(Hypertension. 1999;33:874-878.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Maximum-Likelihood Generalized Heritability Estimate for Blood Pressure in Nigerian Families
From the Loyola University Medical Center, Department of Preventive Medicine and Epidemiology, Maywood, Ill (C.N.R., R.S.C., G.C.), the University of Ibadan, University College Hospital, Ibadan, Nigeria (O.O., M.L., E.O.), and the Institute of Biological Anthropology, University of Oxford, Oxford, UK (R.W.).
Correspondence to C. Rotimi, Loyola University Medical Center, Department of Preventive Medicine and Epidemiology, 2160 S First Ave, Maywood, IL 60153. E-mail crotimi{at}wpo.it.luc.edu
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Abstract |
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Abstract—Elevated blood pressure (BP) is more common in relatives of hypertensives than in relatives of normotensives, indicating familial resemblance of the BP phenotypes. Most published studies have been conducted in westernized societies. To assess the ability to generalize these estimates, we examined familial patterns of BP in a population-based sample of 510 nuclear families, including 1552 individuals (320 fathers, 370 mothers, 475 sons, and 387 daughters) from Ibadan, Nigeria. The prevalence of obesity in this community is low (body mass index: fathers, 21.6; mothers, 23.6; sons, 19.2; and daughters=21.0 kg/m2). The BP phenotype used in all analyses was created from the best regression model by standardizing the age–adjusted systolic blood pressure (SBP) and diastolic blood pressure (DBP) to 0 mean and unit variance. Heritability was estimated by use of the computer program SEGPATH from the most parsimonious model of "no spouse and neither gender nor generation difference" as 45% for SBP and 43% for DBP. The lack of a significant spouse correlation is consistent with little or no influence of the common familial environment. However, the heritability estimate of <50% for both SBP and DBPs reinforces the importance of the nonshared environmental effect.
Key Words: blood pressure • genetics, population • blacks
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Introduction |
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Hypertension is the most common human cardiovascular disease, with a lifetime cumulative incidence approaching 50% in many populations.1 Epidemiological evidence demonstrates a multifactorial cause for this condition,2 3 4 5 with major risk factors including obesity, diet (specifically, high sodium, low potassium, and excess energy intake), stress, and physical inactivity.6 7 8 Genetic factors that confer susceptibility to hypertension are now being identified in several populations.9 10 11 12 Most of these studies, undertaken to define the genetic influences, are being conducted in westernized societies where high levels of exposure to environmental risk factors prevail, especially obesity and excess sodium. In the present study, we reported on the familial patterns of BP in a population sample of Nigerian families.
The prevalence of hypertension in this population is 7% among persons>25 years of age,7 accompanied by low levels of the major risk factors, ie, an average body mass index (BMI) of 21.7 kg/m2 for men and 22.6 kg/m2 for women, sodium excretion of 121 mEq/d, and a sodium/potassium ratio of 2.7:1.7 In addition, the level of physical activity is, on average, higher than that observed among blacks in most social settings in the western hemisphere.
Ethnohistorical data show that the majority of African Americans are descendants of enslaved Africans from the western regions of the continent.13 Within this region lies the present- day Nigeria. Furthermore, the Yoruba ethnic group, from which the participants for this study were selected, represents one of the major tribes that contributed to the European slave trade. The Yorubas, thus, have historic ties to present- day blacks in the western hemisphere, where broad admixture among survivors of the African diaspora has taken place.
We have developed a long-term strategy to understand the origins of the health disadvantage of blacks in the western hemisphere by using the contrasting environments occupied by contemporary populations of African origin. Within the context of the International Collaborative Study of Hypertension in Blacks (ICSHIB), numerous epidemiological, physiological, and genetic data are being collected on family sets in West Africa, the Caribbean, and the United States.7 14 An important focus of this work is to understand better how genes interact with the environment. The analysis presented in this paper represents an evaluation of the familial patterns of BP among Nigerian families.
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Methods |
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Selection of Probands and Relatives
Probands between 35 and 65 years of age were selected randomly from among the participants of an ongoing population survey designed to estimate the prevalence of hypertension and associated risk factors. The age–stratified sampling scheme has been previously described.14 Briefly, a cluster sampling technique known as "probability proportionate to size" was used to recruit approximately equal proportions of men and women from randomly selected clusters. All households within the selected cluster were approached to participate in the study. A total of 10 014 individuals (women=5433, men=4581) were enrolled and examined in the baseline prevalence survey in West Africa (Cameroon and Nigeria, both with urban and rural sites), the Caribbean (Barbados, Jamaica, and St Lucia), UK (Manchester), and in the United States (Maywood, Ill). The family study reported here involved a subset of individuals who participated in the Nigerian survey. A random sample of 510 probands of both genders within the age group of 35 to 65 years along with consenting family members were invited to participate in this second set of examinations; the overall participation rate was 85%. Family recruitment began in 1994 and continued through the spring of 1998.
Measurement
BP was measured by use of a standardized protocol developed for
ICSHIB.14 Briefly, all BPs were measured on the right arm
with an appropriate size cuff with the patient in the sitting position.
