Opioids Does Kratom interfere with Vivitrol (causing pwd)?

[Shant]

I've got a buddy who says he inducted suboxone safely while on Kratom. I'm scheduled for the Vivitrol shot on the 28th and I figured if it didn't mess with the suboxone, maybe not the vivitrol? But logically it doesn't make sense to me that it wouldn't cause PWD. From what I know any opiate/opioid would result in PWD.

What say you, oh superior drug brains?

Thanks a lot

 

[Shant]

I guess this is a tough one. I saw another thread on this very question from may 2017. Some guy'd been on kratom for 2+ years, got clean for 3 weeks, then did a shot of tar the day before (.3) he was to get on vivitrol. He was wondering if he'd fucked himself (i guarantee he did...even with the 3 weeks). But he never updated us. One of the least understood questions atm and he didn't bother to say.

Anyway, just tell me this. I'm scheduled for the shot this Tuesday the 28th. The kratom strain with the highest opiate concentration is supposedly the red stuff. That one happens to have a ridiculously short half life of about 2 hours. Can I take that with vivitrol if I take the kratom 3 days in advance, and ONLY for one day? Prior use, 150mg of tramadol 4 days ago on the 21st. Nothing for 2 days before that. Heroin probably 4 times that month. Mostly tramadol (100-150mg a day) inbetween. Probably a total 0f a week with nothing.

I was also narcaned 4 times in the prior 4 days (for non opioid overdoses ironically...clonidine the fist one, GHB the 2nd...been trying to medicate my way til this Tuesday when I get the shot...and clearly have been miscalculating). Anyway I'm thinking being narcaned (and no they didn't bring me out of my OD with that) 4 times should reduce my chances of getting pwd, no?

Please, someone give me something. You've no idea how badly that Kratom is calling but I simply cannot afford to fuck myself with PWD again. That was literal torture for a day and a half before I could finally feel the heroin I was smoking.

 

[Shant]

Here's that old thread. https://www.bluelight.org/xf/thread...t-i-did-heroin-less-then-12-hours-ago.822286/

 

[Shant]

btw if this belongs in the general forum please feel free to move it.

 

[Shant]

Dang...still nothing? C'mon my brothers, I induct the day after tomorrow and this cell phone is burning a hole in my pocket. Where's Hodor or the rest of the big brains around here? Did I put this in the wrong forum maybe?

 

[Hodor]

I don't think PWD is caused by the opioid interacting with the opioid antagonist/partial agonist; rather the issue is that the suboxone/naltrexone causes a sudden and massive drop in your level of opioid receptor activation.

If a hardcore smackhead who's not already in full withdrawal is administered suboxone,they go from a high level of activation to the maximum level of activation that buprenorphine can provide; since the latter isn't all that high, their opioid receptors are no longer activated to an extent that they could avoid getting sick.

However, if your baseline tolerance is low (i.e. that of someone taking only a few grams of kratom per day), the suboxone may provide enough opioid receptor activation for you not to go into withdrawal. Heck, I would expect someone who's only taking 50 mg of tramadol per day to actually get high if you gave them suboxone.
As I said, this isn't a chemical reaction between an opioid and an antagonist; it's simply your mind and body experiencing less of their opioid receptors getting activated, and the more opioids you're currently on, the sharper and more painful that sudden drop is going to feel.

Now, the issue with naltrexone (vivitrol) is that it's not even partial agonist, but an antagonist. It doesn't provide a mild level of receptor activation like buprenorphine, but blocks it completely. So in this case, even a mild level of tolerance could result in withdrawals.

That said... kratom also seems to target delta opioid receptors, which aren't blocked as effectively by naltrexone, so maybe that might provide some mild effects even if it's getting outcompeted at the Mu-opioid-receptor front.

 

[Shant]

Hodor you are a GOD among men. I've been counting the minutes hoping you;d respond to this question. BTW You have NO idea how useful that last paragraph is to me. NOBODY has information on Kratom and Vivitrol out there. You hear occasional stories that seem dubious but no actual data, You have provided that data just now, so thanks for that. How solid is that data about Kratom and vivitrol would you say?

