Sibling Correlations Research Articles

Analysis of X-ray-induced cell-cycle perturbations in mouse osteosarcoma cells: a two-signal cell-cycle model.

The effects of X-irradiation on mouse osteosarcoma cells have been studied by time-lapse cinematography and the resulting pedigrees have been analysed statistically. It is shown that the irradiation treatment causes three types of cell kinetic lesions: cell death (disintegration), cell sterilization (failure to divide) and proliferation delay. The first two lesions are the most important with regard to survival of the irradiated cell in a clonal assay. Of these two lesions, sterilization appears to be highly correlated for sister cells, while this is not true for cell disintegration. This indicates that cell survival in a clonal assay may be a function of the ratio of the incidences of these two types of lesions. The X-ray-induced proliferation delay was studied in terms of intermitotic time distributions, mother-daughter correlation and sibling correlation in relation to the current cell-cycle phase at the time of treatment. This analysis shows that the effects of irradiation on these cell-cycle characteristics is highly cell-cycle-dependent. A qualitative model to account for the observations is presented.

Family aggregation of high density lipoprotein cholesterol. Collaborative lipid research clinics program family study.

High density lipoprotein cholesterol data on a population-based random sample of 858 white and 72 black probands and their 3935 white and 205 black relatives were collected from nine North American clinics using a common protocol and standardized methodology. Familial associations were examined within clinics for whites and pooled across clinics for blacks. The influence of covariates and varying family size on correlations was examined using several sets of transformed and adjusted values and a variety of weighting schemes. Parent-offspring and sibling correlations were significant in most cases, but spouse correlations were not, suggesting a stronger influence of shared genes than shared environment on high density lipoprotein cholesterol. Adjustment for covariates tended to weaken the correlations, but the effect of variable family size was imperceptible. Although pairs involving pediatric offspring or siblings tended to show higher correlation than their adult counterparts, the differences were not significant. All correlations except father-daughter and brother-brother were homogeneous across clinics in whites. There was no asymmetry in parent-child correlations by the sex of the offspring, but the pooled mother-child correlation was significantly higher than father-child values, suggesting a possible maternal influence on high density lipoprotein cholesterol. No heterogeneity in correlations in high density lipoprotein cholesterol was detected between blacks and whites except for mother-son pairs.

Dental size traits within families: path analysis for first molar and lateral incisor.

Previous works on the inheritance of dental traits have traditionally followed Fisher's model for family data under the assumption that phenotypic similarity between relatives is due solely to genetic factors. This study uses recent causal models that incorporate the contribution of nonrandom environmental sources of variation to familial resemblance on dental size. Path analysis was applied to observed interclass and intraclass correlations of sex-specific parent-offspring and sib pairs in 293 Pima Indian families from the southwest United States. The mesiodistal dimension of an early-forming and stable tooth (first molar) was contrasted with a late-forming and variable tooth (upper lateral incisor) for genetic and familial environmental components of variation. Parameters were estimated according to the XTAU models of Rice et al. (1980) and linear constraints placed upon the parameters were tested. The proportion of variance accounted for by genetic and environmental transmissible factors is estimated to be 52% for the first molar and 35% for the lateral incisor. Neither X-linkage nor sex-specific environmental effects are required to explain the transmission of dental size. Nontransmissible environmental effects that account for sibling correlations are detectable. Furthermore, sex differences are found in correlated sibling environments for the lateral incisor but not the first molar, to explain in part male-female differences in the distributions of the upper lateral incisor size.

Extensions to multivariate normal models for pedigree analysis. II. Modeling the effect of shared environment in the analysis of variation in blood lead levels.

A multivariate normal model for pedigree analysis is applied to blood lead measurements from 617 individuals in 80 families in Melbourne, Australia, studied in 1977-1978. A new method is introduced for estimating time dependence of the family covariance matrix for blood lead levels; this time dependence can be interpreted as arising from the effects of common family environment on blood lead levels. Methods for the testing of assumptions and detection of outlying pedigrees and outlying individuals are applied. No correlation between blood lead levels of spouses was observed, but an effect of shared family environment was suggested by the difference between an estimated sibling correlation of about 0.5 for young sibling pairs living together and of about 0.1 for older siblings no longer living together. As there was no significant polygenic additive effect, the non-zero correlation between older siblings is more likely to be due to continuing effects of (environmental) factors shared in youth, rather than to a polygenic dominant effect. It is estimated that smoking 20 cigarettes per day is associated with an increase of about 12 per cent in blood lead level.

Familial correlations for serial measurements of recumbent length and stature.

