide, with roughly atwentyfold difference between the lowest andthe highest. The table also shows the relativefrequency of admission for gallbladder disease,which very closely pa.-allels that for diabetes. 1.1-fact, the rank correlation is slightly higher than.5 and extremely significant. There is, however,a considerably narrower range of variability than

133

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for diabetes. It can be seen that there is anequally striking association between diabetes andaverage birth weight. Here again the regressionof birth weight on frequency of diabetes, byhospital, is highly significant.

Specifically in regard to diabetes there areseveral pints of interest. First of all, in almosttwo thirds of the Indian hospitals diabetes seemsto represent a significant! y greater proportion ofthe patient population tl an in non-Indian hos-pitals. Most of the major linguistic groups arerepresented in the high and intermediate dia-betes categories with the exception of the Aleut-Eskimo group and possibly the Athabascans.The highest diabetes group is composed of sev-eral different tribes, but most conspicuous arethe so-called five civilized tribes from the south-eastern portion of the country. All had relativelyhighly developed agriculture prior to Europeancontact. Also notable among this group are sev-eral of the southwestern agricultural tribes in-cluding the Pima. It might be suspected thatthese early agriculturists would be the ones mostsusceptible to acculturation and hence wouldhave undergone the most significant changes indietary patterns.

The low-chabetes group is notable for includ-ing all of Alaskathe Aleuts, Eskimos, and

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various Alaskan Indiansand also the Atha-bascan-speaking Navajo and the closely relatedApaches. I think it is noteworthy that the Alas-kan natives and the Navajo are probably theleast acculturated of all the Indians remainingin the United States.

The possibility that their low frequency ofdiabetes is due to the inherent genetic make-upof these groups, indepent:ent of environmentalfactors, cannot be excluded. Likewise, it couldbe argued that birth weight and diabetes arerelated by virtue of both being tne result of aparticular genetic constitution. Alternatively, thebirth-weight gradient might be considered a sec-ondary effect of maternal diabetes. It seems toine, however, that the relationship between gall-bladder disease, birth weight, and diabetes, whenviewed together with the admittedly limitedinformation on cultural variation, suggests atleast one other possibility: the operation of com-mon environmental factors, presumably dietary.To speculate a bit more than is perhaps war-ranted by the data, I would suggest that virtuallyall Indians may be of a genetic constitutionespecially susceptible to diabetes and its expres-sion is the result of dietary and nutritional fac-tors associated with prtsent-day reservation life.

In this regard, it is unfortunate that there are

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'

Frequency of diabetes mellitus and gallbladder disease and mean birth weight in Public Health Service, Divisionof Indian Health Hospitals

HOSPITALS

DIABETES GALLBLADDER ' N 1 EAN

MAJOR (To OF ALL (% OF ALL BIRTH

TRIBES ADMISSIONS) ADMISSIONS WEIGH,' I

Window Rock Area (6 hospitalsNew Mexico, NavajoArizona)

Beicourt, North Dakota Chippewa

Mescalero, New Mexico; White River, Arizona Apache 0-1 1.9 6.(8

Keams Canyon, Arizona Navajo, Hopi

Alaska (7 hospitals) Aleut, Eskimos"Alaskan Indians"

Montana (3 hospitals) Blackfoot, CrowCheyenne, Gros

VentresAssiniboine, Cree

Cass Lakc, Minnesota; Rcd Lake, Minnesota Chippewa

North Dakota, South Dakota, Nebraska "Sioux" 2-3 2.3 6.88(6 hospitals)

Santa Fe, New Mexico; Zuni, New Mexico "Pueblo," Zuni

San Carlos, Arizona Apache

Clinton, Oklahoma; Lawton, Oklahoma Cheyenne, Arapaho,Kiowa, Comanche,Caddo

Sells, Arizona Papago

Cherokee, North Carolina; Tahlequah, CherokeeOklahoma

Claremore, Oklahoma; Pawnee Oklahoma; Cherokee, Creek,Philadelphia, Mississippi Ponca, Choctaw,

Seminole

Talihina, Oklahoma Choctaw, Chickasaw, 4-10 2.6 7.05Cherokee, Creek

Wagner, South Dakota Sioux

Sacaton, Arizona Pima, Papag,i

Shurz, Nevada; Owyhee, Nevada Paiute, Shoshone

Winterhaven, California; Parker, Artzona Cocopa, Mohave,Chemehuevi

Based on 257,320 discharge diagnoses, 1963-1967.t Based on 27,288 births.

135

..,140

no very adequate data avvilable on relativeobesity between tribes or on the increase inobesity that may have occurred in recent years.There is, however, one study that reports ap-proximately a six-kilogram increase in weightamong the Navajo, with no increase in stature,over a twenty-year period. The reservationNavajo, however, are still considered relativelylean in body build, without the great tendencytoward obesity that is seen in some of the othertribes. It would be of considerable interest tofollow Navajos whu have now moved to themajor urban centers and compare them both forobesity and for serum glucose levels with theirpresumably less acculturated counterparts whohave remained on reservations.

My purpose in this discussion has been pri-marily to point up the need not only for detailedstudies of special diseases in specific groups butalso for data gi ing comprehensive coverageover many Indian populations. Certainly, studiesof human adaptation and attempts to understandthe interactions between genotype and changingcultural patterns demand considerable knowl-edge of the variation which may exist withinand between various human ppulations.

If my speculations prove to be correct, diabetesmay become an increasingly important medicalproblem as the acculturation of the AmericanIndian increases. Further, such considerationswould seem important in terms of general plan-ning for dealing with the health problems ofemerging primitive groups.

Acknowledgment

I am grateful to Mr. Abraham Ranofsky. ProgramAnalysis awl Statistics Branch. Division of Indian Health,for furnishing the special tabulations on diabetes andgallbladder disease.

Edmundo Covorrublos

The presentations we have heard this after-noon make it clear that the American Indiansreceived from the conquisatadors a rather heavyburden of evils: biological agents of disease andthe pressure of a different culture, stresses towhich they had to become adapted at the toll

of increased mortality and morbidity figures.Difficult related questions, not yet answered, con-cern the proportion of genes potentially capableof prccoking disease that have passed to theIndians from the other races with which theyare in the process of mixing.

Ail the specific health problems mentioned inthis session are characterized by a complexcausality involving multiple genetic, environ-mental, anti cultural factors. The genetics of a

disease like diabetes is a complicated subject, inwhich no precision as to the part played by geneshas thus far been reached; moreover, diabetesmay represent a genetically heterogeneous groupof disorders.' A similar situation exists forendemic goiter. In the case of malaria, in whichincreased resistence is found among individualsheterozygous for hemoglobin S, other still un-known genetic factors, probably polygenic, maybe involved.2

What I have said in relation to genetic etiologyis paralleled in the field of environmental causes.Thus, the variability of all these diseases is

caused by an interaction of factors that is prob-ably unique in each population, and no geneti-cism or environmentalism will be of real valueto an over-all comprehension of the problems.2

Among the specific questiors raised to-day.should like to point out the associations betweengene distributions and such phenomena as therelationship suggested for Pewenche Indiansbetween nodul.ar goiter and lcwer phenylthio-carbamide thresholds in the group of "tasters"of this substance. Similar results may appearfrom the studies of diabetes and gallbladderdisease among the Pima Indians, in relation toblood groups. Whether or not such associationsare real is to be found in the future, but theymay constitute r.arting points for the analysisof polygenic systems in man. Another interestingquestion here concerns how the epidemiology of

' Rimoin. D. L. Genetics of diabetes mdlitus. Diabetes16:346-351. 1967.

2 Allison, A. C. Genetic factors in resistance to malaria.Ann. N.Y. Acad. Sci. 91:i10-729, 1961.

8 Thoday. J. M. Geneticism and environmentalism. InI. E. Mead (ed.), Biological Aspects of Social Problems.Edinburgh and London, Oliver and Boyd. 1965.

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a disease would be influenced by the distributionof genes, which vary notably from tribe to tribe,as has been shown for blood groups in some ofthe papers submitted today.

The mental diseases present a set of problemseven more formidable in view of the difficultiesof diagnosis due to cultural differences. Oneeffort in this direction was recently made inChile: a new structural theory of psychoses ledto transcultural definitions that made it possibleto distinguish corriderabk differences in the fre-quencies of the proposed types of psychoses be-tween Mapuche Indian patients and the controls.4

Finally, I feel tempted to generalize to othersystems the words of Book5 concerning theetiology of mental illness: ". . my generalmedical and biological background together withmy fragmentary knowledge of psychiatric re-search work has led to the tentative conclusionthat any unitary explanation of the etiologyeven of what is now considered a special typeof mental illness, or a clinical entity, will notcontrib,ite to the advancement of psychiatricresearch."

To sum up, biomedical research among theAmerican Indians is apt to disch new factsthat may be of value both for srecific publichealth policies and for a general understandingof the diseases studied.

General Discussion

Mille: I should like to congratulate Dr. Maron his excellent paper. It seems to me that, lateas the hour is, it woald be wrong to let this goby without emphasizing its importance. As thoseof us here who are working in the field of child.hood malnutrition will agree, the lessons to belearned from his paper are of great importance.

First, I think that we all have to realize thatall groups that have been living in a certain

4 Mufioz, L., J. Marconi, J. Horwitz, and P. Naveil-!An. Cross-cultural definitions applied t' the study offunctional psychoses in Chilean Mapuches, Brit. J. l'sy-arial. 112:1205-1215, 1966.

136iik, J. A. Genetical etiology in mental illness. InCauses of Mental Disorders: A Review of Epidernio-lopical Knowledge. Ncw York, Milbank Memorial Fund,1961.

ecosystem for many centuries have evolved andadapted their own practice of infant feeding,and that z,f we rush in with our own outsideideas without taking these into careful consid-eration we may do very great harm.

Second, there are lessons to be learned,believe, from different groups of people anddifferent traditional systems. I think that we inthe so-called Western world have a considerablebody of dogma in our own infant feeding thatin fact might very well be re-examined in thelight of practice elsewhere. For example, asDr. Behar pointed out, in most of pre-conquis-tador South America and also in Polynesiaanimal milk was not traditionally drunk. Yetpeople there reared childien and fed them per-fectly adequately without it. There are messagesfor us from these differe-,t groups.

Another important aspect of Dr. Behar's paperis the fact that disruption of a culture can veryfrequently have its most sensitive and devas-tating effect on the age group that is most pre-cariously poised physiologically. That, of course,is the young child--the weanling, who is in a

process, if you like, of biocultural transition.When we consider the Indian communities in

the Americas, we should, I think, bear in mindwhat has happened elsewhere in the world. Forexample, the Hadza hunters of northern Tan-zania were surveyed some six years ago andwere found to have a pattern of infant feedingwell adapted to their communitybreast feed-ing, bone marrow, pre-chewed meat, and soforth. Five years later another survey WaS car-ried out, and the pattern of infant feeding andchildhood malnutrition had changed completely.In the first survey there was very little protein-calorie malnutrition. In the second it was verycommon.

What practical messages are there ta be gainedIvoin Dr. Mar's paper? I think thew are these:We. should realize that as well as the rapidspreid of infections due to viruses, such asmeasles, or to bacteria, such as tuberculosis, thespread of inappropriate non-adapted ideas con-cerning inFant feeding can have a very consid.erable effect on local child health and on the

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local pattern of childhood malnutrition. Howcan we try to prevent this? I think that veryprobably, before changes are allowed to occurtoo easily in the dietary habits of AmericanIndian groups, careful thought should be givento whc has been responsible for these changesin the past.

Many of these inappropriate imported changesare iatrogenic, using the term in its wide sense.I think, therefore, that in dealing with theAmerican Indian groups that have been dis-cussed here the infant feeding practices taughtby the health services should be most carefullyadapted to the local circumstances and shouldnot merely be cultural imports from elsewhere.

Furthermore, any imports of foods into thesecommunities through, for instance, food aidprograms undertaken by international agencies,national services, and voluntary organizations,including missions, should be very closely lookedat for whether their hoped-for immediate bene-fits will in fact yield ill effects in the near future.

Lastly, "commerciogenic" malnutrition has tobe mentioned here. It is probably as dangerousto introduce a commercial milk company, a com-pany selling milk and promoting feeding bot-tles, to a community of people who are success-fully breast-feeding as it is to introduce ronslesor tuoerculosis.

Water low. May I ask Dr. Giglio li one ques-tion? Is it your belief that malaria did notoriginally exist in the Amazon forest country?Was it one of the things brought in along withothers?

Gig Both My paper touches on this question.Not that I have any competence to discuss it.I mean, 1. is a moot question whether malariapre-dated the Conquest or was introduced.think the consensus now is that it was intro-duced and that this is probably the reason whythe Ainerindian reacts so much more activelyto malaria infection than the Negro, who hasbeen exposed to it lor ages.

We have no data to go by. Consider the Medi-terranean populations, Nhich were exposed tomalaria for centuries. Certainly there was nosuch total endemic malaria. People suffered from

malaria and died from it and never came toterms with it as the African does. You do findendemic malaria in a few other groupsinnortheastern India, for example. But it is solocalized as to suggest a racial factor in themechanism of holoendemic malaria quite apartfrom length of exposure.

Water low: That is what I am getting atwhether there is a racial factor even with theAmerindian.

Gig lioli: I think so.

Roche: What has been said about care withthe food brought into these areas induces me tosay a few words about the moral issues involvedin studying Innians. These are people who areat our mercy both morally and physically. TheDeclaration of Helsinki on research on humanbeings states that the informed assent of thepeople on whom one is doing research should beobtained. Thi:3 includes research on their internalmilieu, not merely their external milieu. Thepersons responsible for the statement were not,I believe, thinking about this type of studybecause it is practically impossible, as everybodywill agree. to get really informed assent fromthe Indians. Thic means that the burden is onthe investigator, who must exert the utmostrestraint in his investigation to be sure that hisactivity is in no way harmful to :he populationshe is studying.

Cohen: I want to return to the theme of howthese factors might emerge without a basicgenetic alteration. I raise the question whethcrwe are not dealing with the well-known modula-tion effects that derepressors and repressorsmight have on the transcription and translationphenomena. It is now, I think, reasonably welldocumented that the inliuence of a variety ofhormones can lead to the expression of enzymeactivity that is not seen at a lower level of certainhormones.

As a matter of fact, many hormonal patternsare now being explained in molecular biologicalterms of messenger RNA and all that goes withit. This must mean that there is an interplay bya variety of factors on the genetic potential ofan individual to give different degrees of quan-

138

titative expression. I am not sure there would bequalitative changes.

As I listened to many of these presentations,diabetes in Indians and so on, I thought it quiteconceivable that this could be a quantitativevariation of one or another enzyme pattern thatwould lead to a metabolic anomaly of the kind Ihave referred to. Considering the influence ofdiet on a number of these circumstances, I thinkthe question still remains whether the basicgenetic pattern is being significantly altered inthe traditional sense or whether the change istaking place at the modulating level, as it were.

Moderator: A discussion of this would take usrather far afield. I am not vire whether you areusing the term modulation in the sense used bythe bacterial geneticist or whether you are re-ferring to the kind of nature-nurture inter-actions for which we have come to have greatrespect :n man. The idea that in fact the geneticreadout might be different for ourselves thanfor, say, the Indians simply because of the en-vironmental difference is a challenging idea.My first reaction is that the homeostatic mecha-nisms of man are such as to buffer this readoutquite a bit. On the other hand, perhaps weshould devote some thought to trying to putthat idea to some kind of critical test, and cer-tainly one opportunity is in transitional popula-tions. For instance, if it can be documented thatthe polymorphisn.c, which are a readout forproteins, alter ;1 .equency more rapidly in apopulation in cultural transition than can pos-sibly be ascribed to genetic selection, this wouldbe hard evidence that the readout is different.Thac is the kind of eidence that I think itwould take to satisfy most of us.

Cohen: Not to prolong this, it is very clear

that a variety of nutritional states will elicit a

great pattern of enzymatic changes that are notdue to an instantaneous transition of the genes.We know this. Just a simple high carbohydrateintake as against a low, high nitrogen intakeas against low, will cause changes of level ofhigh orders of magnitude. These can be feed-backs of various kinds, but many have hormonalfactors that are known to have their initiatingeffect on the transcription phase in which thegene may be repressed for a particular level ofquantitative operation.

I am only suggesting that before we get tooinvolved in genetic markers as an absoluteknown relationship, which is clearly the case inmany diseases that have been defined in theseterms, we give some thought to the possibilitythat in many of these adaptive phenomena weare dealing with something quite different.

I hope that at some time in the future theremay be a chance to talk at this level as a follow-up to our discussion today. This is where thenew molecular biology may perhaps changesome of our concepts.

Moderaton The final item on the agenda islabeled "Commentary and Summarization."This will be extremely brief. One of the marksof a good meeting is the extent to which oldideas are rescrutinized and questioned, andfrom beginning to tad of this session we havebeen questioning some of our old ideas, begin-ning with the matter of the origins of theAmerican Indians and ending with details ofdisease susceptibility and resistance. The sessionbas been very profitable, and it is my privilegeto thank PAHO for making this gatheringpossible, both financially and in terms of facili-ties.

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144v. V..'t ,

ApFendix

TABULATIONS OF PHENOTYPE AND GENE FREQUENCIES FOR 11

DIFFERENT GENETIC SYSTEMS STUDIED IN THE AMERICAN INDIAN'

R. H. Post, J. V. Neel, and W. J. Scholl

With the impetus given to further geneticstudies of the American Indian by the forth-coming International Biological Program, it is

probable that the next decade will witness asharp increase in investigations of this kind.The literature is already voluminous and scot-tered; it seemed that a compilation of thwestudies which deal with the major genetic poly-morphisms would prove useful in assisting investigators both in planning and facilitatingstudies and in comparing their findings withthose of others. Accordingly. in Tables 1 to 11tabulations are presented for the following sys-tems: ABO, MN, Rh, Kidd, Duffy, Diego, P,Lewis, transferrins, haptoglobins, and Gm.These are all systems exhibiting marked poly-morphism. W. have not included systems, suchas the glucose-6-phosphate dehydrogenase orhemoglobin system, that are polymorphic insome populations but esselitially nonvariant inthe Indian. Nor have we included some systemsthat while probably polymorphic arc still inade-quately defined either genetically or phenotypi-cally, such as sensitivity of taste to phenylthio-carbamide, distribution of hair on phalanges,tongue-rolling, and so on. An effort has beenmade to survey all publications prior to Novem-ber 1967; these are cited in the Bibliography.

I Work supported in part by US. Atomic EnergyCommission Contract AT( 11-1)-1952.

In preparing the tabulations, a recurrent ques-tion in the face of an unusual finding has beenwhether the cause might be racial admixture(i.e., miscegenation). Furthermore, as we havepointed out elsewhere (5), the Indian presentsan unusual challenge to those interested inrecent developments in genetic taxonomy (seeI, 2), but attempts to apply these developmentsmay be vitiated by substantial racial admixture.Accordingly, we have made an effort here toclassify each sample in one of three ways: (1)probably essentially no admixture, (2) non-Indian contribution to the gene pool probablyless than 5 per cent, and (3) non-Indian con-tributiorr to the gene pool probably greater than5 per cent.

As every student of the problem knows, theclassification of certain samples into one of thesethree categories is difficult, and we are sure notonly that there are grounds for issue with somcof our decisions, but also that some of thesedecisions are incorrect and will have to bemodified. In this connection, it should be em-phasized that the decision applies only to theparticular sample that was examined, and notnecessarily to the entire group or tribe. Eachclassification has been based on the history ofthe tribe, the opinion of competent observers, theresults of the genetic studies themselves, and,where given, the author's statement.

ifof 141

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The results of typings for the ABO systemhave been thought to provide especially criticalmaterial for ckcisions regarding admixture. Weaccept the working hypothesis that IB and IA-are not found among American Indians andthat IA, does not occur in South America. How-e-ier, we note that in the few South Americansamples where P3 and 01 do occur, the ratio ofthe frequency of the former to that of the lattertends to be higher th.n in western Europe andAfrica, the presumed origin of these genes. Thepossibility must be recognized that IB was pres-ent in South America in pre-Colombinn times(see also 6), perhaps introduced by trans-Pacificcontacts.

Additional genetic grounds for decisions re-garding sampk purity are the presence of thefollowing antigens, wherever tested for: Kell,Lewis (a), I3errian (Be), Henshaw (He),Lutheran (Lu"), Miltenberger (Mia), Sutter(Js"), V of the Rh system, Verweyst (Vw) ofthe MN system, and Wright (Wr). All of theseare thought to be absent in unmixed Indians,and we have not included tabulations for anyof them. References establishing the virtual orcomplete absence of these traits in samples ofunmixed Indians are listed in Table 12. Wehave felt, on the other hand, and contrary tosome opinions, that the occurrence of Rh-nega-tive individuals (d) need not necessarily indicateadmixture (see 3), although high frequenciesmay be of significance.

In our opinion, many types of critical com-parisons are impossible when there is more than5 per cent admixture in the sample. Only thedata on samples with no admixture, or less than5 per cent admixture, have been incorpoiatedinto Tables 1 to 11, with samples of the firstclass designated by asterisks. The references tosamples with more than 5 per cent admixtureare given in Table 13, which lists the samplesin alphabetic order.

