• N&PD Moderators: Skorpio | thegreenhand

  • Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

cannabinoid addiction

cdin

cdin

Moderator: H&R; Discord Sr. Staff
Staff member
Joined
Jul 26, 2009
Messages
1,479
So , I've been spending time watching these really heart breaking documentaries about kids in the UK
and elsewhere becoming super strung out on the new, potent synth cannabinoids. One of the main sticking points for people
seems to be the withdrawal. We've elucidated the downregulation of CBx receptor systems in the last year, we know
this is a truly addictive physical problem. My question: is there any way we/anyone could come up with a basic
medical protocol for withdrawling people from synth noids? Obviously pushing for marijuana legalization and in fact, marijuana
are the best answers here - but that ignores the problem that made these appealing anyway - legality. So are there any
long acting, legal, non cannabis CB1/2 receptor agonist/antagonists, and what else can be done to assist these people? I note
that ibogaine has reset my cannabis tolerance, so that could be an option, any other ideas?
 
There was a study on Gabapentin in cannabis dependence and it showed promise for treating cannabis addiction - I think that anything that decreases the excitability of the brain will help. I would guess a sodium channel antagonist like oxcarbazepine would probably help too.
 
Ok, so apparently I'm the only one interested in this ;P though it seems like we should be on it, with many people suffering out there.
I was able to find a little data, and this table http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171994/table/T1/ which suggests Lofexidine+ THC works for regular marijuana withdrawals. Perhaps for the noid
crowd we should work from there. I don't think we're going to get around needing to use THC somehow in this process. I would suggest that the first line "suboxone" for synth noid withdrawals
be oral THC preparations, it divorces people from the ROA and is an agonist/antagonist at the receptor site/s (cb1/2 et al). It's pretty cruel that these people with JACKED endocannibanoid systems are just being told
"welp, cold turkey is the only way" also, these compounds(JWH's. AB-CHMNCA etc.) seem to be very hard to "taper" in any effective way, probably due to unknown concentrations/chemicals and ROA. Sorry if I'm
being overreactive here, but I am a HEAVY cannabis smoker, (3 - 7 gr a day indoor, 1gr bho, some edibles, 1 - 2gr bubble hash) and I can say it's pretty uncomfortable to run out, not bad,
but not good. These guys are on compounds THOUSANDS of times more active in the CB systems, I watch and listen and hear what they say - sweats, shakes, vomiting - all the opposites of CB activation, and it happens every
four hours without redosing. That's as bad as a dope habit, I feel like these guys get shrugged off because our general perception of cannabis is so benign, but I've watched kids on the street here in SF and I have seen
people in withdrawals I would EASILY mistake for opioid and was dumbfounded watching them smoke some spice and "get well".
 
Lofexidine and Clonodine have been used successfully in opiate withdrawals for a long time because they shut down the sympathetic nervous system rebound that occurs with withdrawal, I assume the mechanism of action for Cannabinoid withdrawal is the same, seeing as Cannabinoid withdrawal is similar to opiate withdrawal if severe enough.

One might put forth that anything that helps with opiate withdrawals/addiction might help with Cannabinoid withdrawals/addiction.
 
might, but lofexidine and clonidine (IME) BARELY touch the symptoms of opioid withdrawal, the only things that worked for me with that were Ibogaine or a replacement/taper arrangement.
 
which gets me to wondering if anyone has used iboga/aine for synth noid addictions...
 
I used gabapentin for cannabinoid withdrawals, 600 mg 3x a day. Although I wasn't a super heavy smoker, 1g a day of kind. Now I've been sober for 6 months and have a hospital job!

In theory one could use Dronabinol to taper, but in my case when I tried to do that I still felt that cannabis taste and it always made me want to go back to smoking real weed, so it didn't work for me, but it might for others.

A cannabinoid reuptake inhibitor or inhibitor of fatty acid amide hydrolase might do the trick but it doesn't seem like there's alot of money in researching those compounds. The ones that were initially investigated have been dropped for various reasons including safety.
 
I don't think cannabinoids have reuptake inhibitor transporters, might be wrong though. I doubt that they've dropped all research on such enzymes. Big pharma wants desperately to find a synthetic cannabinoid that works better than any phytocannabinoid for psychiatric reasons.

