We have long known the simplest recipe for weight loss: eat less and exercise more. Despite our understanding of the causes of weight fluctuation and the serious health risks associated with obesity, our collective weight continues to rise.
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Researchers have suggested several potential culprits for the ‘obesity epidemic,’ including genetic predisposition, lack of education, and cultural incentives for unhealthy behaviors (such as time and cost savings). However, none of these factors provides a thorough explanation of the problem. Indeed, most of us, regardless of our specific genes, knowledge, and cultures, can relate to the desire to eat too much, and many of us indulge in this temptation, despite our rational understanding of the disadvantages of doing so.
Though there are likely several factors that lead to obesity, it is generally accepted that the most direct cause for obesity is excessive consumption. Thus, the most universal solution for obesity may intervene in the decision making process by modifying feeding choices. A prerequisite for such a solution is an understanding of the neural mechanisms underlying our decisions regarding food.
In response to the complexity of obesity and to the recent controversial declaration by the American Medical Association (AMA) that obesity is itself a disease, Nature featured a comprehensive Outlook issue on the ‘disease’ this month. The collection of articles closed with a discussion of the neural circuits involved in appetite, the elucidation of which has been greatly facilitated in the past few years by the development of optogenetic techniques, which allow for the activation and inactivation of individual neurons using light.
According to Bradford Lowell, a neuroscientist at Beth Israel Deaconess Medical Center in Boston, the hypothalamus, which has long been recognized as the feeding center of the brain, is “a tangle of circuits that look like a Jackson Pollock painting.” The Nature discussion on the physiology of appetite included an explanation of agouti-related peptide (AgRP) neurons and pro-opiomelanocortin (POMC) neurons in the hypothalamus, which stimulate and suppress appetite, respectively. In the 1990s, scientists demonstrated that knocking out the genes for individual appetite stimulator peptides does not affect eating behavior or weight. Further, though full destruction of the AgRP nucleus in mice results in starvation, GABA receptor stimulation of the parabrachial nucleus, which communicates directly with the hypothalamus, reinstates food consumption. It thus appears that mammals have evolved some neural redundancy that increases the chances that we remember to eat.
This research was carried out by Nisha Kaul Cooch, a Senior Contributor for Brain Blogger and founder of BioInnovation Consulting LLC.
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