Last week, Volteface covered reports of a clinical trial accident in France that has left one person brain dead and five more in hospital.

Initially news stories quoted French media reports that suggested it was a cannabis based painkiller or contained cannabinoids.

Some media reports in France claimed the drug was a cannabis-based painkiller and AFP quoted a source “close to the case” who said the drug contained cannabinoids – an ingredient found in cannabis plants. (Source: The Local.fr)

 

The UK media reports only furthered this misconception but many were already sceptical of their accuracy.

Drug policy experts questioned the validity of the details – sensing the media was getting caught up in these initial reports.

 

The Portuguese company behind the trial, Biotrial, released a statement on Friday afternoon.

Throughout the course of the afternoon the reports that cannabis had anything to do with the trial began to fade away.

Dr Doris Payer of the Beckley Foundation wrote an interesting piece on her blog that you can read below.


Don’t believe the hype

by Dr Doris Payer of the Beckley Foundation (Sat 16th Jan 2016)

By now you’ve probably heard about the very unfortunate incident in France, where a Serious Adverse Event in a Phase I Clinical Trial left several people hospitalised, one with irreversible brain damage.

While my condolences go out to all involved, my deference to all the Drug War soldiers, rejoicing that it was a cannabis-derived drug (or even, somehow, cannabis), does not. Hate to tell you, but the news was wrong.

The drug that was being tested had nothing to do whatsoever with cannabis, any of the compounds in it, or anything derived from it. #sorrynotsorry

In fact, they don’t even know what the structure or pharmacological properties of this drug are. (Why they were doing human trials then, if that is true, is a whole other story).

According to the NYT article, which is the most informative and up-to-date I have found, the drug was a “FAAH inhibitor.” Let me break down for you what this means and you will see how ludicrous it is to link the incident to cannabis.

All humans have a brain-chemical system called the endocannabinoid system. The same way we all have a serotonin system, or a dopamine system. The reason you’ve probably heard of the latter but not the former is that the endocannabinoid system was only fairly recently discovered, and we know very little about it. But, we all have one; it’s just part of how the brain normally works.

The reason it has “cannab” in the name, which sounds suspiciously like “cannabis,” is that some of the compounds found in cannabis – called cannabinoids (including THC and CBD) – happen to bind to the receptors in this system. And we knew about cannabinoids before we knew about the system, so the system got named after them – the ENDOcannabinoid system (endo = inside).

(We’ve seen this before, like when we knew about opium before we knew about what it did in the brain, so when we found the brain system that it interacts with, the chemicals got named “ENDOgenous opioids” [including endorphins = endogenous morphine] and the whole thing got called the opioid system. Nothing inherently bad or ‘druggy’ about the system itself.)

What little we know about the endocannabinoid system includes that it has chemicals (“neurotransmitters”) and places for them to bind (“receptors”) – the standard lock-and-key mechanism that lets the brain communicate. So far we have found 2 types of receptors – creatively named CB1 and CB2 – and several neurotransmitters, one of which is called anandamide. Anandamide binds to CB1 receptors. As it happens, so does THC (one of hundreds of compounds in cannabis). So do chemicals like JWH-018 or HU-210 (commonly sold as those terrifying ‘Spice’ variants), and a whole slew of other things that happen to be similar to the chemical “key” that fits in the receptor “lock.”

And that is the closest we get to a relationship with cannabis.

Now, what the drug did was manipulate the levels of anandamide in the brain. Under normal circumstances, anandamide, after being released, gets ‘recycled’ via an enzyme that breaks it down, named FAAH. The drug being tested was a FAAH inhibitor, meaning it prevented the enzyme from breaking down anandamide, which elevated the levels of anandamide in the brain, which somehow led to the consequences we saw.

But we don’t even know if that, specifically, was the culprit. Other FAAH inhibitors have been used in research and clinical trials with no such consequences. So who knows what else this drug was doing.

In any event, see how none of this has to do with cannabis per se? You can’t outlaw anandamide. It’s a brain chemical. You’re producing it RIGHT NOW. I’m sorry one compound in cannabis mimics it but let’s stop making this about cannabis, and focus on figuring out how FAAH inhibition went wrong, shall we?

You can read more by Dr Doris Payer here.

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