Bisphenol A and Metabolic Syndrome

Extract

The rapid increase in obesity in many countries in recent years has been associated with an increase in the prevalence of associated cardiovascular disorders, including type 2 diabetes, hypertension, and dyslipidaemia. Although genetic factors are likely to play a role in an individual’s susceptibility to these disorders (1), this increase in disease prevalence has occurred too rapidly to be a result of a genetic change within a population, and there is general acceptance that the combination of reduced exercise and increased consumption of calorie-rich food are important factors in the development of the conditions. Although it is attractive to believe that it is simply lifestyle changes during childhood/adulthood that are fuelling this epidemic, it is now recognized that the environment experienced in early life can influence susceptibility to cardiovascular and metabolic disorders in later life, including an increased risk of obesity and the “metabolic syndrome” (2).

There is widespread acceptance of the “developmental origins hypothesis,” which suggests that the action of a stimulus or insult during a specific critical period of in utero or early postnatal development can lead to “programmed” alterations in tissue structure and function, predisposing the individual to later disease (2). In this context, therefore, metabolic syndrome disorders in adults may represent a complex interaction between early developmental influences on disease susceptibility and later lifestyle, which builds on the level of predisposition, therefore, more of a “lifetime” than simply a “lifestyle” disorder. Given the widespread exposure of humans to environmental chemicals, is it possible that early life exposure to one or more of these substances during fetal and early postnatal life might underpin the current epidemic of obesity and related metabolic disorders?