Systolic BPs (SBP) and diastolic BPs (DBP) were
recorded to the nearest 2 mm Hg as the first and the fifth
Korotkoff phases with both an electronic device and a standard
mercury manometer.
Data Adjustments
BP measurements were adjusted for the effects of age
separately for fathers, mothers, sons, and daughters to accommodate
observed gender and generational heterogeneity.
Stepwise regression procedures were performed with only terms
significant at the 5% level retained in the model:
Y=ß0+ß1(age)+ß1(age)+ß2(age2)+ß3(age3)+e;
where Y is the observed phenotype (SBP or DBP). Extreme values
(defined as: ¦observed phenotypic value-mean¦>4 SD) were excluded
temporarily in the regression models to prevent excessive influence
from outliers. There was no significant age term for the fathers or
mothers. Age was significant for sons and age2
was significant for daughters. Observed residual variance was examined
for heteroscedasticity due to age effects by regressing
(e2=(Y-[ß0+ß1(age)+ß1(age)+ß2(age2)+ß3(age3)]2))
on another cubic polynomial in age. The data displayed no
heteroscedasticity because none of the regression terms were
significant for any variable in any group. This result indicates
that the error variance does not change with the values of the
independent variables (ie, the age terms).
After extreme observations were restored to the data set, each
measurement in all groups was standardized by use of the relevant
regression models as follows: Z=(Y-
)/SDr,
where is the predicted value and SDr is
the standard deviation for the residual. The standardized residual was
then pooled, ranked and normalized.15 The normalized
scores constituted the BP phenotypes in all analyses.
Statistical Analysis
Eight familial correlations—father-mother (fm),
father-son (fs), mother-son (ms), father-daughter (fd), mother-daughter
(md), son-daughter (sd), son-son (ss), and daughter-daughter (dd)—were
estimated through the maximum- likelihood methods available in the
computer program SEGPATH.16 The 10 models fitted to test
specific hypotheses are displayed in Table 1. Each reduced hypothesis is tested
against the general model by use of the likelihood ratio test computed
as (-2 ln Lreduced)-(-2 ln
Lgeneral); where ln L is log-likelihood. The
likelihood ratio has a 
2 distribution with the
degrees of freedom equal to the number of parameters in the
general model, minus the numbers of parameters in the
reduced model. The most parsimonious model that is generally used in
these analyses represents the combination of all
nonrejected hypotheses and is desirable because it uses fewer
parameters. Maximum heritability
(h2) was estimated under the most
parsimonious model using
h2=(rpo+rsib)(1+rfm)/(1+rfm+2rfmrpo),
where rpo, rsib, and
rfm denote parent-offspring, sib-sib, and
father-mother correlations, respectively.
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Results |
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The 510 nuclear families available for analysis included 320 fathers, 370 mothers, 475 sons, and 387 daughters for a total of 1552 individuals (Table 2). Among these families, both parents and at least 1 offspring were enrolled in 254 (number of individuals=919), 1 parent and at least 1 offspring were available for 178 (n=446), offspring with no participating parents were enrolled in 76 (n=183), and 2 families had only spouses and no participating offspring (n=4). The mean age by generation was 53.0±10.1 for the parents (fathers, 56.0±9.2; mothers, 50.3±10.0) and 26.0±12.7 for the offspring (daughters, 26.2±13.0; sons, 25.9±12.3 years). Daughters made up 45.0% of the offspring generation (Table 3).
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The low prevalence of obesity in this community is evident in the gender- and generation–specific mean BMI values (fathers, 21.6; mothers, 23.6; sons, 19.2; and daughters, 21.0 kg/m2). Although the mothers were 2 BMI units heavier than the fathers, the SBP (P=0.4237) and DBP (P=0.4029) values were not significantly different in the 2 groups. Similarly, although daughters were heavier than sons, mean SBP was not different by gender in the offspring generation, whereas the 2 mm Hg difference in DBP observed was borderline significant (P=0.05). As expected, females had significantly larger hip circumferences compared with males. In contrast to the offspring generation in which daughters had larger waist circumferences compared with the sons, the differences between the mothers and fathers were not statistically significant. All the anthropometric measurements thus reflect the general leanness of this population.
The results of the likelihood ratio tests for the reduced models
are summarized in Table 4 for SBP and
Table 5 for DBP. For both SBP and DBP,
the hypotheses of no familial correlations (ie, all 8 correlations set
to zero), no sibling correlation, no parent-offspring correlations, and
neither sibling nor parent-offspring correlations were rejected.
Consequently, the most parsimonious model for both SBP and DBP was the
combination of model 4 (ie, neither gender nor generation differences)
and model 8 (ie, no spouse correlation). The comparison of the
parsimonious model to the general model resulted in a
2 value of 6.36 for SBP and 8.35 for DBP
(P=0.50 and 0.30, respectively.) The most parsimonious
models thus fit the data very well for both SBP and DBP.
