Increasing obesity is a world-wide health concern. Its most commonly used indicator, body mass index (BMI), consistently shows considerable genetic and shared environmental variance throughout life, the latter particularly in youth. Several adult studies have observed less total and genetically influenced variance with higher attained SES. These studies offer clues about sources of the ‘obesity epidemic’ but analogous youth studies of SES-of-origin are needed. Genetic and environmental influences and moderating effects of SES may vary in countries with different health policies, lifestyles, and degrees/sources of social inequality, offering further clues to the sources of the obesity epidemic. We examined SES-of-origin moderation of BMI variance in the German TwinLife study's cohorts assessed around ages 5, 11, 17, and 23-24, and in the Minnesota Twin Family Study's (MTFS) 11- and 17-year-old birth cohorts assessed longitudinally around ages 11, 17, and 23-24, comparing male and female twins and their parents. Age for age, both sexes’ means and variances were greater in MTFS than in TwinLife. We observed that SES generally moderated genetic influences, more strongly in females, similar to most adult studies of attained-SES moderation of BMI. We interpreted differences in our SES-of-origin observations in light of inevitably-missing covariance between SES-of-origin and BMI in the models, mother-father and parent-offspring BMI correlations, and parental attained-SES-BMI correlations. We suggest that one source of the present obesity epidemic is social change that amplifies expression of genes both constraining SES attainment and facilitating weight gain.
- national differences