TY - JOUR
T1 - Evidence for independent genetic influences on fat mass and body mass index in a pediatric twin sample
AU - Faith, Myles S.
AU - Pietrobelli, Angelo
AU - Nuñez, Christopher
AU - Heo, Moonseong
AU - Heymsfield, Steven B.
AU - Allison, David B.
N1 - Copyright:
Copyright 2015 Elsevier B.V., All rights reserved.
PY - 1999/7
Y1 - 1999/7
N2 - Objective. Insight into genetic and environmental influences on fat mass, independent of body mass index (BMI; kg/m2), is expected to enhance methods for treating pediatric obesity. However, few studies have estimated the heritability of fat mass in pediatric samples, and those conducted have relied primarily on BMI measurements. Present Study. Using bioimpedance analysis, the present study tested a series of hypotheses predicting significant genetic and environmental influences on percent body fat (PBF) above and beyond BMI. Subjects were 66 pairs of twins, including 41 monozygotic and 25 dizygotic pairs, from 3 to 17 years of age. Structural equation modeling tested hypotheses, adjusting for demographic variables. Results. Analyses indicated significant genetic influences on PBF, with genes estimated to account for 75% to 80% of the phenotypic variation. The remaining variation was attributable to nonshared environmental influences. Multivariate analyses revealed sizable genetic correlations and environmental correlations between BMI and PBF (r(g) = .74 and r(e) = .67, respectively), suggesting that some genes and environmental experiences influence both phenotypes. However, analyses confirmed genetic and environmental influences on PBF above and beyond BMI. For example, 62.5% of the total genetic variation in PBF was attributable to genes that influenced PBF but not BMI. Conclusion. There seems to be a substantial genetic contribution to fat mass distinct from BMI in a sample of children and adolescents. Studies testing putative genetic or environmental determinants of pediatric obesity might be strengthened further by including research-based body composition methods.
AB - Objective. Insight into genetic and environmental influences on fat mass, independent of body mass index (BMI; kg/m2), is expected to enhance methods for treating pediatric obesity. However, few studies have estimated the heritability of fat mass in pediatric samples, and those conducted have relied primarily on BMI measurements. Present Study. Using bioimpedance analysis, the present study tested a series of hypotheses predicting significant genetic and environmental influences on percent body fat (PBF) above and beyond BMI. Subjects were 66 pairs of twins, including 41 monozygotic and 25 dizygotic pairs, from 3 to 17 years of age. Structural equation modeling tested hypotheses, adjusting for demographic variables. Results. Analyses indicated significant genetic influences on PBF, with genes estimated to account for 75% to 80% of the phenotypic variation. The remaining variation was attributable to nonshared environmental influences. Multivariate analyses revealed sizable genetic correlations and environmental correlations between BMI and PBF (r(g) = .74 and r(e) = .67, respectively), suggesting that some genes and environmental experiences influence both phenotypes. However, analyses confirmed genetic and environmental influences on PBF above and beyond BMI. For example, 62.5% of the total genetic variation in PBF was attributable to genes that influenced PBF but not BMI. Conclusion. There seems to be a substantial genetic contribution to fat mass distinct from BMI in a sample of children and adolescents. Studies testing putative genetic or environmental determinants of pediatric obesity might be strengthened further by including research-based body composition methods.
KW - Bioimpedance analysis
KW - Body composition
KW - Body mass index
KW - Heritability
KW - Non-shared environment
KW - Pediatric obesity
KW - Twin design
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U2 - 10.1542/peds.104.1.61
DO - 10.1542/peds.104.1.61
M3 - Article
C2 - 10390261
AN - SCOPUS:0033015156
VL - 104
SP - 61
EP - 67
JO - Pediatrics
JF - Pediatrics
SN - 0031-4005
IS - 1 I
ER -