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Cannabis / CBD / THC / cannabidiol / tetrahydrocannabinol


It seems that certain components of the Cannabis plant family have protective properties against Poison/"Vitamin A" toxicity.  Yes, there is the endocannabinoid system and all that...and what if many of the benefits of these cannabinoids may come from a protective effect against Poison/"Vitamin A" toxicity?


Cannabinoids Protect Cells from Oxidative Cell Death: A Receptor-Independent Mechanism

"The antioxidative property of cannabinoids was confirmed by their ability to antagonize oxidative stress and consequent cell death induced by the retinoid anhydroretinol [a form of Poison/"Vitamin A"]. Therefore, cannabinoids act as antioxidants to modulate cell survival and growth of B lymphocytes and fibroblasts."

Cannabis smoke directly breaks down beta-carotene:

Chemical and biological studies of β-carotene after exposure to Cannabis sativa smoke

"Our results showed that the BC [beta-carotene, the main plant form of Poison/"Vitamin A] exposed to CSS [Cannabis sativa smoke] underwent 98.8% degradation and suffered loss of its antiradical activity."

Vitamin E (tocopherols and tocotrienols) are protective against Poison/"Vitamin A" toxicity, it would appear that THC is as well:

Cannabinoid-induced apoptosis in immune cells as a pathway to immunosuppression

"They also performed experiments with α-tocopherol, the most potent isomer of the antioxidant vitamin E and with retinod anhydroretinol, which induces oxidative cell death [form of Poison/"Vitamin A"], either in the presence or absence of THC. Their results demonstrated that similar to the effect of α-tocopherol, and unlike retinoid anhydroretinol , THC was able to protect 5/2 cells [cultured human beta lymphoblastoid cells] from oxidative stress and cell death."

Less Vitamin A in the liver = leaner mice.  There seems to be a connection between the endocannabinoid system and Poison/"Vitamin A".  Pay attention to the bold parts, ignore their theorizing in between:

Transcriptional Regulation of Cannabinoid Receptor-1 Expression in the Liver by Retinoic Acid Acting via Retinoic Acid Receptor-γ*

"Raldh1 knock-out mice are largely deficient in RA [retinoic acid, aka Poison/"Vitamin A"] in the liver (), and it is possible that at the greatly reduced hepatic RA levels, the high fat diet may have failed to induce CB1R expression in tissues involved in metabolic control, and the resulting reduction in endocannabinoid “tone” may have contributed to the lean phenotype of these animals. Further experiments are under way to test this possibility.

Retinoic acid has been implicated in the control of a variety physiological processes, including cellular differentiation, tumor growth, and metabolic processes (). The endocannabinoid system has also been implicated in many of these processes (), which could suggest that some of the pleiotropic actions of RA may be mediated via the endocannabinoid/CB1 receptor system."

This study didn't really contribute anything that I could glean (giving a VA-deficient diet, then a large injection of cannabinoids, then killing the rats isn't going to be that useful for telling us anything long-term):

Changes on metabolic parameters induced by acute cannabinoid administration (CBD, THC) in a rat experimental model of nutritional vitamin A deficiency.


Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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