Compulsive Eating Linked to Same Brain Mechanisms as Drug Addiction

Posted on Jun 17th, 2010 | comments No Comments

The terms "food addiction," "food addict," and "food junkie" have long since been incorporated into the American jargon, but new scientific evidence can now justify their implications in the era of the growing American waistband. A study conducted by the Scripps Research Institute and sponsored by the National Institute on Drug Abuse (NIDA) discovered similarities between the brain mechanisms associated to drug addiction in humans with those of compulsive eating habits and the development of obesity. The study is now available in the online version of Nature Neuroscience journal or its May 2010 print publication.

Researchers Paul J. Kenny and Paul M. Johnson conducted a 40-day experiment using three groups of male rats by providing them with varying amounts and access to high-fat foods. All three groups had unrestricted access to standard lab food, while only two of the groups had access to palatable high-fat foods. Of these two groups, one had access to the high-fat foods for only one hour each day, while the other group had unrestricted access to these foods for 18–23 hours per day. After the 40-day period, all groups of rats were denied access to the high-fat foods. The researchers observed the eating behaviors of all rats throughout the entirety of the experiment by measuring their calorie intake, brain response, and weight gain.

By the end of the experiment, only the group of rats that had had unresticted access to the palatable high-fat foods had developed compulsive eating habits. These rats continued food intake of the high-fat foods even when a conditioned trigger of punishment (shock) was presented to them. In the end, these rats weighed almost twice as much as the rats in the other two groups. Their brain activity demonstrated a dramatic reduction overtime in the type 2 dopamine receptors (D2DR), a key element to the brain’s reward circuitry. This same decrease in dopamine is experienced by cocaine and heroin addicts as addiction worsens. As with substance abuse, a tolerance was built up to the pleasuring effects of the high-fat foods, and therefore required more intake to achieve the same satisfactory level of dopamine release needed to purge cravings.

The unlimited, unrestricted access to the palatable high-fat food alone was enough to cause addiction-like compulsive eating behaviors in the rats and lead to their obese weight levels. The need to compensate a satisfactory level of food intake with overeating can be described as a brain dysfunction called reward deficiency syndrome. The loss of D2D receptors, caused by conditioned high-fat, high-sugar food consumption, created lower dopamine activity and the need to overcompensate food intake to normalize reward circuitry.

Approximately one-third of Americans (33.8%) are obese, according to the Center for Disease Control and Prevention (CDC). Today, both obesity and drug addiction are major health issues for Americans. This study may possibly help health officials understand the physiological conditions suffered by individuals who experience rapid weight gain or obesity. With this new insight, addiction researchers may be able to identify existing substance addiction medications that can also treat overeating behavior.

However, researchers Kenny and Johnson note that the greatest contributor to compulsive eating behavior is environmental factors. The unrestricted availability of high-fat foods can trigger overconsumption and the onset of obesity. The brain is circuited with a natural reward system for such necessary activities as eating; however, when the act of eating is used for recreation (such as "comfort food"), and/or used in excess (as with increased portions or increased servings), the reward system begins to develop an imbalance and requires compensation.

Past research has linked obesity to genetic factors that affect 60–70% of an individual’s body mass index (BMI). However, the drastic increase in obesity levels of the population in the last five decades could not have been caused by a single genome change in such little time. Kenny and Johnson’s study helps researchers understand the obesity epidemic by combining concepts of genetic makeup, behavior, and conditioned environmental factors. Indeed, high-fat, high-sugar foods have grown in portion size and availability to the American public.

The standardization of a fast-food diet has gradually contributed to the health epidemic that America is now faced with solving. Obesity is not only a major threat to one’s physical health, susceptibility to disease, and life expectancy, but it has also been associated with other psychological disorders such as low self-esteem, depression, and anxiety disorders.

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