Fetal Programming of Disease Process in Later Life- Mechanisms beyond Maternal Influence

Cardiovascular disease (CVD) is the leading cause of death worldwide and is the principal cause of early death in developing countries. The acceleration of the epidemic of early CVD is thought to include genetic factors as well as demographic factors such as lifestyle changes and nutritional transitions. CVD prevalence is a consequence of the interaction between the distribution of relative genotype frequencies and environmental exposures of a particular population. Although, the biological determinants of CVD and metabolic disorders in low and middle income countries are likely to be similar to those in affluent countries, the drivers of these determinants are likely to differ. In accordance with the developmental origin of health and disease (DOHaD) hypothesis adverse intrauterine influences such as poor maternal nutrition lead to impaired fetal growth, resulting in low birth weight, short birth length, and small head circumference. These adverse influences are postulated to also induce the fetus to develop adaptive metabolic and physiological responses. These responses, however, may lead to disordered reactions to environmental challenges as the child grows, with an increased risk of glucose intolerance, hypertension, and dyslipidaemia in later life and adult CVD as a consequence. This chapter discusses some of the possible links between programmed development and oxidative stress as one of the underlying mechanisms involved in the DOHaD phenomenon.

Keywords: Antioxidants, Fetal origin, congenital anomalies, premature birth, diabetes, cardiovascular disease, metabolic syndrome,