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Which infancy growth parameters are associated with later adiposity? The Cambridge Baby Growth Study.

ABSTRACT: Background: Highly consistent positive associations are reported between infancy growth and later obesity risk. However, it is unclear whether infancy growth parameters beyond body weight add to the prediction of later obesity risk.Aim: To assess whether infancy length and skinfold thicknesses add to infancy weight in the prediction of childhood adiposity.Subjects and methods: This analysis included 254 children with available data on infant growth from birth to 24 months and childhood adiposity at age 6-11 years measured by DXA. Multilevel linear regression was used to examine the predictors of childhood percent body fat (%BF), with adjustment for sex and age at follow-up visit.Results: Birth weight and weight gain (modelled as changes in z-score) between 0-3 months and 3-24 months showed independent positive relationships with childhood %BF. The addition of gains in infant length and skinfolds between 0-3 months, but not 3-24 months, improved overall model prediction, from 18.7% to 20.7% of the variance in childhood %BF (likelihood ratio test, p < 0.0001), although their independent effect estimates were small (infant length gain: negative trend, partial R-square 0.6%, p = 0.2; skinfolds: positive trend, 1.3%, p = 0.09).Conclusion: Infancy length and skinfolds contribute significantly, but only modestly, to the prediction of childhood adiposity.

SUBMITTER: Ong KK

PROVIDER: S-EPMC7261401 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:OBJECTIVE:Fixed genomic variation explains only a small proportion of the risk of adiposity. In animal models, maternal diet alters offspring body composition, accompanied by epigenetic changes in metabolic control genes. Little is known about whether such processes operate in humans. RESEARCH DESIGN AND METHODS:Using Sequenom MassARRAY we measured the methylation status of 68 CpGs 5' from five candidate genes in umbilical cord tissue DNA from healthy neonates. Methylation varied greatly at particular CpGs: for 31 CpGs with median methylation ?5% and a 5-95% range ?10%, we related methylation status to maternal pregnancy diet and to child's adiposity at age 9 years. Replication was sought in a second independent cohort. RESULTS:In cohort 1, retinoid X receptor-? (RXRA) chr9:136355885+ and endothelial nitric oxide synthase (eNOS) chr7:150315553+ methylation had independent associations with sex-adjusted childhood fat mass (exponentiated regression coefficient [?] 17% per SD change in methylation [95% CI 4-31], P = 0.009, n = 64, and ? = 20% [9-32], P < 0.001, n = 66, respectively) and %fat mass (? = 10% [1-19], P = 0.023, n = 64 and ? =12% [4-20], P = 0.002, n = 66, respectively). Regression analyses including sex and neonatal epigenetic marks explained >25% of the variance in childhood adiposity. Higher methylation of RXRA chr9:136355885+, but not of eNOS chr7:150315553+, was associated with lower maternal carbohydrate intake in early pregnancy, previously linked with higher neonatal adiposity in this population. In cohort 2, cord eNOS chr7:150315553+ methylation showed no association with adiposity, but RXRA chr9:136355885+ methylation showed similar associations with fat mass and %fat mass (? = 6% [2-10] and ? = 4% [1-7], respectively, both P = 0.002, n = 239). CONCLUSIONS:Our findings suggest a substantial component of metabolic disease risk has a prenatal developmental basis. Perinatal epigenetic analysis may have utility in identifying individual vulnerability to later obesity and metabolic disease.

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Which infancy growth parameters are associated with later adiposity? The Cambridge Baby Growth Study.

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