The names of tribes and groups are thosegiven by authors, to which an arabic numeralhas been added in cases of two or more samplesof the same name. Among the civilized popula-tions of Middle and South America, where

tribal organization has long since disappeared,these names may be confusing and occasionallymeaningless. Thus there are two samples ofMayans so called by the authors, an unsatisfac-tory name since several other samples are tabu-lated of Mayan-speaking IndiansChol, Kek-chi, Mam, Pocomam, Quiche, and others. Fivesamples are designated Aymara, two Quechua,and one Chibchan, each of which is a largelinguistic stock including several distinct culturesand several millions of persons. Three linguisticstocks of simpler culwre are similarly employedas names of samplesArawak, Carib, andGuarani. From four to ten samples are desig-nated by tribal names that fall under each ofthese stocks.

The estimates of gene frequencies in thetables that follow were computed on an IBM1130 Model, using programs written in the De-partment of Human Genetics. The ABO pro-gram has been publishesi (4); the other pro-grams are available on iequest. The "goodnessof fit" of the observed phenotype frequencieswith those expected under Hardy-Weinbergequilibrium and with the calculated gene fre-quencies has been tested by chi square. The latterare rot given, but the corresponding probabili-ties when significant are indicated by one ofthree letters in the column to the far left ofeach table, as follows: A- - 0.05>P>0.01; B-0.01>P>0 001; C 0.001>P. The validity ofapplying such X2 tests to small sample:t in whichthe mean coefficient of relationship is probablynot negligible is dubious, but we have followedconvention in this respect.

Names of countries are abbreviated by threeletters and followed by brief indication oflocality, such as that of a state or province,River (R), Mountain (M), Lake (L), or region(N for north, and so on). Exceptions are madefor French Guiana and for Guyana and Suri-nam (formerly British and Dutch Guiana, re-spectively), for which no locality is added, sincetheir areas are small.

In several instances an author has publisheddata on two or more "subtribes" as well as thepooled data of the "tribe." The grounds for

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3

4

recognizing subtribes are seldom clear; theysometimes appear to represent different villagesof the same tribe. In all case!), we have retainedthe author's designation but listed his data underthe main tribal unit, with a cross-referenceunder subtribe. Thus, the data on the Arecunasubtribe of the Pemons will be found under"Pemon-Arecuna" with a cross-reference under"Arecuna."

Genetic marker data have ken published on

a few samples of mixtures of several tribes orgroups that appear to have less than 5 percent non-Indian ancestry. Such data are nottabulated here, but the references are listedapart (Table 14) in alphabetical order of thetribes, together with notes on geographic local-ity, the names of the several tribes included inthe mixture, and our estimate of the amount ofnon-Indian ancestry of the pooled sample.

REFERENCES

1. CAVALLI-SFJRZA, L. L., and A. W. F. EDWARDS.Analysis of human evolution. In S. J. Geerts (ed.),Genetics Today, Vol. 3. Oxford, Pergamon Press,1965, pp. 923-932.

2. CAVALLI-SFORZA, L. L., and A. W. F. EDWARDS.Phylogenetic analysis: Models and estimation pro-cedures. Amer. I. Hum. Genet. 19:233-257, 1967.

3. GERSHOWITZ, H., P. C. JUNQUEIRA, F. M.SA LzAtio, and J. V. NEEL. Further studies on theXavante Indians. HI. Blood groups and ABH-LeaseCretor types in the Sim 6es Lopes and São Marcos

Xavantes. Amer. J. Hum. Genet. 19:502-513, 1967.4. MACCLUER, J. W., R. GRIFFITH, C. F. SING, and

W. J. Sc HULL. Some genetic programs to supplementself-instruction in FORTRAN. Amer. I. Hum.Genet. 19:189-221, 1967.

5. NEEL, J. V., and F. M. SALZANO. A prospectusfor genetic studies of the American Indian. ColdSpring Harbor Symp. Quant. Biol. 29:85-98, 1964.

6. SALZANO, F. M. The blood groups of SouthAmerican Indians. Amer. I. Phys. Anthropo:".15:555-579, 1957.

BIBLIOGRAPHY: GENETIC MARKERS IN THE AMERICAN INDIAN

I. AGUIRRE, F., 0. B. TANDON, and N. S. SCRIM-SHAW. Distribution of blood groups in GuatemalanIndians. Genetics 38:635, 1953.

2. ALLEN, F. W., JR. Inheritance of the Diegofactor. Amer. I. Hum. Genet, 10:64-67, 1958.

3. ALLEN, F. H., JR. Summary of blood groupphenotypes in some aboriginal Americans. Amer.I. Phys. Anthropol. 17:86, 1959.

4. ALLEN, F. W., JR., and J. KORBER. Cited inAlien and Schaeffer, 1935. Univ. N. Mex. Bull. Biol.Ser. 4:2-29, 1935.

5. ALLEN, F. W., JR., and H. D. LARSEN. Heredityof agglutinogens M and N among Pueblo andBlackfeet Indians. J. Immun. 32:301-305, 1937.

6. ALLEN, F. W., JR., and W. SCHAEFFER. Thedistribution of the human blood groups among theNavajo and Pueblo Indians of the Southwest. Univ.N. Mex. Bull. Biol. Ser. 4:2-29, 1935.

7. ALVAREZ, A. G. Comprobaciones biolOgicas enaborigines aigentinos. Com. Hon. ReduccionesIndios (Buenos Aires) Pub. 6:25-34, 1939.

8. ARCE-LARRETA, J. Doscientos determinacionesde grupos sanguineos en los indios del norte delPeril. An. Hosp. (Lima) 3:74-77, 1930.

9. ARCE-LARRETA, J. Grupos sanguineos en elnativo de Los Andes. Rev. Med. Peruana 12:117-120, 1940.

10. ARCILA VELEZ, G. Grupos sanguineos entre los

indios Pliez. Rev. Inst. Etnol. Nac. (Bogotti) 1:7-14,1943. Aos. HLAS 9:53.

. ARC1LA VELEZ, G. Los Caramanta. Univ.Antioquia 20:445-452, 1946. Abs. HLAS 12:50.

12. ARCILA VELEZ, G. Grupos sanguineos de losindios Katios de Antioquia. Bol, Inst. Antrop.(Medellin, Colombia) 1:65-79, 1953. Abs. HLAS19:58.

13. ARENDS, T. Estado actual del cstudio de lashemoglobinas anormales en Venezuela. Sangre(Barcelona) 8:1-14, 1963.

14. ARENDS, T., G. BREWER, N. CHAGNON, M. L.GALLANGO, H. GERSHOWITZ, M. LAYRISSE, J. NEEL,D. SHREFFLER, R. TASAIAN, and L. WEITKAMP. Inter-tribal genetic differentiation among the YanomamaIndians of Southern Venezuela. Proc. Nat. Acad.Sci. 57:1252-1259, 1967.

15. ARENDS, T., and D. A. DAVIES. Absence ofvariants of usual serum pseudocholinesterase (acyl-choline acylhydrolase) in South American Indians.Acta Genet. 17:13-16, 1967.

16. Arends, T., and M. L. GALLANGO. Haptoglobintypes in a Paraujano Indian population. Vox Sang.5:452-461, 1960. Abs. HLAS 24:77.

17. ARENDS, T., and M. L. GALLANGO. Haptoglobinand transferrin groups in Venezuela. Bib?. Haemat.13;379-382, 1962.

18. AREmns, T., and M. L. GALLANOO. Frecuencia

de haptoglobinas en varias poblaciones surameri-canas. Acta Cientif. Venez. 13:116-119, 1962.

19. ARENDS, T., and M. L. GALLANGO. Frequenciesof haptoglobin types in various South Americanpopulations. Bibl. Haemat. 19:463-471, 1964.

20. ARENDS, T., and M. L. GALLANGO. Transferrinsin Venezuelan Indians: high frequenq of a slow-moving variant. Science 143:367-368, 1964.

21 ARENDS, T., and M. L. GALLANGO. 1964. Re-ported in reference 225, P. 286.

22. ARENDS, T., and M. L. GALLANGO. Transferringroups in South American Indians. Bibl. Haemat.23:405-411, 1965.

23. ARENDS, T., and M. L. GALLANGC. Haemoglo-bin types and blood serum factors in British GuianaIndians. Brit. I. Haemat. 11:350-359, 1965.

24. ARTEAGA, C., M. SALAZAR-MALLEN, E. L.UGALDE, and A. ViLEz-ORozeo. Blood agglutinogensof the Mexicans. Ann. Hum. Genet. 16:351-358,1952.

25. BAUMGARTNER, J. Apuntes de LID medicoindigenista sobre !os PiarOa de Venezuela. Bol.Indigen. Venez. II:111-124, 1954.

26. BERG, K. A new serum type in man-the Ldsystem. Vox Sang. 10:513-527, 1965.

27. BERG, K. Further studies on the Lp system.Vox Sang. 11:419-426, 1966.

28. BEST, W. R., M. LAYRISSE, and R. BERMEjo.Blood group antigens in Aymar and Quechuaspeaking tribes from Puno, Peru. Amer. I. Phys.Anthropol. 20:321-329, 1962.

29. BIASUTTI, R. Le razze c i populi della terra.2nd ed. Torino, Unione Tipografico-Editrice Tori-nese, 1957.

30. BroccA, E. Sui gruppi sanguigni degliAmerindi dell' Alto Rio Negro. Rev. Antivp.(Roma) 41:375-376, 1954. Abs. HLAS 20:55.

31. BIOCCA, E., and F. OTTENSOOSER. Estudos etno-hiolOgicos sobre os Indios da região do Alto RioNegro-Amazonas. I. Grupos sanguineos comuns efactores M e N. Arq. Biol. (São Paulo) 28:111-118,1944. Abs. HLAS 10:46,

32. BLUMBERG, B. S., A. C. ALLISON, and B. GARRY.The haptogiobins and hemoglobins of AlaskanEskimos and Indians. Ann. Hum. Genet. 23:349-356, 1959.

33. BLUMBERG, B. S., J. R. MARTIN, F. J. ALLEN, JR.,J. L. WEINER, E. M. VITAGLIANO, and A. COOK.Blood groups of the Naskapi and Montagnais In-dians of Schefferville, Quebec. Hum. Biol. 36:263-272, 1964.

34. BLUMBERG, B. S., L. MELARTIN, R. A. GuINTO,and B. WERNER. Family studies of a human serumisoantigen system (Australia antigen). Amer. J.Hum. Genet. 18:594-608, 1967.

35. BLUMBERG, B. S., and N. M. RIDDELL. In-herited antigenic differences in human serum beta

lipoproteins. A second anti-serum. 1. Clin. invest.42:867-875, 1963.

Boilean Grant, see Grant, J. C. B.36:Bo No-SoP SHLM and A. G. BEARN. The dis-

tribution of haptoglobin sub-types in various popu-lations. Amer. 1. Hum. Genes. 16:477-483, 1964.

37. BOYD, W. C. Blood groups. Tabu lae Biolog.(Hague) 17:113-240, 1939.

38. BOYD, W. C. Blood groups of American In-dians. Amer. I. Phys. Anthropol. 25:215-235, 1939.

39. BOYD, W. C. Blood groups of South AmericanIndians. Handbook S. Amer. Indians 3:91-95, 1950.

40. BOYD, W. C., and L. G. BOYD. The bloodgroups and types of the Ramah Navajo. Amer. I.Phys. Anthropol. 7:569-574, 1949.

41. BREAZEALE, E. L., R. A. GREENE, and L. J.KANTOR. Blood groups of the Papago Indians. 1.

lmmun. 40:161-162, 1941.42. BROWN, K. S., B. L. HANNA, A. A. DAHLBERG,

and H. H. STRANDS/WV. The distribution of bloodgroup alleles among Indians of southwest NorthAmerica. Amer. J. HUM. Genet. 10:175-195, 1958.

43. BUETTNER-JANUSCH, j., J. R. BOVE, and N.YOUNG. Genetic traits and problems of biologicalparenthood in two Peruvian Indian tribes. Amer. I.Phys. Anthropol. 22:149-154, 1964.

44. BUETTNER-JANUSCFI, J., H. GERSHOWITZ, L. J.

PosPisIL, and P. WILSON. Blood groups of selectedaboriginal and indigenous populations. Nature 188:153-154, 1960. Abs. HLAS 24:74.

45. CABANNES, R., A. BEURRIER, and B. MONNET.Etude des proteines, des haptoglobulines et destransferrines chez les indiens de Guyane Francaise.Nouv. Rev. Pram.. HZmat. 5:247-260, 1965.

46. CABRERA, M. A. Breve estudio sobre la reparti-ciOn de los grupos sanguineos entre nuestra pobla-ciOn. Salud y Asistencia (Guatemala) 3:16-17, 1950.

47. CARVALHO, J. C., P. DE LIMA, and E. GALVA.O.ObservaOts zoolOgicas e antropolOgicas na regiãodos formadores do Xingti. Avulso Mus. Nac. 5,1949.

48. CHIASSON, L. P. Gene frequencies of the Mic-mac Indians. J. Hered. 54:229-236, 1963.

49. CHOWN. B., and M. LEWIS. The ABO, MNSs,P, Rh, Lu, Kell, Le, Fy and Kidd blood groups andsecretor status of thc Blackfoot Indians of Alberta,Canada. Amer. 1. Phys. Anthropol. 11:369-384,1953.

50. CHOWN, B., and M. LEWIS. The blood groupand the secretor genes of the Stoney and SarceeIndians of Alberta, Canada. Amer. I. Phys. An-thropol. 13:181-190, 1955.

51. CHOWN, B., and M. LEWIS, The blood groupgenes of the Cree Indians and the Eskimos of theUngava District. Amer. 1. Phys. Anthropol. 14:215-224, 1956.

52. CHOWN, B., and M. LEWIS. The Kell antigen

144

in American Indians, Amer. I. Phys. Anthropol. 15:149-156, 1957.

53. CHOWN, B., and M. LEWIS. Blood groups in

anthropology. 13u1. Nat. Mus. Canada No. 167,Contrib. Anthropol., 1958.

54, CHOWN, 13., M. Ltwis, and H. KAITA. TheDiego blood group system. Nature 181:268, 1958.

55. CLEVE, H., and A. G. BEARN. Studies on thegroup specific component of human serum. Genefrequencies in several populations. Amer. I. Hum..Genet. 13:372-378, 1961.

56. CLEVE, H., R. L. KIRK, W. C. PARKER, A. G.BEARN, L. E. SCHACHT, W. KLEINMAN, and W. R.HORSFALL. Two genetic variants of the group-specific component of human serum: Gc Chippewaand Gc aborigine. Amer. 1. Hum. Genet. 15:368-

379, 1963.57. COCA, A. F., and 0. DEIBERT. A study of the

occurrence of the blood groups among the Ameri-can Indians. J. lmmun. 8:487-491, 1923.

58. COLLIER, W. A. The MN blood groups in theArawaks of Matta, Surinam. Docum. Med. Geogr.Trop. (Amsterdam) 7:359-360, 1955.

59. COLLIER, W. A., and W. AMSTELVEEN. DieBlutgruppen des Bevolkerung von Surinam. VoxGuyanae (Paramaribo) 1:85-89, 1954.

60. COLLIER, W. A., J. FROS, and J. F. A. SCHIPPER.Blood groups of some American Indian settlements.Docuni. Med. Geogr. Trop. (Amsterdam) 4 :225-226, 1952.

61. COLLIER, W. A., A. E. WOLFF, and A. E. G.ZAAL. Blood groups of some American Indian set-tlements. Docum. Med. Geogr. Trop. (Amsterdam)4:92-95, 1952.

62. CORCORAN, P. A., F. H. ALLEN, JR., A. C.ALLISON, and B. S. BLUMBERG. Blood groups ofAlaskan Indians and Eskimos. Amer. I. Phys. An-thropol. 17:187-193, 1959.

63. CORCORAN, P. A., D. L. RABIN, and F. H.ALLEN, JR. Blood groups of 237 Navajo schoolchildren at Pinon Boarding School, Pinon, Arizona.Amer. J. Phys. Anthropol. 20:389-390, 1962.

64. CORDOVA, M. S., R. LISKER, and A. LORIA.Studies on several genetic hematological traits ofthe Mexican population. XII. Distribution of bloodgroup antigens on twelve Indian tribes. Amer. 1.

Phys. Anthropol. 26:55-56, 1967.65. DA SILVA, E. M. Grupos sanguineos comuns

e fatores M e N em indios Cane la (Ramkokamekra)do Maranhio. Rev. Mus. Paul. n.s. 2:271-274, 1948.Abs. HLAS 14:48.

66. DA SILVA, E. M. Blood groups of Indians,whites and white-Indian mixtures in southern MatoGrosso, Brazil. Amer. 1. Phys. Anthropol. 7:575-586, 1949.

67. DA SILVA, E. M., R. PATIii0 SALAZAR, R.PIMENTA DE MELLO, and W. 0. CRUZ. Distribuicio

de grupos sanguineos comuns (AB) c incidenciado fator Rh etc. de Duque de Caxias (Estado doRio). 0 Hosp. (Rio de Janeiro) 34:649-655, 1943.

68. DEL Rio M., J. A. ContribuciOn al estudio delos grupos sanguineos en Colombia. Tesis, Facultadde Medicina, Universidad Nacional de Colombia,(Bogota), 1930.

69. Di Az UNGRIA, A. G. DE. Los grupos sanguineosdel sistema MN en poblaciones indigenas de Vene-zuela. Folio Antrop. (Caracas) 3:1-26, 1962.

70. DOBBLIN, T. D., and J. F. MOHN. The bloodgroups of the Seneca Indians. Amer. I. Hum. Genet.19:700-712, 1967.

71. DUQUE GOMEZ, L. Grupos sanguineos entrelos indigenas del Departamento de Caldas. Rev.Inst. Etnol. Nat% (Bogota) 1:623-653, 1944. Abs.

HLAS 10:47.72. EISEN, B. and C. F. ABILDoAARD. Hemoglobin

electrophoretic patterns and blood groups of SanBias Indians. Vox Sang. 5:560-561, 1960.

73. ESCOBAR, J. J. Distribuci6n de los grupos san-guineos en el Valle del Cauca, Repdblica de Co-lombia. Bibl. Haemat. 10:315-316, 1959.

74. ETCHEVERRY, R., C. GUZMAN, C. REGONESI,N. MURANDA, and N. DURAN. Blood groups andother genetic blood characters in the Atacamenos.Rev. MM. Chil. 1966. In press.

75. ETCHEVERRY, R., N. MURANDA, C. GUZMAN,

C. REGONESI, N. DURAN, J. ROJAS, J. VILLAGRAN, and

E. BORIS. Blood groups in Indians of Tierra delFuego. Nature 214:211-212, 1967.

76. FERNANDES, J. L. "Notas hemato-antropolOgi-cas sôbre os Casingangues de Palmas." Rev. MZ'd.Parand. (Brazil) 8:1-8, 1939.

77. FERNANDES, J. L., P. C. JUNQUEIRA, H. KALMUS,

F. OTTENSOOSER, R. PASQUALIN, and P. WISHART.P.T.C. thresholds, colour vision and blood factors

in Brazilian Indians. I. Kaingangs. Ann. Hum.Genet. 22:16-21, 1957.

78. FERNET, P., G. LARROUY, and J. RUFFIf. Etude

hémotypologique des populations indiennes de

Guyane Francaise. II. Les groupes seriques dusysteme Gm. Bull. Wm. Soc. Anthrop. (Paris) 7:119-123, 1964.

79. FIGUEROA, E. R. Resultado de algunas investi-gaciones del Rh. Arch. Venez. Pueric. Pediat. 11:

42, 1948.80. FLORY, L. L. Haptoglobin types of the Nez

Perce Indians. Nature 197:577-578, 1963.

81. FUENTES, L. G. Distribución de los grupossanguineos en indios guatusos de Costa Rica. Rev.Biol. Trop. 9:131-140, 1961.

82. GALLANGO, M. L., and T. ARENDS. Incidenceof Gma and Gml genes among Venezuelan Indiansand mestizos. Hum. Biol. 35:361-365, 1963.

83. GALLANGO, M. L., and T. ARENDS. Incidence

145

1446

of Gm factors among various South Americanpopulations. Bibl. Ramat. 19:472-477, 1964.

84. GALLANGO, M. L., and T. ARENDS. Inva genefrequency in Venezuelan Indians. Bibl. Haemat.23:400-405, 1965.

85. GALLANGO, M. L., and T. ARENDS. El sistemade grupos sericos Gc: sus variantes fenotipicas y sudistribución mundial. Acta. Cient. Venez. 16:120-127, 1965.

86. GALLANGO, M. L., and T. MENDS. Inv (a)serum factor in Venezuelan Indians. Transf. 5:457-460, 1965.

87. GATES, R. R. Blood groups of Canadian In-dians and Eskimo. Amer. 1. Phys. Anthropol. 12:475-485, 1929.

88. GATES, R. R. The blood groups and otherfactors of the Micmac Indians. I. Roy. Anthropol.Inst. 68:283-298, 1938.

89. GATES, R. R., and G. E. DARBY. Blood groupsand physiognomy of British Columbia coastal In-dians. 1. Roy. Anthropol. Inst. 64:23-44, 1934.

