1085

of feed, (5) volume per unit birth-weight, (6) dura-tion of feed, and (7) ambient oxygen concentration.There was no apparent relation with the one excep-tion of volume of feed per unit of birth-weight(r=0-81, n<001).

Discussion

Early feeding of low-birth-weight infants is nowan established routine in most special-care nurseries.Hypoglycaemia and jaundice are lessened in infantsfed as early as 2 hours after birth compared withthose fed later.2,3 The amounts of feed given byindwelling nasogastric tubes have also been increasedwith apparently only slight disturbance to the infant.This method of feeding applies to babies of very lowbirth-weight or to larger infants who are ill, especi-ally those with respiratory distress.The physiological capacity of infants to tolerate

such regimens has been doubted.4 Bauman 5 demon-strated that early feeding of dextrose and hypotonicsaline solution to low-birth-weight babies resulted ina greater frequency of dyspnoea. Regurgitation aftertube-feeds was reported in a third of babies fedwithin 2 hours of birth.2 In another report, theinhalation of vomit was a

" disturbingly frequentnecropsy finding" in a group of infants in whomthere was an increased mortality among " early-fed "infants compared with a

" later-fed " group 3 Re-

gurgitation of milk into the lower half of the ceso-phagus and altered or abnormal patterns of breathinghave been demonstrated after nasogastric tube-

feeding 6; however, in this study exceptionally largefeeds were given over a short time (60 ml. per kg.at 20 ml. per minute). Russell and Feather studiedhealthy term babies and found no significant effectof feeding on respiratory mechanics. They concludedthat feeding does not necessarily cause respiratoryembarrassment in all newborn infants but felt thatthe point at which adverse effects do appear shouldbe determined. They believed that the various fac-tors involved might include the size and maturity ofthe infant, the volume of feed, the time taken forfeed, and the route by which feed is given.The striking fall in Pao2 after tube-feeding is

unlikely to be due to hypoventilation, since P aco2 fell.We did not measure tidal air, but the increased

respiratory-rate suggests compensatory hyperventila-tion as a consequence of hypoxaemia, with recoveryby the end of the 30-minute study period. The dropin P.c.v. and total proteins can be explained by slighthaemodilution, but the results exclude fluid changesin or out of the vascular compartment after the feedof an order that might invoke cardiorespiratoryresponses or blood-gas changes.We have demonstrated a transient but significant

fall in Pa02 after nasogastric tube-feeding in a groupof ill, newborn infants, recovering from respiratorydistress. In infants with already precariously 10’-’

resting oxygen tensions before feeds, such disturb-ances would be of special importance and migh1explain some of the cyanotic spells or apnoeic attack!that are observed after feeds. Our findings do n01provide sufficient evidence to explain the mechanisnof this disturbance.

We thank Prof. J. P. M. Tizard, Dr N. R. C. Roberton, am

Dr J. D. Baum for their advice; and Mr P. Rolfe for technicalassistance.

Requests for reprints should be addressed to V. Y. H. Y.

REFERENCES

1. Rolfe, P. Bio-med. Eng. 1971, 6, 402.2. Smallpiece, V., Davies, P. A. Lancet, 1964, ii, 1349.3. Wharton, B. A., Bower, B. D. ibid. 1965, ii, 969.4. ibid. i, 791.5. Bauman, W. A. Pediatrics, Springfield, 1960, 26, 756.6. Barrie, H. Lancet, 1968, ii, 1158.7. Russell, G., Feather, E. A. Archs Dis. Childh. 1970, 45, 325.

Reviews of Books

Human Chromosomes

E. H. R. FORD, department of anatomy, University of

Cambridge. London: Academic Press. 1973. Pp. 381. S7.