On your primary point (theory), it makes sense but if true, then wouldn't everyone go into PWD, or at least a very uncomfortable, if short, phase? Well we already know that;s not the case, no?

 

[Shant]

Hey Hodor my dude, is it true that post naltrexone (the vivitrol shot has finally worn off completely), the receptor sites are actually extra sensitive, and this has even resulted in overdose deaths?

 

[Shant]

Sorry for the rapid volley of questions Hodor, but if you're in a sharing mood I'm simply going to capitalize. I really wish I had that Kratom data a little sooner as I just cheated and smoked a little tar. About 5 puffs and I threw the rest away, It had to literally be $5 worth of dope. I did this about 6 hours ago. I'm scheduled to get the vivitrol shot on Tuesday the 28tn. Prior to the heroin, I was clean for the previous 3 days, 150mg of tramadol the day before that, and intermittently between 100mg of tramadol one day and nothing the next day, and this is how its been for the last month. What do you think, did I fuck myself? Is there any way I'm avoiding PWD? Thanks man

 

[Nicomorphinist]

Anything involving an antagonist is going to reduce tolerance and the overdose deaths I have heard of were associated with rapid opioid detoxification, so naltrexone in theory can do the same thing. People do take tiny doses of naltrexone, naloxone, and in some cases nalorphine along with narcotic analgesics to slow down development of tolerance and it works through the antagonist kicking opioid molecules off of a certain absolute number of receptors which is miniscule compared to the number of receptors being agonised by the painkiller.

The buprenorphine causes precipitated withdrawal by, as a partial μ opioid agonist, occupying close to 100 per cent of those receptors and having a high affinity for them, and antagonising the κ and δ opioid receptors. I think that reintroducing nalorphine and it esters as medications that can be prescribed and mixed into combination products would be very helpful -- nalorphine has agonist as well as antagonist activity and may be good in like a Suboxone for people wanting to get clean, get maintained, or kick down but also have diagnosed severe pain; another narcotic invented in 1966 but lost in the mists of time, myrophine, 3-acetyl, 6-myristylmorphine, probably does that job better than buprenorphine so a myrophine-nalorphine mixture would be even better.

Kratom having actions which are different in some respects than morphine, for example, and certainly ones which are unknown, probably some activity not considered narcotic and therefore it will be impacted less by opioid antagonists, to a degree that varies from one person to another. I had indeed wondered if the differences amongst naltrexone, naloxone, nalmefene, nalorphine, diprenorphine, nalorphine dinicotinate, nalodeine &c may allow various agonists to get some work done via the δ opioid receptor, as well as the newly discovered ζ opioid receptor, and the ones suspected to exist that I am sure they will find soon (λ, ε, θ, ι, ξ, φ, ψ, χ, γ, β, α opioid and still others) and some narcotic painkillers which work with the antinociceptive and NMDA systems, opioid-like receptor, and the σ receptor . . . then there is the μ₃ opioid receptor, a type of receptor which seems to work only with morphine and appears to have developed along with the body's ability to make morphine endogenously . . . then other agents with higher affinities than the antagonists and partial agonists, and above a certain level of affinity agonise the receptors to a different and greater degree, like 14-methoxymetopon, which appears to actually, literally, stick a part of its molecule deeper into the μ₁ and μ₂ opioid receptors and may agonise the μ₃ opioid receptor to a notable degree . . . there may be some fentanils, ampromides, benzimidazoles, bridged oripavine derivatives, morphazones, and other 14-dihydromorphinone opioids which can do this also . . .

