AbstractPurpose of review
Postprandial lipemia (PPL), the prolonged increase in plasma triglyceride-rich lipoproteins following food consumption, is an independent risk factor for cardiovascular disease. Genetic variation, environment and the interplay between these direct an individual's postprandial lipid response. From such interplay, inducible and reversible epigenetic changes arise. Increasing evidence suggests epigenetic variation contributes to postprandial response in lipids and risk.Recent findings
Diet and exercise are central agents affecting postprandial lipemia - triglyceride, but heterogeneity of the findings warrant more and larger studies. Several epigenetic loci identified from a human intervention study account for a substantial proportion of PPL phenotype variation, but the burden to conduct an intervention study of postprandial responses likely limits translation to personalized nutrition.Summary
The impact of both DNA methylation patterns and environmental factors such as diet, exercise, sleep and medication on PPL is multifaceted. Discovery of interactions that modify the association between CpG (oligodeoxydinucleotide) methylation and postprandial phenotypes is unfolding.