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PREVENTIVE MEDICINE 4, 5 18-525 (1975)

The Framingham Offspring Study. Design

and Preliminary Data1

MANNING FEINLEIB, WILLIAM B. KANNEL, ROBERT J. GARRISON,

PATRICIA M. MCNAMARA, AND WILLIAM P. CASTELLI

Epidemiology Branch, Division of Heart & Vascular Diseases,

National Heart and Lung Institute, National Institutes of Health,

Bethesda, Maryland 20014

The Framingham Heart Study included 1644 spouse pairs as part of the original cohort.The new Framingham Offspring Study consists of examination of the offspring of these

matings. Over 5000 offspring and their spouses have been identified and invited to an exam-ination at the Framingham Heart Study facilities. Approximately 82% of the offspring stilllive in the New England area. Response rates for those living in New England are currentlyabout 80%. Due to vigorous efforts to contact offspring who have moved from NewEngland, it is estimated that over 20% of this group will also be examined. Comparison ofage-specific means for the original cohort in 1950 and the offspring in 1972 show apparentreductions in blood pressure, serum cholesterol, and cigarette smoking in the offspring. Incontrast, height in men and women and relative weight in men show significant increases inthe offspring. Methodologic differences may account for certain o f these changes, but it ispossible that the observed reduction in the major CHD risk factors may result from gener-

ally increased health awareness in this sample or the institution of primary preventionmeasures.

The Framingham Heart Study was started in 1949 with the examination of5209 persons aged 30 to 62 (l-3). The survivors of this group have been exam-ined every 2 yr since then and are currently undergoing the thirteenth biennialcycle with 24 yr of follow-up. In the original cohort there were 1644 spousepairs. The children of these marriages form the basis of the current study, whichwe have called the Framingham Offspring Study. During the past 4 yr these off-spring, aged 12 to 60, have been invited for physical examinations at the Fram-ingham Heart Study facilities. The two major aims of the Framingham Offspring

Study are, first, to determine whether there have been secular changes in thelevels of risk factors between the two generations of persons and, second, toexamine the presence of familial and genetic effects in determining the levels ofthese risk factors. The timing of the Framingham Offspring Study was not coin-

cidental. By allowing 22 yr to elapse between the two studies, the offspring wereexamined at approximately the same ages that their parents were when theywere first examined as part of the original heart study. The statistical summariesof this report are based on incomplete data and should be construed as prelimi-

nary.Table 1 shows the sampling frame for the offspring study. The 1644 spouse

pairs in the original cohort consisted of 1387 pairs who had one or more children

1 Presented at the Conference on Cardiovascular Disease Epidemiology, Tampa, F lorida, March1975.

518

Cowright 0 1975 by Academic Press. Inc.

All rights of reproductionn any form reserved.



FORUM: CARDIOVASCULAR DISEASE EPIDEMIOLOGY 519

TABLE 1

THE FRAMINGHAM OFFSPRING STUDY SAMPLE

1644 spouse pairs in Framingham Heart Study cohort1387 pairs had one or more children

227 pairs had no children30 pairs unknown

1921 ndividuals with no spouse in the study cohort330 had CHD or lipid abnormality and at least one child163 others had one or more offspring volunteer

1880 otal number of eligible families

and 257 pairs who were either childless or of unknown fertility. The remainderof the original cohort consisted of 192 1 individuals who did not have a spouse inthe study cohort. From among these, 330 had CHD or a lipid abnormality as de-

termined by the Fredrickson typing and also had at least one child. Their off-spring were also invited for examination. In addition, there were 163 individualswho had one or more offspring who volunteered to come in for examination as aresult of the local publicity given to the offspring study. Thus, our sample con-sists of the offspring of 1880 eligible families. In future analyses the spouse pairsample will be treated separately, but for this preliminary report all availabledata were utilized.

