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Long term Cannabinoid Use and why it's impossible to wean off them

Whether it was 20 pills or one hit, it's pure shit to smoke pills.

I was probably being generous with the 95% filler estimate. It's probably closer to 99% filler which means that your pure cannabinoid smoking experience is close to that of shwag weed with a bunch of seeds and stems. After all, there is about that much PURE THC in shwag. I'm sure that high felt "amazing".

Your pills are MAXIMUM 10mg THC and 99% shit that shouldn't be smoked.

BTW, for comparison purposes, a single SMALL dab on average contains 30-40mg of THC in it. I can easily get several hundred mgs of THC in my lungs at any moments notice within a couple of seconds %)

But you know, you like to smoke pills and stuff?
 
Ugh what don't you get, it was for the experience TO SMOKE PURE THC it was worth smoking the other stuff

The dab contains other cannabinoids that interfere alter the high and you should understand this

You are clearly not understanding

I was interested in the effects of pure THC by itself without the other cannabinoids in it to alter the high... so I didn't give a fuck about the other shit in the pills because I only did it once so stop lecturing me about it
 
I want to let people know who have read the threads dealing with smoking and holding in cannabis smoke:

when I smoke cannabis smoke...when holding in I either breathe in a massive breath of oxygen at either around 6 - 7 or 10 seconds so oxygen deprivation is not a factor and I have cannabinoids right not, my am 2201 was replaced - the benzo was an accident - and the increase in effects is a truth

And dronabinol is a pure form of thc and by pure form of thc I mean it lacks other cannabinoids and by other cannabinoids I mean the phytocannabinoids - the cannabinoids in marijuana. The only way to do this is dronabinol

And marinol is full of sesame oil. Those are the inactive ingredients. So it is natural
 
^Chhh it was a lot longer in the other thread where you were constantly unable to prove anything...! I smoked MJ daily for a few years and have smoked synthetic cannabinoids daily for at least a couple of months if not three or four with no real WD. I guess I'm just lucky.

The only thing you can do is stop smoking like that. No ones going to be able to give you a 100% verified reason when there's no research/evidence to back it up.
 
Back to your topic GWB, I myself have been consuming SC thinking these were normal, natural cannabinoïds in the form of hash for 2 years, daily, in a junky-like fashion, from my 15th to my 17th approx. I quitted everything (SCs, alcohol, benzos and Speed/X) after a heavy binge-drinking, speeded-up and smoked up summer; all at once. This sudden deprivation of self-medication precipitated schizophrenic like symptoms and a heavy-duty psychosis, along with lethargy, anxiety, depression and irritability. I ended up losing contact with +150 peeps I used to hang out with. These symptoms lasted for about 6 months, and I had to be hospitalized in a specialized departement of neuro-psychiatry. All in all, I'm telling you this because they (the group of 6 highly competent neuroscientifics and psychiatrics etc) concluded that the SCs that I used daily had caused a gigantic desensibilisation at my endocannabinoïd receptors (the CB1 and CB2, plus some other ones in your belly, muscles and all the nerve tissues in your body) that are known to regulate (along with a lot of other stuff) dopaminergic (+norepinephrine, the "stress" molecule), serotonergic and GABAergic function in your body, but also immune system functions, hormonal functions and a lot of other vital stuff. This de-sensibilisation had led to a state of "no-control" of my body over these mecanisms, as the natural endocannabinoïds my body was throwing out weren't "strong" enough to behave as agonists at these receptors. To make it short:

SCs fuck up the way your endocannabinoïds affect your body, turning it into a unresponsive son of a bitch to what it normally should be working with. Why? Because as you said, SCs are "full agonists" and at some receptors, even "irreversible" (look it up).


More than 18 months later, and having researched the subject like no other motherfucker could have, I can tell you that the best way to go would be to "train" your CB receptors to function normally again. Keep in mind that they take part in the regulation of almost everything in your body, from hunger to sleep, immune-system to bowel function, etc. You can do that by starting to withdraw in a very simple way: You lower the dose you consume /day and the time in between each dosing by a 5% every day. Keep doing so until you consume 1/10 of the minimal active dosage (in the 1/10 of a mcg for ADB-FUBINACA, e.g); eventhough you don't think that it affects you (you won't feel a high with such small dosages), it has been proven that microdosing does help lowering withdrawal effects and that it helps re-establishing the responsivity of your receptors (they "seek" activity from compounds; if you went from x10000 in power to x1, it's normal they don't "find" the activity, but if you go from x10000 to x9990 to x9980 etc, they'll stay "responsive" in a fashion that permits you to slowly quit).
I myself understood this much later, with the help of psychiatrists, a biologist and a lot of introspection and research.
My dopaminergic system is fucked-up (not unlike parkinson patients) in a way that I have to be treated with ADHD medication to function normally (my cognitive, memory and pleasure systems have lost more than 1/2 their "normal" potency, compared to baseline people), but that I could only start months after my last psychotic and anxiety symptoms flushed away, for security reasons. (ADHD treatments can worsen anxiety and social withdrawal).

