Upshot of Epigenetics and Famine on Metabolic Syndrome

Abstract

Chronic diseases are stimulated in the womb through adaptations acquired by the fetus in response to malnutrition. Maternal malnutrition during early pregnancy, in relation to low birth weight as well as uterine growth restriction, may adversely influence offspring metabolism and health. Parental nutritional imbalance, either through global nutritional manipulation or deficiencies in specific nutrients, predisposes the offspring to metabolic disease. Exposure to environmental factors in early life can influence the developmental process as well as long-term health in humans. The famine affected fertility, weight gain during pregnancy, maternal blood pressure, infant size at birth and development of the central nervous system, are associated with an increased risk of adult-onset metabolic syndrome. The point to ponder over here is how these risk factors interact at the cellular level so as to cause disease? Here, epigenetic epidemiology enables researchers to explore critical links between genomic coding, modifiable exposures and the manifestation of the disease phenotype. Extensive epidemiologic studies have suggested that adult disease risk is associated with adverse environmental conditions (famines) to which the mother is exposed to early in development.