Endocrine Disruptors and Obesity

Obesity is an epidemic in children and adults worldwide and is associated with comorbidities including diabetes, metabolic syndrome, heart disease and cancers. In the past, obesity has been considered the result of an imbalance between caloric intake and expenditure. However, more recent research has shown the roles of genetics, the endocrine system, and environmental toxins on obesity development. The DOHaD Hypothesis holds that prenatal and early life nutrition affect the development of obesity, and that there are critical periods of development during which environmental factors can cause phenotypical changes that result in increased susceptibility to diseases later in life. The Obesogen Hypothesis proposes that environmental chemicals, termed “obesogens,” promote obesity by acting to increase adipocyte commitment, and differentiation or by altering the regulation of metabolism, appetite and satiety. These effects often begin during development, and lead to obesity later in life. Many obesogens are endocrine disrupting chemicals that interfere with normal endocrine regulation of metabolism, adipose tissue development and maintenance, appetite, weight and energy balance. Endocrine disruptors are abundant in our environment, used in everyday products from food packaging to fungicides. This review explores the genetic, endocrine, and environmental factors that promote obesity in order to better understand their contribution to the obesity epidemic.