Nutrition and Fetal Origins of Diseases in Adults

Abstract

Accumulating evidence suggests that the early-life environment has lasting effects on health and disease into adulthood. The current concept of developmental origins of adulthood disease has expanded beyond the original observation by Barker and colleagues correlating low birth weight with adulthood cardiovascular and metabolic disorders. Notably, the fetal-neonatal nutritional environment has a significant role in influencing an individual’s wellness in adulthood. During critical periods of fetal and neonatal development, tissues and organ systems are most vulnerable to nutrient deficiencies. Through fetal programming mechanisms such as epigenetic modification, a biochemical process that regulates gene expression without altering the genetic code, developing tissues adapt to nutrient-poor environments to preserve normal development of critical organ systems, including the brain. However, these programmed adaptations can have negative long-term health consequences if the postnatal environment does not match the fetal-neonatal environment in which the programming occurred. These long-term adverse health outcomes constitute the true cost to society, in both increased medical costs and the indirect cost of lost productivity. Here we review the effects of nutrient deficiencies on fetal programming and subsequent health outcomes, as well as the potential mechanisms that underlie fetal programming. This review contains 3 Figures, 2 Tables and 115 references Key words: critical period, epigenetics, fetal programming, iron, long-chain polyunsaturated fatty acids, neurodevelopment, nutrient deficiency, protein-energy, vitamins, zinc