90. GERSHOWITZ, H. The Diego factor amongAsiatic Indians, Apaches and West African Negroes.Amer. J. Phys. Anthropol. 17:195-200, 1959.

91. GERSHOWITZ, H., P. C. JUNQUEIRA, F. M. SAL-ZANO, and J. V. NEEL. Further studies on theXavante Indians. III. Blood groups and ABH-Leasecretor types in the Sim Oes Lopes and Sao MarcosXavantes. Amer. 1. Hum. Genet. 19:502-513, 1967.

92. GIBLETT, E. R. The plasma transferrins. Prog.Med. Genet. 2:34-63, 1962.

93. GIBLETT, E. R., and W. R. BEST. Haptoglobinand transferrin types in Peruvian Indians. Nature192:1300-1301, 1961.

94. GONZALEZ-VALLARINO, G. Frecuencia de losfactores ABO y Rh en pobladores del Peril. Sangre':31-33, 1958.

95. GOODNER, K. Incidence of blood groups amongthe Maya Indians of Yucatan. J. Immun. 18:433-435, 1930.

96. GRANT, J. C. B. Anthropometry of the Chipe-wyan and Gra Indians of the neighborhood of LakeAthabasca. Nat. Mus, Canada Bull. 64, Anthrop.Ser. 14 (Ottawa), 1930.

97. GRANT, J. C. B. Progress in an anthropometricsurvey of the Canadian aborigines. Fifth Pacific Sci.Congr. B 2:2, 1933.

98. GRANT, J. C. B. Anthropometry of the Beaver,Sekani and Carrier Indians. Nat. Mus. Canada Bull.81, Anthrop. Ser. 18 (Ottawa), 1936, pp. 1-37.

99. Ottity, M. Pop and W. S. LAUGHLIN. Bloodgroups of Caddoan Indians of Oklahoma. Amer, 1.Hum. Genet. 12:86-94, 1960.

100. HANNA, B. L., A. A. DAHLBERG, and H. H.STRANDSKOV. A preliminary study of the populationhistory of the Pima Indians. Amer. 1. Hum. Genet.5:377-388, 1953.

101. HENCKEL, K. 0., A. CASTELLI, and J. DALBORGO. Algunas observaciones acerca de la propor-ción de los grupos sanguineos M y N de los indiosMapuches. Bol. Soc. Biol. (Concepci6n) 15:37-41,1941.

102. HULSE, F. S. Blood types and mating pat-terns among northwest coast Indians. Southwest 1.Anthropol. 11:93-104, 1955.

103. HULSE, F. S. Linguistic barrier to gene flow.Amer. I. Phys. Anthropol. 15:235-246, 1957.

104. HuLss, F. S. Ripples on a gene pool. Theshifting frequencies of blood-type alleles amongthe Indians of the Hupa reservation. Amer. 1. Phys.Anthropol. 18:141-152, 1960.

105. JUNQUEIRA, P. C. Personal communication toT. Arends, reported in reference 17.

106. JUNQUEIRA, P. C., and P. J. WISHART. Bloodgroups of Brazilian Indians (CaraMs). Nature 177:40, 1956.

107. JUNQUEIRA, P. C., P. J. W15HART, F. OTTEN-SOWER, R. PASQUALIN, P. L. FERNANDEZ, and H.KALMUS. The Diego factor in Brazilian Indians.Nature 177:41, 1956.

108. JUNQUEIRA, P. C., H. KALMUS, and P. WISH-ART. P.T.C. thresholds, colour vision and bloodfactors of Brazilian Indians. II. Carajis. Ann. Hum.Genet. 22:22-25, 1957.

109. KAHN, M. C. Blood grouping of 336 UpperAucaner Bush Negroes and 70 Alukuyana Indiansin Dutch Guiana. J. Immun. 31:377-385, 1936.

110. KAKLAMANI, E., and E. J. HOLBOROW. Secre-tor and Lewis gene frequencks in Blackfeet Indians.Vox. Sang. 8:231-234, 1963.

I 1 I. KRAUS, B. S., and C. B. Wi-taL. Microevolu-tion in a human population: tudy of socialendogamy and blood type distributions among thewestern Apache. Amer. Anthropol. 58:1017-1043,1956.

112. LANDSTEINER, 1(.3 and P. LEVINE. 011 theracial distribution of some agglutinable structuresof human blood. J. Immun. 16:123-131, 1929.

113. LANDSTEINER, K., A. S. WIENER, and G. A.MATSON. Distribution of the Rh factor in AmericanIndians. 1. Exp. Med. 76:73-78, 1942.

114. LARROUY, G.,Y. MARTY, and J. Ruani. Etudehémotypologique des populations indiennes de laGuyane Française. I. Les groupes erythrocytaires.Bull. Mini. Soe. Anthrop. (Paris) 7:107-117, 1964.

115. LAYRISSE, M. Anthropological considerationsof the Diego (Dia) antigen. Amer. 1. Phys. An-thropol. 16:173-186, 1958.

116. LAYRISSE, M. Per rnmunication toJ. V. Ned, 1967.

117. LAYRISSE, M., arid 1"system. Steps in the invest+,4at1o1group system. Blood 12:115-122, 195

118. LAYRISSE, M., T. ARENDS, and

The Diegoa new blood

7.R. DomiNotnz-

146

et.14t0

Sisco. Nuevo grupo sanguineo encontrado endescendie.ntes de indios. Acta. Med. Venez. 3:132-138, 1955.

119. LAYRISSE, M., T. ARENDS, and R. DOMiNGUEZ-Sisco. Investipci6n del factor Diego en indiosvmezolanos. Importancia clinica y antropológica.Bibl. Haemat. 2:773-776, 1955.

120. LAYRISSE, M., T. ARENDS, and J. WILBERT.Peculiar distribution of the Diego factor among theWarrau. Nature 181:118-119, 1958.

121. LAYRISSE, M., and Z. LAYRISSE. Frequency ofthe new blood group antigen Jsa among SouthAmerican Indians. Nature 184:640, 1959.

122. LAYRISSE, M., Z. LAYRIS4E, E. GARCIA, andJ. PARRA. Genetic studies of the new Rh chromosomeDcel (Rol) found in a Chibcha tribe. Vox Sang.6:710-719, 1961.

123. LAYRISSE, n, Z. LAYRISSE, E. GARCIA, andJ. WILBERT. Blood group antigen tests of the YaruroIndians. Southwest. J. Anthropol. 17:198-204, 1961.

124. LAYRISSE, M., Z. LAYRISSE, E. GARCIA, andJ. WILBERT. Blood group antigens of the PemonIndians of Venezuela. Amer. I. Phys. Anthropol.20:411-420, 1562.

125. LAYRISS2, M., Z. LA YRISSE, E. GARCIA, J.

WILBERT, and J. PARRA. New Rh phenotype Dccele1f,found in a ChibckIn Indian tribe. Nature 191:503-504, 1961.

126. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.Blood group antigen tests of the Yupa Indians ofVenezuela. Amer. Anthropol. 62:418-436, 1960.

127. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.Blood group antigens among the Paraujano. Amer.I. Phys. Anthropol. 18:131-139, 1960.

128. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.The blood group antigens in Goajiro Indians. Amer.I. Phys. Anthropol. 19:255-262, 1961.

129. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.Blood group antigen tests of the Waica Indians ofVenezuela. Southwest I. Anthropol. 18:78-93, 1962.

130. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.

Tim. blood groups of northern continental Caribs.Hum. Biol. 35:140-166, 1963.

131. LAYRISSE, M., Z. LAYRISSE, and J. WILBERT.

Blood group antigen svidies of four Chibchantribes. Amer. Anthropol. 65:36-55, 1963.

132. Lf.YRISSE, M., Z. LAYRISSE, and J. WILBERT.Blood group antigen tests of the Bari Indians ofVenezuela. Hum. Biol. 36235-245, 1964.

133. LAYRISSE, M., and J. WILBERT. Absence ofthe Diego antigen, a genetic characteristic of earlyimmigrants of South America. Science 134:1077-

1078, 1961.134. LAYRISSE, M., and J. WILBERT. Indian So-

cieties of Venezuela. Caracas, Instituto Caribe deAntropologia y Soeiologia, 1966. (Monograph 13)

135. LAYatssis, M., J. WILanT, and T. ARENDs.

Frequency of blood group antigens in the descend-ants of Guayqueri Indians. Amer. I. Phys. An-thropol. 16:307-318, 1958.

136. LEHMANN, H., A. CEBALLOS ARA00, andM. CHAVES. Grupos satiguineos entre los indiosKwaiker. Biol. Arqueol. (Bogota') 2:227-230, 1946.Abs. HLAS 12:51.

137. LEHMANN, H., L. DUQUE, and M. FORNA-GUERA. Grupos sanguineos entre los indios Guam-biano-Kokonuko. Rev. Inst. Etnol. Nac. (BogotOI:197-208, 1943. Abs. HLAS 9:54.

138. LEITE, G. M., M. 0. VILLELA, and V. S.VEGAS. A distribuigio de alguns fatOres de grupossanguineos em indios brasileiros do Alto Xingti.Rev. Paul. Med. 53:370-372, 1958.

139. LEVINE, P., G. S. MATSON, and H. F.SCHRADER. Distribution of blood groups and antigenM among Indian Blackfeet and Blood tribes. Proc.Soc. Exp. Biol. Med. 33:297-299, 1935.

140. LEVINE, P., E. A. ROBINSON, M. LAYRISSE,

T. ARENDS, and R. DOMINGUEZ-SISCO. The Diegoblood factor. Nature 177:40-41, 1956.

141. LEVINE, V. E. The blood groups of AlaskanIndians. Amer. I. Phys. Anthropol. 9:238, 1951.

142. LEWIS, M. Further observation on the bloodfactor Dia. Nature 178:1125, 1956.

143. LEWIS, M., H. AYUKAWA, B. CHOWN, andP. LEVINE. The blood group antigen Diego in NorthAmerican Indians and in Japanese. Nature 177:1084,

1956.144. LEWIS, M., B. CHowN, and H. KAITA. Further

observations on the blood factor Dia. Nature 178:1125, 1956.

145. LEWIS, M., J. A. HILDRES, H. KA/TA, and

B. CHOWN. The blood groups of the KutchinIndians at Old Crow, Yukon Territory. Amer. I.

Phys. Anthropol. 19:383-389, 1961.146. LIMA, P. E., DE. Grupos sanguineos dos

indios do Xingii. Bol. Mu:. Nac. (Rio de Janeiro)11:1-4, 1950.

147. LIPSCHUTZ, A., G. MOSTNY, and L. ROBIN.

The bearing of ethnic and genetic conditions onthe blood groups of three Fuegan tribes. Amer. I.Phys, Anthropol. 4:301-312, 1946.

148. LISKER, R., and E. R. GIBLET?. Studies onsr,veral genetic hematological traits of Mexicans. Xl.

Red cell acid phosphatase and phosphoglucomutasein three Indian groups. Amer. I. Hum. Genet. 19:

174-177, 1967.149. LISKER, R., G. ZARATE, and E. RODRIGUEZ.

Serum polymorphism in several Indian tribes. Amer.I. Phys. Anthropol. 27:27-32, 1967.

150. LOVETT, C. A. Haptoglobin and Gc types in

Haida Indians. Vox Sang. 12:151-153, 1967.LOUREIRO-FERVANDES, lee Fernandes, J. L.

151. MARROQUIN, J. Particularidades antropol6gicas

147

j4§1

a

del indigena pundio. Rev. Mus. Nac. (Lima) 15:13-32, 1946.

152. MARTINEZ SILVA, R., and A. SORIANO LLERAS.Grupos sanguineos de los indios Guajiros. Rev. Fac.Med. (BogotA) 28:10-14, 1960.

153. MARTINg, A. V. and T. BASTOS. SObre adistribuick dos grupos sanguineos entre os indiosbotocudos do Rio Doce. Brasil Med. 49:108-109,1935.

154. MATSON, G. A. Unexpected differences indistribution of blood groups among AmericanIndians. Proc. Soc. Exp. Biol. Med. 30:1380-1382,1933.

155. MATSON, G. A. Blood groups and ageusia inIndians of Montana and Alberta. Amer. J. Phys.Anthropol. 24:81-89, 1938.

156. MATSON, G. A. Blood groups and ageusia inIndians of northern Alberta. Amer. J. Phys. An-thropol. 27:263-267, 1940.

157. MATSON, G. A. Distribetion of blood groupsamong the Sioux, Omaha and Winnebago Indians.Amer. J. Phys. Anthropol. 28:313-318, 1941.

158. MATSON, G. A. Personal communication toJ. V. Ned, 1967.

159. MATSON, G. A., E. A. Kocx, and P. LEVINE.A study of the hereditary blood factors among theChippewa Indians of Minnesota. Amer. I. Phys.Anthropol. 12:413-426, 1954.

160. MATSON, G. A., P. LEVINE, and R. F.SCHRADER. Distribution of the subgroups of A andM and N agglutinogens among the Blackfeet In-dians. Proc. Soc. Exp. Biol. Med. 35:46-47, 1936.

161. MATSON, G. A., and C. L. PIPER. Distribudonof the blood groups, M-N, Rh types and secretorsamong the Ure Indians of Utah. Amer. 1. Phys.Anthropol. 5:357-368, 1947.

162. MATSON, G. A., and H. F. SCHRADER. Bloodgrouping among Blackfeet and Blood tribes ofAmerican Indians. 1. Immun. 25:155-163, 1933.

163. MATSON, G. A., and H. F. SCHRADER. Distri-bution of the four blood groups among the liteIndians of Utah. Proc. Utah Acad. Sci. Arts Lett.18:101-103, 1941.

164. MATSON, G. A., H. E. SUTTON, R. ETCHEVERRY, J. SWANSON, and A. ROBINSON. Distributionof hereditary blood groups among Indians in SouthAmerica. IV. In Chile. Amer. 1. Phys. Anthropol.27:157-194, 1967.

165. MATSON, G. A., H. E. SUTTON, J. SWANSON,and A. R. ROBINSON. Distribttion of haptoglobin,transferrin, and hemoglobin qpes among Indiansof Middle America. Southern Mexico, Guatemala,Honduras, and Nicaragua. Hum. Biol. 35:474-483,1963.

166. MArsorr, G. A., H. E. SUTTON, J. SWANSON,and A. R. ROBINSON. Distribution of haptoglobin,transferrin, and hemoglobin types among Indians

of Middle America. In British Honduras, CostaRica, and Panama. Amer. J. Phys. Anthropol. 23:123-130, 1965.

167. MATSON, G. A., H. E. SUTTON, J. SWANSON,A. ROBINSON, and A. SANTIANA. Distribution ofhereditary blood groups among Indians in SouthAmerica. I. In Ecuador. Amer. I. Phys. Anthropol.24:51-70, 1966.

168. MATSON, G. A., H. E. SUTTON, J. SWANSON,and A. ROBINSON. Distribution of hereditary bloodgroups among Indians in South America. II. InPeru. Amer. I. Phys. Anthropol. 24:325-349, 1966.

169. MATSON, G. A., H. E. SUTTON, J. SWANSON,and A. ROBINSON. Distribution of hereditary bloodantigens among Indians in South America. III. InBolivia. Amer. J. Phys. Anthropol. 25:13-33, 1966.

170. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood group antigens among the Mayaand non-Maya Indians in Mexico and Guatemala.Amer. J. Phys. Anthropol. 17:49-74, 1959.

171. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among AmericanIndians in Middle America. I. Lacandón and otherMaya. Amer. Anthropol. 63:1292-1322, 1961.

172. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Indians inMiddle America. II. Tzotzil and other Maya. Amer.1. Phys. Anthropol. 21:1-14, 1963.

173. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Indians inMiddle America. III. In Guatemala. Amer. I. Phys.Anthropol. 21:301-317, 1963.

174. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Indians inMiddle America. IV. In Honduras. Amer. 1. Phys.Anthropol. 21:319-333, 1963.

175. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Indians inMiddle America. V. In Nicaragua. Amer. I. Phys.Anthropol. 21:545-559, 1963.

176. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Indians inMiddle America. VI. In British Honduras. Atner. 1.Phys. Anthropol. 22:271-284, 1964.

177. MATSON, G. A., and J. SWANSON. Distributionof hereditary biood antigens among Indians inMiddle America. VII. In Costa Rica. Amer. J. Phys.Anthropol. 23:107-122, 1965.

178. MATSON, G. A., and J. SWANSON. Distributionof hereditary blood antigens among Indians inMiddle America. VIII. In Panama. Amer. 1. Phys.Anthropol. 23:413-426, 1965.

179. MATSON, G. A., and J. SWANSON. Blood groupantigens among Indians in British Honduras. Bibl.Haemat. 13:320-326, 1965.

180. MAzzA, S. Los factores M y N en sangre de

indigenas del Chaco Argentino. Soc. Arg. Patol.Region. 3:1916-1918, 1939. Abs. HLAS 6:61.

181. MAZZA, S., and I. FRANKE. Grupos sanguineosde indios y de aut6ctonos del norte argentino. Pren.Med. Argent. 14:408-409, 1927.

182. MAzzA, S., K. SCHURMAN, and H. GUT-DEUTSCH. 1933. Cited in Steffan and Wellisch, 1936.

183. MELARTIN, L. and B. S. BLUMBERG. AlbuminNaskapi: a new variant of serum albumin. &Fence153:1664-1666, 1966.

184. MEZA ARRAC C., J. STAEDING, and A. NA-J AMK1N. Investigación del sistema Diego en lapoblación chilena. Sangre 3:360-365, 1958.

185. MonN, J. F., R. M. LAMBERT, and C. M.ZmIJEwsKI. Incidence of the blood group antigenDia in the Tuscarora Indians of North America.Nature 198:697-698, 1963.

186. MONTENEGRO, L. Blood groups in TucanoIndians. Hum. Biol. 39:89-92, 1967.

MONT IEL, see Ntez Montiel.187. MOURANT, A. E., A. C. Kopic, and K.

DOMAN I EWSKA-SOBCZAK. The ABO Blood Groups:Comprehensive Tables and Maps of World Distribu-tion. Springfield, Illinois, Charles C Thomas, 1958.

188. NAGEL, R., R. ETCHEVERRY, C. GUZMAN, E.COVARRUBIAS, A. HILLE, and A. MON TE NEGRC . Hapto-globin types in the Mapuche Indians of SouthernChile. Preliminary report. Rev. Med. Chile 90:863-865, 1962.

189. NAGEL, R., and R. ETCHEVERRY. T3.pes ofhaptoglobins in Araucanian Indians of Chile '''ature197:187-188, 1963.

190. NEEL, J. V., F. M. SALZA NO, P. C. NQUEIRA,

F. KEITER, and D. MAY URY-LEWIS. Studies on theXavante Indians of the Brazilian Mato Grosso.Amer. I. Hum. Genet. 16:52-140, 1964.

191. Nico, C. A study of the blood g oups amongthe American Indians. J. lmmun. 11:A9-322, 1926.

192. NOVELO, G., M. SALAZAR MALLiN, and T.KORNHA USER. Caracteristicas de los aglutin6genosde grupos sanguineos de los indigenas mexicanos.Bibl. Haemat. 19:256-262, 1964.

193. Nt'n1Ez MONTIEL, J. T., R. A. ARTEAGA.PEREZ,and A. E. N6r1Ez MONTIEL. Estudios hematológicosen grupos indigenas del Estado Zulia. SistemasABO, MN, Rh, Duffy, Kell y Diego. Acta Cient.Venez. 8:10-13, 1957.

194. N6F4Ez MONTIEL, J. T., and A. E. N6izazMONTIEL. El factor Diego y otros sistemas (Rh-Fir,ABO, MNSs) en los indios rionegrinos. Acta. Cient.Venez, 8:134-136, 1957.

195. N6izaz MONTIEL, A. E., and J. T. N6 FiEZMONTIEL. Investigachin del factor Diego y otrosfactores hemAticos (ABO, Rh-Hr, MN, Duffy yKell) en los indios macoitas de la Sierra de Peril&Zulig-Maracaibo. Sangre 3:38-43, 1958.

196. ONE170, A. E., and F. J. CASTILLO. LOS

grupos sanguineos en lov araucanos. Rev. Inst. Bact.(Chile) 1:17-24, 1930.

197. OTTENSOOSER, F., and R. PASQUALIN. Bloodtypes of Brazilian Indians. Amer. J. Hum. Genet.1:141-155, 1949.

198. PAEz Pin; C., and K. FREUDENTHAL. Grupossanguineos entre los indios sibundoy, santiaguelios,kwaiker, e indios y mestizos de los arredores dePasto. Rev. Inst. Etnol. Nac. (Bogota) 1:411-415,1944. Abs. HLAS 10:47.

