In my recent review on vitamin D and allergy I introduced the rather new concept of epigenetic priming of the offspring’s vitamin D system. I could find only a limited number of studies supporting this view. Fortunately, there is a new study published today that gives me some support. Using a twin design the authors (AJCN. First published ahead of print May 30, 2012 as doi: 10.3945/ajcn.112.035683) find
Our results suggest that maternal circulating 25(OH)D is the most significant regulator of neonatal circulating 25(OH)D concentrations, with underlying genetic factors playing a limited role.
It is certainly hard to understand how early life events are leading to later disease. Here is an incredible nutrigenomics story done in agouti mice:
We find that the somatic epigenetic state of Avy is affected by in utero methyl donor supplementation only when the allele is paternally contributed. Exposure to methyl donor supplementation during midgestation shifts Avy phenotypes not only in the mice exposed as fetuses, but in their offspring. This finding indicates that methyl donors can change the epigenetic state of the Avy allele in the germ line, and that the altered state is retained through the epigenetic resetting that takes place in gametogenesis and embryogenesis. Thus a mother’s diet may have an enduring influence on succeeding generations.