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Table 6 summarizes the parameter estimates for SBP and DBP under both models. The maximum heritability was estimated as 45% for SBP and 43% for DBP under the most parsimonious model. Although these estimates represent the effect of both genetic and familial environmental factors, the nonsignificant spouse correlations suggest that the majority of the effect is due to shared genetic factors.
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Discussion |
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The main contribution of this study is the use of genetic epidemiology methods to estimate the proportion of BP variability that is determined by transmissible factors (ie, shared environmental and shared genetic factors) in a population sample of nuclear families from West Africa. Heritability was estimated from the most parsimonious model as 45% for SBP and 43% for DBP. To the best of our knowledge, this represents the first attempt to use standard statistical genetic methods to estimate the degree of familial clustering of BP in Nigerian families. In general, relatively few studies have reported data on familial clustering of BP in black families. Furthermore, data on familial aggregation of BP in black populations of sub-Saharan Africa is nonexistent. The paucity of information on the impact of genes on BP variability in sub-Saharan Africa can be attributed to several factors, including the general notion that the prevalence of hypertension remains low. Recent epidemiological data on hypertension and associated complications (eg, stroke) from different communities in this region of Africa now suggest the need to modify this assumption.7 17 18 19 Other reasons for the paucity of data on the genetic contribution to BP variability are lack of resources and the degree of complexity involved in conducting family studies. Given the level of research funding available to most researchers in sub-Saharan Africa, investigators would be hard- pressed to find adequate local support for a large-scale family study. Several important advantages to study in this geographic region can be identified, however. Family size tends to be large, and generation time is relatively short. Families tend to reside in close geographic proximity, and participation rates are often high. The low prevalence of hypertension and the subsequent rarity of treatment make analysis of BP as a continuous trait more informative.
Our estimates of maximum heritability are in general agreement with previously reported estimates for both black and white families.4 20 21 22 23 24 25 26 27 28 29 30 In 1983, Moll and colleagues reported heritability of 35% and 53% for SBP and DBP in their cohort of black families from the Detroit Project.20 The corresponding estimates for whites in the same study were 43% for SBP and 38% for DBP. Recently published heritability estimates from the HERITAGE family study were 68% for SBP and 65% for DBP, estimates higher than we observed.21 Whether these population differences are real or statistical variability is not immediately apparent. Different sampling strategies may also be partially responsible for the observed difference; for example, families included in the HERITAGE family study were required to be sedentary. In addition, some of the differences in heritability estimates may be because of the adjustment strategies for concomitant variables (eg, gender and age) used.
Although some studies have reported significant spouse correlations, especially for SBP,29 30 none were observed in the present study, an indication that most couples from this Nigerian community were discordant in relevant environmental determinants of BP or that error in measurements of BP obscured detection of small effects. Similarly, there were no significant differences between parent-offspring and sib-sib correlations, also suggesting a lack of shared environment unique to the siblings, not shared with the parents, which have physiological relevance. Similar observations were reported among black and white families included in the HERITAGE family study.21
Despite a high transmissibility estimate from published reports,
as well as this study, a sizable proportion of the BP variation
(
55% for the present study) remains unexplained. Most of this
unexplained variance is probably due to a combination of measurement
error, intraindividual variation, and factors which do not cluster in
families. Measurement error could be reduced by performing repeated
measurement at shorter or longer intervals. Unfortunately,
epidemiological methods to assess environmental exposures have limited
precision when the goal is cross-sectional characterization of
individuals. Because genetic factors and environmental exposures are
likely to interact, explaining variance at either dimension should
enhance treatment and prevention strategies. Widespread expectation now
exists that genetic markers could enhance the precision with which
individual risk of hypertension is predicted. Of the potential
candidate loci, the strongest case for susceptibility of human
hypertension now exists for genes encoding components of the
renin-angiotensin system.9 10 11 12 A collaborative
investigation of the angiotensinogen (AGT) gene in
siblings from Utah and Paris found both linkage and association of AGT
molecular variants (M235T and T174 M) with hypertension.10
Although the association between the molecular variants of the AGT gene
and hypertension status in blacks has been
inconsistent,31 32 33 we recently reported an
association between 235T and plasma level of
angiotensinogen among Nigerians, and hypertensives had
higher plasma AGT level than the control subjects.33
Evidence of strong heritability of BP in the family sets, reported
here, suggests that molecular determinants should be identifiable given
ongoing improvement in laboratory methods.
In summary, this study provides evidence of familial resemblance of BP in a population with a low prevalence of hypertension having historic ties to blacks in the western hemisphere. Although parameter estimates vary from one study to another, these data reinforce the general consensus that a large proportion of the phenotypic variation in BP is genetically determined. Family studies of hypertension and associated risk factors in populations of the African diaspora may contribute to a better understanding of the complex interaction between genetic and environmental factors leading to hypertension.
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Acknowledgments |
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This research was supported by grants from the National Heart, Lung, and Blood Institute (HLB45508, HLB52075, HLB53353).
Received August 6, 1998; first decision September 3, 1998; accepted December 2, 1998.
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