199. PALATNIK, M. Seroantropologia argentina.Sangre 11:395-412, 1966.

200. PALIsTNIK, M. Grupos sanguineos en ran-queles de Argentina. Sangre 1968. In press.

201. PA NTIN, A. M., and P. C. jUNQUEIRA. Bloodgroups of Brazilian Indians. Amer. 1. Phys. An-thropol. 10:395-405, 1952.

202. PANTIN, A. M., and R. K ALLSE N. The blaodgroups of the Dieguefio Indians. Amer. 1. Phys.Anthropol. 11:91-96, 1953.

203. PARKER, W. C., and A. G. BEARN. Hapto-globin and transferrin gene frequencies in a Navajopopulation: a new transferrin variant. Science 134:106-108, 1961.

204. PAULOTTI, 0. L. Los Toba. ContribuciOn a lasomatologia de los indigenas del Chaco. Runa 1:9-96, 1948.

205. PAULOTTI, 0. L., and L. G. ALEGR1A. Grupossanguineos de los nativos de la Puna jujelia. An.Mus. Arg. C'ien. Nat. (Buenos Aires) 41:21-28,1943.

206. Rums, F. P., B. B. VICTORS, and M. W.DODSON. Distribution of blood groups among theEskimos, Indians and whites of western Alaska.Amer. 1. Hum. Genet. 5:252-256, 1953.

207. PEDRE IRA, C. M., 1. 1. S. PE IXOTO, and L. R.DE CASTRO REGINA. GrUpOS sanguineos de rema-nescentes do tribo kariri (kiriri) de Mirandela,Bahia. 55o Paulo, Atas do Primeiro Simpóseo Sul-Americano de Genetica, 1961, pp. 315, 316. Abs.HLAS 25:67.

208. PEDitEntA, C. M., L. I. S. PEixoTo, andL. M. G. I. ROCHA. Determinagio de grupos san-guineos em indios patax6s do vale do rioBahia. Anais Ia. Reuniiio Brasileira Genética Hu-mana, 1958, pp. 84-88, Abs. F1LAS 22:80.

209. POLLITZER, W. S., R. C. HARTMA NN, H.Moon, R. ROSENFELD, H. SMITH, S. HAKIM, P. J.SCHMIDT, and W. C. LEYSHON. Blood types of theCherokee Indians. Amer. 1. Phys. Anthropol. 20:33-43, 1962,

210. POLLITZER, W. S., D. S. PHELPS, R. E.WAGGONER, and W. C. LEvstioN. Catawba Indians:morphology, genetics and history. Amer. 1. Phys.Anthropol. 26:5-14, 1967.

211. RAHM, G. Los grupos sanguineos de los

araucanos (mapuches) y de los fueguinos. Invest.Prog. Med. (Madrid) 5:160, 1931.

212. RAMOS DE ANDRADE, R., C. LASCANO, and M.ZARATE. GrUPOS sanguineos (ABO) de los indios ymestizos de los airededores de Quito. Humanitas(Quito) 1:19-21, 1959. Abs. HLAS 23:78.

213. REICHELZOLMATOFF, A., and G. REICHEL-DOLMATOFF. Grupos sanguineos entre los indiospijao del Tolima. Rev. Inst. Etnol. Nac. (Bogota)1:507-520, 1944.

214. REYNAFARIE, C. El factor Rh y otros grupossanguineos en los indios peruanos. Anal. Fac. Med.Univ. Nac. S. Marcos (Lima) 40:573-584, 1957.

215. REYNAFARJE, C., J. PAURA, and V. P1MENTEL.El factor Diego y otros grupos sanguineos en losindios de la sierra y selva peruana. Arch. lnst.An dina. 1:14-22,1965.

216. RIBEIRO, L., W. BERARDINELLI, and E. M.ROITER. Grupos sanguineos dos indios guaranys.Arch. Med. Leg. ldent. (Rio de Janeiro) 5:59-65,1935.

217. RIDE, L. Anthropological studies amongstNorth American Indians from British Columbia.Caducens 14:205-216, 1935.

218. RIFE, D. W. Blood groups of Indians incertain Maya areas of Central America. 1. Immun.22:207-209, 1932.

219. ROBINSON, J. C., C. LEVENE, B. S. BLUMBERG,and J. E PIERCE. Serum alkaline phosphatase typesin North American Indians and Negroes. 1. Med.Genet. 4;96-101, 1967.

220. RODRIGUEZ, H., E. Q. DE Ronaioutz, A.LOMA, and R. LISKER. Estudios sobre algunas carac-teristicas hematolOgicas heredittirias en la poblaciOnmexicana. I. Grupos sanguineos en tarascos, nahoasy mixtecos. Rev. invest. Clin. (Mexico) 14:319-328,1962.

221. RODRIGUEZ, H., E. DE RODRIGLEZ, A. LORIA,and R. LUKER. Studies of several genetic hematologi.cal traits of the Mexican population. Hum. Biol. 35:350-360, 1963.

RODRIGUEZ, M. L. G. DE, see Gallango, M. L.222. ROPARTZ, C. Personal communication to

Gallango and Arends, 1965 (reference 86).223. RuPPti, J., G. LARROUY, and H. VERGUES.

Himatologie comparie des populations amerindi-ennes de Bolivie et phinomenes adaptifs. Nouv. Rev.Franc. d'Himat. 6:544-552, 1965.

224. SACCHETTI, A. Studi ematologici nella zonadel Lago Titicaca, Bolivia. Riv. Antrop. 40:189-231,1953.

225. SAccHErri, A. Hamatologisch-anthropolo-gische Untersuchungen an eingeborenen Popula-tionen der Anden. Anthrop. Anz. 26:279-293, 1963.

226. SALAZARMALLEN, M. El aglutin6geno 'Lewis'en la sangre de los mexicanos. Bol. Inst. Baud. Mid.Biol. (Mexico) 7:25-28, 1949. Abs. HLAS 16:45.

227. SALAZARMALLEN, M., and T. ARIAS. Inheri-tance of Diego blood group in Mexican Indians.Science 130:164-165, 1959.

228. SALAZAXMALLEN, M., and R. HERNANDEZ DE

LA PORTILLA. Existencia del aglutin6geno Rh en loshématies de 250 individuos mexicanos. Rev. Soc.Mex. Hist. Nat. 5:183-185, 1944.

229. SALAZAR-MALLEN, M., and G. MARTINEZ.Estudio sobre la frequencia del factor Rho endiferentes grupos de habitantes de la ReptiblicaMexicana. Rev. Mid. Hosp. Gen. (Mexico) 9:1-4,1947.

230. SALZANO, F. M. The blood groups of SouthAmerican Indians. Amer. 1. Phys. Anthropol. 4:555-579, 1957.

231. SALZANO, F. M. Studies on the CaingangIndians. III. Blood groups. Amer. 1. Phys. Anthropol.19:391-404, 1961.

232. SALZANO, F. M. Salivary secretions of Indiansfrom &Liu Catarina, Brazil. Amer. J. Hum. Genet.16:301-310, 1964.

233. SALZANO, F. M Blood groups of Indiansfrom Santa Catarina, Brazil. Amer. I. Phys. An-thropol. 22:91-106, 1964.

234. SALZANO, F. M., and D. C. SHREFFLER. TheGc polymorphism in the Caingang Indians of Brazil.Acta Genet. 16:242-247, 1966.

235. SALZANO, F. M., and A. G. STEINBERG. TheGm and Inv groups of Indians from Santa Catarina,Brazil. Amer. J. Hum. Genet. 17:273-279, 1965.

236. SALZANO, F. M., and H. E. SUTTON. Hapto-globin and transferrin types in southern BrazilianIndians. Acta Genet. Statist. Med. (Basel) 13:1-8,1963.

237. SALZANO, F. M., and H. E. SUTTON. Hapto-globin and transferrin types of Indians from SantaCatarina, Brazil. Amer. 1. Hum. Genet. 17:280-289,1965.

238. SANDOVAL, L., and C. HENCKEL. The ABO,MNS and Rh-Hr blood groups of the MapucheIndians of Cautin Province, Chile. Hum. Biol. 26:324-329, 1954.

239. SANDOVAL, L., C. 0. HENCKEL, and L.Givovicx. Grupos, subgrupos y factores Rh san-guineos en los indios mapuches de la Provincia deCautin. Notas Inst. Mus. Univ. Nat% de La Plata, 11,Antrop. 35:283-299, 1946.

240. SAN MARTIN, M. Equipos sanguineos y factorRh en Ull grupo dc nativos del Departamento deJunin. Anal. Fac. Med. (Lima) 34:276-279, 1951.

241. SANTIANA, A. LOS grupos sanguineos de losindios del Ecuador. Notas Mut. La Plata 9(30):431-438, 1944. Abs. HLAS 10:47.

242. SANTIANA, A. LOS grupos sanguineos de losindios del Ecuador: comunicación definitiva. Anal.Liniv. Cent. (Quito), 325 and 326, pp. 1-50, 1947-1948. Abs. HLAS 13:33.

.464

vrt.,

1,

243. SANTIANA, A. Los indios del Ecuador y suscaracteristicas serológicas. Terapia 10:13-18, 1952.

244. SCARO, J. L. Investigación del factor Diegoen aborigines de la Quebrada de Humahuaca. Rev.Soc. Argent. Biol. 34:71-74, 1958.

245. SCOTT, E. M., I. W. DUNCAN, V. EKSTRAND,and R. C. WRIGHT. Frequency of polymorphic typesof red cell enzymes and serum factors in AlaskanIndians and Eskimos. Amer. 1. Hum. Genet. 18:408-411, 1966.

246. SHim, B. S., and A. G. BEARN. The distribu-tion of haptoglobin subtypes in various populations,including subtype patterns in some nonhuman pri-mates. Amer. J. Hum. Genet. 16:477-483, 1964.

247. SHREFFLER, D. C., and A. G. STEINBERG.Serum protein groups and the SC1 trait of saliva inthe Sitniies Lopes and Sio Marcos Xavantes. Amer.1. Hum. Genet. 19:514-523, 1967.

SILVA, DA, see DA SILVA.SILVA, R. M., see MARTINEZ SILVA, R.248. SILVER, R. T., J. M. HABER, and A. KELLNER.

Evidence for a new allele in the Kidd blood groupsystem in Indians of northern Mato Grosso, Brazil.Nature 186:481, 1960.

249. SILVER, R. T., J. M. HABER, and A. KELLNER.Blood studies of jungle Indians of the upper XinguRiver, Mato Grosso, Brazil. Bibl. Haemat. 13:167-169, 1962.

250. SNYDER, L. H. Human blood groups: theirinheritance and racial significance. Amer. 1. Phys.Anthropol. 9:233-263, 1926.

251. SOCARRAS DEL Rio, J. A. ContribuciOn alestudio de los grupos sanguineos en el Pei ti. Rev.Cienc. (Lima) 32, 1930. Cited in Sacchetti, 1953.

252. SOCARRAS DEL Rio, J. A. Contribución alestudio de los grupos sanguineos en Colombia. Univ.Nac. Col. (Bogota), 1930. Citcd in Sachetti, 1953.

253. SORIANO-LLEXAS, A., and R. MARTINEZ SILVA.Estudios immunohematológicos entre los indiosIloreos. Rev. Pan Med. (Bogota) 28 (7-9):101-106,1960.

254. STEFFAN, P., and S. WELLISCH. Die geogra-phische Verteilung der blutgruppen. Z. Rassen-physiol. 5:180-5, 1932; 6:28-36, 1933; 7:176-185,1935; 8:38-47, 1936.

255. STEINBERG, A. G., M. S. CORDOVA, and R. Lis-KER. Studies on several genetic hematological traitsof Mexicans. XV. The Gm allotypes of some Indiantribes. Amer. J. Hum. Genet. 19:747-756.

256. STEINBERG, A. G., R. STAUFFER, B. S. BLUM-BERG, and H. FUDENBERG. Gm phenotypes and geno-types in U.S. whites and Negroes; in American In-dians and Eskimos; in Africans, and in Microne-sians. Amer. I. Hum. Genet. 13:205-213, 1961.

257. STEINBERG, A. G., R. STAUFFER, and H. Fun-ENDERG. Distribution of Gma and Gm-like among

Javanese, Djuka Negroes and Oyama and Carib In-dians. Nature 185:324-325, 1960.

258. SUAREZ MORALES, 0., B. BRODER, and A.LOAYZA. Antigenos de grupos sanguineos en indioschipayas de Bolivia. Anal. Acad. Nac. Cien. quad. 2,Cien. Nat. (La Paz) pub. 4, pp. 1-9, 1964.

259. SUAREZ MORALES, 0., E. LINARES I., andJ. GUTIERREZ B. Grupos sanguineos en poblacionesdel altiplano andino con bocio endémico. Anal.Acad. Nac. Cm. quad. 2, Cien. Nat. (La Paz)pub. 5, pp. 1-10, 1965.

260. SurroN, H. E,, G. A. MATSON, A. R. ROBIN-SON, and A. W. KOUCKY. Distribution of haptoglo-bin, transferrin and hemoglobin types among In-dians of southern Mexico and Guatemala. Amer. I.Hum. Genet. 12:338-347, 1960.

261. SurroN, H. E., J. V. NEEL, F. B. LIVING-STONE, G. BINSON, P. KUNSTADTER, and L. E. TROM-

BLEY. The frequencies of haptoglobins in five popu-lations. Ann. Hum, Genet. 23:175-183, 1959.

262. TEJADA, C., M. SANCHEZ, M. A. GUZMAN, E.BREGNI, and N. S. SCRIMSHAW. Distribution of bloodantigens among Guatemalan Indians. Hum. Biol.33:319-334, 1961.

263. TEJADA, C., M. SANCHEZ, M. GUZMAN, N. S.SCRIMSHAW, and E. BREGNI. Blood groups in Mayanpopulation. Abstract. Rec. Genet. Soc. Amer. 28:102,1959.

264. THOMAS, J. W., M. A. STUKEY, H. S. ROBIN-SON, J. P. GOFTON, I). 0. ANDERSON, and J. N. BELL.Blood groups of the Haida Indians. Amer. 1. Phys.Anthropol. 22:184-192, 1964.

265. URIZAR, R. Grupos sanguineos de zutoctonosdel Chaco Paraguayo. Amer. Indigena 2:49-50, 1942.

266. VELA, C. Los grupos sanguineos en Quito.Quito, Imp. Univ. Central, 41, 1933.

267. VELLARD, J. Contribution A Isetude des in-diens Uru ou Kotssuns. Tray. Etud. And. 1:191-209,1949. Abs. HLAS 17:33.

VIANNA MARTINS. SCC MARTINS.

268. WALKER, M., F. H. ALLEN, and M. T. NEW-MAN. Blood groups of Cakchiquel Indians fromSumpango, Guatemala. Amer. I. Phys. Anthropol.25:239-242, 1966.

269. WEiss, P. Estudio sabre los lamistas; su gruposanguineo; algunas prucbas psico-tecnicas. Rev. Mus.Nac. (Lima) 18:19-41, 1948. Abs. HLAS 15:48.

270. WIENER, A. S., J. ZEPFDA, E. B. SONN, andH. R. POLIVKA. Individual blood differences in Mexi-can Indians, with special reference to the Rh typesand Hr factor. 1. Exp. Med. 81:559-571, 1945.

271. WITKOP, C., and J. GAISER. Genetic bloodstudies. Bethesda, Maryland, NIH, Interdepart. Coin-tee. Nutrit. Nat Defense, 1960.

151A, 1

153

:r7

CODE

General

1. An asterisk following the name of a tribe or groupindicates essentially no Negro or Caucasian admixture.

2. When two or more samples are presented from atribe or group of the same name (whether from thesame or different authors), each sample is arbitrarilyassigned a serial number. This appears in column 14unless the sample is pooled from several areas or sub-tribes, in which case "P" appears in column 14 prrcededby the serial number in column 13. (Subsamples arcpresented separately, also, whenever available.) "P"stands for "pooled."

Abbreviations of nations andother abbreviations

Nations

ArgentinaBoliviaBrazilCanadaChileColombiaCosta RicaEcuadorGuatemalaHondurasNicaragua

ARGBOLBRZ

CANCHLCOLCOSECDGUAHON

colonies and

PanamaParaguayPeru.SalvadorUnited StatesVenezuela

Colonies

British HondurasFrench GuianaGuyanaSurinam

Other abbreviations

NorthEastSouth; Saint;

SierraWestMountain(s)Another; OthersRiverLakeDeltaIsland (s)Pooled data,

from severalsamples

PANPARPRUSALUSAVEN

BRHFRGGUYSUR

M(TS)ANO

I(S)

TABLE 1A.

TRIBE OR GROUP

THE Alio A2. e. Ale 0 GENE pAroueNcres.As OLTEAmmeo wtt., AN71.40 ANT1A1. AND ANIP4

SENA.

NATION

REGION

REF

SAMPLE

PHENOTYPES

GENE FRovENcits

PSIZE

0Al

A2

8Alt

A29

Al

A2

et0

ACAWA10*

GUY

130

90

90

00

00

00.000

0.000

0.000

1.000

AGUARUNA*

PRO

R MARANON

1.68

151

151

00

00

00.000

0.000

0.000

1.000

ALACALUP 9

CHL

MAGELLAN

164

44

41

30

00

00.035

0.000

0.000

0.965

APACHE* 1

USA

ARIZ

042

179

105

74

00

00

0.234

0.000

0.000

0.766

APACHE 2

USA

NEW MEX

090

108

59

48

12

20

0.266

0.006

00019

0.7011

ARAWAK*

SUR

060

88

87

00

20

00.000

0.000

0.006

0.994

"MECUM

SEE

PERON

ATACAMENOS 1

CHL

ANTOPAGST

164

80

73

30

40

00.019

0.000

0.029

0.999

ATHAPASCAN 1

USA

ALASKA

062

78

74

40

00

00.026

0.000

0.000

0.974

mla/KOMA

ANO*

BRZ

S CATRINA

233

122

121

00

10

00.000

00000

0.004

0.996

AYMARA* 1

PRU

PUNO

028

58

58

00

00

00.000

0.000

0.000

1.000

AYMARA* 3

PAU

PUNO

168

93

93

00

00

00.000

0.000

04000

1.000

AYMARA* 4

POL

3 AREAS P

169

903

491

71

20

006007

0.003

0.002

0.987

BARI*

VEN

W ZULIA

132

126

126

00

00

00.000

0.000

0.000

1.000

BRIM/.

COS

SALITRE

177

SO

50

00

00

00.000

0.000

04000

10000

CARECAR*

COS

UJARPAS

177

62

62

00

00

00.000

0.000

0.000

1.000

CAINGANG

BRZ

R G SUL

231

341

334

41

20

00.006

0.001

0.003

0.989

cAlcommet i

GUA

I. ALTI1LM

171

150

142

40

40

00.013

0.000

0.013

0.973

cAlmstoucLA 2

GUA

SOLOLA

170

99

00

00

00.000

0.000

0.000

1.000

cAlconourt 3

GUA

SUMPANGO

268

137

112

20

30

00.007

0.000

0.011

0.981

CAMARACOTO

SEE

PEMON

CAMPA*

PRU

R umeAme

168

89

89

00

00

00.000

0.000

0.000

1.000

CAYAPA* 2

LCD

R CAYAPAS

167

244

240

00

40

00.000

0.000

0.008

0.992

CHACORO*

BOL

R YATA

169

14

14

00

00

00.000

0.000

0.000

1.000

CHAMA*

BOL

R MADIDI

169

30

30

00

00

00.000

0.000

0.000

1.000

CHAHULAA

PEA

CHIAPAS

024

63

63

00

00

00.000

0.000

0.000

1.000

CHEROKEE*

USA

N CARLINA

209

78

75

01

20

00.000

0.006

0.013

0.980

CHOCO*

PAN

DARIEN

178

80

SO

00

00

00.000

0.000

0.000

1.000

COLORADO* 2

LCD

S DOMINGO

167

36

36

00

00

00.000

0.000

0.000

10000

CUIVA*

WEN

APURE

134

82

82

00

00

00.000

0.000

0.000

1.000

CUM* 2

PAN

S BLAS 15

178

388

388

00

00

00.000

0.000

0.000

1.000

DIEGUENO

USA

CAL

202

'18

56

10

10

00.009

0.000

0.009

0.982

GOAJIRO 3

WEN

W ZULU,.

128

119

1.14

30

20

00.013

0.000

0.00$

0.979

GuAmtso.

