The Barker hypothesis: implications for future directions in toxicology research

Purpose of reviewThis review covers the past year's papers germane to the Barker hypothesis. While much of the literature has centered on maternal and developmental nutrition, new findings have emerged on the ability of toxic exposures during development to impact fetal/developmental programming. Recent findingsMost papers lend strong support to the idea that the intrauterine and early postnatal periods are sensitive to endogenous and exogenous influences on metabolic programming. These studies rely on birth weight or other size metrics as a surrogate for nutrition during development. Not only low-protein but also high-fat or high-carbohydrate diets are linked to adverse metabolic profiles in animal studies. Nutritional intervention studies in animals show that antioxidant or essential fatty acid supplements may combat development of the metabolic syndrome. Developmental exposures to the endocrine disrupting chemical vinclozolin cause male germ cell abnormalities in offspring that are transmitted to subsequent generations through an epigenetic mechanism. SummaryThese studies solidify the scientific basis of the Barker hypothesis and extend its tenets to developmental toxicology. Long-term, latent effects of developmental toxicant exposure have rarely been considered to date, and work is needed to understand how such effects may occur.