Familial correlation coefficients were calculated for recumbent length or stature measured serially on participants in the Fels Longitudinal Growth Study and for short-term serial or cross-sectional measurements on relatives of participants. Pairs of relatives are compared at the same chronological ages from 1 to 18 years in 1-year increments and again in adulthood. First-degree relatives are more similar than second- or third-degree relatives at all ages. Sibling correlations are consistently higher than parent-offspring correlations, except after age 15, when they become very similar. For the most part, these results agree with those of cross-sectional studies finding higher sibling than parent-offspring correlations. Familial correlations tend to decrease during adolescence, perhaps due to differences among relatives in timing of growth spurts. Trends observed in bivariate plots of correlations over age are confirmed by multivariate analysis of correlations for different types of relatives at different ages. The largest amount of variation in familial correlations is due to the degree of relationship, although the amount of genetic similarity is difficult to separate from the effects of common family environment and generational differences. Age, sex and generation also play a role in multivariate prediction of the magnitude of familial correlations.

Maternal nutrition supplementation during pregnancy interferes with physical resemblance of siblings at birth according to infant sex

A randomized controlled double-blind study of nutrition supplementation of pregnant and lactating women was conducted in Suilin township, Taiwan. Pregnant mothers were randomly assigned to one of two treatment groups consisting of either a high (800 kcal and 40 g protein) calorie daily supplement or a placebo. For each mother treatment began following the delivery of her first study infant, continued throughout the lactation period; and through the pregnancy and lactation of her second study infant. Comparisons of sibling-sibling anthropometric correlations at birth between groups show that among the placebo group the sibling correlations are statistically significant and of the same magnitude seen in previous studies ( ∼ 0.5), while among high calorie siblings correlations are unusually low and often not significant. This is particularly true for male fetuses, suggesting that the latter are more sensitive to nutritional environmental variations in utero, than are female fetuses. Reduction in familial correlations, presumed measures of genetic influence, in nutritionally stressed populations, will occur when the environment of relatives differ, but are not due to malnutrition per se.

Family resemblances in personality.

Parent-offspring regressions, sibling correlations, and other measures of family resemblance in personality were computed for 54 personality traits, assessed by several psychometric personality tests as part of the Hawaii Family Study of Cognition. Considering all scales, the results suggest that a small familial/heritable component exists with regard to individual differences in personality, but did not demonstrate that some domains of personality are more familial or heritable than others.

Familial associations of lipids and lipoproteins in families of hypercholesterolemic probands.

We used the Princeton School Family Study hypercholesterolemic recall group to assess whether, and to what degree, the identification of hypercholesterolemic subjects could be improved through the phenomenon of familial lipid and lipoprotein aggregation. A second aim was to assess whether within-family lipid and lipoprotein correlations outlasted the period of shared family environment. Approximately twice as many (as expected) siblings and offspring of hypercholesterolemic probands had plasma total and low density lipoprotein cholesterol levels greater than the 90th and 75th percentiles respectively, emphasizing how identification of hypercholesterolemic subjects can be facilitated by use of the phenomenon of familial aggregation of plasma total and low density lipoprotein cholesterol. After exclusion of the hypercholesterolemic probands from calculations of within-family correlations, and use of natural log transformations for the probands' first-degree relatives' lipids as required, most father/pediatric offspring and mother/pediatric offspring correlations for lipids and lipoprotein cholesterols were significant, while most parent/adult offspring correlations were not significant. All pediatric sibling correlations for lipids and lipoprotein cholesterols were significant; most adult sibling correlations were not significant. The loss of significance and consistency in sibling and parent/offspring lipid and lipoprotein correlations in adults who no longer shared a common household environment points to environmental influences on total, high, and low density lipoprotein cholesterol in kindreds with a hypercholesterolemic proband.

Parent-offspring and sibling lipid and lipoprotein associations during and after sharing of household environments: The Princeton School District Family Study

The specific aim of this report was to determine whether, and to what degree, parent-offspring and sibling associations for lipids and lipoproteins outlast the period of shared household environment. Intrafamilial lipid-lipoprotein associations were assessed in two and three generation kindreds in the Cincinnati Lipid Research Clinic's Princeton School District Family Study. Intrafamilial lipid-lipoprotein associations were evaluated in parents and their pediatric (<20-yr-old) offspring, parents and their adult (≥20-yr-old) offspring, and in pediatric and adult siblings. The cohort included 177 randomly recalled probands (70 pediatric and 55 adult whites, 36 pediatric and 16 adult blacks) and their spouses and first-degree relatives. Altogether, 963 subjects were studied. For parents and their pediatric and adult offspring, total plasma cholesterol and low density lipoprotein cholesterol (C-LDL) were, for the most part, significantly correlated. There was no consistent pattern of higher correlations for parents and their pediatric offspring compared to parents and their adult offspring for any of the lipids and lipoprotein cholesterols except for high density lipoprotein cholesterol (C-HDL). Parents and their pediatric offspring had higher correlations for C-HDL than parents and their adult offspring. All pediatric and adult sibling correlations for lipids and lipoproteins were significant with the exception of C-HDL in adult siblings. There also was no consistent pattern of higher sibling lipid or lipoprotein correlations when pediatric siblings were compared to adult siblings, except for C-HDL correlations which were higher in pediatric siblings in both races. Whatever the relative contributions of genetics and environment to the association of lipid-lipoprotein values between parents and offspring and between siblings, the magnitude of the association (except for C-HDL) appears to outlast the period of the shared household environment.