VEN

APURE

134

109

107

10

10

00.005

0.000

0.005

00990

GUARANI* 2

PRZ

S CATARIN

233

34

34

00

00

00.000

0.000

0.000

1.000

GUAYM1*

PAN

N W COAST

178

240

240

00

00

00.000

04000

0.000

1.000

GUAYO*

SEE

WARAO

HOPI AND TEMA

USA

NEW mu

042

123

115

39

00

00.012

0.021

0.000

0.966

HUASTEC* 1

MEX

VERA CRUZ

024

52

52

00

00

00.000

0.000

0.000

16000

ICA

!NAPA*

COL

SEE

S REV

YUPA

131

114

110

10

10

00.013

0.000

0.004

0.982

1SCONAHUA* 2

PRO

R UCAYALI

168

14

14

00

00

00.000

00000

0.000

1.000

JIVARO* 2

ECD

ARAP/COS

167

233

233

00

00

00.000

0.000

0.000

1.000

KARAPALO ANO*2

BRZ

MA GROSSO

201

7$

73

00

00

00.000

0.000

0.000

1.000

KEKCH1 1

GUA

COPAN

171

162

154

41

21

00.016

0.003

0.009

0.972

KEKCHI* 2

ORH

'mow

176

119

117

20

00

00.008

04000

0.000

0.992

LACANDON* /

MEX

CHIAPAS

170

33

32

10

00

00.015

0.000

0.000

0.985

LACANDON* 2

MEX

ENIAPAS

171

61

61

00

00

000000

0.000

0.000

1.000

MAC0/7A*

SEE

YUPA

MACUSHI*

MAKIRITARE* 1

GUY

WEN

S BOLIVAR

130

130

11986

119

elA

0 o0 o

0 o0 o

0 o0.000

0.000

0.000

0.000

0.000

0.000

1.000

1.000

HAP t

GUA

SAN JUAN

171

116

112

31

00

00.013

0.004

0.000

0.982

MAN 2

GUA

HUEHUETGO

170

24

22

20

00

00.043

0.000

0.000

0.957

MAPUCHE 2

CHL

LONOUIMAY

163

141

130

91

10

00.032

0.004

0.004

0.919

mAR1COPA*

USA

ARIZ

042

3$

38

00

00

00.000

0.000

0.000

16000

MOJAVE*

USA

ARIZ

042

117

109

70

10

00.030

0.000

0.004

0.969 I

NASKAP/

NAVAJO 2

NAVAJO 4

OTOMI*

PANAAEP

PARIAI*

PEKIN*

3P

ARECUNA*

CAMARACOTO*

TAUREPANs

CAN

USA

USA

MEX

veN

SEE

YEN

VEN

VEN

VEN

Quenec

AR/2

ARIZ

HIDALGO

w mouvAlit

YUPA

LA SABANA

LA SABANA

LA SABANA

LA SARANA

033

042

063

024

130

124

124

124

124

PIAROA* 1

YEA

APUAE

134

PIMA*

USA

ARIZ

042

P/A0*

PAU

R UNMAN,'

168

QUECHUA 1

ECD

NORTHERN

167

QUECHUA 2

ECD

CENTRAL

167

QUICHE 1

GUA

S CENTRAL

170

RAMA

NIC

RAMA CAT

175

SANEMA*

SEE

YANOMAMA

BECOYA

ECD

CUYARENO

107

SNAOARUA

SEE

YUPA

SHIP1B0* 1

PAU

A UCAYALI

166

S/R/ONO*

ROL

R MACHUPO

169

SUMO*

NIC

E COAST

175

TAUREPAN

SEE

PEMON

TERRAPAS*

COS

TERRARA

177

'VICUNA*

PRU

R AMAZON

168

TOTONAC 1

MEX

VERA CRUZ

024

TOTONAC 2

MEX

VERA CRUZ

170

Yumemo.

cot

COCUY NTS

131

TZELTAL*

MEX

CHIAPAS

170

bro.

TZOTZIL* 1

MEX

CHIAPAS

171

7207271* 2

MEX

CHIAPAS

170

uyr 1

usA

UTAH

163

UTE 2

USA

UTAH

161

MAMA*

SEE

YANOMAMA

WAP15HANA

GUY

134

WARAO*

VEN

ORINOCO D

134

GUAYOm

YEN

ORINOCO D

120

WIMIKINA*

VEN

OR/NOCO 0

120

XAVAATE*

3P

elu

MA GROSSO

091

YAGUA*

PAU

R AMAZON

168

VANOMAMA.

10P

vem

s sottvAN

014

SANEMA40

VEN

S BOLIVAR

134

WA1CA*

YEN

S BOLIVAR

129

VARURO*

VEN

APURE

123

YUMA.

USA

ARIZ

042

YUPA.

39

VEN

E ZUL/A

130

IRAPAA 2

VEN

E ZULIA

126

MACOITAII

VEN

E ZULIA

126

PARIQI9

VEN

E ZULIA

126

SMAPARUm

VEN

E 2ULIA

126

;0

152

101

50

01

00

0.181

0.000

0.003

0.815

106

61

45

00

00

0.241

0.000

04000

0.759

237

173

61

30

00

0.116

0.007

0.000

0.854

81

76

50

00

00.031

0.000

0.000

0.969

33

33

00

00

00.000

0.000

0.000

1.000

267

267

00

00

00.000

0.000

0.000

1.000

70

70

00

00

00.000

0.000

0.000

1.000

109

109

00

00

00.000

0.000

0.000

1.000

111

111

00

00

00.000

0.000

0.000

1.000

489

395

93

00

10

0.101

0.000

0.001

0.898

90

90

00

00

00.000

0.000

0.000

1.000

732

217

50

90

10.011

0.002

04022

0.964

C

372

354

13

14

00

0.01$

0.001

0.005

0.975

203

188

13

02

00

0.033

0.000

0.005

0.962

36

37

10

00

00.013

0.000

0.000

0.987

AA

48

00

00

00.000

0.000

0.000

1.000

142

141

00

10

00.000

0.000

0.004

0.996

27

27

00

00

00.000

0.000

0.000

1.000

101

103

00

00

00.000

0.000

0.000

1.000

40

40

00

00

00.000

0.000

0.000

1.000

122

122

00

00

00.000

0.000

0.000

1.000

150

142

50

30

00.017

0.000

0.010

0.973

45

41

10

20

00.034

0.000

0.011

0.954

100

98

10

10

00.005

0.000

0.005

0.990

111

110

10

00

00.005

0.000

0.000

0.995

80

79

10

00

00.006

0.000

0.000

0.994

91

69

00

20

00.000

0.000

0.011

0.903

118

135

30

00

00.011

0.000

0.000

0.989

104

102

20

00

00.010

0.000

0.000

6.990

119

119

00

00

00.000

0.000

0.000

1.000

127

127

00

00

00.000

0.000

0.000

1.000

81

81

00

00

00.000

0.000

04000

1.000

72

72

00

00

00.000

0.000

0.000

1.000

539

539

00

00

00.000

0.000

0.00C

1.000

99

00

00

00.000

0.000

0.000

1.000

572

572

00

00

00.000

0.000

0.000

1.000

156

156

00

00

00.000

0.000

0.000

1.000

141

141

00

00

00.000

0.000

0.000

1.000

102

102

00

00

00.000

0.000

0.000

1.000

182

167

14

01

00

0.039

0.000

0.003

0.988

176

176

00

00

00.000

0.000

0.000

1.000

138

138

00

00

00.000

0.000

0.000

1.000

ys

76

00

00

00.000

0.000

0.000

1.000

74

74

00

00

00.000

0.000

0.000

1.000

24

24

00

00

00.000

0.000

0.000

1.000

"04

r,4.

0? '-

e.00

4O04

4

TAGLE 118.b

TME A. D AND 0 RENE FREOUENCIES AS DETERMINED GT ANTP"A AND ANTI'M SERA*

TOE SIGNIFICANT DEPARTURE FROM

NARD,WEINSERO EQUILIORIUN NOTED IN THE COLUMN HEADED P IS IN EACN CASE OCCASIONEDLARSELY SY THE OCCURRENCE

OF ONE ON NONE TYPE AS PERSONS IN A SAMPLE WHERE EXPECTATION FOR THIS EVENT IS VERY LON.

TR/RE OR GROUP

NATION

REGION

REF

SAMPLE

PHENOTYPES

GENE FREQUENCIES

SIZE

0A

RA8

A8

ALACALUF 1

CHL

MAGELLAN

074

45

42

30

00.034

0.000

0.966

ALACALUF* 2

CHL

MAGELLAN

147

99

00

00.000

0.000

1.000

ALKUYANAM

SUR

109

70

70

00

00.000

0.000

1.000

ANDIDO

ARG

JUJUY

205

209

198

80

30027

0.007

0.966

CATACAMENOS 2

CHL

CASPANA

074

60

58

02

00.000

0.017

0.983

ATACAMENOS 3

CHI.

TOCONCE

074

SO

47

30

00.030

0.000

0.970

AYMARA* 2

ROL

MOCOMOCO

259

100

94

51

00.025

0.005

0.970

RAKAIRI*

BRZ

MA GROSSO

146

109

108

10

00.005

0.000

0.995

ROR000*

PRI

MA GROSSO

197

119

119

00

00.000

0.000

1.000

ROTOCUDOR

BRZ

MI GERAIS

153

35

35

00

00.000

0.000

1.000

CAIUA*

SRI

MA GROSSO

197

237

237

00

00.000

0.000

1.000

CAMAYURA*

&NZ

MA GROSSO

146

60

60

00

00.000

0.000

1.000

CANAR/

tco

CANAR

242

1726 1646

53

20

70.018

0.008

0.974

CCARA

ECD

IMBAOURA

242

1838 1754

59

16

90.019

0.007

0.974

C

CARAJAP

BRZ

ST ISAREL

108

66

$6

00

00.000

0.000

1.000

CARIB 1

COL

CALDAS

071

540

519

17

40

0.016

0.004

06979

CARIB 2

SUR

061

177

169

44

00.011

0.011

0.977

CARIR* s

SUR

060

104

104

00

00.000

0.000

1.000

CARINA*

VEN

ANZOATEGI

118

170

169

10

00.003

04000

0.997

CAYAPA* 2

LCD

R CAYAPAS

243

62

62

00

00.000

0.000

1.000

CHAGUANCO ANO*

ARG

SALTA

181

120

120

00

00.000

0.000

1.000

CHINANTEC

MEX

OAXACA

064

21

21

00

00.000

0.000

1.000

CHIPAYA 1

804.

LA PAZ

259

100

94

51

00.025

0.005

0.970

CNIPAYA* 2

801

SASAYA

258

77

77

00

00.000

01000

1.000

CHIPPEWA

USA

MINN

159

161

141

20

00

0.064

0.000

0.936

CHOL

NES

CHIAPAS

064

152

135

16

10

0.054

0.003

0.943

CHONTOL

MEX

TARASCO

064

101

88

10

30

0.051

00015

0.933

CHULUPI* 1

ARG

SALTA

182

55

55

00

00.000

0.000

1.000

CNULUPI 2

ANG

SALTA

180

282

269

12

10

0.022

0.002

00976

COLORADO* I

ECU

S DOMING.)

243

97

97

00

00.000

0.000

1.000

CORA*

NES

NAYARIT

064

96

93

30

00.016

0.000

0.984

CREEC

CAN

ALRERTA

096

33

33

00

00.000

0.000

1.000

CUNA* I

PAN

S RLAS IS

072

$9

$9

00

00.000

0.000

1.000

ENERILLON4

FRG

114

39

39

00

00.000

0.000

1.000

GOAJIRO* I

VIM

ii ZULIA

118

152

151

10

00.003

0.000

0.997

GOAJIROP 2

VEN

M ZULIA

193

488

4e8

oo

o0.000

0.000

1.000

GUARANI* 1

RAZ

Ft G SUL

216

107

107

00

00.000

01000

1.000

GUATUSO*

COS

ALAJUELA

081

65

65

00

00.000

0.000

1.000

HUASTEC 2

MEX

VERA CRUZ

064

76

72

04

00.000

0.027

0.973

HUICHOL

MEX

JALISCO

064

71

71

00

00.000

0.000

1.000

IRAPA* 1

SEE

YUPA

ISCOMAHUA* 1

PRU

R UCAYALI

043

16

16

00

00.000

0.000

1.000

JIVARO* 1

ECD

ARAPICO

243

111

111

00

00.000

0.000

1.000

KARAPALO* I

BRZ

MA GROSSO

146

81

61

00

00.000

04000

1.000

KUAIKER

COL

PUTUMAYO

136

172

165

43

00.012

0.009

0.979

KUTCHIN

USA

ALASKA

145

114

113

01

00.000

0.004

0.996

LLOREOS*

COL

R ATRATO

253

81

81

00

00.000

04000

1.000

MACA

PAR

CHACO

265

111

108

12

00.005

0.009

0.986

MACOITA* I

SEE

YUPA

MACU*

RRZ

AMAZONAS

031

99

00

0n.000

0.000

1.000

MAN

POOL 9

GUA

M AND SW

262

70

65

32

00.022

0.014

0.963

MAPUCME 1

CHL

LONOUIMAY

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431/4.

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RATION

REGION

REP

SAmPti

SIZE

ANTIC +

4411.c

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202

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00

028

10

00

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114

36

00

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00

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106

00

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SEE

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201

73

00

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90

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SEE

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40

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262

235

20

163

12

31

70

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94

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113

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114

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LISTRO to MIS 'MM. IN Imam ofty

was EMPLORMO In. 102. 100 AND IN THE REMAININO. THREE

ANISSIRA

WERE EMPLONTO tANTIC. ANTWO. ANTI.41 bUT THE CALCUtATIONS

LIMITED TO THE O COMPONENT.

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REGION

REF

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SIZE

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RH+

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197

103

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102

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161

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THE JK(A) Akk JK115) GENE FREQUENCIES, AS DETERMINED WITH

ANIP.JKIA) AND AN11..',8(t8

SERA.

TRIM OR GROUP

NATION

REGION

REF

SAMPLE

PHENOTYPES

GENE FREQUENCIES

SIZE

A48

A-8+ A484

JKA

JK8

ACAWA104

ARECUNA4

GUY

sEE

PERON

130

90

22

24

44

0.489

0.511

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171

141

23

47

71

0+415

0.585

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209

77

17

22

36

0.468

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173

154

24

57

71

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171

61

424

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0036

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173

112

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62

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033

152

41

54

17

0.523

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237

64

49

124

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0.468

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267

57

70

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124

70

17

23

30

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0.543

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124

109

10

26

73

0.427

0.573

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124

108

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21

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134

109

743

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0.335

0.665

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N1C

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175

36

4S

24

0.444

0.556

SUMO*

RIC

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175

103

22

26

55

0+481

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TAUREPAIMI

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TZOT2IL*

1MEX

CHIAPAS

171

79

13

23

43

0.437

0.563

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S BOLIVAR

229

141

34

17

90

0.560

0.440

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VEN

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223

202

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25

54

0.490

0.510

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41,1

1;44

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TARLE 411.

THE JKIA/ AND JIM,/ GENE FREQUENCIES. AS DETERMINED %arm ANTI..JKIA1 SERUM.

(THERE IS A SINGLE STUDY I114I

WITH THE USE OF ANTIJKIBI ONLY

THIS OAS MOT BEEN TABLED).

TRIBE OR GROUP

NATION

REGION

REF

SAMPLE

SIZE

PHENOTYPES

A+

A..

GENE FREQUENCIES

JKA

JK6

AGUARUNA*

PRU

* MARANON

166

151

67

64

0.254

0.746

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CML

MAGELLAN

164

44

30

14

0.436

0.564

ATACAMENOS

1CHL

ANTOFAGST

164

80

44

36

0.329

0.671

ATHABASCAN

1USA

ALASKA

062

78

60

18

0.520

0.480

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PRU

PUNO

028

100

51

49

0.300

0.700

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PRU

PUN°

168

93

60

35

0.404

0.596

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SOL

3 AREAS P

169

503

315

188

0.389

0.611

BARI*

VEN

W ZULIA

132

TO

54

16

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0..478

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COS

SALITRE

177

50

26

24

0.307

0.693

CARECAR*

COS

UJARRAS

177

62

45

17

0.476

0.524

CAKCHIOUEL*

2GUA

SOLALA

170

99

a1.000

0.000

CAKCH/OUEL

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SUMPANGO

268

137

74

63

0.322

0.67$

CAMPA*

PRU

R URUBMBA

168

89

67

22

0.503

0.497

CAYAPA* 2

LCD

R CAYAPAS

167

244

207

37

0.611

0.389

CHACOB0*

SOL

R VATA

169

14

11

304437

0.463

°AMA*

SOL

R MADMI

169

30

14

16

0.270

0.730

CHOCO*

PAN

DARIEN

178

00

53

27

0.419

0.581

COLORADO* 2

ECD

$ DOMINGO

167

316

24

22

0.423

0.577

CUNA* 2

PAN

$ BLAS IS

178

388

256

132

0.417

0.583

GOAJIRO 3

VEN

W ZULIA

128

1111

99

20

0.590

0.410

GUMMI*

PAN

N W COAST

178

240

61

179

0.136

0.864

ICA

COL

S NEVADA

131

113

104

90018

0.282

/NAPA*

SEE

VUPA

ISCONAMUA*

2PRU

R UCAYALI

168

14

95

0.402

0.598

JIVARO* 2

LCD

ARAPICOS

167

233

154

79

0.418

0.582

KEKCHI* 2

INN

TOLEDO

176

119

73

46

0.378

0.622

LACANDON* I

MEX

CHIAPAS

170

33

21

12

04497

0.603

MACOITA*

SEE

VUPA

MACUSHI*

GUY

130

119

90

29

0.506

0.494

MAKIRITARE*

1VEK

S BOLIVAR

130

86

47

39

0.327

0.673

NAM 2

GUA

HUEHUETGO

170

24

21

30.646

0.354

NAM 3

GUA

W AND SW

262

70

23

47

0.181

0.819

MAPUCHE 2

CHL

LONOUIMAY

164

141

30

111

0.113

0.887

NAVA* 5

GUA

E PETEN

263

80

56

24

0.452

0.548

PANARE*

VEN

W BOLIVAR

130

33

30

30.699

0.301

PARINI*

SEE

YUPA

PIRO*

PRU

R URUBMBA

168

90

63

2/

0.452

0.548

POCOMAM ANO

GUA

CENTRAL

262

40

25

15

0.388

0.612

QUECHUA 1

ECD

NORTHERN

167

220

154

74

0.430

0.570

cortmem 2

LCD

CENTRAL

167

572

220

152

0.361

0.639

QUICHE 1

GUA

S CENTRAL

170

203

179

24

0.656

0.344

QUICHE 2

GUA

S CENTRAL

262

60

48

32

0.367

0.633

SECOVA*

ECO

CUYABENO

167

48

29

19

0.371

0.629

SHAPARU*

SEE

YUPA

SHIP180* 1

PRU

* UCAYALI

168

142

103

39

0.476

0.524

SIRIONO*

BOL

R MACHUPO

169

27

22

50.570

0.430

TERRABAS.

COS

TERRA8A

177

40

18

22

0.258

0042

TICUNA*

PIM

R AMAZON

168

122

91

31

0.496

0.504

TOTONAC 2

MEX

VERA CRUZ

170

45

35

10

0.529

0.471

TUCANO 2

SRL

AMAZONAS

186

20

812

0.225

0.775

TUNES°.

COL

COCUY MIS

131

98

84

14

0.622

0.378

TZELIAL.

'ex

CHIAPAS

170

111

84

27

04007

0.493

TZOTZIL* 2

melt

CHIAPAS

170

91

69

22

0.508

0.492

WAP/SMANA

GUY

134

119

104

15

01,645

0.355

XAVANTE*

3P

BRZ

MA GROSSO

091

445

296

149

0.421

0.579

i* ..TlirvisepoirmvIkTom,..,-,,,,

04'1 .1.4 ,te'ZIIIIPIO

1.40900

26600

*OZ

,Z

9ZI

vilnz 3

WAA

40WWWWWS

996*0

setipc

II

£9

9ZI

lerva 3

Nu

ININW4

00S*0

0000

IL

IL

9ZI

lulu 3

W3A

Z *V1IO2,06

66Z00

6000

zt

9ZI

ICI

9ZI

vilnz 1

W3A

Z 41ANWVI

9660

99900

zz

96;

ILI

061

vilAZ I

w3A

df

orkA

WOO

ZZ60

06t

0,9

016

9t0

WWWWW3 S

W3A

WO!

414,100WWA

ILVO

62600

6S

ITWOrowW il

mid

svOSIWA

0,41,44t

TABLE S.

THE MAI AND FV(8) GENE FREQUENCIES. AS DETERMINED eV TESTING WITH ANT14..FYIAI SERUM.