Preliminary response in the offspring study as of January 1975 is shown inTable 2. The identity and location of 4190 offspring are known. An additional500, approximately, are known to be dead. To date 2732 offspring from 1219families have been examined, or 65% of all of those alive. About 82% of the4 190 identified offspring live in the New England Area, and of these, 26 10 or76%, have been examined. As would have been predicted, the examination ratefor those who live outside of New England has been rather low, and to date only122 of these 769 persons, or 16%, have been examined at the Framingham facil-ities. To test whether those who live outside of New England and have not par-ticipated are similar to the others, special examinations have been arranged forat least 50 persons through the cooperation of local lipid research centers. Thiswill raise the non-New England examination rate to approximately 22%. The

examination offered to the offspring is similar to that taken by their parentsduring the last 24 yr, with the major difference being that all of the offspring areexamined in the morning in a fasting state so that we are able to obtain fastingblood for lipoprotein phenotyping.

TABLE 2

PRELIMINARY RESPONSE-THE FRAMINGHAM OFFSPRING STUDY

4190 offspring alive and locatable2732 offspring from 1219 amilies examined3421 of 4190 offspring (82%) live in New England2610 of 3421 (76%) have been examined

122 of 769 (16%) not living in New England have been examined50 examined at LRCs will raise non-New England examination rate to 22%



520 FEINLEIB ET AL.

For the purposes of this initial report, data will be presented on 1837 of theoffspring who are between the ages of 30 and 61, the same age range as theirparents were in when first examined 24 yr ago. The age and sex distribution ofthe offspring who are over the age of 30 in comparison with the age and sex dis-

tribution of the parental generation is shown in Table 3. Since the data are notcomplete or organized into family groups, this report will present the data simplyin terms of the age and sex trends. Thus, for example, the 832 persons in thecohort who were between 30 and 39 in 1950 will be compared with the 434 off-spring in this age group in 1971-1975. These members of the initial cohort arenot necessarily the fathers of these male offspring but were simply in the sameage group at the initial examination. It should be appreciated that in terms oftheir years of birth, the youngest members of the original cohort were born in the19 10’s, as were the oldest members of the offspring generation. This will becomeapparent when we examine some of the risk factors to follow.

The cardiovascular risk factors that are available on both the parental and off-spring generation can be divided into two categories: those that have been con-

sistently measured, such as in height, weight, and cigarette smoking, and thosefor which there may have been appreciable variability in the techniques ofmeasurement during the past 25 yr or consistent examination differencesbetween the offspring and the cohort.

Figure 1 shows the change in height between the parental or cohort generation

and the offspring. A fairly consistent trend is seen, with the sons being approxi-mately 1 in. taller than their fathers were about 25 yr ago, whereas the womenare approximately l/z in. taller than their mothers were. As mentioned earlier, theyoungest members of the cohort and the oldest members of the offspring genera-tion belong to the same generation in terms of year of birth, namely, the 1910’s.It is seen that these two groups are approximately the same height for both menand women. If we follow each of the decades of birth, there has been an increasefrom about 66.5 in. among those men born in the 1890’s to a mean height of 69in. among those men born in the 1930’s, while for the women the change overthese 50 yr has been from about 61.75 to 63.25 in.

Figure 2 shows the difference in mean relative weight between the two genera-tions. Relative weight at Framingham is defined in terms of the median weight

for a given height in the parental or cohort generation. Because it is defined interms of the median, the mean relative weight is slightly greater than 100%.Even with this adjustment for height, the male offspring are approximately 5%

TABLE 3

NUMBER OF SUBJECTS IN FRAMINGHAM STUDIES BY AGE, SEX, AND GENERATION

30-39 40-49 50-l

Men

Cohort

offspringWomen

Cohort

Offspring

832 779 725

434 336 114

1037 963 873

432 403 118



522 FEINLEIB ET AL.

ORT

iPRlN0WOMEN

FIG. 3. Framingham Offspring Study-proportion smoking cigarettes (22 SE) for cohort and off-

spring generation by age and sex.

proportion observed in the offspring generation. In women there seems to be aninteraction effect. Among the older women in the parental generation, there werevery few smokers, and it seems that it wasn’t until the 1930’s or 1940’s thatwomen started to smoke appreciably. This effect seems to have carried over tothe older women in the offspring generation, but the younger women are smok-ing less than women of the same age a generation ago. Those women who wereage 30 when fhst seen in the cohort examinations have also reduced their smok-ing habits, as have the men, and now only 43% of them smoke, which is quite

consistent with the figure seen in the offspring data.As Fig. 4 indicates, the changes in cholesterol levels between the two genera-tions also seem to be in the direction to indicate that we might expect a loweringof the heart disease rates in the current offspring generation. In each age groupfor men and for women, the offspring have mean cholesterol levels approxi-mately 15 mg% lower than the parental generation. Although this trend is con-sistent, a word of caution is indicated because there may have been consistent