THIS is a good enough book to be worth criticising insome detail. It deals with all aspects of human cyto-genetics-the biological background, techniques, clinical

syndromes-and gives some value judgments. A book ofthis size cannot deal with all these facets in depth, but thebalance is good and adequate references are given. Thereare some very interesting sections with an original way ofthinking. For example, Dr Ford points out the imprecisionin the estimates so far given for the incidence of chromosomeabnormalities. Even samples of many thousands are smallfor incidence levels of the sort found in Down’s andKlinefelter’s syndromes. It is surprising, then, that theauthor presents the interesting but very preliminary dataon non-random occurrence of certain chromosome abnor-malities as evidence that they may be virus induced: byDr Ford’s own standards these fluctuations must be con-sidered as statistical variations until we have many moredata. He concludes that from the clinical point of viewhuman cytogenetics has been of relatively little value sofar. On the other hand, he considers that the scientificcontributions have been considerable, and that ultimatelysuch studies will " add greatly to the quality of life livedby future generations ". Many will disagree. Ford arguesthat most autosome abnormalities can be diagnosed clini-cally (and the patients are going to die anyway) and that youcannot do anything about the sex-chromosome abnor-malities which often do require a cytogenetic diagnosis.Yet a firm diagnosis will prevent further unnecessaryinvestigation and can often remove the worry of relativesthat an inherited abnormality is involved. Is cytogeneticsgoing to bring us a better life ? True, it has cleared upsome very dark corners and opened up new possibilities,but mutation testing is not going to be the future of cyto-genetics. Bruce Ames’s microbial system with addedmammalian microsomes is a better bet for that. Now allthis is good stuff-well worth discussing, so it must beessentially a good book-but there is some very curiouslogic and some odd errors. Throughout the book theXga blood-group is called a hxmoglobin; and the groupingof pure gonadal dysgenesis under Turner’s syndrome andthe division of Hurler’s syndrome into a sex-linked and anautosomal recessive form are open to criticism. Dr Ford

acknowledges that the word mongol offends some people,but he decides to use it all the same. In several places it isassumed that if a chromosomal trisomy is compatible withsome sort of development, though imperfect, then therecannot be many genes of importance on that chromosome.However, in the extreme case of the plant Datura, alltwelve trisomics are known to be viable-does this meanthat we have a karyotype totally devoid of genes of anyconsequence ?

This book will have its place. It will be compared with

1086

J. L. Hamerton’s Human Cytogenetics (1971). It is not asgood at present, but it is half the price, and if the authorcould get some good critical editing done, the secondedition might take a lot of beating as the standard workfor students and non-specialists.

The Freud/Jung LettersEdited by WILLIAM MCGUIRE. Translated by RoLF MAN-HEIM and R. F. C. HULL. London: Routledge & KeganPaul. 1974. Pp. 650. E7.95.

ANYONE who expects the quality of this work to matchthat of the volume of Jung’s letters, published last year,is going to be very disappointed. In scope, in the range of

subjects, in compassion and humanity, the new work issadly inferior, and there is little in it to remind one of thepsychological discoveries and the literary excellence of whichboth writers were capable. The collection is, surprisingly,almost complete, and the lack of stern editing means thatall too many pages are taken up by trivia-arranging con-ferences and meetings; negotiations with publishers;decisions about the contents of periodicals; abuse ofenemies (" gang of cut-throats ....... a ghastly crowd,reeking of vanity, Janet the worst of the lot ", Friedlander," that liar and clown ... has been puking again ", MortonPrince, " an arrogant ass "; and later of erstwhile sup-porters such as Stekel and Adler and the ambivalent

Eugen Bleuler (" prickly eel "). Altogether there are 164letters from Freud and 196 from Jung, dated from April,1906, to the acrimony and break-up of 1912-13. Several,particularly from the honeymoon period, are charming,generous, and self-revealing-notably a Freud letter of

September, 1907, in which he contrasts their respectivepersonalities, and Jung’s letter eight weeks later whereinhe analyses his religious "crush" for Freud. Inklings oftrouble to come occur as early as 1909 with the beginningsnot only of Jung’s interest in precognition, myths, alchemy,and astrology, a world where Freud could not follow veryfar, but also with a reference to " the oppressive sense ofyour paternal authority ". Indeed, although the eventualbreak ostensibly came from a doctrinal squabble about themeaning of the words incest and libido, the crack wasinherent in the two men’s differing make-up. The rigidFreud could not tolerate any challenge to his authorityor to the immutability of the rules of the human mind thathe discovered (" You must think that I am playing thePope again, fulminating against heretics "). His " dearfriend and heir " was quite incapable, on the other hand, ofbowing to authority if his ideas and discoveries led him ina contrary direction. Both, incidentally, claimed thatpsychoanalysis was scientific, but Freud at least adds " Iwas not cut out for inductive investigation ... my wholemake-up is intuitive ". For the devoted this work must beread as an act of natural piety. For the rest of us it speaksonly of " old, unhappy, far-off things, and battles long ago ".It is easy to agree with Jung that what he called " thataccursed correspondence " is " not particularly important "

and to regret that after his death publication in this form wasdecided on by the two families.