TRIBE OR GROUP

NATION

REGION

REF

SAMPLE

PHENOTYPES

GENE FREQUENCIES

SIZ:0

A*

A.,,

'VA

FVe

ACAWAIO*

GUY

130

76

14

0.606

0.394

AGUARUNA*

PRU

A MARANON

168

151

137

14

0.696

0.304

ALACALUF 3

CHL

MAGELLAN

164

44

38

60.631

0.369

APACHE 2

USA

NEW ME%

090

84

58

26

0.444

0.556

ABECUNA*

SEE

PEMON

ATACAMENOS I

CHL

ANTOFAGST

164

80

6$

12

0.611

0.387

ATHABASCAN I

USA

ALASKA

062

78

77

0.887

06113

AWEIKOMA ARO*

BRZ

S CATKINA

233

109

7$

31

0.467

0.533

AYMARA* 1

PRO

PUNO

028

58

54

0.737

0.263

AYMARA* S

PIM

PUNO

168

93

0.656

0.344

AYMARA*

80L

3 AREAS P

169

503

4:1

1:

0.822

0.178

BARI*

VEN

W ZULIA

132

70

46

24

0.414

0.586

BRIBRI*

COS

SALITRE

177

50

45

50.684

0.316

CABECAP*

COS

UJARRAS

177

62

56

60.689

0.311

CAKCHIQUEL I

GUA

L ALTITLN

171

ISO

135

15

0.684

0.316

CAKCHIOUEL* 2

GOA

SMOLA

170

99

01.000

0.000

CAKCHIOUEL 3

GUA

SUMPANGO

268

137

125

12

0.704

0.296

CAMARACOTO*

SEE

PEMON

CAMPA*

PPU

R URUBAMB

168

89

86

10.816

0.184

CABAjA*

BRZ

S ISABEL

108

40

27

13

0.430

0.570

CAYAPA* 2

CHAC000*

ECD

mot

R CAYAPAS

* YALTA

167

169

244

14

229

22

15 2

0.752

0.622

0.248

0.378

'N

BOL

R MADIDI

169

30

30

01.000

0.000

H::::EE*

USA

N ARLINA

209

78

62

16

0.547

0.451

CHIRANTEC

CHIPPEWA

CHOCO*

mex

USA

PAN

0A.'4CA

MINN

DARIEN

064

159

178

20

161 80

17

15871

3 3 9

0.613

0.864

0.665

0.387

0.136

0.335

CHOL

MEX

CHIAPAS

064

137

126

11

0.717

0.263

CHONTOL

HEX

TABASCO

064

101

90

11

0.670

06310

COLORADO* 2

ECD

S DOMINGO

167

36

29

70.559

0.441

CORA*

MEX

NAYARIT

064

96

95

I0.898

0.102

CUIVA*

VEN

APURE

134

82

72

10

0.651

0.349

CUNA* 2

PAN

S BIAS IS

17$

388

343

45

0.659

0.141

DIEGUENO

USA

CAL

202

58

52

60.678

0.322

EmER1LL04*

FRG

114

27

15

12

0.333

0.667

BOAJIRO 3

VEN

W ZULIA

125

119

106

13

0.669

0.131

QUAHIBO*

VEN

APURE

134

109

102

70.747

0.253

iUARAN14, 2

OUAYOI*.

6R2

PAN

S CATRINA

N W COAST

233

178

33

240

23

183

10S7

0.490

0.513

0.550

0.487

GUAY0*

HUASTEC 2

SEE

MEX

WARAO

VERA CRUZ

064

75

67

80.673

0.327

HUICHOL

MEX

JALISCO

064

69

62

70.681

0.319

ICA

COL

S NEVADA

131

113

107

60.770

0.210

IRAPA* 1

S EE

YUPA

IRAPA* 2

SEE

VUPA

ISCONAHUA* I

PRU

R UCAYALI

043

16

10

60.388

0.612

ISCONAHUA* 2

PRO

K UCAYALI

168

14

68

0.244

0.756

JIVARO* 2

LCD

ARAP1COS

167

233

192

41

0.580

0.420

KALAPALO ANO*2

ORZ

MA GROSSO

201

73

071

0.000

1.000

KOICHI 1

GUA

CO/INN

173

162

136

24

0.615

0.385

KEKCHI* 2

BAH

TOLEDO

176

119

112

70.757

0.243

LACANDON* I

MEX

CHIAPAS

170

33

32

I0.826

0.174

LACANDON* 2

MEX

CHIAPAS

171

60

57

30.776

04224

MACOITA* I

SEE

YUPA

MACOITA* 2

SEE

YUPA

MACUSMI*

GUY

130

119

106

Il

0.696

0.104

MAKIN/TABF*

1VIM

c ROLtVA*

148

86

81

10.813

0.187

PAM I

MAN 2

MAN 5

CHLGUA

$AN JUAN

W AND SW

HUEHUETGO

GU11

GUA

NASKAPT

KAMA 3

USAFRG

:4511:EC

VERA CRUZ

MAPUCHE 2

NEX

GUA

LONOUIMAY

MAZATEC 1

MAYA* 3

MEX

MEX

OAXACA

PUEBLA

E WEN

MANUA 1

CAN

OAYANA*

NAVAJO 4

FRG

FRG

::::::"

OYANP1*

YEN

yytItIVAR

sp

YEN

SEE

PARINI*

VEN

'ENO**

VEN

LA SABANA

ARECUNA*

VEN

LA SABANA

CAMARACOTO*

TAUREPAN*

USA

VEN

iivi:BANA

LA SABANA

OUICHC 1

RANA

POCOMAM

ounmuA 1

QUICHE 2

PIMA*

PIRO*

OUCCHUA 2

PIAROA* 1

GU

A

GUA

GUA

NIC

SEE

PRU

ECD

ECD

RANA CAT

R URUBANB

S CENTRAL

CENTRAL

NORTHERN

SOUTHERN

$ CENTRAL

1....

SAMNA*

E:Zig::

R UCAYALI

SECOYA*

SNIP1150* 2

NIC

NO

SHAPARU*

SHIPIBO* 1

PRU

B OL

TAUREPAN*

SEE

: =gig

EP:ZIT

ita/

SIRIONO*

SUMO*

11144

TERRABAS*

TICUNA*

ETERRAIA

is3

TOTONAC 2

NEX

BR?

VERA CRUZ

R AMAZON

TOTONAC 3

COL

PUEBLA

Ttlit

T1:;;k: 1

NEX

N EX

CHIAPAS

TUCANO 2

*EX

:51grr:;S

WAPISHANA

VEN

VACUA*

YANOMANA*

HAVANTE*

YABARANA*

WATCA*

WINIK/NA*

SANENA*

10P

sp

VEN

VEN

PRU

VEN

VENYEN

VEN

R AMAZON

RIO

:111ZIA

MANAPIARE

i EFfili

CHIAPAS

CHIAPAS

WA/CA*

GUY

VEN

YANDNAMA

SEE

GUAY0*

3P

BR?

WARAO*

VEN

ORINOCO D

YUPA

VARURO*

IRAPA* 1

11111:

1E 12!!!

IRAPA* 2

YEN

PARINI*

OEX

I 2ULIA

MACOITA*

1MACOITA*

VEN

VEN

VEN

ZAPOTEC

SHAPARO*

OAXACA

I ZUL1A

E 2UL1A

263

252

120

70

170

24

III

116

114

71

064

136

164

141

064

41

064

141

033

152

114

22

114

74

063

237

130

33

124

247

124

70

124

124

109

108

134

$1

042

184

166

90

062

262

175

167

167

167

170

232

372

203

48

3780

$0

168

142

043

10

179

103

169

27

170

177

156

20

122

16$

40

170

111

131

100

064

4579

170

91

171

80

120

72

193

168

014

134

130

129

123

491

156

141

176

154

1029

134

119

120

81

134

127

134

14

091

539

126

138

195

117

126

78

064

105

126

24

126

74

ss

22

52

18

24

0110

6

2::

16 7

103

33

129

12

40

I

123

14

149

3

14

850

24

3o

3

:::::

0.773

1:1;26:

0.156

0.000

0.507

0.708

:::::

0.572

::1411;

0.860

0.276

0.724

0.314

0.603

0.569

0.301

::::1

0.699

:::$269

IS

211

0.267

0.271

0.733

0.345

0.655

0.833

4o

21

179

376

14

220

12

344

183

20

65

13

4133

2$ 4 7

:::::63

17

138

466

4

98

527

0

43

2

I12

37

3104

18

94

17

SO

10

7s

0

113

876

6

70

2

434

57

14

Iii

497

37

co

0

102

17

74

7IIS

12

11

3425

114

112

26

63

54

53

2$

62

12

0.:773

:3:15

WS,

:::::

0.567

0.606

:OE

:::::

:::::

0.314

0.671

0.761

00132

0:06:312ii

0.000

0.618

0016: 778590

0.726

0.274

0.616

0.000

:3::

iiiii

0.775

0.704

0.776

!!!!!

!!!!!

:::::

0010:1460309099102

:::::

0.413

0.706

0.533

0.00':

0.341

:::::

00.22::

0.622

0.307

0.525

06506

:::6:

0.608

0.434

0.566

0.321

:::::

82

23

le

6Eili

0.500

0.468

,I

JA

laat.

f-

rovr

.,.11

fam

olot

,w

et1,

$10.

.r.,g

TABLF 6.

THE DICAI AND DUB) GENF FREOUFNCIES. AS DETERMINED BY TESTING WITH A% ANT1...011A/ SERUM.

TRIBE OR GROUP

NATION

REGION

ACAWAI0*

GUY

PRu

R MARANO%

AGUARUNA.

ALACALUF* 3

CHL

MAGELLAN

APACHE 2

USA

NEW MEX

ARECUNA*

SEE

PEMON

ATACAMENCS I

CHL

ANTOFAGST

ATHABASCAN 1

USA

ALASKA

AMEIKOMA ANO*

BRZ

S CATRINA

AYMARA* 1

PRU

PU40

AYMARA* 2

BOL

MOCOMOCO

AYMARA* e

PRU

PU40

AYMARA* 4

BARI*

BOL

3 AREAS P

AVEM

W ZULIA

R/RRI*

COS

SALITRE

CAMECAR*

COS

UJARRAS

BRZ

R G SUL

CAINGANG

CAKCHIOUEL I

GUA

L ALTITL4

CAKCHIQUEL* 2

GUA

SDLOLA

CAMARACOTO.

VEN

LA SABANA

CAMPA*

PRU

R URUBAmB

CARAJA*

BRZ

S ISABEL

CARINA*

VEN

MONAGAS

CAYAPAr 2

BOL

R YATA

CH6C060.

ECD

R CAYAPAS

CHAMA*

(SOL

R MADID/

CHEROKEE*

USA

N CARL/NA

CHINANTEC

MEX

OAXACA

CHIPPEWA

CHOCO*

IX

:11:7E4

LCHO

MEX

CHIAPAS

CHONTOL

MEX

TABASCO

COLORADO* 2

ECD

S DOMINGO

mom.

Hex

NAYARIT

CUIVA*

VEN

APURE

WU

' 2

PAN

S BIAS IS

EMERILLON*

FRG

GOAJIRO* I

VEN

M ZULI6

GOAJIRO 3

VEN

M 2046

GUAHIBO* 2

GUAHIBO* 2

VEN

APURE

VEN

APURE

GUARANI*

PAZ

S CATRINA

GUAYMI*

PAN

4 W COAST

GUM*

SEE

MARAO

HUASTEC 2

MEX

VERA CRUZ

HUICHOL

MEX

JALISCO

ICA

COL

S NEVADA

IRAPA* I AND 2

SEE

YUPA

ISCONAHUA* I

PRU

R UCAYALI

ISCONAH0A* 2

PR0

R UCAYALI

JIVARO* 2

ECO

ARAPICOS

KEKCH/ 1

GUA

CORM

KEKCHI* 2

BRH

TOLEDO

LACANDON* I

Hex

CHIAPAS

LACANDON* 2

MEX

CHIAPAS

MACOITA* 1 2

MACUSHZ.

SEE

YUPA

GUY

MAKIRITARE* 1

VEN

$ BOLIVAR

MAN 1

GUA

SAN JUAN

REF

SAMPLE

SIZE

130

90

168

151

164

44

090

108

164

80

062

78

233

109

028

58

259

100

168

93

169

491

132

126

177

50

177

62

231

257

171

150

170

5

124

109

168

89

100

36

118

170

167

240

169

14

169

30

209

78

064

14e

20

148

178

60

064

54

064

89

167

36

064

96

134

82

178

317

114

28

110

152

128

119

134

209

116

76

233

34

178

240

064

70

064

72

131

112

043

16

168

14

167

233

173

122

176

117

170

33

171

61

130

119

130

86

171

116

PHENOTYPES

GENE FREQUENCIES

DIA+ DIA

37

53

12

:39

044

4104

773

078

59

SO

10

48

496

!:

4::

g1:g

062

1!

1:i

19

90

38

51

13

23

50

120

21

219

410

22

8

07e

416

16

132

53

27

747

17

72

I35

23

73

062

24

293

424

8144

12

107

23

86

11

65

14

20

I239

565

29

43

47

65

412

410

7115

37

196

P109

11

22

10

51

34

85

26

60

104

17

DIA

DIB

0.233

0067

0.041

0.959

0.000

1.000

0.019

0.981

0.045

0.955

0.000

14000

0.323

0.677

0.090

0.910

0.020

0.980

04084

0.916

0.050

0.950

0.000

1.000

0.000

1.000

0.000

1.000

0.152

06848

0.044

0.956

0.000

1.000

0.091

0.909

0.243

0.757

0.201

0.799

0.160

0.640

0.045

0.955

0.155

0.845

0.484

0.516

0.000

1.000

0.105

0.695

0.056

0.946

0.419

0.581

0.067

0.933

0.101

0.899

0.014

0.986

0.128

0.872

0.000

1.000

0.039

00961

0.074

0.926

0.027

0.973

0.052

04948

0.112

0.688

0.075

0.925

0.233

0.767

0.002

0.998

0.036

0.964

0.227

0.773

0.238

0.762

0.134

0.866

0.155

0.845

041083

0.917

0.029

0.971

0.035

0.965

0.184

04816

0.086

0.914

0.155

0.845

0.165

0.635

0.053

0.947

ei*

"Ver,

d.

11114-7

414

PAM 2

MAPUCHE 2

MAYA*

MAZATEC 1

MANUA I

MANUA 1

NASKAPI

NAVAJO 4

OAYANA.

PARIRI*

PERON.

30

ARECUNA*

CAMARACOTO*

TAUREPAN*

PIAROA. 1

PIAROA* 2

PIRO*

POCOMAM ANO

QUECHUA 1

QUECHUA 2

QUICHE 1

QUICHE 2

RAMA

RIONEGPINO*

SANEMA.

SECOU*

SHAPARU*

SHIPIRO* 1

SHIPIBO* 2

SIRIONO,

SUmO*

TAUREPAN.

TERRABASs

TICUNA*

TOTONAC 2

TOTONAC 3

TUCANO 2

TUNERO.

TZELTAL*

TZOTZIL.

1

TZOTZIL* 2

WAICA.

WAP1SO4NA

WARAO*

GUAYG*

WINIKINA*

XAVANTE.

3P

YABARANA.

VAGUA*

YANOHAMA.

10P

SAME48*

WAICA*

YARURC*

YUPA.

3P

IRADA* 1

IRAPA* 2

MAC0f7A* 1

MACOIIA* 2

PAR1RI*

RIONEGRINO.

SHADARU*

ZAPOTFC

GUA

CHL

GUA

MEX

MIX

REX

CAN

g:

FRG

FRG

V::

VEN

VEN

VEN

VFN

VEN

'YEN

PRU

GUA

ECO

ECO

GUA

GUA

MK

SEE

SEE

PRU

PRU

am.

NIC

SEE

COS

PRU

REX

MEX

BRZ

COL

MEX

MEX

REX

SEE

WY

VEN

VEN

VIM

BR1

VEN

PRU

VEN

VIM

VEN

VEN

VEN

VEN

VEN

YEN

VEN

VEN

VE4

VI%

4FX

W AND SW

LONQUIMAY

E PETER

OAXACA

PUEBLA

VERA CRUZ

QUEBEC

ARIZ

W BOLIVAR

YUPA

LA SABANA

LA SABANA

LA SABANA

LA SABANA

APURE

AMAZONAS

R URUBAMR

CENTRAL

NORTHERN

SOUTHERN

S CENTRAL

S CENTRAL

RAMA CAY

19UPA

YANOMAMA

CUYARENDO

RUrA:ALI

R UCAYALI

R MACHURO

E COAST

PEMON

TERRABA

R AMAZON

VERA CRUZ

PUEBLA

AMAZONAS

COCUY

MrS

CHIAPAS

CHIAPAS

CHIAPAS

YANOMAMA

ORINOCO D

ORINOCO

ORINOCO

MA GROSSO

MANAPIARE

R AMAZON

S BOLIVAR

5 BOLIVAR

S BOLIVAR

APURE

E ZULIA

E ZULIA

E ZU11A

E ZULLA

E ZULIA

E zuLtA

E ZULIA

F ZULIA

OAXACA

262

164

269

064

064

064

033

063

114

114

114

130

124

124

124

124

134

134

168

262

167

167

170

262

175

167

168

043

169

175

177

168

170

064

186

131

170

171

170

114

114

120

120

091

134

168

014

134

129

/23

130

193

121

195

126

126

194

126

064

70

130

120

136

32

128

152

237

9198 30

33

28770

109

108

111 2490

80

220

3554680

37

48

141 70

27

103

40

122

41

49

131

100

1118086

119

127

81

72

538 14

571

156

141

102

176

44

138

117

78 74

125 24

105

23 536

16 2

1813

11

17

34

11

19

78

251934

19 3

13 17

50

92 8

25 0 9

9142 1

11 0

4.4 9 4

46 I

11

1513

33 0 3 0

164 9 2 0 9 0 5 46 0 3 24 1725

31 6

15

47

125

84

120

SO

110

119

226

7464 19

14

209

459074

92

2157

63

178

26338

5537

39

50

2826

92

100

6573

86

127

78

72

374 5 7

57!

147

241 97

110 44

135 93 6149

94

1890

0.181

0.019

0.163

0.061

0.032

0.073

0.044

0.023

0.098

0.192

0.204

0.349

0.147

0.198

0.091

0.172

0.090

0.065

0.204

0.113

0.116

0.139

0.091

0.171

0.000

0.099

0.405

0,367

0.019

04055

0.000

0.200

0.111

0.042

0.194

0.005

0.051

0.099

0.079

0.150

0.000

0.019

0.000

0.166

0.402

0.118

04000

0.029

0.000

0.025

0.141

0.000

0.01

10108

0.116

0.186

04133

0.154

0.074

0.619

0.981

0.817

0.939

0.966

0.927

0.956

0.977

0.902

0.806

0.796

0.651

0.853

0.802

0.909

0.828

0.910

0.935

0.796

0.887

0.884

0.861

0.909

0.829

1.000

0.901

0.595

0.631

0.981

0.945

1.000

0.600

0.889

0.958

0.806

0.995

0.949

0.901

0.921

0.850

1.000

0.981

1.000

0.834

0.598

0.882

1.000

0.971

1.000

0.975

0.859

1.000

0.989

0.892

0.884

0.814

0.667

0.866

0.926

,%

dew

* '

..4...

1a.4

0,34

11A

4

TARLE 7.

THE P GENE FREQUENCIES. AS DETERMINED 87 TESTING WITH AN ANTI*0 SERUM. FOR

LOWER CASE P.

TRIBE OR GROUP

NATION

REGION

REF

SAMPLE

PHENOTYPES

SIZE

PI

P2

oPP0 READ CAPITAL P AND FOR *Pop

GENE FREQUENCIES

PP

ACAWAIO*

GUY

130

90

64

26

0.463

0.537

AGUARUNA*

Pm

R MARANON

168

151

140

11

0.730

0.270

ALACALUF 3

CHL

MAGELLAN

164

44

25

19

0.343

0.657

APACHE 2

USA

NEW MEX

090

61

35

26

0.147

0.653

ARECUNA*

SEE

PEMON

ATACAMENOS

CHL

ANTOFAGST

164

80

61

19

0.513

0.4to7

ATHABASCAN I

USA

ALASKA

062

77

14

63

0.095

0.905

AWE1KOMA ANO0

BR2

S CATRINA

253

122

41

81

0.185

0.815

AYMARA* 1

PRU

PUNO

028

58

21

37

',.201

0.799

AYMARA* 3

PRU

MAO

168

95

92

10.896

0.104

AYMARA* 4

SOL

3 AREAS P

169

503

434

69

0.630

0.370

emu.

VEN

W ZUL1A

132

70

32

38

0.263

0.737

BRI8k146

COS

SALITRE

177

SO

42

80.600

0.400

CASECAR*

COS

UJARRAS

177

62

61

10.873

0.127

CAINGANG

BR!

R G SUL

231

166

73

93

0.252

0.748

CARCHIOUEL 1

GUA

L ALTITLN

171

150.