A while ago, there was this kid everyone called Deeper; his given name may have been Deepak or something similar. One night, he stays after school for running in the hallway and at the end as he was getting ready to leave, he asked the teacher, Ms Take, if she would take off her clothes . . . he figured there were even odds on it, given that earlier in the day when there were not enough pinballs and marbles to go around when doing experiments with inclined planes, she got out some Ben Wa Balls.
"No, that is not a good idea" she said
-- Please, just for me?
She got a frisson from the transgression and subversion it would be, and decided she would do it, after all Deeper was one of the more diligent and tractable students
"skirt too"
--Why
"Just for me?"
-- Well, OK
So this continues for a short time, then Deeper picks up a 45-cm ruler and says:
"Can I stick this ruler up your arse?"
-- No
"Please, just for me?"
So in goes the ruler, and it was cold and quite a bit of shock & awe set in almost instantaneously.
"Deeper! Deeper!" she yelled

 

[Shant]

Anything involving an antagonist is going to reduce tolerance and the overdose deaths I have heard of were associated with rapid opioid detoxification, so naltrexone in theory can do the same thing. People do take tiny doses of naltrexone, naloxone, and in some cases nalorphine along with narcotic analgesics to slow down development of tolerance and it works through the antagonist kicking opioid molecules off of a certain absolute number of receptors which is miniscule compared to the number of receptors being agonised by the painkiller.

The buprenorphine causes precipitated withdrawal by, as a partial μ opioid agonist, occupying close to 100 per cent of those receptors and having a high affinity for them, and antagonising the κ and δ opioid receptors. I think that reintroducing nalorphine and it esters as medications that can be prescribed and mixed into combination products would be very helpful -- nalorphine has agonist as well as antagonist activity and may be good in like a Suboxone for people wanting to get clean, get maintained, or kick down but also have diagnosed severe pain; another narcotic invented in 1966 but lost in the mists of time, myrophine, 3-acetyl, 6-myristylmorphine, probably does that job better than buprenorphine so a myrophine-nalorphine mixture would be even better.

Kratom having actions which are different in some respects than morphine, for example, and certainly ones which are unknown, probably some activity not considered narcotic and therefore it will be impacted less by opioid antagonists, to a degree that varies from one person to another. I had indeed wondered if the differences amongst naltrexone, naloxone, nalmefene, nalorphine, diprenorphine, nalorphine dinicotinate, nalodeine &c may allow various agonists to get some work done via the δ opioid receptor, as well as the newly discovered ζ opioid receptor, and the ones suspected to exist that I am sure they will find soon (λ, ε, θ, ι, ξ, φ, ψ, χ, γ, β, α opioid and still others) and some narcotic painkillers which work with the antinociceptive and NMDA systems, opioid-like receptor, and the σ receptor . . . then there is the μ₃ opioid receptor, a type of receptor which seems to work only with morphine and appears to have developed along with the body's ability to make morphine endogenously . . . then other agents with higher affinities than the antagonists and partial agonists, and above a certain level of affinity agonise the receptors to a different and greater degree, like 14-methoxymetopon, which appears to actually, literally, stick a part of its molecule deeper into the μ₁ and μ₂ opioid receptors and may agonise the μ₃ opioid receptor to a notable degree . . . there may be some fentanils, ampromides, benzimidazoles, bridged oripavine derivatives, morphazones, and other 14-dihydromorphinone opioids which can do this also . . .

A while ago, there was this kid everyone called Deeper; his given name may have been Deepak or something similar. One night, he stays after school for running in the hallway and at the end as he was getting ready to leave, he asked the teacher, Ms Take, if she would take off her clothes . . . he figured there were even odds on it, given that earlier in the day when there were not enough pinballs and marbles to go around when doing experiments with inclined planes, she got out some Ben Wa Balls.
"No, that is not a good idea" she said
-- Please, just for me?
She got a frisson from the transgression and subversion it would be, and decided she would do it, after all Deeper was one of the more diligent and tractable students
"skirt too"
--Why
"Just for me?"
-- Well, OK
So this continues for a short time, then Deeper picks up a 45-cm ruler and says:
"Can I stick this ruler up your arse?"
-- No
"Please, just for me?"
So in goes the ruler, and it was cold and quite a bit of shock & awe set in almost instantaneously.
"Deeper! Deeper!" she yelled

OK the story at the end is baffling lmao but OK why not. Probably went right over my head. So bottom line, you are saying one should be able to take Kratom everyday for several days, right up to the day of induction, and not suffer PWDs?

