ArticleNature communications2026
Distinct genetic profiles influence body mass index between infancy and adolescence.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Early-life body mass index and adult fat distribution: a life-course Mendelian randomisation study.BMJ open · 2026Article
- Late Preschool BMI Acceleration as the Strongest Predictor of Childhood Cardiometabolic Risk at School Entry: A Dual-Trajectory Cohort Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Body mass index (BMI) changes throughout life with age-varying genetic contributions. We use a random regression model to investigate the genetic contribution to BMI trajectories from ages one to 18 years in 6,291 ALSPAC participants with 65,930 repeated BMI measurements. Here we show the estimated SNP-based heritability of BMI at 9.5 years is 28.4% (SE = 4.8%), and 23.8% (SE = 4.2%) for rate of change in BMI from one to 18 years. The genetic correlations between early childhood and adolescence are low (genetic correlation between two and 17 years is 0.108 [SE = 0.146]). We find that the first principal component of the trajectory, explaining 89% of genetic variation, captures effects which increase in magnitude from early childhood to adolescence and then plateau. A second axis explaining 9% of the genetic variance has opposite effects on BMI between early and later ages. Our findings demonstrate the value of RRMs to reveal age-specific genetic influences on BMI across development.
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