Part II: Modernization effects on familial aggregation of Samoan blood pressure: A preliminary report

Abstract Familial correlations of blood pressure corrected for age, sex, and body weight are described in, and compared among, four Samoan samples which differ in exposure to modern life. An initial assessment of the genetic effects on blood pressure variation is performed in the most traditional sample. The juvenile sibling correlation of systolic pressure increases with modernization, whereas the adult sibling systolic correlation decreases with modernization. It is suggested that there is an increased interfamilial and decreased intrafamilial variation in environment as modernization increases. The preliminary estimate of the additive genetic effects, .25, is discussed in terms of the environmental variation in traditional life.

Sibling correlations and genetic estimates for selected blood variables in French Canadian children.

Selected blood variables were studied in 165 French Canadian boys and girls aged 6–15 years from the Center for Research on Human Growth at the University of Montreal. Venous blood samples were obtained between 1968 and 1971, and results closest to 10 years of age are retained for the present analysis. A maximum of 124 pairs of sibs were studied for hemoglobin concentration, hematocrit, total cholesterol, concentration of carotene, vitamin A and serum iron, iron-binding capacity, and saturation of transferrin. Sibling correlations ranged from essentially zero (0.06; hematocrit) to 0.51 (carotene) with the effect of age controlled. An estimate of the contribution of nonbiological factors to covariation between sibs was attempted through statistical control of the following seven indicators: education of father and of mother, occupation of father and of mother, total family income, size of household, and dollars spent on food per capita per week. This procedure lowered correlations by a substantial amount, particularly serum iron concentration, iron-binding capacity, and percentage saturation of transferrin (about 0.20 correlations units). Only cholesterol (0.30) and carotene (0.42) maintained a moderate positive coefficient. Broad heritability estimates computed after such statistical controls of nonbiological familial effects ranged from zero to 0.84. Total genetic effects for cholesterol, in this normolipemic population, reached a fairly high value of 0.60.

Sibling resemblance in mental ability: a review.

Empirical evidence on sibling resemblance in intelligence published since 1915 in the United States and Europe, including more than 27,000 sibling pairs, is reviewed. The results of these investigations are presented in tables showing the date, investigator, test, sample size, and correlations found for each specific study. Collectively, the results are highly consistent with the polygenic hypothesis and the conclusion that genetic factors are the major source of individual differences in intelligence. The most likely estimate of the sibling correlation for IQ in the population is +0.49.

Estimation of the correlation between relatives

Suppose, to take a simple example, we have a set of sibships. Each individual (sib) has a certain measured character x. We wish to estimate the interclass (or sib–sib) correlation for this character. Our model is as follows. In sibship s the observed values x are supposed drawn from a distribution with (true) mean ms and variance vs. The sibships are drawn from a population of sibships, so that the ms have a mean M and variance B, and the vs have mean A. (We also suppose that the number ns of sibs in sibship s is independent of ms and vs.) The interclass correlation is then easily seen to beρ = B/(A + B).The obvious way to proceed is to estimate A and B first, and then find ρ. Take a sample of k sibships. In sibship s the observed mean is and the deviance (sum of squares of deviations) δs. Let n = σ ns = the total number of individuals in the sample, and δ = σ δs = the total deviance within sibships. Proceed iteratively as follows:

Estimation of the correlation between relatives

Suppose, to take a simple example, we have a set of sibships. Each individual (sib) has a certain measured character x. We wish to estimate the interclass (or sib–sib) correlation for this character. Our model is as follows. In sibship s the observed values x are supposed drawn from a distribution with (true) mean m s and variance v s . The sibships are drawn from a population of sibships, so that the m s have a mean M and variance B, and the v s have mean A. (We also suppose that the number n s of sibs in sibship s is independent of m s and v s .) The interclass correlation is then easily seen to be ρ = B/(A + B). The obvious way to proceed is to estimate A and B first, and then find ρ. Take a sample of k sibships. In sibship s the observed mean is and the deviance (sum of squares of deviations) δ s . Let n = σ n s = the total number of individuals in the sample, and δ = σ δ s = the total deviance within sibships. Proceed iteratively as follows:

Transient environmental effects detected in sibling correlations.

