AIM: Familial loading for alcohol dependence (AD) and variation in genes reported to be associated with AD or BMI were tested in a longitudinal study. MATERIALS & METHODS: Growth curve analyses of BMI data collected at approximately yearly intervals and obesity status (BMI > 30) were examined. RESULTS: 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. CONCLUSION: Variation at loci implicated in addiction may be influential in determining susceptibility to increased BMI in childhood and adolescence.
AIM: Familial loading for alcohol dependence (AD) and variation in genes reported to be associated with AD or BMI were tested in a longitudinal study. MATERIALS & METHODS: Growth curve analyses of BMI data collected at approximately yearly intervals and obesity status (BMI > 30) were examined. RESULTS: 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. CONCLUSION: Variation at loci implicated in addiction may be influential in determining susceptibility to increased BMI in childhood and adolescence.
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