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An adequate intake of vitamin B 12  during pregnancy plays an important role in offspring neurodevelopment, potentially via epigenetic processes. We used a two-step Mendelian randomization approach to assess whether DNA methylation plays a mediating and causal role in associations between maternal vitamin B 12  status and offspring’s cognition. Firstly, we estimated the causal effect of maternal vitamin B 12  levels on cord blood DNA methylation using the maternal  FUT2  genotypes rs492602:A &gt; G and rs1047781:A &gt; T as proxies for circulating vitamin B 12  levels in the Avon Longitudinal Study of Parents and Children (ALSPAC) and we tested the observed associations in a replication cohort. Secondly, we estimated the causal effect of DNA methylation on IQ using the offspring genotype at sites close to the methylated CpG site as a proxy for DNA methylation in ALSPAC and in a replication sample. The first step Mendelian randomization estimated that maternal vitamin B 12  had a small causal effect on DNA methylation in offspring at three CpG sites, which was replicated for one of the sites. The second step Mendelian randomization found weak evidence of a causal effect of DNA methylation at two of these sites on childhood performance IQ which was replicated for one of the sites. The findings support a causal effect of maternal vitamin B 12  levels on cord blood DNA methylation, and a causal effect of vitamin B 12 -responsive DNA methylation changes on children’s cognition. Some limitations were identified and future studies using a similar approach should aim to overcome such issues.

human molecular genetics

Exploring a causal role of DNA methylation in the relationship between maternal vitamin B 12  during pregnancy and child’s IQ at age 8, cognitive performance and educational attainment: a two-step Mendelian randomization study