If your willing to stop, tell yourself that the worst is only just starting, and that it's gonna take at least 6 months of your life to "function" normally again, be it sleep, cognition, beeing able to have fun , or just not craving that stuff any longer, w/out taking in account the long weeks you'll have to go through to slowly reduce the consumed amounts in order to re-establish a as good a possible functionning receptor system.

EDIT: If you can, and have the money it'll take, try doing this "reducing daily consumed dosage" thing with natural weed, and not dronabinol, which might just be worse than some SCs out there (precipitates schizophrenia even faster in predisposed patients).

LaGaf
 
I was prescribed dronabinol the first two times during withdrawals and nabilone the second.

And it's interesting to hear it took you six months. It always took me three months. And it just confirms that the people that are naysayers about month long withdrawals are completely wrong.

I'm utterly sorry about the trials and awfulness you went through and effects you suffered because of it. You have my condolences. Here's to staying clean
 
And BTW, have you noticed any cravings? E.g, have you started consuming again? , And if so, have you noticed any help from a treatment with drone?
I heard from some people it was pretty different from MJ or SCs.
Take care, and good luck
 
I received cannabinoids today after not having any in three months. I have not used them months and do not find them Moorish.

They produce similar effects to THC but they produce similar effects to crack in terms of craving. from a treatment with drone?

I wish help?!?! would stop harassing me. I have dozens of harassing PMs from him, even ones from him threatening to call the police on me for using drugs. I would be careful around him people.
 
I don't see how these are respiratory depressants... I just smoked a large dose and my respiratory rate skyrocketed.
 
I agree with the idea of a really slow taper to minimize kindling, it could be a combination of excess CB receptor down regulation and excess kindling downstream at play here.

Is it true that some of the full agonists are irreversible agonists? That would be asking for some serious kindling if that was the case.
 
Are we really continuing this ambiguous conversation by using terms like "full agonist" without specifying a damn thing else?

You guys know that THC happens to be a full agonist too, right?

http://www.ncbi.nlm.nih.gov/pubmed/20417220


Please be specific about the drugs you are talking about because no one here can read minds.
 
It's unique because THC is unique, just as is all cannabinoids are unique.

THC does have full agonist properties however they are specific to the CB1 receptor as it relates to GABA, just as I linked you to.

So, by lumping all full agonist together without detail or specifics you see you are not differentiating a damn thing.

Again, noone can read your mind. Tell us what drug you are talking about.
 
It is a partial agonist and only elicits a partial bioloigical response. This is why it doesn't cause seizures; because it doesn't fully inhibit GABA like the full agonisit synthetic cannabinoids do.
 
w01fg4ng said:
Are we really continuing this ambiguous conversation by using terms like "full agonist" without specifying a damn thing else?
You guys know that THC happens to be a full agonist too, right?
http://www.ncbi.nlm.nih.gov/pubmed/20417220
Please be specific about the drugs you are talking about because no one here can read minds.
Click to expand...

Affinity for the receptor in question is not the same thing as efficacy in activating downstream signaling pathways, which could be different in different cell types or even species. There are cases where the CB1 receptor is coupled to inhibitory pathways, and then also cases where it is coupled to excitatory pathways.

Regarding THC vs. synthetic cannabinoids and why discussing efficacy is important, it could be that some synthetic cannabinoid has even higher efficacy than THC at inhibiting GABA - this would mean that after you inhibit the GABA, the glutamate downstream of that GABA really has a chance to ramp up. Or alternatively, if the synthetic cannabinoid is an irreversible agonist, then cases where the synthetic cannabinoid is binding to a CB1 receptor coupled to an inhibitory pathway could be partially to blame for kindling effects, because the irreversible agonist would diminish the amount of CB1 receptor mediated inhibitory tone.

Anyways, if it is an irreversible binding agonist and it is forming covalent bonds and such with the receptor then that should be preserved across CB1 receptors.
 
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