 

[Shant]

BTW, what in God's name do you guys do? I guess you're obviously chemists or students perhaps? I'm very interested in going back to school and researching opioid receptors. Maybe work for a drug company. But I heard it's a pretty hard core field and there's lots of math involved (always a weakness)

 

[Shant]

as well as the newly discovered ζ opioid receptor, and the ones suspected to exist that I am sure they will find soon (λ, ε, θ, ι, ξ, φ, ψ, χ, γ, β, α opioid and still others)

This sounds interesting, Is there a story there?

 

[Nicomorphinist]

OK the story at the end is baffling lmao but OK why not. Probably went right over my head. So bottom line, you are saying one should be able to take Kratom everyday for several days, right up to the day of induction, and not suffer PWDs?

If I were in that situation I would not worry as much about something under a week because it takes weeks to months of taking something like that every day because, caeteris paribus, there is not a notable level of physical dependence generated.

Since I took kratom steadily over a day and a half at most and my others doses were all one offs and never had anything but a few 100 μg doses of naltrexone to see if it was better than DXM in reducing hydromorphone tolerance, it is hard for me to draw any conclusions from that. The differences that kratom has versus morphine, smack &c are still being discovered (and that research may very well lead to new discoveries about the nervous system and pharmacology -- provided it can be done. Controlling and outlawing Kratom like is being called for the rehab gangsters who want the government to fill inpatient detox beds for them and the whole programme at five or six figures each time will make it very hard, but it just means that the medical communities of Germany, France, Austria, and Switzerland, maybe Canada and Japan, will take the lead on kratom and other opioid-type things, whilst the US continues heading back to the Dark Ages. Fine. Fuck anybody that gullible and venal.)

 

[Nicomorphinist]

This sounds interesting, Is there a story there?

The ζ opioid receptor, also known the first Opioid Growth Factor receptor, appeared from what I have seen to maybe have effects bearing similarity to δ and μ opioid receptors . . . it sounds as if the currently suspected λ, ε, or the ι opioid receptor would be the next to be characterised.

 

[Mycophile]

I don't think PWD is caused by the opioid interacting with the opioid antagonist/partial agonist; rather the issue is that the suboxone/naltrexone causes a sudden and massive drop in your level of opioid receptor activation.

If a hardcore smackhead who's not already in full withdrawal is administered suboxone,they go from a high level of activation to the maximum level of activation that buprenorphine can provide; since the latter isn't all that high, their opioid receptors are no longer activated to an extent that they could avoid getting sick.

However, if your baseline tolerance is low (i.e. that of someone taking only a few grams of kratom per day), the suboxone may provide enough opioid receptor activation for you not to go into withdrawal. Heck, I would expect someone who's only taking 50 mg of tramadol per day to actually get high if you gave them suboxone.
As I said, this isn't a chemical reaction between an opioid and an antagonist; it's simply your mind and body experiencing less of their opioid receptors getting activated, and the more opioids you're currently on, the sharper and more painful that sudden drop is going to feel.

Now, the issue with naltrexone (vivitrol) is that it's not even partial agonist, but an antagonist. It doesn't provide a mild level of receptor activation like buprenorphine, but blocks it completely. So in this case, even a mild level of tolerance could result in withdrawals.

That said... kratom also seems to target delta opioid receptors, which aren't blocked as effectively by naltrexone, so maybe that might provide some mild effects even if it's getting outcompeted at the Mu-opioid-receptor front.

I'm a bit confused by this comment because I don't understand the science behind everything, but I am seeing a psychopharmacologist and just started taking naltrexone to block me from being able to use both kratom and drink alcohol.

It's not a 100 percent PERMANENT choice, but i have trouble moderating with both kratom and alcohol, so i am trying to be as clean as possible and have now gone 1 month without kratom and over 3 weeks without booze.

Now ID' ASSUME this doctor knows more about drugs overall than you, though maybe not, but she doesn't know as much about kratom as us, but she told me i would have to get over my kratom wd completely before going on naltrexone or else i would get precipitated withdrawals, so i went 7 days without kratom before taking it and had no issues.

Do you think she was right that I would have had worse kratom wd had i not done this?


Also, she says that naltrexone will block kratom, and MOSTLY block the enjoyment from alcohol.