Detection of environmental effects in sibling correlation is difficult. Mueller (1978) has proposed that transient environmental effects should be associated with a decrease in the sibling correlation with increasing age difference between members of a pair of adult sibs. The present report suggests that an environmental effect can also be detected by partialing out environmental indicators from correlations between sibs measured at the same chronological age. Correlations for 12 variables were computed between 208 pairs of 10-year-old French-Canadian sibs from Montreal. Partialing out seven socio-economic indicators from these correlations resulted in significant changes for three skeletal measurements as well as for body weight and triceps skinfold. These results differ from those reported earlier. The proposed method may be sufficiently sensitive to detect environmental effects, provided simple assumptions are met.

Heritability estimates of somatotype components based upon familial data.

Somatotype components were obtained in 239 French-Canadian families from Montreal. Endomorphy, mesomorphy and ectomorphy were anthropometrically assessed in the Health and Carter system. All three components were available in 208 pairs of siblings, while only ectomorphy was estimated in 507 parent-child pairs. Sibling correlations reached 0.40 for endomorphy, 0.30 for mesomorphy, and 0.38 for ectomorphy. Partialling out the effects of 7 socioeconomic indicators permitted an estimate of common familial environment upon covariation between relatives. Residual sibling correlations yielded broad heritability estimates (HB) of 0.50 for endomorphy, 0.42 for mesomorphy and 0.54 for ectomorphy. Narrow heritability (HN) for ectomorphy, controlling for familial indicators, was approximately 0.36 including a positive contribution from assortative mating.

Genetic and environmental influences on growth of Philadelphia Black and White schoolchildren.

Sibling correlations in body size and composition are considered in 114 pairs of American Black and 101 pairs of White sibs, ranging in age from 6 to 12 years. Correlations were similar in the two races. Sibling resemblance was more or less similar for skeletal measurements (0.35-0.48), limb circumferences (0.41-0.43), and skinfolds (0.31-0.41). Age difference between members of a pair was found to affect the sibling correlations, especially for measurements of low genetic control. This is taken as evidence for environmental contributions to sibling resemblance. Higher sister-sister similarities in fat (as compared to brother-brother) were evident in Blacks (as they were in a rural South American sample) but not in Whites. This pattern could arise from similar sex-role differentiation in these two cultures (Afro and Latin American) or similar expression of sex-limited genes under less favourable environmental conditions.

Familial resemblance for specific cognitive abilities

Measures of familial resemblance (spouse correlations, regressions of offspring on midparent, single-parent/single-child correlations, and sibling correlations) are presented for members of the two largest ethnic groups tested in the Hawaii Family Study of Cognition. Median spouse correlations (corrected for differences in test reliability) for 15 individual tests of specific cognitive abilities are 0.15 and 0.12 for Americans of European and of Japanese ancestry, respectively. With regard to the regressions of offspring on midparent value, corresponding median values are 0.50 and 0.35. Results of hierarchical multiple regression analyses, as well as the ordering of single-parent/single-child and sibling correlations, provide no evidence to support the hypothesis that spatial ability is influenced by a sex-linked, recessive gene.

The Influence of "Family Background" on Intellectual Attainment

Family background frequently has been found to have long-term effects on adult intellectual, occupational, and economic outcomes. Since families differ both genetically and environmentally, it has been difficult to interpret family effects in studies of individuals or biological relatives. This study includes samples of adoptive and biologically-related families with children between 16 and 22 years of age. We regressed child IQ on several family demographic variables, on parental IQ, and on natural parent characteristics (for the adopted children) to estimate the degree of genetic bias in the coefficients on measured family background. The results indicate that there is little effect of those family environmental differences studied on IQ differences among the adolescents in the SES range of working to upper middle class. Parent-child and sibling correlations further indicate that genetic differences among families account for the major part of the long-term effects of 'family background on IQ.

A Reply to Fahey, Kamitomo, and Cornell

Fahey, Kamitomo, and Cornell (1978) dispute our conclusion that genetic factors are more important than environmental events for the development of individual differences in language skills. They argue that our data are confounded by ceiling effects due to the slightly older average age of our DZ twins and siblings, by invalidity of our language measures, and by the use of a DZ twin correlation rather than a sibling correlation in our formula to estimate the heritability of language ability. We will show their criticisms are contradicted