Wasting Syndrome/Cachexia:  HIV, Cancer, Crohn’s, Parkinson’s, Nausea

The appetite stimulant effects of cannabis were reported in the literature as early as 1845.  THC (CB1 Agonist) stimulates appetite when present in low levels.  High levels interfere with the mechanical aspects of feeding due to the psychotropic and sedative effects of THC.  CB1 receptors are found in the brain and central nervous system, in fat cells, and in the liver.

  • The hypothalamus is the area of the brain responsible for appetite and is rich in CB1 receptors.  Animal experiments confirm that activation of these receptors with anandamide trigger feeding activity, while blockade impairs appetite.  The cannabinoid equivalent to anandamide is thc, which has psychotropic effects.  Low levels of thc also trigger appetite, but high levels impair actual feeding activity in animals due to the psychoactive properties.
  • In fat cells, CB1 receptors modulate lipid metabolism and promote fat deposition.  An adverse effect in humans is obesity and metabolic syndrome, however blockade holds promise for treatment.  In situations where the patient is nutritionally compromised, as in wasting syndrome and cachexia due to diseases such as HIV and Cancer, these CB1 effects on lipids and appetite hold promise to reverse the nutritional deficiency and return the patient to a healthier body weight.
  • CB1 receptors in the liver predispose the patient to ‘fatty liver’ due to the effects on lipid metabolism.
  • Skeletal muscle CB1 receptors play a role in promoting insulin resistance and metabolic syndrome/type 2 diabetes.
  • The endocannabinoid system is involved in the suckling activities of newborns.

Proper nutrition is essential for a healthy immune system.  Cachexia results with the energy expenditure of the body outstrips the intake of nutrition- one example known to many people is emphysema where the lungs do not properly absorb oxygen resulting in rapid breathing to increase the amount of air available for exchange- the resulting work outstrips the patient’s ability to take in nutrition and the body weight falls. Furthermore, age and hormonal related changes in appetite and absorption of nutrition (and deposition of fat), also play a part.  When compounded by chronic disease, this effect becomes significant enough to require treatment.

Increasing the caloric intake and fat deposition by activation of the CB1 receptors holds promise to reverse the nutritional deficits caused by the stress of chronic disease.  Selective or general blockade of CB1 receptors holds promise for the treatment of metabolic syndrome, fatty liver, and insulin resistance in type 2 diabetes. Selective blockade of hypothalamic receptors may find use as an appetite suppressant in the treatment of obesity.

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