Abstract
Familial loading for alcohol dependence (AD) and variation in genes reported to be associated with AD or BMI were tested in a longitudinal study. Growth curve analyses of BMI data collected at approximately yearly intervals and obesity status (BMI > 30) were examined. High-risk males were found to have higher BMI than low-risk males, beginning at age 15 years (2.0 kg/m(2) difference; p = 0.046), persisting through age 19 years (3.3 kg/m(2) difference; p = 0.005). CHRM2 genotypic variance predicted longitudinal BMI and obesity status. Interactions with risk status and sex were also observed for DRD2 and FTO gene variation. Variation at loci implicated in addiction may be influential in determining susceptibility to increased BMI in childhood and adolescence.
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