The Fetus and Newly Born Infant

Influences of the Prenatal Environittent. ROGER E. STEVENSON,M.D., University of Texas Medical School at Houston.St. Louis: Mosby. London: Kimpton. 1973. Pp. 391.$30.25; E13.60.

IN his introduction Dr Stevenson delineates the hazardsof intrauterine life. More deaths occur during this periodthan during the fifty years after birth. Even more depressingis the number of mentally and physically handicappedchildren-damaged before they are born-who cannot

take their place as responsibly functioning members ofsociety. This book defines such harmful influences and

examines their effect on mother and infant. The materialis classified sensibly with separate parts for immunology,chemical influences, infection, and prenatal nutrition." Other influences " covers such topics as radiation andmaternal malignant disease. Cigarettes head the list ofadverse effects of drugs: alcohol and drug addictionfollow closely. Each factor is evaluated separately, and itseffect on mother and child is discussed. Reference listsare concise and follow each section: full use is made oftables and photographs. Attention is drawn to topicswhich might benefit from further research. The compre-hensive index is adequately cross-referenced. The sectionson maternal metabolic derangements and neonatal hepatitisare very clear. A disproportionately large amount of spaceis devoted to syphilis. Effects of the contraceptive pill arenot mentioned-surely appropriate for inclusion in a

future edition ?-and there are several typographical errors.More seriously, a dose of thyroxine quoted is a thousandtimes too large. Who would derive most use from thisbook ? Certainly anyone involved in prenatal paediatrics&mdash;whether their prime concern is for mother or baby. Itwould be particularly useful as a reference and informationsource for senior obstetric and paediatric staff when facedwith an unusual situation in pregnancy whose implicationsfor fetal development are not widely known. Recommenda-tion is easier because the text is clear and fluent, and,despite its list-like format, it does not read like a catalogue.

Leprosy for Students of MedicineANTHONY BRYCESON, department of medicine, AhmaduBello University, Zaria, and Roy E. PFALTZGRAFF, AdamawuProvincial Leprosarium, Garkidua, Nigeria. Edinburgh:Churchill Livingstone. 1973. Pp. 152. El.50.

THIS book well fulfils the declared purpose of its authors.It provides for medical students in Africa a generallysound introduction to the subject, in which the newer

knowledge of immunology serves as the conceptual back-ground for the clinical presentation. Much that formerlyseemed irrational or inexplicable is now becoming clearer,as the predominant role of cell-mediated immunity indefence mechanisms becomes better understood. Thestudent of today wishing to embark on the study of leprosyshould have available a text that links leprosy with othermycobacterial diseases and emphasises its rationality ratherthan its unique features. This book will help him. Thereis much more in it than students in the Western worldwill have time for, but they would find it readable anddependable once they dipped into it. The diagrams arehelpful in elucidating the text; the same cannot be saidof many of the black-and-white photographs. It is unusualin a book of this nature to find so many misprints andmis-spellings.

A.M.A. Drug Evaluations (2nd ed. Acton, Mass:Publishing Sciences. London: Pharmaceutical Press. 1973.

Pp. z22; C10.50).-For the price of the mark-upagainst the dollar the European distributors could haveprovided a simple cross-index of drug names. Theyhave not, however, and this must, for British andother readers, detract from the compendium’s usefulness.Otherwise the entries-under twenty broad and ninety-two finer groupings-are compact and nicely set out, andthere is a useful adverse-reactions index. The book is

compiled by the Department of Drugs of the AmericanMedical Association.

New Editions

Clinical Laboratory Medicine. 2nd ed. By R. Ravel. Chicago:Year Book. London: Lloyd-Luke. 1973. Pp. 486.$9.95, S5.

Medical Disorders in Obstetric Practice. 4th ed. By Cyril G.Barnes. Oxford: Blackwell. 1974. Pp. 509. E7.

1087

THE LANCET

Tuberculosis Retreats&mdash;SlowlyTUBERCULOSIS declines in Britain, but too slowly.