Would you agree with this?


I hope you do, because what is making it easier not to give in to taking kratom or drinking is knowing or at least strongly believing that if i do it will lead to no high or significant buzz, so there's no point, but if I found out otherwise i would be upset.

But despite Kratom's only being a partial agonist, like suboxone, though subs are much stronger i think, my psychopharmacologist still says it would probably block most if not all the enjoyment from kratom because it still hits the opioid receptors.

Would you agree with her ?

Also, i did not get vivitriol shots but take 50mgs or oral naltrexone daily.

Funny cause i am thinking that people here are hoping that they can still get high on kratom or drunk while on naltrexone, but I am 100 percent hinging my hopes on the belief that it DOES at least MOSTLY block MOST of the pleasurable effects from Kratom and alcohol, and again, it would seem it would to a large extent interfere with the kratom high.

Maybe it might not interfere with some of the stimulant action of kratom that is atypical, but i am assuming it would significantly interfere if not completely block one's ability to really enjoy kratom, and that's exactly what i want, and i like that the washout period of naltrexone is only about 2 days according to my doctor so i'd just have to skip the naltrexone for 2 days to get high off the kratom, which is why i chose the pills and not the shot, but she says if i did so i'd have to be VERY careful to be sure that if i went back to kratom my withdrawals were close to 100 percent over and i was no longer physically dependent on the kratom before going back to the naltrexone or else it would put me into precipitated withdrawals and make me much much more uncomfortable.

 

[Shant]

Well the one question you have there that I'll give you my 2 cents on is that the naltrexone should have no trouble blocking Kratom. But there are what, 22 strains? With wildly varying half lives. And you occasionally see people say they can still feel the Kratom, but I really question that. For one, Kratom isn't as euphoric as your usual agonists to begin with, so even if some of the Kratom makes its way their receptor sites, it would be dulled to the point where you wouldn't feel what little euphoria is left (if any) anyway. But I'm not like the brains around here, can't give you any of the actual science. More of an experience and gut feeling play.

As far as your doctor telling you even with Kratom you'd need a full 7 days before vivitrol/naltrexone, you have to realize that 7 days is the minimum that they're always gonna quote. Basically, this is what they all say: 7 days for pills, heroin, & Kratom, 10-14 for suboxone, and the full 14 for methadone. She wasn't telling you it's 7 days for Kratom because she actually knows that to be the actual number, it's a catch all. There's no research for her to base that number on, so the only way she'd actually know that is if somebody told her he/she was on Kratom 6 days ago and still got PWDs when he/she inducted. And that patient could easily be lying or exaggerating. So if I was you, I'd be very specific with your questions if you really wanna know what that doctor knows. You'll probably be disappointed.

As I said, my buddy insists he took Kratom the same day and for several days up to the date of induction with no PWD. I know, it's a 3rd party random guy on the internet, but lol unfortunately that and personal experience is about the best information we have right now with Kratom & naltrexone. We need the people who actually try these things to post detailed analyses, time-stamped and/or maybe even recorded. Get some actual reliable experience reports. Until then, we're all guinea pigs.

 

[sekio]

Kratom is going to have mostly mitragynine as an active component, there isn't a massive variation in alkaloid content between varieties, at least from my first-hand analysis (GCMS of chlorofor:ethanol extract of kratom leaf). A recent study showed that most of the activity actually comes from metabolic activation of mitragynine to 7-OH-mitragynine.

Kratom is not a partial agonist, it is a full agonist. One of the classic 'proofs' that showed that mitragynine was indeed an opioid was that its effects were reversed by naloxone. Naltrexone would do the same. It just has a much longer duration of action. At best you'd be left with a mild adrenergic stimulant along the lines of low dose yohimbine - probably not very pleasant or useful.

Presumably if you were on a high enough dosage of kratom, you'd get some sort of precipitated withdrawal. But between the short half-life and comparatively low dose when compared to "recreational" heroin usage, I would think that as little as 24 hours after dosing you should be fine when it comes to opioid antagonists. The only time precipitated withdrawals are a concern is initially, switching from full-agonists to partial-agonists or antagonists. Once you are taking naltrexone on a regular basis, if you "slip" you will not get sick but rather ... nothing will happen.

