The Connection Between Anorexia, Bulimia, and Marijuana
An imbalance in brain chemistry.
Posted April 9, 2012 | Reviewed by Ekua Hagan
Eating is very pleasurable. Our brain has evolved to produce feelings of euphoria when we eat because eating makes it more likely that we will survive to pass on our genes—which in turn will induce the next generation to enjoy eating as well. Yet, for some people, eating can induce feelings of anxiety and fear. Food, or even the expectation of food, makes someone with anorexia nervosa feel terribly uncomfortable; the only thing that can reduce this anxiety is to avoid food completely. Surprisingly, in spite of their intense mental efforts to avoid food they are often preoccupied with thoughts of it, or thoughts of preparing it for others. Food never truly loses its influence over our brain!
Bulimia shares some features with anorexia; these people alternate between a careful restriction of eating and an almost complete loss of self-control. When these people lose control they may quickly consume a few thousand calories, thus experiencing the gustatory pleasure of eating; subsequently, they force themselves to purge causing injury to their esophagus and teeth. Both stages of this process can be rewarding because of their ability to suppress depressive feelings and instill a sense of control over their bodies.
Anorexia and bulimia may be due to an imbalance in brain chemistry. A recent study published in Biological Psychiatry provided some intriguing insights into the role played by the brain’s own endogenous marijuana neurotransmitter system, called the endocannabinoid system. Without a doubt, exogenous marijuana can certainly affect one's mood and feeding behavior. Somehow, the normal function of the endocannabinoid system becomes impaired in people with either anorexia or bulimia.
The regulation of appetite and feeding behaviors are complex phenomenon involving our brain, peripheral organs, and the numerous pathways that connect them. Considerable evidence suggests that the endogenous endocannabinoid system has an important role in signaling rewarding events, such as eating. A group of scientists from the Katholieke Universiteit Leuven in Belgium used positron emission tomography (PET) to investigate the status of the endocannabinoid system in the brains of thirty women with anorexia or bulimia and compared their results to scans of age-matched control women.
The scientists discovered that the brain’s marijuana-like neurotransmitter system was significantly underactive in women with either anorexia or bulimia in a part of the brain that is responsible for the integration of the taste of food with our emotional response to eating. Essentially, these women could not fully experience the pleasure of food and thus developed inappropriate rituals and responses to it. This same brain region, called the insula, has been previously linked to other eating disorders.
The insula allows us to integrate the sensory aspects of food, such as taste, flavor, and oral texture, as well as how hungry we feel; it also responds to food’s rewarding properties. The insula processes information on a wide range of sensations that determine how we feel, including pain, temperature, sensual touch, stomach pH, and intestinal tension (such as constipation). Integration of these internal feelings provides a blended sense of the state of the entire body. The insula is the place in the brain where our sensory experience (from eating), our emotions (in response to eating) and thoughts (about why should not be eating!) come together.
Our brain’s endocannabinoid system normally controls how much pleasure we derive from sensory experiences; it then motivates us to repeat the experience again and again. An obsessive interest in food coupled with an inappropriate emotional response is consistent with a dysfunction in the brain’s endocannabinoid system. This new information might help identify new targets for medications that may help reverse the symptoms of anorexia and bulimia.
© Gary L. Wenk, Ph.D. Author of Your Brain on Food (Oxford Univ Press)