Up to 1969 notifications of respiratory tuberculosishad been decreasing fairly steadily by 9% or 10%a year. But between that year and 1971 the annualdecrease fell to only 2%; and in women there wasno decrease at all.1 There is evidence that this

slowing-down is largely due to immigration. In a

survey in 1971, 32% of those notified were bornoutside the British Isles.2 For those born in Indiathe rate was 27 times higher than for those born inEngland and Wales, and for persons born in Pakistanit was 54 times higher. Between 1965 and 1971there had been a decrease in notification-rates of

43% (7% a year) among persons born in the BritishIsles but an increase of 68% among those born inAfrica, India, and Pakistan.

Probably much of the tuberculosis in Asian

immigrants becomes manifest within the first few

years after their arrival. They come from countrieswith a high prevalence of the disease and a high riskof infection. The rational procedure is to X-ray andtuberculin-test all immigrants from these countriessoon after they arrive. The tuberculous could betreated and the uninfected vaccinated; spread ofinfection would be reduced and the disease woulddecline. But search for tuberculosis in new

immigrants is still not compulsory. It should be.The intention is not to debar entry to the tuberculous-as is done in some countries-but to offer themtreatment before they take their rightful place in thecommunity. This is not racial discrimination; it issimply humane.Treatment of those with manifest tuberculous

lesions is not difficult, nor is B.C.G. vaccination.

1. Registrar-General’s Statistical Review for 1971. H.M. StationeryOffice, 1973.

2. British Thoracic and Tuberculosis Association. Tubercle, 1973,54, 249.

Both can easily be absorbed into the work of the >

country-wide chest-clinic service. This service is

probably by no means overworked at present; andin future it should be even less occupied withtuberculous patients, for there is now ample evidencethat long-continued

" observation " of adequatelytreated patients is unnecessary. It is doubtfulwhether, for the benefit of either themselves or thecommunity, patients need be examined again afterproperly prescribed and apparently regularly takenchemotherapy has been completed.3 3 Clinicattendances could be drastically reduced.The prevention of relapse in those infected but

without manifest lesions is not so simple. Chemo-

therapy can undoubtedly reduce the risk of spreadfrom the small inapparent foci (the evidence hasbeen critically summarised by FEREBEE 4), but thereare practical difficulties. The use in Great Britainof this form of chemotherapy-erroneously called

chemoprophylaxis-has lately been examined by theJoint Tuberculosis Committee of the British Thoracicand Tuberculosis Association.5 In young children

(those under 5, for instance) with large tuberculinreactions it is now common practice to give chemo-therapy. The risk of spread is relatively large andthe numbers to be treated are small. In older childrenthe risk is smaller and the numbers are larger. The riskof developing manifest tuberculous lesions is probablyaround 2 per 1000 per year 6; so 1000 childrenwould have to take antituberculosis drugs to prevent20 from acquiring manifest lesions in the next 10years, if the treatment were 100% effective. Withinfected but otherwise healthy adults the risk iseven smaller, probably in the order of 0-15 per1000 per year. 7 So 10,000 would need to be treatedto prevent only 15 cases within 10 years.

If treatment consisted merely of a single injec-tion-as does prevention of the disease with B.C.G.vaccination-or a few days’ taking of pills, and ifthere were no unpleasant effects of the drugs, thedecision to apply the procedure on a large scalewould be relatively simple. But the tleatment isneither short nor free from risk. So the expectedbenefit to the community must be set against thepossible ill effects in the individual. The risks of

unpleasant effects are certainly not great. Whenisoniazid was used alone, in a large-scale controlledtrial carried out by the International Union againstTuberculosis in several European countries, gastro-intestinal symptoms caused treatment to be stoppedin around 4 per 1000, and 3 per 1000 showed someevidence of liver damage. 8 If the risk of liver

damage is of the same order in Britain-and there is

3. Tubercle, 1973, 54, 247.4. Ferebee, S. H. Adv. Tuberc. Res. 1969, 17, 28.5. Joint Tuberculosis Committee. Tubercle, 1973, 54, 309.6. Medical Research Council. Br. med. J. 1963, i, 973.7. Svandova, E. Bull. int. Un. Tuberc. 1972, 47, 129.8. Tubercle, 1973, 54, 321.