Are Eating Disorders Regulated by Our Endocannabinoid System?

We humans enjoy many things—especially eating. (And occasionally marijuana.) Yet sometimes, our relationship with food becomes quite distorted. A recent study investigated the interaction between our brain’s endogenous cannabinoid system (eCB) and our brain’s reward system and how this interaction might underlie the altered eating habits of people with anorexia nervosa.

The current study monitored and then correlated the neural activity within the brain’s principal reward center, the nucleus accumbens, with levels of the body’s two main endocannabinoids, AEA and 2-AG. The researchers predicted that circulating levels of AEA and 2-AG have an impact on how our pleasure center communicates with the rest of the brain and how these communications influence our eating behavior and our body mass index (BMI). BMI was used as an indicator of the severity of the anorexia.

The authors further speculated that aberrant eating behavior might be due to dysfunctional reward processing in the brain’s pleasure center, i.e. the nucleus accumbens. The nucleus accumbens receives projections from brain regions that influence both the motivation to eat (“wanting”) and the hedonic evaluation of food (“liking”). [To read more about this topic, see Your Brain on Food.]

What The Study Discovered

The nucleus accumbens of patients with anorexia nervosa showed decreased neural activity in response to seeing tasty foods as compared to healthy controls. The patients with anorexia nervosa reported not “wanting” to be motivated by food stimuli for fear of gaining weight. In contrast, their nucleus accumbens increased its neural activity when the subjects were viewing pictures of people who were underweight. Looking at tasty foods was not pleasurable while looking at skinny people was pleasurable.

The current study also discovered patients with anorexia nervosa showed abnormal alterations in how their brain’s pleasure center communicates with the insula, a brain region that is responsible for processing our enjoyment of touch, taste, sounds, etc. This brain region may also mediate the association between eCB and BMI. The authors suggested that in patients with anorexia nervosa, this aberrant communication process could be responsible for the development of maladaptive eating behavior and distorted perceptions surrounding hunger, satiety, and body weight and shape.

The study further discovered that AEA and 2-AG may play distinct and independent roles in regulating BMI by influencing how we experience the pleasure of eating. Their findings indicated that an increase in AEA concentrations promoted weight gain, while an increase in 2-AG tended to counteract the weight gain. In both healthy control subjects of those with anorexia nervosa, BMI is distinctly regulated by circulating levels of AEA and 2-AG.

The increased levels of AEA in patients with anorexia nervosa might represent an attempt by the brain to improve eating behavior and favor gaining weight. These changes suggest that the brain made some compensatory changes as a consequence of chronic starvation.

These findings could have important clinical implications for the development of new therapeutic strategies aimed at maintaining a healthy weight, as a treatment for weight disorders.