Naltrexone has been reported to reduce alcohol consumption/cravings as well but I don't think it actually blocks the inebriating effects of alcohol. Maybe some of the rewarding effects will be reduced, but nothing like the total removal of most effects from any opioid.

 

[Shant]

Great shit, thank you.

 

[Mycophile]

Kratom is going to have mostly mitragynine as an active component, there isn't a massive variation in alkaloid content between varieties, at least from my first-hand analysis (GCMS of chlorofor:ethanol extract of kratom leaf). A recent study showed that most of the activity actually comes from metabolic activation of mitragynine to 7-OH-mitragynine.

Kratom is not a partial agonist, it is a full agonist. One of the classic 'proofs' that showed that mitragynine was indeed an opioid was that its effects were reversed by naloxone. Naltrexone would do the same. It just has a much longer duration of action. At best you'd be left with a mild adrenergic stimulant along the lines of low dose yohimbine - probably not very pleasant or useful.

Presumably if you were on a high enough dosage of kratom, you'd get some sort of precipitated withdrawal. But between the short half-life and comparatively low dose when compared to "recreational" heroin usage, I would think that as little as 24 hours after dosing you should be fine when it comes to opioid antagonists. The only time precipitated withdrawals are a concern is initially, switching from full-agonists to partial-agonists or antagonists. Once you are taking naltrexone on a regular basis, if you "slip" you will not get sick but rather ... nothing will happen.

Naltrexone has been reported to reduce alcohol consumption/cravings as well but I don't think it actually blocks the inebriating effects of alcohol. Maybe some of the rewarding effects will be reduced, but nothing like the total removal of most effects from any opioid.

This is odd, because i asked like 30 people on here who have used suboxone and kratom and ALL of them said that even 2mgs of suboxone would get them WAY WAY higher than even the max amount of the strongest kratom, and that they feel that suboxone wd is worse than kratom wd, and advised me NOT to take suboxone to get off of kratom when offered it.

Would you agree with them?

And if Kratom is a full agonist, though others on here have told me it's a partial agonist, then would you not agree that it is not as strong as suboxone, and if not, then how could suboxone be a stronger opioid than kratom?

My doctor wanted to give me suboxone to wean me off kratom and i think i wisely refused because EVERYONE on here says that suboxone is a stronger high than kratom, so if you agree that subs are stronger than kratom but are still a partial agonist, then how would you account for that, or do you really think kratom gets one higher than suboxone?

And from what I have heard from MOST people you are partially correct about alcohol, in that most people say it greatly reduces the enjoyment of alcohol, but one DOES still get drunk but not nearly the same kind of euphoric drunk and it requires much more effort and generally becomes much easier to cut oneself off after a few drinks rather than just drinking more and more.

This is how the ''Sinclair Method'' if you have ever heard of it works, where people are told to ONLY drink while on naltrexone, and that due to less enjoyment being produced, eventually cravings are lessened by not asssociating drinking with as much pleasure.

I'm trying to simply not drink for not, but at some point i will put it to the test, as it is apparently not dangerous to drink on naltrexone as long as one doesn't over do it to make up for any blocked effects.

I think one's mileage may vary and some say they still enjoy booze a lot on naltrexone, but most i've spoken to say that it really makes it very hard to fully enjoy drinking while on naltrexone and that they just tend to kind of ''give up'' after a few drinks cause it isn't really giving them the full buzz they are used to, but that no, it doesn't COMPLETELY block alcohol like it does with opioids, and that the physical effects of inebriation still occur, but not nearly so much of the enjoyment.

I'll have to test it out at some point, and if that's not good enough there's antabuse but i'm not really a stone cold alcoholic and have now not drank for a month but only taken naltrexone half of those days, just figuring that knowing i have it there and can take it will make me not so likely to drink or use kratom, and though i am not planning on permanent sobriety, i think i'll go a long time this time and probably be able to abstain and or moderate with both kratom and alcohol much more easily from now on now that i have naltrexone.