America has a growing problem with obesity that raises concerns about the future health of the nation. Additional, the incidence of childhood obesity is steadily increasing as well, which puts youth at an increased risk for a number of conditions later in life including high blood pressure, high cholesterol, cardiovascular disease, type 2 diabetes, bone and joint problems, sleep apnea, and psychological problems. The cause of obesity appears to be simple: overnutrition. People are consuming more calories than they are burning off, which causes them to gain weight as body fat. But is the cause really that simple? The article, “Is obesity a brain disease” argues that obesity is caused by overnutrition but the brain may be responsible for releasing signals that propagate the biological trap of obesity.
Often, overeating and obesity is seen as an issue of lack of willpower. People are told to choose to eat less and choose healthier food options. However, scientists have found that early exposure to high-fat and high-sugar diets increases the likelihood that a person will prefer that type of diet as an adult. Even pre-natal exposure via the mother’s diet during gestation may impact the feeding behavior of an individual later in life. Preferences for high fat and sugar diets have long lasting effects for individuals. For example, glucose sensing and use of insulin is impaired in individuals that are chronically exposed to overnutrition. Dysregulation of glucose metabolism plays a role in the development of type 2 diabetes. Studies using fMRI, an imaging technique to study functionality, have found there are differences between the activity in obese brains versus normal brains. Obese brains became more activated by food stimuli and more rewarding signals were sent in the brain in response to food. What causes the differences in desires for food and activity in the brain? There are two neuron types in the brain that control appetite. POMC neurons increase appetite, and these are the neurons that are overactivated in obese individuals. On the other hand, NPY/AGRP neurons have the opposite effect of decreasing appetite and are less active in obese people than average weight individuals.
Based on these facts, things are looking pretty grim because the brain is contributing to a person’s likelihood to overeat to form a biological trap. Is there any chance to break this vicious cycle? Our class investigated several ways to treat obesity as a brain disease and break the cycle. First it has been shown that eating healthy foods decreases appetite by increasing hormone signals to the brain. Another healthy lifestyle choice includes maintaining a regular sleep schedule. Regular sleep prevents decrease in metabolic rate, increases glucose levels and changes in insulin response. POMC neurons are a potential target for pharmacological intervention. By decreasing activation of POMC neurons, appetite would be suppressed in obese people. The differences in the brain can be changed to an extent by losing weight and maintaining a normal BMI. Scientists have found that there is a difference in brain activity between individuals that successful dieted and individuals that are still obese. However, not all of the differences in the brain caused by obesity can be reversed in all cases. Ultimately, our society needs to understand the consequences of eating fast food, constantly being on-the-go, and exposing kids to unhealthy food from a young age. Education will be another important tool in breaking the cycle for future generations.
My Brain Made Me Do It…Obesity As a Brain Disease?