116

34

0.524

0.476

CAKCH2OUEL 3

GuA

suMPANGO

268

137

85

52

0.384

0.616

CAMARACOTO*

SEE

DEMON

CAMPA*

PRU

R URUBMPA

168

89

66

23

0.492

0.508

CAYAPA* 2

ECD

R CAYAPAS

167

244

134

110

0.329

0.671

CHACOBO*

ROL

R YATA

169

14

14

02.000

0.000

CHAMA*

BOL

R MADIDI

169

30

20

10

0.423

0.577

CHEROKEE*

USA

N CARLINA

209

7$

65

13

0.592

0.408

CHINANTEC

MEX

OAXACA

064

20

012

0.225

0.775

CHIPPEWA

USA

MINN

159

161

136

23

0.606

0.394

CHOCO*

PAN

DAR/EN

178

80

63

17

0.539

0.461

CHOL

MEX

CHIAPAS

064

150

47

103

0.171

0.829

CHONTOL

MEX

TABASCO

064

101

SS

46

0.325

0.675

COLORADO* 2

ECO

S DOMINGO

167

36

29

70.559

0.441

CORA*

MEX

NAYAR/T

064

96

74

22

0.521

0.479

CUIVA*

VEN

APURE

134

82

64

18

0.531

0.469

CORA* 2

PAR

S 81.AS IS

178

388

328

60

0.607

0.393

DIEGUENO

USA

CAL

202

58

33

25

0.343

0.657

EMERILLON*

FRG

114

73

40,244

0.756

GOAJIRO 3

VEN

w ZULIA

128

119

63

56

0.314

0.686

GUAHIBO*

VEN

APURE

134

109

67

42

0.379

0.621

GUARAN/* 2

8R1

S CATRINA

233

34

24

20

0.458

0.542

GUAVW*

PAN

N W COAST

178

240

197

43

0.577

0.423

HUASTEC 2

MEX

VERA CRUZ

064

75

56

19

0.497

06503

mu/CHOL

REX

JALISCO

064

72

67

40.763

0.237

ICA

COL

S NEVADA

131

113

41

72

0.202

0.798

/RAPA*

SEE

YUPA

ISCONAHuA* 2

PRU

R UCAYALI

168

14

14

01.000

0.000

JIVARO* 2

ECD

ARAPICOS

167

231

181

50

0.537

0.463

KALAPALO ANO*2

BRZ

MA GROSSO

201

73

30

43

0.233

0.767

KEKCHI I

GUA

COBAN

173

162

137

25

0.607

0.393

KEKCHI* 2

BIM

TOLEDO

176

119

106

23

0.669

0.331

LACANDON. 2

MEX

CHIAPAS

170

33

24

90.478

0.522

LACANDON* 2

MEX

CHIAPAS

171

61

47

14

04521

0.479

MACOITA*

SEE

YUPA

MACUEHI*

GUY

130

119

79

40

0.420

0.580

MAK/RITARE* 1

VEN

S BOLIVAR

130

86

57

29

0.419

0.581

MAM 1

GUA

SAN JUAN

172

116

89

27

0.518

0.482

MAP 3

GUA

W AND SW

262

70

38

32

0.324

0.676

MAPUCHE 2

CHL

LONOU1MAY

164

141

137

40.832

0.168

MAYA* 1

GUA

E PETEN

261

120

85

35

0.460

0.540

MAZATEC I

MEX

OAXACA

064

136

43

93

0.173

00827

MANUA I

MEX

PUEBLA

064

41

23

18

0.337

0.663

NOWA 1

MEX

VERA CRUZ

064

141

102

39

0.474

0.526

NASKAPT

CAN

OUEBEC

033

152

108

44

0.462

0.538

NAVAJO 4

USA

ARIZ

B63

237

142

95

0.367

0.633

OYANA*

FRG

114

99

46

53

0.268

0.732

PALIKOUR*

FRG

114

75

38

37

0.298

0.702

PANARE*

VEN

M BOLIVAR

130

33

825

0.130

0.870

PARIRt*

SEE

YUPA

PERON*

3P

VEN

LA SABANA

124

287

149

138

0.307

0.693

ARECUNA*

VEN

LA SABANA

124

70

36

34

0.303

0.697

CAMARACOTO*

VEN

LA SABANA

124

109

54

55

0.290

0.710

TAUREPAN*

VEN

LA SABANA

124

108

59

49

0.326

0.674

PIAROA* 1

VEN

APURE

134

111

84

27

0.507

0.493

PIRO*

PRU

R URUBMAA

168

90

75

15

0.592

0.408

POCOmAM ANO

GUA

CENTRAL

262

80

59

21

0.486

0.512

ouemA 1

LCD

NORTHERN

167

221

204

17

0.723

0.277

QUECHUA 2

ECD

CENTRAL

167

372

338

34

0.698

0.502

QUICHE 2

GUA

$ CENTRAL

262

80

55

25

0.441

0.559

RAMA

NIC

RAMA KAY

115

37

31

60.597

0.403

SANEMA*

SEE

YANOMAMA

SECOVA*

ECD

CUYABENO

167

48

29

19

0.371

0.629

SMAPARU*

SEE

YUPA

SM/PI11041 2

PRU

R UCAYALI

168

142

109

33

0.518

0.482

SIRIONO*

Mt

R MACHUPO

169

27

20

70.491

0.509

SUMO*

NIC

E COAST

175

103

64

39

0.385

0.615

TAUREPAN*

SEE

PERON

TERRABAS*

COS

TERRABA

177

40

38

204776

0.224

TICUNA*

PRU

R AMAZON

168

122

121

I0.909

0.091

TOTONAC 2

MEX

VERA CRUZ

170

45

27

18

0.367

0.633

TOTONAC 3

MEX

PUEBLA

064

79

50

29

0.394

0.606

TUNE90*

COL

COCUY MT5

131

100

54

46

0.322

0.678

TZELTAL*

REX

CHIAPAS

170

101

68

33

0.428

0.572

MUM* 1

MEA

cHiApAs

171

80

67

13

0.597

0.401

TZOTZIL* 2

ME%

CHIAPAS

170

75

54

21

0.471

0.529

MAICA*

SEE

YANOMAMA

WAAAO*

VEN

ORINOCO 0

134

127

59

88

0.168

0.832

XAVANTE*

3P

6R2

MA GROSSO

091

538

468

70

0.639

0.361

YAGUA*

PRU

R AMAZON

168

99

01.000

0.000

VANOMAMA*

10P

YEN

S BOLIVAR

014

570

427

143

0.499

0.501

SANEMA

VEN

S BOLIVAR

134

156

79

77

0.297

0.703

%MICA*

VEN

S BOLIVAR

129

141

81

60

0.348

0.652

YARURO*

VEN

APURE

123

102

62

40

0.374

0.626

YUPA*

3P

VEN

E ZULIA

130

176

76

100

0.246

0.754

!PAPA*

VEN

E 2ULIA

126

138

74

64

0.319

0.681

MACOITA*

VEN

E ZULIA

126

78

44

34

0.340

0.660

PARINI*

VEN

E 2ULIA

126

74

23

51

0.170

0.830

SHAPARU*

VEN

E ZULIA

126

24

915

0.209

0.791

ZAPOTEC

MEX

OAXACA

064

105

41

64

0.219

0.781

TAMA sae

Twit THENOTT01 TIONINcIts POO Two MI6 AMEN, A$ OCTIONINOD DT TOOTING WITH ANTI-LOIAI AND ANTIeramil

MA. UNE PAIONINCIts CANNOT me SouTIMELY CoMPOID OtCAult tilt Allim SWIM MOUS wmICK IS NOCOASAMV TO

SOON CALCULATIONS SAS NOT OCTIENNINSO PON ROST SAMPLCS*

TRIBE OR GROUP

NATION

REGZON

REF

SAMPLE

PHENOTYPES

PHENOTYPE FREQUENCIES

SIZE

MA.. A+90.

148.1.

AS A+O A.41+

AGUARUNA4

PRU

R MARANON

168

151

28

0123

0.185 0.000 0.115

ALACALUF 3

CHL

MAGELLAN

164

44

10

034

0.227 0.000 06773

APACHE 2

USA

NEW MEX

090

49

10

039

0.204 0.000 0096

ATHAAASCAN 1

USA

ALASKA

062

77

40

73

0.052 0.000 0.948

AYMARA* 5

PRU

PUNO

168

93

40

89

0.043 0.000 0.957

AYMARA* 4

SOL

3 AREAS P

169

503

48

2453

0.095 0.004 0.900

RRIRRI*

COS

SALITRE

177

SO

16

034

0.320 0.000 0.680

CARECAR.

COS

UJARRAS

177

62

20

042

0.323 0.000 0.677

CAXCNIOUEL.

1GUA

I. ALTITLN

171

150

27

1122

0.180 06007 0.812

CAKCHIOUEL*

2GUA

SOLALA

170

94

05

0.444 0.000 0.556

CAMPA.

PRU

R URUOMAA

160

89

32

057

0.360 0.000 0.640

CNACOSOs

SOL

R TATA

169

14

00

14

0.000 0.000 1.000

-,......

CVAMA*

sot

p MA010/

169

30

11

019

0.367 0.000 0.611

4CHOCOM

PAN

DARIEN

178

SO

27

IS

35

0.337 0.225 04.437

1/44

.11..

COLORADO* 2

CORA* 2

ECD

PAN

S DOMINGO

S ALAS IS

167

178

36

11

0388

173

025

215

0.306 0.000 0.694

0.446 0.000 0.554

GUAYm/*

PAN

N W COAST

178

240

123

0117

0.512 0.000 0.488

TSCONANUAC 2

PRU

R uCAYALI

168

14

30

11

0.214 0.000 0.766

JIVARO* 2

ECO

ARAPICOS

167

233

106

0127

0.455 0.000 0.545

KEKCHI 1

GUA

COAAN

171

162

32

0130

0.198 0.000 0.802

KEKCHI* 2

ORH

TOLEDO

176

119

91

024

0.765 0.000 0.235

LACANDON* 1

MEX

CH/APAS

170

31

10

023

0.303 0.000 0.697

LACANDON. 2

MEX

CHIAPAS

171

61

90

52

0.148 0.000 0.052

NAN I

GUA

SAN JUAN

171

116

34

082

0.293 0.000 0.707

MAM 2

GUA

HUEHUETGO

170

24

51

18

0.208 0.042 0.750

MAPUCHE 2

OIL

LONQUIMAY

164

141

18

0123

0.128 0.000 0.872

NASKAP1

CAN

OUEREC

033

152

25

0127

0.164 0.000 0.836

NAVAJO

USA

ARIZ

043

237

24

1212

0.101 0.004 0.895

PIRO*

PRU

R URUBMSA

168

90

IT

073

0.189 0.000 0.812

QUICHE 1

GUA

S CENTRAL

170

203

42

2159

C 407 0.010 0.782

ouecHuA 1

ECD

NORTHERN

167

231

73

0158

0416 0.000 0.684

OUECHUA 2

ECD

CENTRAL

167

168

110

0258

0.299 0.000 0.701

RANA

Nrc

RAmA KAY

175

37

21

016

0.568 0.000 0.412

SMIP/O0e 1

PAU

A UCAYALI

168

142

29

0113

0.204 0.00 0.796

srlitrono*

rim

R NACHUPO

169

27

40

23

0.148 0.000 0.652

SUMO*

NIC

E COAST

175

103

37

13

53

0.359 0.126 0.515

TERRABAS*

COS

TERRAAA

177

39

16

023

0.410 0.000 0.590

TICUNA.

PRu

R AMAZON

168

122

20

120

0.016 0.000 0.984

TOTONAC 2

MEX

VERA CRUZ

170

45

60

37

0.178 0.000 0.822

1?ELTALC

HEN

CHIAPAS

170

111

26

184

0.234 0.009 0.757

T2OTZ/L' 1

MEX

CHIAPAS

171

80

13

067

0.163 0.000 0.837

rzortiLe 2

MEX

CHIAPAS

170

91

16

273

0.176 0.022 0.801

KAYANYE*

3P

8R2

MA GROSSO

091

338

64

102

172

0.189 0.302 0.508

YAGUA6

PRU

R AMAZON

168

90

09

0.000 0.000 1.000

...4.

646a

teN

iVid

At t

aidi

bihk

4/6.

itiom

aii 4

1* li

airt

4+4.

4,64

4. 4

4.

4.-

04'

TAIDLE s.

THE PHENOTyPE FREQUENCIES FOR THE LEwIs SYSTEm. As DETERMINED BY TESTING WITH ANIPoLEIAI.

GENE FREQuENCIES

CANNOT BE ROUTINELY COMPUTED BECAUSE THE ABH SECRETOR STATUS WHICH IS NECESSARY TO SUCH CALCULATIONS WAS NOT

DETERmINED FOR MOST sAmPLES.

TRIBE OR GROUP

NATION

REGION

REF

SAMPLE

SIZE

PHENOTYPES

A+

A-

PHENOTYPE FREQUENCIES

A+

A-

ACAWAIO*

ARECuNA*

GUY

SEE

PEMON

130

90

090

0.000

1.000

ATACAmENOS 1

CHL

ANT0FAGs7

164

80

278

0.025

0.975

AWEIKOMA ANO

AYMARA* 1

BRZ

PRU

$ CATRINA

PUNO

233

028

11858

69 0

49

58

0.585

0.000

0.415

1.000

BARI*

YEW

W ZULEA

132

70

070

0.000

1.000

CAMARACOTO*

SEE

PERON

VEN

APuRE

134

$2

082

0.000

1.000

02=

3VEN

W ZULIA

128

119

0119

0.000

1.000

GUAMIBO*

YEN

APURE

134

109

1108

0.009

0.991

GUARANI* 2

VEN

S CATR/NA

233

34

22

12

0.647

0.353

ICA

TAMPA.

COL

SEE

S NEVADA

yupA

131

113

C113

0.000

1.000

1SCONANUA. 1

PRU

P UCAYALI

043

16

016

0.000

1.000

MACO/TA*

MACUSHI*

GUY

130

119

0119

0.000

1.000

MAKIRITANE* 1

VEN

S BOLIVAR

130

86

086

0.000

1.000

OTOmi*

PANARE*

mEx

VEN

HIDALGO

W NDLIVAR

024

130

8133

8 073 33

0.099

0.901

PARIRI*

SEE

YUPA

0.000

1.000

PEmON*

3P

vEN

LA SABANA

124

267

1286

0.003

0.997

ARECLINA*

VEN

LA SABANA

124

70

070

0.000

1.000

CAMARACOTO*

vEN

LA SABANA

124

109

1108

0.009

0,991

TAuREPAN*

VEN

LA SABANA

124

100

0108

0.000

1.000

P/AROA* I

VEN

APURE

134

81

081

0.000

1.000

SANEmA*

SEE

YANOMAMA

SECOYA*

sMAPARU.

LCD

SEE

CuYABENO

YuPA

167

48

048

0.000

1.000

SHIP1B0* 2

PRU

R UCAYALI

043

70

070

0.000

140000

7AuREPANw

SEE

PEmON

TuNE80*

ng: :

coL

SEE

VEN

COCUY mTs

YANOMAMA

ORINOCO 0

131

134

99

127

0 0

99

127

0.000

0.000

1.000

1.000

YANOMAMA

SANEMA4

vEN

s 801.1vAR

134

1F6

0156

0.000

1.000

MAMA*

YEN

5 BOLIVAR

129

141

0141

0.000

1.000

YARURO*

VEN

APuRE

123

102

0102

0.000

1.000

YUPA*

3P

'..EN

E 2ULIA

130

176

0176

0.000

1.000

1/100,4A*

N co

VEN

VEN

E ZULIA

E ZULIA

126

126

13678

2 0136

78

0.014

0.000

0.986

1.000

PARIRI*

YEN

E ZULIA

126

74

00.000

1.000

soAPARu*

vEN

E ZuL1A

126

24

024

0.000

1.000

4

1

TARLE 9.

THE TRANSFERRIN PHENOTYPES AND GENOTYPES.

BECAUSE THE 404C PHENOTYPES ARE SO MANY BUT YET INDIVIDUALLY

SO RARE. GENE FREQUENCIES ARE GIVEN POR C AND FOR ALL

OTHERS COMBINED (EXPRESSED IN THE TABLE AS I:K.

TR/BE OR GROUP

NATION

REGION

REF

SAMPLE

SIZE

801

82C

PHENOTYPES

802C

C COCHI

CO1

DI DCHI

GENE FREQUENCIES

1.C

ACAWAIO*

GUY

022

64

00

084

00

00

0.000

1.000

AGUARUNA6

PRU

R MARANON

16$

151

00

0151

00

00

00000

10000

ALACALUF* 3

CHL

MAGELLAN

164

45

00

043

00

00

0.000

1.000

ATACAMENOS 1

CHL

ANTOFAG5T

164

76

00

079

00

00

0.000

2.000

ATHABASCAN

USA

ALASKA

092

49

00

049

00

00

0.000

1.000

AWEIKOMA ANO*

8RZ

S CATARNA

227

37

00

037

00

00

0.000

1.000

AYMARA* I

PRU

PUNO

093

56

00

056

00

00

0.000

1.000

AYMARA* 5

PRU

PUNO

168

71

00

071

00

00

06000

1.000

AYMARA* 4

SOL

3 AREAS P

169

71

00

071

00

00

00000

1.000

BARI*

VEN

W ZULIA

022

71

00

054

17

00

00.120

0.880

BRIBRI4

COS

SALITRE

237

38

00

053

50

00

0.066

0.934

CABECAR*

COS

UJARRAS

266

25

00

024

10

00

0.020

00980

CAINGANG

BRZ

R G SUL

236

116

01

0115

00

00

0.004

0.996

CAKCHIQUEL 1

GUA

I ALJUILN

165

150

00

0142

09

00

04027

0013

CAKCHIQUEL* 2

GUA

SMOLA

260

10

00

010

00

00

0.000

1.000

CAMPA.

Pnu

A URUBAmn

168

99

00

093

00

00

0.000

1.000

CAYAPAr

ECD

R CAYAPAS

167

226

00

0206

020

00

0.044

0.956

CHIAPANECA 1

MEX

CHIAPAS

165

40

00

038

02

00

0.025

0.975

CHIAPANECA 2

mEx

CHIAPAS

260

47

00

045

02

00

0.021

0079

CHINANTECO

MEX

OAXACA

165

53

00

350

00

00

0.028

0.972

126

CHOCO*

PAN

DARIEN

166

74

00

014

00

00

0.000

1.000

41

CHOL 2

COLORADO* 2

MEX

ECO

CHIAPAS

S DOMINGO

260

167

1636

0 00 0

0 01636

0 00 0

0 00 0

0.000

0.000

16000

1.000

CUNA* 2

PAN

5 ALAS IS

166

174

00

0174

00

00

0.000

1.000

;Ch

GUAH190*

GUARAN/*

VEN

BR2

APURE

$ CATARNA

022

237

11230

0 00 0

0 0112

90

0 00 0

0 00 0

0.000

0.000

1.000

1.000

GUAYMIA

PAN

N W COAST

166

204

00

0180

024

00

0.059

0.941

IRAPA*

SEE

YUPA

2SCONAHUA4 1

PRU

R UCAYALI

043

16

00

016

00

00

0.000

1.000

JIVARO* 2

ECD

ARAPICOS

167

221

00

0220

01

00

0.002

0.998

KEKCHI 2

GUA

COUR

165

162

00

0153

09

00

0.020

0072

KEKCHI* 2

BRH

TOLEDO

166

65

00

158

05

10

0.062

0.938

LAC/000mm 1

mEx

cHIAPAS

260

31

00

031

00

00

0.000

1.000

LACANDON* 2

mEx

CHIAPAS

165

59

00

10

49

00

00

04085

0015

MACOITA*

SEE

YUPA

MACUSHI*

GuY

022

116

00

0116

00

00

0.000

1.000

MAKIRITARE* 1

VEN

S ROLIVAR

022

54

00

054

00

00

0.000

1.000

MAP 1

GUA

SAN JUAN

165

116

00

0112

04

00

0.017

0.983

HAM 2

GUA

HUEHUETNG

260

27

00

027

00

00

0.000

1.000

MAYA 4

BRH

TOLEDO

166

212

00

0195

016

10

0.042

0.956

NAVAJO 3

USA

ARIZ

203

230

01

16

213

00

00

0.037

0.963

PARIRI

SEE

YUPA

PEMON4

3P

VEN

LA SABANA

022

96

00

096

00

00

0.000

1.000

PIAROAP 1

VEN

APURE

022

77

00

052

20

05

00.195

0.805

PIRO*

PRU

4 URUBAMB

168

86

00

083

03

00

0.017

0.963

QUECHUA

2P

ECO

N ANO CEN

167

192

00

0165

027

00"

0.070

06930

QUICHE 1

GUA

S CENTRAL

260

94

00

192

01

00

0.011

0.989

RAMA

NIC

RAMA CAY

165

37

00

025

0A

40

0.216

0.784

SANEMA*

SHIRISHAKA4

VEN

S BOL/VAR

022

74

00

074

00

00

0.000

1.000

SECOYA4

ECO

CUYABENDO

167

46

00

047

01

00

0010

0.990

SMAPARU

SEE

YUPA

SHIPIBO* 1

PRU

R UCAYALI

168

129

00

0129

00

00

0.000

1.000

SHIP180* 2

PRU

R UCAYALI

043

70

00

070

00

00

0.000

1.000

SHIRISMANA4

SEE

SANEMA

SUMO-4r-

-NIC-

-E COAST-

165

101

0----0

-0-408-

43

0--

00

0.000

10100

029

20

00.032

0.968

TERRABAS*

COS

TERRABA

166

32

00

0TICUNA*

PRU

R AMAZON

168

122

00

0122

00

00

06000

1.000

TOTORAC 2

MEX

VERA CRUZ

260

4$

00

045

00

00

0.000

1.000

TZELTAL*

MEX

CHIAPAS

260

97

00

097

00

00

0.000

2.000

TZOTZIL* 1

MEX

CHIAPAS

265

79

00

075

04

00

0.025

0.975

720711L* 2

MEX

CHIAPAS

260

88

00

167

00

00

0.006

0.994

MAICA*

SEE

YANOMAMA

WAPISHANA

GUY

022

116

00

0116

00

00

0.000

1.000

WARRAU*

VEN

ORINOCO 0

022

123

00

0121

20

00

0.008

0.992

XAVANTE*

3P

WIZ

MA GROSSO

247

521

00

0521

00

00

0.000

1.000

YAGUA*

PRU

AMAZON

168

90

00

90

00

00.000

1.000

YANOMAMA*

10P

VEN

S BOLIVAR

014

450

00

0428

00

20

0.005

0.995

WAICA*

VEN

S BOLIVAR

022

136

00

0236

00

00

0.000

1.000

YUPA*

2P

VEN

E 2ULIA

020

91

00

038

38

00

15

0.374

0.626

!PAPA* 2

VEN

E ZULIA

017

89

00

084

05

00

0.028

0.972

MACOITA* 2

VEN

E ZULIA

027

42

00

038

04

00

0.048

0.952

PARIRI44

VEN

E ZULIA

020

69

00

027

27

00

15

0.413

0.5*/

SHAPARU*

VEN

E ZULIA

020

22

00

011

11

00

00.250

0.750

2APOTEC

MEX

OAXACA

260

80

00

278

00

00

0.013

0.987

ZOOM

REX

CHIAPAS

165

31

00

029

02

00

0.032

0.968

fele

:-.

