The endocannabinoid system, part of the body’s onboard cell-signaling network, is recognized to be involved in the regulation of feeding and energy balance, and cannabinoid type-1 neural receptors (CB1s) are expressed in many brain regions that control food intake. Animal and human studies indicate that CB1 agonists enhance appetite and increase the perceived reward value of food. Conversely, CB1 antagonists have been shown to inhibit food intake. Combined with existing clinical and preclinical evidence, it is reasonable to hypothesize a link between defects in the endocannabinoid system and eating disorders, and consider the development of drugs that modulate this system in eating disorder-related pathologies.
There appears as well to be an association of CB1 and FAAH endocannabinoid gene polymorphisms with anorexia nervosa and bulimia nervosa. In human trials, anorexic and bulimic patients show significantly higher frequencies of the AG genotype and the A allele of the CB1 1359 G/A SNP than do healthy control subjects. Similarly, the AC genotype and the A allele of the FAAH cDNA 385C to A SNP are significantly more frequent in anorexic and bulimic individuals. A synergistic effect of the two SNPs is evident in anorexia nervosa, but not in bulimia nervosa, however.
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The foregoing is a report on trends and developments in the cannabinoid industry. No product described herein is intended to diagnose, treat, cure or prevent any disease or syndrome.
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