SCOPE: Dietary fat correlates with bone mineral density (BMD). We tested the association between fat intake and BMD, and tested if fat intake modified the degree of genetic influence on BMD and bone speed of sound (SOS). METHODS AND RESULTS: We included 622 twins aged 7-15 from South China. Data on anthropometry, dietary intake, BMD, and SOS were collected. Quantitative genetic analyses of structural equation models were fit using the Mx statistical package. The within-pair intraclass correlations for BMD in dizygotic twins were nearly half of that for monozygotic twins (intraclass correlations = 0.39 versus 0.70). The heritability of BMD and SOS were 71 and 79%. Phenotypic correlation between fat intake and SOS was significant (r = -0.19, p = 0.04). SOS was negatively correlated with fat intake in boys (r = -0.11, p = 0.05), but not in girls. Full Cholesky decomposition models showed SOS has a strong genetic correlation with fat intake (rA = -0.88, 95% confidence interval = -0.94, 0.01); the environmental correlation between fat intake and SOS was weak (rE = -0.04, 95% confidence interval = -0.20, 0.13). Fat intake modified the additive genetic effects on BMD. CONCLUSION: Genetic factors explained 71 and 79% of individual variance in BMD and SOS, respectively. Low fat intake counteracts genetic predisposition to low BMD.
SCOPE: Dietary fat correlates with bone mineral density (BMD). We tested the association between fat intake and BMD, and tested if fat intake modified the degree of genetic influence on BMD and bone speed of sound (SOS). METHODS AND RESULTS: We included 622 twins aged 7-15 from South China. Data on anthropometry, dietary intake, BMD, and SOS were collected. Quantitative genetic analyses of structural equation models were fit using the Mx statistical package. The within-pair intraclass correlations for BMD in dizygotic twins were nearly half of that for monozygotic twins (intraclass correlations = 0.39 versus 0.70). The heritability of BMD and SOS were 71 and 79%. Phenotypic correlation between fat intake and SOS was significant (r = -0.19, p = 0.04). SOS was negatively correlated with fat intake in boys (r = -0.11, p = 0.05), but not in girls. Full Cholesky decomposition models showed SOS has a strong genetic correlation with fat intake (rA = -0.88, 95% confidence interval = -0.94, 0.01); the environmental correlation between fat intake and SOS was weak (rE = -0.04, 95% confidence interval = -0.20, 0.13). Fat intake modified the additive genetic effects on BMD. CONCLUSION: Genetic factors explained 71 and 79% of individual variance in BMD and SOS, respectively. Low fat intake counteracts genetic predisposition to low BMD.
Authors: E W Gregg; A M Kriska; L M Salamone; R L Wolf; M M Roberts; R E Ferrell; S J Anderson; L H Kuller; J A Cauley Journal: Osteoporos Int Date: 1999 Impact factor: 4.507
Authors: R M Hoffman; L A Lawrence; D S Kronfeld; W L Cooper; D J Sklan; J J Dascanio; P A Harris Journal: J Anim Sci Date: 1999-12 Impact factor: 3.159
Authors: I Kato; P Toniolo; A Zeleniuch-Jacquotte; R E Shore; K L Koenig; A Akhmedkhanov; E Riboli Journal: Int J Epidemiol Date: 2000-02 Impact factor: 7.196