Mohammed El Sharkawy, Janine F Felix, Veit Grote, Trudy Voortman, Vincent W V Jaddoe, Berthold Koletzko, Leanne K Küpers
Journal: Epigenetics 2024;19(1):2299045
PMID: 38198623
Diet in early life plays an important role for future health through epigenetic mechanisms which may be mediated by DNA methylation. Compared to plant protein, higher intake of animal protein in early life has been associated with a higher risk of childhood obesity. The aim of this meta-analysis was to evaluate whether DNA methylation may mediate this risk. 2 studies were included in this epigenome-wide association study meta-analysis, including 1183 infants for the animal protein analysis and 1181 for plant protein. Most infants were not breastfed. Protein intakes (as percent of total energy intake) were measured at age 12-14 months, using food diaries in one and food frequency questionnaires in the other study. DNA methylation was measured in early and late childhood, 2-6 years and 7-12 years, respectively. Potential confounding factors were adjusted for, including total energy intake, age and sex, as well as maternal factors. Animal protein intake was associated with DNA methylation in 2 sites in late but not early childhood, whilst plant protein intake was associated with DNA methylation at 2 different sites in early but not late childhood. The results differed between girls and boys. One of the methylation sites associated with animal protein intake is thought to be involved in glucose tolerance, lipid storage and obesity-induced insulin resistance. The authors concluded that further research into the epigenetic pathways linking protein intake and health outcomes is required.
BACKGROUND
Higher early-life animal protein intake is associated with a higher childhood obesity risk compared to plant protein intake. Differential DNA methylation may represent an underlying mechanism.
METHODS
We analysed associations of infant animal and plant protein intakes with DNA methylation in early (2-6 years, = 579) and late (7̄-12 years, = 604) childhood in two studies. Study-specific robust linear regression models adjusted for relevant confounders were run, and then meta-analysed using a fixed-effects model. We also performed sex-stratified meta-analyses. Follow-up analyses included pathway analysis and eQTM look-up.
RESULTS
Infant animal protein intake was not associated with DNA methylation in early childhood, but was associated with late-childhood DNA methylation at cg21300373 ( = 4.27 × 10¯, ) and cg10633363 ( = 1.09 × 10¯, ) after FDR correction. Infant plant protein intake was associated with early-childhood DNA methylation at cg25973293 ( = 2.26 × 10, ) and cg15407373 ( = 2.13 × 10, ) after FDR correction. There was no overlap between the findings from the animal and plant protein analyses. We did not find enriched functional pathways at either time point using CpGs associated with animal and plant protein. These CpGs were not previously associated with childhood gene expression. Sex-stratified meta-analyses showed sex-specific DNA methylation associations for both animal and plant protein intake.
CONCLUSION
Infant animal protein intake was associated with DNA methylation at two CpGs in late childhood. Infant plant protein intake was associated with DNA methylation in early childhood at two CpGs. A potential mediating role of DNA methylation at these CpGs between infant protein intake and health outcomes requires further investigation.
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