Marijuana is abused for the effects it has on the central nervous system and usually produces a euphoric calming sensation. In addition, marijuana use has been anecdotally reported to cause hunger and urge to eat colloquially referred to as the “munchies”. The munchies often cause marijuana abusers to consume foods that they normally would not have eaten. The active ingredient in marijuana that is thought to cause its euphoric and its appetite stimulant effects is a compound known as delta-9 tetrahydrocannabinol (THC). Pharmaceutical companies have taken advantage of this known appetite stimulant effect of THC by producing synthetic THC analog medications that have similar effects. Dronabinol, also known as Marinol, is a synthetic THC medication that is approved by the U.S. Food and Drug Administration for the treatment of anorexia in AIDS patients and for the treatment of nausea and vomiting in patients receiving chemotherapy. In addition, a second synthetic THC medication called nabilone (or Cesamet) is available in Canada for the treatment of nausea and vomiting. The human body has endogenous molecules that serve as neurotransmitters and hormonal regulators that are similar to THC and are known as endocannabinoids. Endocannabinoids regulate food intake, energy balance, and activate the reward center of the brain. THC binds to the endocannabinoid receptor to produce its euphoric and appetite stimulant effects. Researchers, lead by Dr. Daniele Piomelli, have discovered that the endocannabinoid signal in the gut regulates dietary fat intake. Their results were published in the journal Proceedings of the National Academy of Sciences. The researchers fed rats diets that contained high levels of sugar, protein, or fat and studied the effects on endocannabinoid regulation and metabolism. When the rats ate a lipid or fat based meal, the endocannabinoid levels were mobilized and increased in the small intestine by alteration in enzymatic activity. Rats that were fed a diet containing only protein or only carbohydrates did not show this change in the small intestinal endocannabinoid metabolism. Rats that were fed a nutritionally complete meal had similar effects to the diet that was high in fat or lipid content. In addition, rats that were fed a diet high in fat consumed more of the feedings compared to the other types of diets. When the researchers surgically resected the vagus nerve, which controls intestinal digestive activity, the increased endocannabinoid mobilization was abolished. Furthermore, local infusion of an endocannabinoid receptor blocker (rimonabant) into the small intestine of the rats caused the increased feeding of the fatty diet to slow and stop. The researchers also infused a second endocannabinoid receptor antagonist and this also slowed the increased feeding of the fat rich diet. The researchers wrote, “Our findings identify the gut endocannabinoid system as a critical component of the positive feedback mechanism that drives fat intake and suggest that therapeutic strategies aimed at restraining small intestinal endocannabinoid activity might help to selectively reduce the overeating of fatty foods”. This is an intriguing physiological discovery and sheds light upon the regulatory elements that control and drive food intake. Future research will focus on development of drugs that block intestinal endocannabinoid metabolism as a way to treat binge eating, over eating syndromes, and obesity.
Nicholas V. DiPatrizio el al. “Endocannabinoid signal in the gut controls dietary fat intake” PNAS published online July 5, 2011