Monday, April 28, 2008

Nerve Gas in Place of Cannabis? Scary.

OK, this possibility is a long way off according to the experts. However, it's a damn scary prospect in my opinion.

Organophosphorus Nerve Agents are those things that were developed in World War 2 and have been used in warfare, pesticides and terrorism ever since; tabun, sarin, soman, GF, and VX are just a few.

Thankfully, the discovery that OGs affect cannabinoid receptors in the brain was just something that scientists thought about as possible and then tested their theories on mice recently (as reported in US News Health section):

"This has great potential but it's years away from human application," said one expert, Dr. Dennis J. Patin, associate professor of clinical anesthesiology at the University of Miami Miller School of Medicine. "I expect that some drug company will research further," he said.

And John Casida, senior author of the paper in the April 27 issue of Nature Chemical Biology, stressed that his team "report new fundamental mechanistic discoveries on the cannabinoid system, rather than proposing a medicine or treatment."

Well, thank your preferred god for that methinks.

I'm no scientist, but from what I could decipher in the report at NCB, certain organophosphate compounds act directly on the brains cannabinoid receptors, resulting in effects that are the same as cannabis, leading some to think that there could be a future in using some derivative of these compounds as a pain relief substitute for cannabis. That is, pot like pain relief but without the high.

For the medicotech geeks among you, here is the Abstract:

Delta-9-Tetrahydrocannabinol (THC), the psychoactive ingredient of marijuana, has useful medicinal properties but also undesirable side effects. The brain receptor for THC, CB1, is also activated by the endogenous cannabinoids anandamide and 2-arachidonylglycerol (2-AG). Augmentation of endocannabinoid signaling by blockade of their metabolism may offer a more selective pharmacological approach compared with CB1 agonists. Consistent with this premise, inhibitors of the anandamide-degrading enzyme fatty acid amide hydrolase (FAAH) produce analgesic and anxiolytic effects without cognitive defects. In contrast, we show that dual blockade of the endocannabinoid-degrading enzymes monoacylglycerol lipase (MAGL) and FAAH by selected organophosphorus agents leads to greater than ten-fold elevations in brain levels of both 2-AG and anandamide and to robust CB1-dependent behavioral effects that mirror those observed with CB1 agonists. Arachidonic acid levels are decreased by the organophosphorus agents in amounts equivalent to elevations in 2-AG, which indicates that endocannabinoid and eicosanoid signaling pathways may be coordinately regulated in the brain.