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diabetes drug to help drug addiction?

asecin

Bluelighter
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Apr 13, 2005
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according to this article; https://medicalxpress.com/news/2019-11-diabetes-drug-relieves-nicotine.html
what do you think about this, considering it was actually injected instead of oral use. any possibility it might work oral route too considering this medication is in general prescribed through oral route. what do you think of the chances of helping with addiction in humans??
i wonder about this though "This receptor, PPARγ, is found in areas of the brain involved in drug addiction". Do you know anything else out there thats easier to obtain that works on PPARy with perhaps some possibility it might help with addiction??
 
hmm from wiki i get this; The phytocannabinoid cannabidiol (CBD) has been shown to activate PPAR gamma in in vitro and in vivo models.
so its possible CBD, besides the fact its been advertised for relaxation, could actually have some benefit in threating addictive behavior? do you think its possible?
 
That study has a few isaues that make it hard to generalize to hunans:
1. direct injection of drug into the brain is a very unusual route of administration
2. it's only tested in nicotine dependency, which may not generalize to opioids, cocaine, amphetamine, PCP or whatever other drug that produces habituation
3. it's in rats, which are known to behave differently than humans, there are tons of potential therapies that work in mice/rats but fail in primatss or humans.

so yeah, this is by no means a miracle cure discovered but it is a promising stepping stone on the way to more immediately applicable studies.


as for CBD it is known to be a good anxiolytic, it turns out it can help reduce drug cravings in heroin users[ref]. It can definitely help and has a very mild side effect profile so it's worth looking at but I would, again, not expect to have miracles from just taking CBD alone.


fun fact 1: Ibuprofen is a PPARy ligand.
fun fact 2: PPARd (delta) activators have been investigated as doping agents as they increase exercise performance and encourage fat loss/muscle gain.
 
Echoing some of the above post, cant react it coz im a dirty greenlighter.

Drawing conclusions from intracranial (referred to IC hereafter) injection on small mammals is generally bad science.

This is the reason we believe amanitas to be a neurotoxic shroom when they arent. Muscimol deemed fine medically but due to a test whereby rats were given an IC dose of ibotenic acid, its other constituent, it acted as a neurotoxin. In reality some ibo acid gets metabolised into muscimol (and no doubt a couple of other minor metabolites), and the rest gets excreted renally.

There are usually several metabolic processes standing between oral ingestion and eventually reaching the brain, you are often "high" on something else entirely.

IC shouldnt be used as much in the way of evidence unless it pertains to being the only viable ROA- which to be honest i cant think of an example in humans of IC administration (less so as the only viable) outside of maybe neural surgery? we use IV, and for drugs that dont cross the blood brain barrier its a spinal tap [citation needed for some of the above]. I could maybe see examples whereby one would want to see what intracranial application of an already endogenous-and-present-in-the-brain compound would have in way of effect maybe emulating brain injury etc but im just postulating here for fun.

Also as mentioned not all addiction mechanisms are born alike and usually theres an entourage of them that need addressed, and polydrug addictions are a thing too. Nicotinic acetylcholine receptors tend to be the target of nicotine dependency treatments like that one whatsitcalled is it wellbutrin? cant remember, anyway that doesnt translate to treatment vs other drugs because its only staving off craving for activation of that particular receptor, none of the psychological attributes. Opioid receptors are the primary target of ibogaine, though maybe someone will correct me here i believe it can be effective in other addictions? Other therapies that arent necessarily involving using substances look to tackle dopamine and compulsion as well for e.g.

Theres many methodologies and to be honest there are few straight fixes (however ibogaine is one that i can think of lol) that dont require accompanying therapy or support/guidance. Making a lot of addiction treatment equatable with other mental health treatments. Its a complex "disease" (its not a disease -or a choice- btw thats an archaic term even though its the accepted one) and isnt innately reliant on a mechanism to be problematic. Its far more than often rooted in environmental stressors or trauma, or mental health conditions. In the instance of smoking schizophrenics in particular find a great deal of relief from psychotic symptoms from a cigarette habit. also theres significant research pointing towards individuals who have a certain expression of the DeltaFosB gene being predisposed to addictive tendancies.

The fact that the rats' DOC was nicotine was just incidental to the experiment. Forcing a small mammal to become addicted to your poison of choice then testing what makes it want only that particular thing less only tells you what helps alleviate some of the physical symptoms of cravings for, or withdrawl *from that drug*. Not withdrawl from homeostasis. Not withdrawl from the fact you had a compulsion to fill time. None of the many factors that contribute to what addiction actually is.

We may see an intracranial nicorette product yet, but an addiction cure or even treatment here would be quite a reach.
 
Ibogaine's receptor potency is nAChR > sigma2 >> SERT > NMDA > MOR, KOR, DAT > sigma1, 5HT3 >> 5HT2a according to wiki so it is certainly not primarily an opioid, more technically it's a dissociative, antinicotinic, and SRI as well as an opioid, and a weak psychedelic.

Its metabolite noribogaine (aka O-desmethyl ibogaine) is a more potent mu/kappa ligand as one may expect from going from OMe to a free phenol. Unfortunately it is more potent at KOR than at MOR and is also very potent at SERT (10fold higher affinity compared to ibogaine)... probably responsible for some psychedelic effects.
 
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