OBJECTIVES: To investigate the contributions of genetic and environmental factors to the development of relative weight during the growth period. DESIGN: Longitudinal twin study. SUBJECTS: Two-hundred and thirty-one monozygotic and 144 dizygotic complete male twin pairs born between 1973 and 1979 were measured annually from birth to 18 years of age. RESULTS: Body mass index (BMI, kg/m(2)) at age 18 correlated with BMI at age 1 (r=0.32, 95% confidence intervals (CI) 0.21-0.42), and this correlation increased steadily up to age 17 (r=0.91, 95% CI 0.89-0.93). Major part (81-95%) of these trait correlations was attributable to correlate additive genetic factors, but also unique environmental correlations were present during the whole-growth period. The correlation between ponderal index (kg/m(3)) at birth and BMI at age 18 was small (r=0.09, 95% CI 0.02-0.15) and totally because of correlated unique environmental factors. CONCLUSIONS: Our results suggest persistent genetic regulation of BMI from age 1 to 18. However, environmental factors, not shared by siblings, also affected the correlations of BMI. A small specific environmental correlation was found between ponderal index at birth and BMI at age 18, which may reflect the effect of neonatal environmental factors on adult BMI. A challenge to the future research is to identify chromosome regions and specific genes regulating the development of BMI as well as environmental factors affecting BMI through the growth period independently or interacting with genetic factors.
OBJECTIVES: To investigate the contributions of genetic and environmental factors to the development of relative weight during the growth period. DESIGN: Longitudinal twin study. SUBJECTS: Two-hundred and thirty-one monozygotic and 144 dizygotic complete male twin pairs born between 1973 and 1979 were measured annually from birth to 18 years of age. RESULTS: Body mass index (BMI, kg/m(2)) at age 18 correlated with BMI at age 1 (r=0.32, 95% confidence intervals (CI) 0.21-0.42), and this correlation increased steadily up to age 17 (r=0.91, 95% CI 0.89-0.93). Major part (81-95%) of these trait correlations was attributable to correlate additive genetic factors, but also unique environmental correlations were present during the whole-growth period. The correlation between ponderal index (kg/m(3)) at birth and BMI at age 18 was small (r=0.09, 95% CI 0.02-0.15) and totally because of correlated unique environmental factors. CONCLUSIONS: Our results suggest persistent genetic regulation of BMI from age 1 to 18. However, environmental factors, not shared by siblings, also affected the correlations of BMI. A small specific environmental correlation was found between ponderal index at birth and BMI at age 18, which may reflect the effect of neonatal environmental factors on adult BMI. A challenge to the future research is to identify chromosome regions and specific genes regulating the development of BMI as well as environmental factors affecting BMI through the growth period independently or interacting with genetic factors.
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