title: Familial resemblance for body composition measures: the HERITAGE Family Study.
abstract: A sex-specific familial correlation model was used to assess the heritable contributions to several measures of body composition in 86 sedentary white families participating in the HERITAGE Family Study. For this study, sedentary families were recruited, tested for a battery of measures, endurance exercise trained for 20 weeks, and remeasured. This sample is unique in that activity level was controlled for in these families at baseline measurement. In this report, three body composition variables measured at baseline were analyzed, two indexing adiposity (total subcutaneous fat based on eight skinfold measurements [SF8] and percent body fat measured by underwater weighing techniques [%BF]) and one assessing fat free mass ([FFM] derived from underwater weighing). The maximal heritabilities for SF8 (34%) and %BF (62%) were consistent with those reported in previous studies. There were no sex nor generation differences in the familial correlations, and the spouse correlation was significant, consistent with the hypothesis that the familial aggregation reflects genetic and familial environmental factors. However, the results for FFM were very different. The most parsimonious pattern of familial resemblance was consistent with mitochondrial inheritance (i.e., mother-offspring and sibling correlations were equal and were larger than those for spouse and father-offspring pairs). Under the mitochondrial hypothesis, 39% of the variance was accounted for by familial/genetic effects. However, under a nonmitochondrial hypothesis, which could not be ruled out, 65% of the FFM phenotypic variance was accounted for by familial/genetic factors. This high heritability level, as compared with results from previous studies, is consistent with the hypothesis that activity may constitute an important environmental determinant of FFM. These alternative hypotheses for FFM warrant further investigation using complex multilocus-multitrait segregation models, which allow for major genetic, polygenic, and environmental sources of variance, as well as interactions among them.
authors.affiliation: Division of Biostatistics, Washington University Medical School, St. Louis, MO 63110, USA.
authors.forename: T
authors.initials: T
authors.lastname: Rice
authors.forename: E W
authors.initials: EW
authors.lastname: Daw
authors.forename: J
authors.initials: J
authors.lastname: Gagnon
authors.forename: C
authors.initials: C
authors.lastname: Bouchard
authors.forename: A S
authors.initials: AS
authors.lastname: Leon
authors.forename: J S
authors.initials: JS
authors.lastname: Skinner
authors.forename: J H
authors.initials: JH
authors.lastname: Wilmore
authors.forename: D C
authors.initials: DC
authors.lastname: Rao
mesh_terms: D000273:Adipose Tissue; D000293:Adolescent; D000328:Adult; D000368:Aged; D001823:Body Composition / Q000235:genetics*; D004272:DNA, Mitochondrial; D005260:Female; D014644:Genetic Variation; D006801:Humans; D008019:Life Style; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012885:Skinfold Thickness
chemical_list: D004272:DNA, Mitochondrial