Gabapentin seems to useful for withdrawal from addictive substances in general, but it's not going to do all the work of course.
 
It was my understanding that the endogenous cannibinoids might not be plentiful enough for a reuptake inhibitor or enzyme inhibitor to be of too much use.

One of the problems with cannabis withdrawal is rebound glutamate, I would venture to guess that kindling occurs with long term use and that there could be some serious glutamate rebound upon withdrawal. I think the reason why Gabapentin was shown to work for cannabis withdrawal is probably related to its ability to decrease glutamate release via calcium channel antagonism (one of the supposed mechanisms for its pain relief).

I suppose more to the point would be one of the glutamate antagonists that have found use in epilepsy. I'd be curious about NMDA antagonists, if I recall correctly they've found use in alcohol withdrawal where there is similar glutamate rebound, though NMDA plays some weird role in alcohol withdrawal with alcohol being an NMDA antagonist itself.
 
Well the recent tragedy in France that left someone brain-dead was the result of an FAAH inhibitor in phase one trials. When other primates were given it, there was no such problem detected, so goes the story.

I mean yeah gabapentin stops excytosis (sp?) but I wasn't aware it was known to work on any neurtransmitter/modulator/hormone in particular, except maybe substance P, which interestingly enough opiates block the action of. Does anyone know what the small neurotransmitter usually thought to be co-localized with substance P is?

Glutamate, along with various cannabinoids, seems to be the hot topic in psychiatry today. Very cool stuff. Glutamate is pretty funky, though. Lots of complexity depending on location, metabotropic or ionotropic, glial cell presence, and receptor subtype/subunit.
 
My concern here, though, would be doing a disservice to harm reduction by substituting with a worse addiction. While the acute withdrawals from the synth noids seem to be quite severe - a short course of gabapentin may be advisable(if indeed glutamate is what causes the seizure/tick activity, seems a good guess though), but I would be very worried about people picking up a gabapentin habit. I've watched it happen a few times and it seems invariably to be a really bad idea...
 
Unfortunately anything that really gets at the roots of this excess glutamate issue is probably going to be intoxicating, benzo users are in much the same situation regarding glutamate antagonists, which have been reported to produce similar effects to benzos (hence the glutamate antagonist Perampanel is schedule 3).

personally I'd rather have my friends be addicted to Gabapentin rather than synthetic Cannabinoids.
 
good point. So we've come to : cannabis and gabapentin for excess glutamate to mitigate synth noid withdrawals. Man, that's pretty limited. It's especially bad because most of the people in the situation were there due to abject poverty/cannabis being too goddamn expensive. Really unfortunate.
 
Yeah it's a pretty shitty situation :/ sodium channel antagonists might help and depakote in particular is very inexpensive. It's not a drug you'd want to be on for a decade though, there can be serious side effects. Typically it's used for bipolar mania, and I imagine Cannabinoid withdrawal is probably similar in presentation.
 
From what I have observed in video and firsthand here in SF is it presents more like a combo opiate/benz withdrawal but very sudden. The kids I know, 4 - 6 hours after last dose would begin to sweat, heave, get twitchy - if I didn't know better I would say they were coming off dope, however it lacks the lethargy - in fact the brain-zapping awakeness is what made me say "it's like opiates x benzo wd"
 
Sodium channel antagonists like carbamazepine I know specifically have proven effective in studies for benzo withdrawal, so maybe that because of the similarity between noid and benzo withdrawal, sodium channel antagonists are indicated. Oxcarbazepine would probably be my drug of choice, eslicarbazepine as it becomes more available. Carbamazepine and then Depakote would be my cheaper suggestions.

Cannabis receptors are mainly inhibitory so it makes sense that you would get over excitation on the rebound just like benzos.
 
To reply to the comments about the bial failure, there are many other faah inhibitors that exist and do not exhibit the toxicity of their compound. The theories of the toxicity of bial's lead seem to think that it may have redox cycled like paraquat, and caused the lesions that way, but it still kind of a mystery.

Faah inhibitors are a promising way to increase endocannabanoid tone, but I feel that the simultaneous use of cannabis along with a faah inhibitor would be the best bet for weaning somebody off of a full agonist synth noid.
 
You must log in or register to reply here.
Top