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non-addictive opiates

MurphyClox said:
So now we are talking about the definition of "opiate". You are of course correct, "opiates" are substances solely from opium poppy. Well, tramadol is completely synthetical (and therefore an "opioid") but it was accepted in the discussion as well. So, I suggested salvinorin A.

If we are strictly talking about what the thread opener asked ("non-addictive opiates") and we strictly stick to the definition, then I second apomorphine ;)

Peace! Murphy
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hey, cocaine addicted monkeys will shoot it.


I refuse to use the whole opiate oid thing anymore. Its pointless, the distinction is meaningless. We've got things call opiates that don't bind to any opiate receptor, only bearing the name because this plant decided to produce them too.

urg.
 
zekethemusicman said:
di-hydro et-orphine? Believed to be thousands of times more pyschologically addictive than morphine, but carry nill physical dependency:\

Its an opiod tho...fully synthetic. All opiates carry dependency as a side-effect, as do the vast majority of oids im sure...
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No it's not, it's a semi-synthetic opioid derived from thebaine, which is an opiate.
 
MurphyClox said:
Peace! Murphy

Edit: And btw, the question is very inaccurate. Are you looking for agonists or antagonists? Compounds that just act on the µ-receptor or are kappa- and delta-ligands allowed, too? Are you aware of the definition of the term "opiate"? Maybe a rhetorical question
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yeh you beat me to it. Naltrexone binds strongly to opiate receptors, but does not cause an increase in intercellular CAMP levels. Hence, naltexone is an opiate and it sure as shit aint addictive.
 
Inrvizion said:
What he said ^^^^ THERE IS NO OPIATE THAT IN NON ADDICTIVE, the less addictive ones are the partial agonists Such as buprenorphine which I am currently taking for opiate maintenance, and let me tell you, it doesn't get you "HIGH" it just gets me ...
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Generally the "high" is a function of drug levels in plasma with time; the quicker the levels increase, the stronger the high is preceived to be, though no doubt there are exceptions to this rule
 
Hammilton said:
I refuse to use the whole opiate oid thing anymore. Its pointless, the distinction is meaningless. We've got things call opiates that don't bind to any opiate receptor, only bearing the name because this plant decided to produce them too.
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And I completely agree. The distinction between "opiates" and "opioids" is somehow outdated. But I was practically forced to explain it just once more...
 
Hammilton said:
For opiates though, I'm not aware of any full agonists not blocked by a suitable partial agonist (obviously affinity is a big issue, but o-desmethyltramadol has a high affinity) so it seems that there is significant overlap for all known mu agonists and antagonists aside from the *inorin's. Tramadol itself has negligible affinity, and the m1 metabolite is mostly or entirely responsible for the opioid effects. I honestly don't know if tramadol itself is a partial agonist, but it seems unlikely.

Oh wait, I'm thinking about the kappa receptor in that *inorin bit. I know salvinorin is not entirely blocked by buprenorpine (a kappa antagoist), at least with a high enough dose (8mg dose, taken ~18-20 hours previous only partially blocked a 5mg smoked salvinorin a dose. The measurement is not 100%, there may be a 1/2mg off +/- , from my 20mg/ml solution- if you weren't on suboxone, it'd be difficult to measure that solution well enough.



IGNVS: I'm not aware of any opiates making 'false receptors'- some types of tumors, yes, but not opiates. It'd be an intresting concept, but AFAIK, it's false. There are some studies indicating that receptor proliferation may be involved in tolerance, but theres a lot more to it that that.

And re: "one that dosnt [sic] fuck with your neurochemistry so that you dont get w/d's'

You can't take a drug that doesn't mess with your neurochemistry. Taking a psychoactive drug means messing with your neurochemistry, that's sort of the definition, you know?

There are some opiates that bind to the ORL receptors that produce less or no tolerance. I think bromidol and methydol are both strong ORL agonists (or is it antagonists you want here? I forget!!)
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thanks for your reply.

i know there arent 'fake receptors' but thats the term i was taught.
its like something to where you need more of a chemical to fill all the receptor sites.
how does tolerance here work?
also i didnt mean not alter your neurochemistry, i guess thats what i said tho. ahhum.. i was trying to find the right word for no tolerance. im not exactly sure how the whole thing works.

and i know there was a thread where they were talking about rediculously strong opiates thousands of times stronger than morphine where someone was talking about mu agonists that didnt give you tolerance issues. if someone could point me in the right direction that would be cool
 
pholcodine or loperamide

opioids not opiates.

