Genetic and Environmental Contributions to Childhood Growth in Stature and Lifetime Overweight Risk.

Abstract

P09 The prevalence of childhood overweight and obesity in the US continues to increase. Epidemiological studies have shown that children who mature earlier tend to have an increased risk of being overweight in adulthood. Acknowledging that measures of overweight and patterns of human growth are under moderate to strong genetic control, we examined the nature of these associations using a bivariate variance components approach to estimate the genetic and environmental correlations between lifetime overweight status and parameters of the adolescent growth spurt. Serial stature data from 490 participants in the Fels Longitudinal Study were used to derive three adolescent growth curve parameters: peak height velocity (PHV), age at PHV, and height at PHV. Three categories of lifetime overweight status were determined from over 16,000 serial observations according to age at onset of overweight: early-onset overweight (BMI >25 kg/m 2 before age 25 y), late-onset overweight (BMI >25 kg/m 2 after age 25 y), and never overweight (never having a BMI measurement >25 kg/m 2 ). Those classified as overweight also needed to meet certain criteria (i.e., maintenance of BMI >25 kg/m 2 in 80% of all subsequent visits following the first presentation). Heritability estimates (h 2 ) for the adolescent growth parameters are h 2 =0.54 for PHV, h 2 =0.74 for age at PHV, and h 2 =0.92 for height at PHV. Heritability estimates for lifetime overweight status range from 0.52-0.57 depending upon the age at onset categorization. Although all of the traits examined are highly heritable, preliminary analyses reveal little effect of shared genes between the adolescent growth curve parameters and the lifetime overweight status categories; the genetic correlations are low and insignificant. There is, however, a statistically significant negative environmental correlation (ρ e =-0.40) between age at PHV and the lifetime overweight status category contrasting never overweight with early/late overweight. These results suggest that environmental influences on the timing of the adolescent growth spurt may be more influential in predicting adult risk of overweight than shared genetic factors.