TABLE 10.

THE HAMTOGLOBIR PHENOTYPES AND GEMF FRFOUEMENS*

IN THE COMPUTATION OF THE LATTER. THE AHAPTOGLOGINEMIA

PHENOTYPES AND THE °OTHER' PHENOTYPES HAVE BEEN OMITTED.

TRIBE OR GROUP

NATION

REGION

REF

SAMPLE

size

1.=.1

2.-1

PNENOTYPES

2.-1M

0OTHER

GENE FREQUENCIES

PHP1

HP2

ACAWA10*

GUY

018

87

38

42

05

20

0.494

0.306

AGUARUNA*

PRU

R MARANON

148

151

50

78

045

00

0.457

0.545

ALACALUF* 3

CHL

MAGELLAN

164

43

13

14

015

10

06476

0026

APACHE. 2

USA

NEW MEX

261

98

54

47

017

00

0.587

0.413

ATACAMENOS 1

CHL

ANIOFAGST

164

79

32

42

05

00

0.671

0.329

ATHABASCAN 1

USA

ALASKA

032

202

551

98

063

33

0.429

0.571

ATHABASCAN 2

USA

ALASKA

245

104

13

:44

041

00

0.565

0.435

ATHABASCAN 3

USA

ALASKA

032

284

SI

89

0136

80

0.346

0.654

AWE1KOMA ANC*

8R2

S CATRINA

237

122

53

40

117

10

0.464

0.336

AYMARA* 1

PRU

POMO

093

56

24

24

04

00

0.714

0.246

AYVARA* 3

PRU

PUNO

168

71

36

26

08

10

0.700

0.300

AYMARA* 4

ece.

3 AREAS P

169

71

56

26

08

10

0.700

0.300

BRIM*

CO3

SALITRE

237

38

113

024

00

0.197

0.803

CAPECAR*

COS

UJARRAS

146

25

414

07

00

0.440

0.560

CAINGANG

ERZ

R G SUL

236

326

103

110

12

21

00

0.75e

0.242

CAKCIONEL I

GUA

I ALT1TLN

165

150

56

73

018

30

04629

0471

CAKCHIOUEL* 2

GUA

SOLOLA

260

20

44

01

10

0.467

0.595

CAMPA*

PRU

R URUSAMR

148

93

33

37

023

00

0.554

0.444

CAVAPA44 2

ECD

R CAVAPAS

147

226

98

97

024

03

0.457

0.543

CEARA

8R2

NOT REPTD

105

24

413

25

00

0.477

0.523

CHIAPANECA 1

MEX

CHIAPAS

240

47

21

20

15

00

0.674

0.324

CHIAPANECA 2

MEx

CHIAPAS

145

35

816

011

00

0.457

0.543

CN1NANTEC 2

CHOCO*

MEX

PAN

OAXACA

DARIEN

145

144

5374

5

III

29

28

0 019

24

0 40 0

0.368

0.457

0.432

0.543

CHOL 2

*COLORADO

2HEX

(CD

CHIAPAS

$ DOMINGO

145

147

16

34

928

4 80 0

3 0

0 00 0

0.484

0.809

0.312

0.111

CUNA* 2

GUANARIRO*

PAM

VEN

S BLAS 13

AMAZDNAS

166

017

17419

19

15

83 4

4 040 0

8 00 0

0.173

0.895

0.627

0440S

GUAH160*

VEN

APURE

134

117

55

45

015

20

0.674

0.324

GUARANI* 2

ON2

S CATRINA

237

34

915

09

10

0.500

0.500

GUMMI*

PAN

N W COAST

166

204

SO

91

033

00

0.415

04,385

HA!DA

CAN

OUEEN C I

150

413

113

221

079

00

0.541

0.459

IRAPA*

SEE

YUPA

ISCONAHUA* 1

Pou

R UCAYALI

043

16

I13

02

00

0.469

0.531

JIVARO* 2

ECD

ARAP1COS

167

222

92

100

028

20

04445

0055

KWH/ 1

GUA

CONN

165

162

74

66

022

00

0.641

0.3311

KEKCHI* 2

8RH

TOLEDO

166

45

24

24

013

20

0.587

0.413

LACANDON, 1

MEX

CHIAPAS

260

31

24

40

03

00.929

0.071

LACANDON. 2

MEX

CHIAPAS

165

59

49

90

01

00.922

0.071

MACOM*

SEE

YUPA

MACUSNI*

GUY

018

129

20

54

027

18

00.465

0.535

MAKIRITARE* 1

YEN

S BOLIVAR

019

85

12

30

037

40

0.342

0.658

MAKIRITARE. 2

YEN

AMAZONAS

017

59

27

18

014

00

0.610

0.390

MAR 1

GUA

SAN JUAN

265

226

31

55

224

40

0.532

0.468

NAN 2

OUR

SAN JUAN

260

27

811

08

00

06500

0.500

MAYA 4

15104

TOLEDO

166

212

92

94

026

00

0.656

0.544

NAVAJO 5

USA

ARIZ

203

261

57

119

087

00

0.443

0.557

PANARE.

VEN

it BOLIVAR

023

32

216

0II

30

0.343

0.655

NEN0N.

39

VEX

LA SABANA

019

214

40

113

049

12

00.4741

0.522

91040149 1

VEX

APURE

019

94

54

33

06

10

0.764

0.232

61906

PAU

R UBURAMO

168

86

29

41

016

00

0.574

0.424

QUECHUA

20

ECD

N AND CEN

147

192

112

66

09

50

04775

0.225

QUICHE 1

SUA

S CENTRAL

260

94

36

46

012

00

06428

04472

RAMA

'SAWA*

PIC

SEE

RAMA CAY

YAMOR AMA

165

37

19 _

12

.....

06

00

0.676

.......___0.324

111

ittSWA.-

SHIRIBO. 1

SNIPING* 2

SUMO.

rEaaanas,

TICUNAs

TLINGIT

TnTORAC 2

T2ELTAL*

TZOTZZL* 1

TZOTZIL* 2

NAIEA*

WAPISMANA

XAVANTE*

YAGUA*

YANOMAMA*

SAMEMA*

WAICA

YARURO*

YUPA IRAPA* 2

MACOITA* 2

2APOTEC

3P

10p

tab

CD

PRO

PRU

NIE

COS

PRO

USA

MCX

MEK

McX

mcX

SEE

GUY

BRZ

PRU

YEN

VEN

VEN

VEIN

VEN

VEN

VEN

AMA

*...0....AmoNXEINISIMI818118.80/11MMWeellbaditig ME5"44-

CUMEN00

167

48

14

23

11

00

0.531

0.469_

UCAYALI

169

129

54

58

17

00

0.643

0.357

R UCAYALI

043

70

25

41

4O

00.650

0.350

E COAST

TERRA8A

165

166

10811

SI 9

49 14

127 8

0 00 0

0.519

0.516

0.481

0.484

R AMAZON

168

122

60

45

17

00

0.676

0.324

ALASKA

VERA CRUZ

032

260

92

45

16

14

38

23

26 a

1 01

0.438

0.567

0.562

0.433

CHIAPAS

260

97

31

54

12

00

0.598

0.402

CHIAPAS

165

80

35

36

70

00.675

0.325

CHIAPAS

260

se

31

44

13

00

0.602

0.398

YANOMAMA

018

120

34

56

022

60

0.553

0.447

MA GROSSO

247

521

114

254

1139

13

00.475

0.525

R AMAZON

168

92

31

00.418

0.562

5 POLIVAR

014

425

301

109

0Is

00

0.836

0.164

S BOLIVAR

017

19

15

40

00

00.995

0.105

80L/VAR

019

139

84

48

04

30

0.794

0.206

APURE

019

103

42

46

013

20

0.644

0.356

E ZULIA

019

93

57

11

50

00.760

0.220

E ZULIA

017

129

151

077

00

0.205

0.795

E 2UL/A

017

74

12

40

022

00

0.432

0.568

OAXACA

260

60

22

40

117

00

0.532

0.468 4 4 ,

7A8LE 11. THE GM PNENOYYPES AND GENE FREQUENCIES. AS OASE0 ON TESTING WITN ANTIGMCA), ANTI...GA(8)s ANDANTI0418(X/ SERA.

TR/8E OR GROUP

NATION

REGION

REP

SAMPLE

PHENOTYPES

SIZE

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GENE FREQUENCIES

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ACAMAIO*

GUY

063

64

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0.524

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ATHAPASCAN 1

USA

ALASKA

256

91

02

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33

0.172

0.8107

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119

04

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06279

06703

06017

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34

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0.233

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FRG

RR2

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078

233

40

34

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0.209

06216

0.791

0.739

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0.045

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GUY

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116

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53

63

0.263

0.737

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062

122

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91

31

06496

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76

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0.517

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078

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36

60

0.207

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0.166

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642

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464

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TABLE 12. Data on genes that are probably absent in Indians who have no Caucasian or Negro admixtureTabulation restricted to samples in which non-Indian ancestry is believed to be less than 5 per cent, as listed inTable I. Samples with relatively high frequencies that may be due to technical problems are starred (*).

Lutheran

Among 32 samples tested with anti-Lu a alone, 28 contained no case of Lu(a+). They are reported in thefollowing seventeen references: 33, 63, 126, 128, 129, 167, 168, 169, 170, 171, 173, 175, 176, 177, 178, 209,

1

4ind 268. The 4 exceptions are:

ribe or Group Area Reference Sample Size Lu(a-F-)ymara Bolivia: Yungas 169 120 1

una Panama: San Blas Is, 178 388 2leguefio U.S.A.: California 202 58 2alapalo (2) (*) Brazil: Mato Grosso 201 73 12

639

Among six samples tested with both anti-Lu and anti-Lu b, no case of tither Lu(a+) nor of Lu(b-) wasevealed (References 33, 176, 177 and 178).

Kell

Among 40 samples tested with anti-K serum alone, 28 contained no positives, and may be considered to consistholly of hotnozygous kk cases. They are reported in seventeen references: 42, 64, 74, 81, 90, 114, 132, 134,

45, 171, 175, 195, 223, 231, 262, 263, and 268. The 12 exceptions are:

ribe or Group Area Reference Sample Size K+thabascan U.S.A.: Alaska 3 206 1

weikoma Brazil: Sta. Catarina 233 122 3araji Brazil: Sta. Isabel 108 35 7hol Mexico: Chiapas 64 137 4ara Mexico: Nayarit 64 96 6ieguefio U.S.A.: California 202 56 6uastec Mexico: Vera Cruz 64 75 2uichol Mexico: Jalisco 64 70 2

Kalapalo (2) (*) Brazil: Mato Grosso 201 73 17aztec ( I) Mexico: Oaxaca 64 136 1

Nahua (3) Mexico: Vera Cruz 64 141 3Irapa (1) Venezuela: E. Zulia 193 153 3

1,300

Among 74 samples tested with both anti-K and anti-k sera, 70 contained no case of Kell positive and may bcconsidered to consist of homozygous kk individuals only. They are reported in references: 23, 28, 33, 43, 90, 123,124, 126, 129, 130, 131, 134, 164, 167, 168, 169, 170, 171, 173, 176, 177, 178, 233 and 262. The 4 exceptionsare:

Tribe or Group Area Reference Sample Size K+Cherokee U.S.A.: No. Carolina 209 78 I

Chippewa (*) U.S.A.: Minnesota 159 161 24-IGoajiro Venezuela: W. Zulia 128 119 1

/Navajo (4) U.S.A.: Arizona 63 237 4

I

595

All of the 30 K-positive cases were heterozygous Kk except two of the four Navajos, who were KK.

30

Wright

1 Among 41 samples tcstcd with anti-Wra serum, not one contained a positively reacting case. References: 63, 91,1164, 167, 168, 169, 171, 173, 175, 176, 177, 178, 209, 231, and 233.

181

'184

TABLE 12-Continued

Miltenberger

Among 40 samples tested with anti-Mia serum, only one contained positive cases. A sample of 232 Quechuas atCalderon, in northern Ecuador (ref. 167), contained four Mia+ individuals, two of whom were related as fatherand son. Relationship of the other two was not ruled out. Thc other 3 9 sarnplcs arc reported in references 1 64, 167,168, 169, 170, 171, 173, 175, 176, 177, 178 and 179.

Verweyst

Among 37 samples tested with anti-Vw serum, only one contained a positive case-in a sample of 162 KekchiMayans in Cobin, Guatemala (ref. 173), ow.: individual was Vw+. The other references are 91, 164, 167, 168,169, 171, 175, 176, 177, 178, and 2 09.

"V" (in Rh-hr ,system)

Among 28 samples tested with anti-V serum, only two samples contained positive cases. Among 12 Kekch stested at CobAn, Guatemala (ref. 173), two were V+, and among 45 Totonacs (sample 2) at Vera Cruz, Mcxi o(ref. 170), one was V+. The other samples are referred to in 2 8, 1 67, 170, 171, 175, 176, 17 7, 178, and 20

Berriens

Among 18 samples tested with anti-Bea serum not one positive case was found. References arc: 167, 1 71, 17176, 177, 178, and 209.

Sutter

Among 15 simples tested with anti-Jsa serum, only one contained a positive case-one individual in a sample t119 Goajiros, sample no. 3, in western Zulia State in Venezuela (ref. 12 8). Other references are: 2 8, 126, 16171, 173, 176, 177, and 209.

182

465

TABLE 13. Tribes and groups estimated to have more than 5 per cent of non-Indian ancestry. Some tribes listedhere will be found also among one or another ot tables 1-11. Such duplication resu;ts: from two or more sampleshaving been drawn from the same tribe, whether by the same or by different workers, one or more samples indi-cating less than 5 per cent non-Indian ancestry and one or wore indicating more than 5 per cent non-Indian ad-mixture.

TRIBE OR GROUP COUNTRY REFERENCES TRIBE OR CROUP COUNTRY REFERENCES

Surinam 109 Chorotega Nicaragua 165, 175Ank; Argentina 2 05 Choroti Argentina 182, 254Apache U.S.A. 42, 90, 111 Colla Argentina 182, 199, 254Arawak Surinam 58 Cora Mexico 192

Araucanian Cree Canada and(see also U.S.A. 51. 97, 143, 155, 156"Mapuche") Chile 189, 196, 211, 2 37 Crow U.S.A. 250

Atacamenos Chile 74, 164 Cuna Panama 72

Athabascan U.S.A. 62, 87, 98, 250 Dogrib U.S.A. 98Aymara Bolivia;

Peru 223; 225 Emerillon French Guiana 114

Beaver U.S.A.; Flathead U.S.A. 154, 155

Canada 62, 98, 156 Galibi French Guiana 114

Blackfeet U.S.A.; 5, 49, 110, 139 Goajiro Venezuela andCanada 154, 155, 160, 162 Columbia 128, 134, 152

Blood U.S.A.; 49, 139 Guambiano Colombia 137Canada 154, 160, 162 Guarani Brazil 216

Boruca Costa Rica 177 Guatuso Costa Rica 81

Botocudo Brazil 153 Guayqueri Venezuela 134, 135

Cachama Venezuela 118, 119 Haida Canada 102, 150, 264Caddo U.S.A. 99 Hopi 42, 250Caingang Brazil 76, 77 Huichol Mexico 192

Canela Brazil 22, 65, 146 Hupa U.S.A. 104

Caraja Brazil 106, 107 Ica Colombia 22, 134Caramanta Colombia 11 Itonama Bolivia 1 69Carib Surinam 257 Itza Maya Mexico 1 70. 2 ouCarrier Canada 98

Catawba U.S.A. 2 10 Jicaque Honduras 1 65. 1 74

t Catio Colombia 12 Kansas U.S.A. 1 12

Catopaxi Ecuador 242 Kariri Brazil 207Ceara Brazil 17, 18 Karok U.S.A. 104Chaguanca Argentina 181, 254 Katios Colombia 12

Chamacoco Argentina 181, 254 Keresan U.S.A. 4

Chemehuevi U.S.A. 42 Kitamaat Canada 2 17

Cherokee U.S.A. 209, 250 Klallam Canada 102Chiapaneca Mexico 170, 260 Kuaiker Colombia 136, 198Chibcha Colombia 252 Kokonuko Colombia 137Chibcha Peru 251 Kutchin U.S.A. 145Chickasaw U.S.A. 112, 250 Kwakiutl Canada 89, 102, 217Chinanteco Mexico 165, 187Chirrya

vyan

ChippewaChiriguano

BoliviaU.S.A.U.S.A.Argentina

25896, 98, 14352, 56, 159

181, 254

LacandonLamistasLencaLloreos

MexicoPeruHondurasColombia

171

2691 65, 174

253

Choctaw U.S.A. 57, 112, 25(' U.S.A. 102

Chol Guatemala; Chile 74, 101, 184, 1 88, 1 89,Mexico 64, 170, 171, 2 60, 2 62 196,211,238,239

Chontol Mexico 64 Mataco Argentina 7, 1 82, 254

183

TABLE 13-Continued

TRIBE OR CROUP COUNTRY REFERENCES TRIBE OR GROUP COUNTRY REFERENCES

Maya

MextizoMicmac

Br. Hondurasand MexicoMexico

Canada

95, 170, 171, 176, 218170

33, 88

Quinault

Ramkokamekra

Sac and Fox

U.S.A.

Brazil

U.S.A.

104

65

250Miskito Nicaragua 165, 175 Sal ish U.S.A.; Canada 62, 87, 89,Mixe Mexico 64, 165 102, 141Mix tec Mexico 64, 221 Sapelo Canada 219Mojave U.S.A. 2 Sarcee Canada 50Montagnais Canada 33, 219 Sekani Canada 98Mor Bolivia 169 Scnaca U.S.A. 70Muckleshoot Canada 102 Seri and Yaqui Mexico 192,221Muskhogean U.S.A. 112, 250 Shoshone U.S.A. 250

Sibundoy Colombia 198Nab ua Mexico 221 Sioux U.S.A. 154, 157,250NaskapiNavajo

CanadaU.S.A.

33, 183, 2194. 6, 40, 42, 63,

SlaveStoney

CanadaCanada

87, 97, 98, 15650, 97, 98, 155191, 203 Subtiaba Nicaragua 165,175Ne7, Puce U.S.A. 80 Swinomish U.S.A.; Canada 102, 103Nootka Canada 102

Tacana Bolivia 169Oajana Surinam 187Tarahumara Mexico 187,221Oka nagon U.S.A.;Tarasco Mexico 24.221Canada 102, 103 Tariana Brazil 31Omaha U.S.A. 157 Tcwa (Pueblo) U.S.A. 4Ona Chile 211 Tinnch U.S.A. 206Otomi Mexico 187, 226, 229 Tlaxcalteca 144.xico 227Oyama Surinarn 257 Tlingit U.S.A. 62, 141, 187Oyampi French Guiana 114 Toba Argentina 182,199,204,254

Paéz Colombia 10, 22, 131, 137 Toltec Mexico 270Panzaleo Ecuador 241 Totonac Mexico 170Paraujano Venezuela 16. 17.127, 134 Towa (Pueblo) U.S.A. 5, 6Patax6 Brazil 208 Tru mai Brazil 249Paya Honduras 165. 174 Tsimshian Canada 102,217Pawncc U.S.A. 99 Tulalip Canada 102Pehuciche Chile 189, 254 Tungurahua Ecuador 242Pchuenche Chile 74, 254 Tuscarora U.S.A. 185Penobscot U.S.A. 3 Uru Peru 267Piegan Canw , 155 the U.S.A. 161, 163Pijio Colombia 213Pilagi Argentina 182, 199, 254 Wichita U.S.A. 99Pima U.S.A. 42, 100 Winnebago U.S.A. 157Ponca U.S.A. 250 Wintun U.S.A. 104Pueblo New Mexico 4, 5, 6, 39, 40 Yagan Chile 75Puruhi Ecuador 242 Yakima U.S.A.; Canada 102, 103Quechua Ecuador; 3. 28, 93, 167, 168, Yamana Chile 74

Peru 214, 723, 244 Yaqui and Seri Mexico 192,221Quillacinga Colombia 198 Yurok U.S.A. 104

Quilieute U.S.A.; Canada 102 Zapotec Mexico 64, 170, 187,260

184

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document resume - eric · document resume. rc 006 143. biomedical challenges presented by the...

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