Tara Mossberg
April 20, 2010
NTR 104 Final Paper

Addiction, as defined by Merriam-Webster is “a compulsive need for and use of a habit-forming substance characterized by tolerance and by well-defined physiological symptoms upon withdrawal; broadly: persistent compulsive use of a substance known by the user to be harmful.” More often than not in society, addiction tends to be assimilated with drug and/or alcohol use and occasionally habits, such as gambling, shopping, and sex. Coinciding with the recent up rise of obesity, a new term has been coined: food addiction. ‘Food addiction’, a contemporary term used to describe a biogenetic condition and pathological disorder, is a compulsive, excessive craving for and consumption of food. Inane as it may seem, those who are overweight or obese have since begun to accredit this issue to their compulsive eating and ever-increasing waistlines. A fine line lies between whether such a condition should be dismissed as an additional scapegoat for those unwilling to alter their lifestyles, or if it should, in fact, be recognized as a genuine, reputable medical problem. Recent research has embarked on the study of this behavioral manifestation, thereby confirming the validity of food addiction. Certainly gives the term ‘chocoholic’ a new meaning. A recently published study in Nature Neuroscience utilized forty-two lean rats as test subjects to assess similarities the in brain changes between drug addiction and compulsive eating. Three groups of rats were first formed: one group subsisting on a healthy balanced diet (“chow only”), another receiving healthy food, but with limited access to high-calorie food for one hour per day (“restricted access”), and the third being offered healthy meals, but with unlimited access to the junk food provided (including Ding-Dongs, cheesecake, donuts, pizza, bacon, sausage, etc.; the “cafeteria diet”). Additionally, the rats were trained to expect a minor shock when exposed to a light. Given unlimited access, the rats in the third group began to develop a predilection for the junk food, and quickly became obese. As the experiment persisted, the expanding group of rats ceased to respond to the potential danger inflicted in favor of continuing to indulge in their snacks. “A defining characteristic of overweight and obese individuals is that they continue to overeat despite the well known negative health and social consequences... Development of feeding behavior that is insensitive to negative outcome is analogous to the compulsive drug-taking behavior seen in human drug addicts, which is similarly impervious to negative consequences.”1 When evaluated, it was found that the rats in the first two groups shared similar caloric profiles, while the rats in the third group exhibited a caloric intake of nearly twice that of the aforementioned two groups. Upon further inspection, “although the restricted-access and chow-only rats maintained approximately the same daily caloric intake, restricted-access rats obtained only ~33% of their daily calories from chow, indicating that they developed binge-like feeding behavior and consumed ~66% of their daily caloric intake during their 1 h access session to the cafeteria diet.”1 The “cafeteria diet” group was at one point no longer offered junk food in favor of the healthier diet. The two weeks following were characterized by their refusal to eat anything at all. Conclusively, the study successfully showed a comparable correlation between downregulated dopamine levels in the brain of the obese rats as there would exist in humans suffering from drug addiction; “our data indicate that obesity and drug addiction may share underlying hedonic mechanisms and may arise from similar neuroadaptive responses in brain reward circuits.”1
It comes as no surprise that the ease in which we can access the foods contributing to an unhealthy lifestyle is considered an important environmental contributor to the current