The herb Cannabis sativa (C. sativa) has been used in China and on the Indian subcontinent for thousands of years as a medicine. However, since it was brought to the UK and then the rest of the western world in the late 19th century, its use has been a source of controversy. Indeed, its psychotropic side effects are well reported but only relatively recently has scientific endeavour begun to find valuable uses for either the whole plant or its individual components. Here, we discuss evidence describing the endocannabinoid system, its endogenous and exogenous ligands and their varied effects on feeding cycles and meal patterns. Furthermore we also critically consider the mounting evidence which suggests non-∆(9) tetrahydrocannabinol phytocannabinoids play a vital role in C. sativa-induced feeding pattern changes. Indeed, given the wide range of phytocannabinoids present in C. sativa and their equally wide range of intra-, inter- and extra-cellular mechanisms of action, we demonstrate that non-∆(9)tetrahydrocannabinol phytocannabinoids retain an important and, as yet, untapped clinical potential.

Hepatic portal vein (HPV) infusion of the medium chain fatty acid caprylic acid (CA; 2.3 mg/min, 40 microl/min) for 90 min beginning at dark onset in 18-h food-deprived male rats reduced the size of the first nocturnal meal about 40% (P < 0.01) and reduced 24-h food intake by about 15% (P < 0.001). Identical infusions into the vena cava affected neither initial meal size nor food intake. HPV CA infusion attenuated the postprandial decreases in plasma free fatty acids (P < 0.01) and beta-hydroxybutyrate (P < 0.01). HPV CA infusions did not significantly reduce nocturnal saccharine intake in a two-bottle conditioned taste aversion test, and there was no association between the saccharine intake on the test day and the feeding-inhibitory effect of CA on the conditioning day. HPV CA infusion did not affect plasma concentrations of corticosterone or of the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha. HPV CA infusion did not increase plasma concentration of the liver enzyme alanine aminotransferase, but did increase plasma concentration of gamma-glutamyl transferase, although not into the pathophysiological range. These data indicate that CA acts in the liver to produce a signal that inhibits feeding and that this inhibitory effect may be related to increases in hepatic fatty acid oxidation rather than be the result of aversion or toxicity.

Prolonged chewing of food can reduce meal intake. However, whether prolonged chewing influences intake at a subsequent eating occasion is unknown. We hypothesised that chewing each mouthful for 30s would reduce afternoon snack intake more than (a) an habitual chewing control condition, and (b) an habitual chewing condition with a pauses in between each mouthful to equate the meal durations. We further hypothesised that this effect may be related to effects of prolonged chewing on lunch memory. Forty three participants ate a fixed lunch of sandwiches in the laboratory. They were randomly allocated to one of the three experimental groups according to a between-subjects design. Appetite, mood and lunch enjoyment ratings were taken before and after lunch and before snacking. Snack intake of candies at a taste test 2h after lunch was measured as well as rated vividness of lunch memory. Participants in the prolonged chewing group ate significantly fewer candies than participants in the habitual chewing group. Snack intake by the pauses group did not differ from either the prolonged or habitual chewing groups. Participants in the prolonged chewing group were less happy and enjoyed their lunch significantly less than participants in other conditions. Appetite ratings were not different across groups. Rated vividness of lunch memory was negatively correlated with intake but there was no correlation with rated lunch enjoyment. Prolonged chewing of a meal can reduce later snack intake and further investigation of this technique for appetite control is warranted.