Freethought & Rationalism Archive

godfry n. glad · 07-23-2003, 12:10 PM

Thanks, ps418. I actually meant all other recreational drugs, including alcohol.

Your comments reinforce my existing suspicions on both counts.

godfry

ps418 · 07-23-2003, 12:23 PM

Quote:

Originally posted by godfry n. glad
Now, if you wish to gain weight, it might be helpful, as I understand it acts as an appetite stimulant for a large number of users. Which is another reason those on chemotherapy find its use agreeable.

Yes, the appetite-stimulant effect is apparent in rodents also, but only if you offer certain types of food, particularly sweet foods. THC does not appear to increase intake of standard 'chow.'

THC's appetite stimulating effect is interesting because it provides a tool to study the physiological basis of hunger and satiety, which might come in hand in the battle against obesity. Lots of people would like to know how to affect appetite, either to increase it or decrease it.

And as it turns out, the endocannabinoid system plays a major role in regulating hunger, and also plays a role in regulating levels of the hormon leptin. (Endo)cannabinoids and leptin seem to act in opposite directions (e.g. Di Marzo et al, 2001). THC just boosts the system towards the I-could-eat-a-horse end of the appetite spectrum.

The question then naturally arises: can you decrease appetite by antagonizing CB1 receptors? We already know that THC produces most of its affects by agonizing CB1 receptors, and that one of its most consistent effects is increase in hunger. Experiments in mice using a CB1 antagonist show that indeed this reduces food intake, so it may be that there will be CB1 antagonist treatment for obesity. Given how nasty ephedra and amphetamines are, and how many health problems can be atributed to obesity, this could be good news. Or it could turn out that the side effects of CB1 antagonism could be bad, Time will tell.

Patrick

Di Marzo et al., 2001. Leptin-regulated endocannabinoids are involved in maintaining food intake. Nature 410, 822-825.

Quote:

Leptin is the primary signal through which the hypothalamus senses nutritional state and modulates food intake and energy balance. Leptin reduces food intake by upregulating anorexigenic (appetite-reducing) neuropeptides, such as alpha-melanocyte-stimulating hormone, and downregulating orexigenic (appetite-stimulating) factors, primarily neuropeptide Y. Genetic defects in anorexigenic signalling, such as mutations in the melanocortin-4 (ref. 5) or leptin receptors, cause obesity. However, alternative orexigenic pathways maintain food intake in mice deficient in neuropeptide Y. CB1 cannabinoid receptors and the endocannabinoids anandamide and 2-arachidonoyl glycerol are present in the hypothalamus, and marijuana and anandamide stimulate food intake. Here we show that following temporary food restriction, CB1 receptor knockout mice eat less than their wild-type littermates, and the CB1 antagonist SR141716A reduces food intake in wild-type but not knockout mice. Furthermore, defective leptin signalling is associated with elevated hypothalamic, but not cerebellar, levels of endocannabinoids in obese db/db and ob/ob mice and Zucker rats. Acute leptin treatment of normal rats and ob/ob mice reduces anandamide and 2-arachidonoyl glycerol in the hypothalamus. These findings indicate that endocannabinoids in the hypothalamus may tonically activate CB1 receptors to maintain food intake and form part of the neural circuitry regulated by leptin.

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07-23-2003, 12:10 PM	#111
godfry n. glad Banned Join Date: Aug 2001 Location: portland, oregon, usa Posts: 1,190	Thanks, ps418. I actually meant all other recreational drugs, including alcohol. Your comments reinforce my existing suspicions on both counts. godfry

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