Environmental Epigenetics and Obesity: Evidences from Animal to Epidemiologic Studies

Obesity is a major health problem today that grows into a global epidemic. Obesity has been associated with increased risk of many non-communicable diseases, such as type-2 diabetes mellitus, hypertension, cardiovascular diseases and cancer. There are multiple factors that cause obesity. Accelerated lifestyle, fast food, unhealthy eating habits and sedentary lifestyle have been considered as the major risk factors of overweight and obesity development. It has been suggested that genetic factors may play an important part of the onset of obesity. However, the observed rapid rise of obesity worldwide has occurred too rapidly to be solely explained by fixed genomic variation in combination with adult lifestyle factors. Epigenetic modifications can be programmed in the intrauterine environment and can be modulated by environmental influences including diet besides genetic influences. It has been widely accepted that genes together with adult lifestyle factors determine the risk of developing non-communicable diseases. Animal study models have demonstrated that epigenetic alternations early in life lead to obesity later in adult life. Natural human experiment, such as Dutch famine study, also suggested that peri-conceptional and peri-natal nutrient deficiency resulted in overweight or obesity later in life. The results from epidemiologic studies are less consistent. This chapter reviewed the evidence from animal studies, ecologic evaluation, to epidemiologic studies to assess whether there is a causal relationship between epigenetics modification from diet and environmental exposure and obesity. Challenges and opportunities to improve the future study design in human are explored.