I +

a&m @U m+ ab* (w 60,AOE AOE

FIG. 4. Framingham Offspring Study-mean serum cholesterol (&2 SE) for

generation by age and sex.

cohort and offspring




changes in the laboratory determinations of cholesterol during the last 25 yr. Ifwe use the approach we used previously to examine the longitudinal trends inthe youngest members of the cohort, we find that among the women, those cur-rently aged 50 in the parental generation had cholesterol levels about the same

as women aged 50 in the offspring generation. This would indicate that forwomen there has been a consistent lowering of cholesterol levels. When thesame analysis is done for the men one finds that those men who were currentlyaged 50 in the cohort had cholesterol levels that were almost identical with themen who were aged 50 at examination 1 in the cohort and are still considerablyhigher than the offspring who are aged 50. A determination of whether thisapparent decrease in mean cholesterol level is real or the result of a systematicchange in laboratory procedure will have to await further analysis of datacollected on the cohort.

The trends in mean blood pressure levels, as shown in Figs. 5 and 6, also

suggest a possible lowering of a significant risk factor between the two genera-tions. Among the men there has been approximately a 5 to lo-mm drop insystolic pressure and an even greater drop among the women. When we look atthe longitudinal effects, we find complete overlapping between the men who arecurrently age 50 in the cohort and the offspring in the same age group. Althoughthis seems to confirm the consistency of the differences, a word of caution is duehere. If we examine the longitudinal trends of blood pressure in the cohort, as

shown in Fig. 7, we note that there was an examination effect in the cohortgeneration so that the systolic and diastolic blood pressures dropped from thefirst to the third examinations and did not begin to increase with age until after

the third examination. This could be due to a stress factor that was presentduring the first two examinations. By the third examination the subjects had ap-parently become acclimated to the examination routine, and we are able to dis-cern thereafter the more typical aging effect of gradually rising blood pressure.

MEN- COHORT

---- OFFSPRlNOWOMEN

P

*oE AQE

FIG. 5. Framingham Offspring Study-mean systolic blood pressure (k2 SE) for cohort and off-spring generation by age and sex.



524 FEINLEIB ET AL.

I I I

so-39 4349 50, 2x-59 4-W 6Qt

AGE AGE

FIG. 6. Framingham Offspring Study-mean diastolic blood pressure (?2 SE) for cohort and off-

spring generation by age and sex.

The fact that the offspring had lower values than their parents may be due to agenuine difference between the generations, but we should also be aware that itmay be due to the fact that the offspring are already somewhat familiar with theexamination procedures. Since their parents have participated in the study forseveral years, the offspring may already be somewhat acclimated; thus, their

blood pressures may already reflect the same kind of drop that was noted fortheir parents during the second and third examinations. Therefore, before we can

i

----WOMEN

125

-MEN

FIG. 7. Framingham Offspring Study-mean blood pressure by examination and sex for personstaking all examinations.




definitely say that there has been a change in blood pressure among the off-spring, we should have data from one or two more examinations. It should alsobe noted that for diastolic pressure, the men showed almost no differencebetween the cohort and offspring generation, while among the women a drop of

about 5 mm was noted.REFERENCES

1. Dawber, T. R., Kannel, W. B., and Lyell, L. P. An approach to longitudinal studies in a commun-ity: The Framingham Study. Ann. N. Y. Acad. Sci. 107, 539-556 (1963).

2. Dawber, T. R., Meadors, G. F., and Moore, F. F., Jr. Epidemiological approaches to heart

disease: The Framingham Study. Amer. J. Pub. Health 41, 279-286 (195 1).

3. Gordon, T., and Kannel, W. B. The Framingham, Massachusetts, Study 20 years later, in “TheCommunity as an Epidemiologic Laboratory: A Casebook of Community Studies” (I. J.Kessler and M. L. Levin, Eds.), p. 123. Johns Hopkins Press, Baltimore, 1970.

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