OBJECTIVE: Obesity has some genetic basis but requires interaction with environmental factors for phenotypic expression. We examined contributions of gender-specific parental adiposity and smoking to adiposity and related @entity65 in adult offspring. DESIGN: Cross-sectional general population survey. SETTING: Scotland. @entity1 : 1456 of the 1477 first generation families in the Midspan Family Study: 2912 parents (aged 45-64   years surveyed between 1972 and 1976) who had 1025 sons and 1283 daughters, aged 30-59   years surveyed in 1996. MAIN MEASURES: Offspring body mass index (BMI), waist circumference (WC), cardiometabolic risk (lipids, blood pressure and @entity413 ) and @entity65 as outcome measures, and parental BMI and smoking as determinants. All analyses adjusted for age, socioeconomic status and family clustering and offspring birth weight. RESULTS: Regression coefficients for BMI associations between father-son (0.30) and mother-daughter (0.33) were greater than father-daughter (0.23) or mother-son (0.22). Regression coefficient for the non-genetic, shared-environment or assortative-mating relationship between BMIs of fathers and mothers was 0.19. Heritability estimates for BMI were greatest among @entity1 with mothers who had BMI either <25 or >= 30   kg/m(2). Compared with offspring without @entity28 parents, offspring with two @entity28 parents had adjusted OR of 10.25 (95% CI 6.56 to 13.93) for having WC >= 102   cm for @entity1 , >= 88   cm @entity1 , 2.46 (95% CI 1.33 to 4.57) for @entity209 and 3.03 (95% CI 1.55 to 5.91) for @entity951 and/or @entity583 (p<0.001). Neither parental adiposity nor smoking history determined adjusted offspring individual cardiometabolic risk factors, @entity6 or @entity64 . Maternal, but not paternal, smoking had significant effects on WC in sons (OR=1.50; 95% CI 1.13 to 2.01) and daughters (OR=1.42; 95% CI 1.10 to 1.84) and @entity209 OR=1.68; 95% CI 1.17 to 2.40) in sons. CONCLUSIONS: There are modest genetic/epigenetic influences on the environmental factors behind adverse adiposity. Maternal smoking appears a specific hazard on @entity28 and @entity209 . A possible epigenetic mechanism linking maternal smoking to @entity28 and @entity209 in offspring is proposed. Individuals with family histories of @entity28 should be targeted from an early age to prevent @entity28 and complications.

Contributions of maternal and paternal adiposity and smoking to adult offspring adiposity and XXXX : the Midspan Family Study.

@entity1 :: ('9606', 'Species') :: ['women', 'PARTICIPANTS', 'men'] @entity64 :: ('MESH:D020521', 'Disease') :: ['stroke'] @entity28 :: ('MESH:D009765', 'Disease') :: ['obesity', 'obese'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetes'] @entity951 :: ('MESH:D000787', 'Disease') :: ['angina'] @entity65 :: ('MESH:D002318', 'Disease') :: ['cardiovascular disease', 'cardiovascular risk'] @entity209 :: ('MESH:D008659', 'Disease') :: ['metabolic syndrome'] @entity583 :: ('MESH:D009203', 'Disease') :: ['myocardial infarct'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity65 :: (MESH:D002318,Disease) :: ['cardiovascular risk']
