How THC promote appetite – support cancer, palliative care and HIV treatment

The cannabinoid compound tetrahydrocannabinol (THC), one of cannabis main active ingredients, is also the main reason why cannabis can boost appetite : by partially binding to and thus activating cannabinoid receptor type 1 (CB1).

In the different body tissues it occupies, CB1 acts in slightly different ways, several of which increase appetite. CB1 can be found in the following areas:

• The basal ganglia, where it may enhance eating pleasure.
• The limbic forebrain, where it may enhance food palatability.
• The stomach and small intestine, which both regulate ghrelin (an appetite-stimulating hormone that speeds digestion).
• The hypothalamus and rhombencephalon, two sections of the brain that help regulate food intake.

By activating CB1, THC increases appetite through the following known mechanisms:

• It may decrease your levels of peptide tyrosine tyrosine (PYY), thus increasing your levels of ghrelin, thus increasing your appetite.
• It activates the mTOR (mammalian target of rapamycin) pathway, thus increasing your levels of ghrelin, thus increasing your appetite.
• It activates a subset of neurons called proopiomelanocortin neurons (POMCs). These neurons can suppress hunger (primary pathway) and/or increase appetite (secondary pathway), to various degrees. Recent research on CB1 has revealed that dronabinol, a synthetic form of THC, can stimulate the secondary pathway without stimulating the primary one.

Current evidence suggests that regular cannabis use promotes weight gain.

THC might be useful for increasing body weight in some clinical populations (such as people with HIV wasting, cancer wasting, or anorexia nervosa).

• References
•  a b Cota D, et al. Endogenous cannabinoid system as a modulator of food intake. Int J Obes Relat Metab Disord. (2003)
• Riggs PK, et al. A pilot study of the effects of cannabis on appetite hormones in HIV-infected adult men. Brain Res. (2012)
• Bermudez-Silva FJ, et al. The cannabinoid CB1 receptor and mTORC1 signalling pathways interact to modulate glucose homeostasis in mice. Dis Model Mech. (2016)