Edit: Just realized you want to get hi... my bad.
 
fixingahole said:
Apomorphine? =D
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not an opiate...it doesnt bind to opioid receptors...its a strong dopamine d2 agonist. Its based around a opioid molecule, but is not an opioid in the pharmalogical or medical meaning.

as for loperamide...its still addictive..just physically only, in that if you take it for months on end, and then stop, you are going to be glued to the toliet for a while, as you will be physically dependant on it.
 
as for loperamide...its still addictive..just physically only, in that if you take it for months on end, and then stop, you are going to be glued to the toliet for a while, as you will be physically dependant on it.
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That is just speculation, and user reports say otherwise.
 
If loperamide was used consistently over long enough periods of time, there could certainly be some physical withdrawal symptoms...
 
Physical dependence after longtime loperamide ("to be glued to the toilet for a while") is certainly reported in the literature.
 
I was under the impression that tolerance to Mu2 mediated antiperistaltic effects did not produce a tolerance linear with that to the euphoriant, antinociceptive and respiratory depression?
 
Limpet_Chicken said:
I was under the impression that tolerance to Mu2 mediated antiperistaltic effects did not produce a tolerance linear with that to the euphoriant, antinociceptive and respiratory depression?
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Have to admit, I don't follow entirely. I'm not aware of any mu mediated antiperisitaltic effect that follows linearly with other effects.

tolerance to Mu2 mediated resp depression is definitely not linearly correlated with euphoriant effects- a la propoxyphene.
 
I do find it interesting that some of buprenorphine's effects seem to linger longer without dose increases than with other opioids. For instance I have spoken to people who have taken the same dose of buprenorphine for treatment-resistant depression for 4+ years, without much diminishment of the efficacy. Besides the mu agonism that is partial, I am sure kappa-antagonism is doing something here, though I'm not sure what.

I would still love to see someone's experiences with long-term memantine + opioid use, perhaps in an antidepressant interest. Memantine, as I've mentioned many times in other threads, has (strangely indeed) very much counteracted the development of tolerance to mood/motivating effects for dextroamphetamine for me, so much that I am still experiencing them fully 10 weeks at a chronic, stable, therapeutic dose. I notice a little tolerance, which 1 day off weekly repairs. In the past for me, after 2-4 days of dosing with dextroamphetamine, the effects on mood and motivation from a stable dose have completely dissipated, requiring continual dose increases if I wish to maintain them, which eventually is not possible due to adrenaline-related side effects. There is no question for me that what I am experiencing is different from that situation.

Now, NMDA antagonism and opioid tolerance actually has some direct research done on it, so I'm surprised more people haven't experimented on themselves. Memantine, being a partial antagonist, is in theory much more manageable and less cognitively impairing than full NMDA antagonists during their duration of effect ... for me this seems to be true.
 
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What I was trying to say, and failing miserably, was that the tolerance develops quickly to the euphoriant (if any) effects of propoxyphene and other opiates, but tolerance to constipative effects doesn't, and was asking if perhaps along with the respiratory depression, the antiperistaltic effects were also mediated by Mu2

Note to self: do not post while tripping on ayahuasca

Further note to self: do not assume wether tripping or not, that people can read your mind.

Sorry folks=D:P
 
I believe Mu2 is more potent constipative, but as 7OHMIT is Mu1 selective (noted to be in literature though I do not know to what degree) and also causes decreased peristalsis, though less so than non-selective Mu opiates, I assume Mu1 must have this capacity but to a lesser degree

also this may be so with overall tolerance potential, charactistic pruritus, and other negative effects...?

obviously a main visible component of Mu1 over Mu2 is a far higher threshold and lower ceiling for sedative/narcotic characteristics

i believe this is the reason for a generally stimulating effect in many users in a large dose range and not some other theories...though nothing's in stone here =D
 
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