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Has anyone else experienced spontaneous full remission of opiate addiction w/o w/d?

Troglodyte

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A very strange thing is happening to me. unfortunately i've been addicted to opiates for the better part of 15 years with the normal attributes of dante's hell when trying to quit. But 6 days ago, saturday, i did heroin. Then the next day, sunday, i waited to get sick so i could switch back to buprenorphine, but it never happened. Monday, tuesday, wed, thurdsay(today)...nothing. it just never happened. im utterly confused...and grateful. but i dont understand what it. its amazing. Last night, wed, i did get some rls and akasthesia, but totally tolerable. i never got any discomfort of my skin, no temp fluctuation, nausea, vomiting...nothing. every other time ive tried to quit has been unfathomably horrible. so this makes so little sense to me.

At the moment im not going to share what was co-administered, because those things can easily kill you/me and i dont want to promote people dying because they think they can recreate what happened to me, and those coadministered substances might have nothing to do with it.

I know im beyond lucky, for one of the first times in my life. But i'm trying to find out if this has ever happened to anyone else or am i a truly singular phenomenon. i havent been able to find anything online thus far. apparently spontaneous remission means something else in the context of opiate addiction and i'm having some trouble figuring out good keywords to search for such cases. has this happened to you or anyone you know or have even heard of?
 

DoctorMolecule

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A very strange thing is happening to me. unfortunately i've been addicted to opiates for the better part of 15 years with the normal attributes of dante's hell when trying to quit. But 6 days ago, saturday, i did heroin. Then the next day, sunday, i waited to get sick so i could switch back to buprenorphine, but it never happened. Monday, tuesday, wed, thurdsay(today)...nothing. it just never happened. im utterly confused...and grateful. but i dont understand what it. its amazing. Last night, wed, i did get some rls and akasthesia, but totally tolerable. i never got any discomfort of my skin, no temp fluctuation, nausea, vomiting...nothing. every other time ive tried to quit has been unfathomably horrible. so this makes so little sense to me.

At the moment im not going to share what was co-administered, because those things can easily kill you/me and i dont want to promote people dying because they think they can recreate what happened to me, and those coadministered substances might have nothing to do with it.

I know im beyond lucky, for one of the first times in my life. But i'm trying to find out if this has ever happened to anyone else or am i a truly singular phenomenon. i havent been able to find anything online thus far. apparently spontaneous remission means something else in the context of opiate addiction and i'm having some trouble figuring out good keywords to search for such cases. has this happened to you or anyone you know or have even heard of?
The mind plays a big role in interpreting the classic withdrawal symptoms. Normally if you feel some malaise/ head cold and you?re not taking opiates you just shake it off like a typical illness.
Get a runny nose and watery eyes 8 hours after using and the mind instantly goes to that hell Dante describes. You start reading into symptoms etc.

When I was using H, sometimes I?d initially buy a whole bundle and have plenty left over to get high the next day (even forgoing my nightly 10p dose) and wouldn?t suffer any withdrawals until the next morning. And there were times I had to forgo my nightly dose cause I ran out, and would be suffering early onset withdrawals.
Yeah the mind can be a powerful ally or enemy
 

Troglodyte

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It absolutely can. 20+ years ago when i was 17 (holy shitchrist the years fly by) I had acquired a sizable brown jar of morphine sulfate compounding powder(yes, it was pretty sweet). it was the first time i was addicted, but i didn't know it at the time. And i mean it was a sizable jar, my friends and i were snorting morphine, just kinda whenever, for probably 6-7 months. I hadn't ever been addicted and at the time i just wasnt thinking about it. When i ran out, i honestly didn't think twice, which is hilarious to me in retrospect. Then i got sick, pretty uncomfortable, but wasnt on deaths door. I figured it was the flu and took 1 personal day, and then i just wanted to hang out with my friends, i was 17(or was it 16...). so i pushed thru it and went out, tho i remember being told i didn't look so hot. it wasn't til a few weeks after that i put it all together and realized that, SURPRISE, i just ran out of a giant jar of morphine and the next day i got pretty sick...there might be a connection! But it just wasn't a really big deal because i didn't realize it's connotations and didn't have expectations.

But i just don't think that could be applicable here. I was expecting to get sick, just like every other time. I get really...REALLY sick. I dont know if it's something i did with the ingestion of other things simultaneously, which is a weak theory, but what else is there? I did get hit in the head with that mallet... but that happens all the time. i got nothing...

But if someone could figure it out, as unlikley as that may be, could that not help, like, everybody under 50 in the united states?
 

Troglodyte

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today is the 4th day with out any opiates, just 1.75g of phenibut, which is low for me when i use it, and maybe 3.2g of gabapentin, which is way low vs when i usually use it.
Tho on a side note, i don't get intoxicated in any way from gabbies, but after a 3 or maybe even 4 year gbl addiction in my youth, it's kinda the only thing that makes me feel like completely normal me again

And today i felt remarkably good considering. But im achy, some rls, last night the rls kinda rolled into akasthesia territory for a lil bit. That's what the phen and gabbies are for. And my mood is a bit flat. i wanted to get in touch with people and go out, but when it came to it i just didn't feel i had the head for it(plus most of my friends are old bastards and it's wednesday). But thats NOTHING, and before last night i had literally no ill effects, i actually felt pretty good. Did someone low dose ibogaine me? my friends are such jokers...

so confused. i got nothing...
 
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DoctorMolecule

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I don?t get high from Gabbies either, but god are they a life saver during WD?s. So really you?re just curious why you only have very minor withdrawals this time in comparison to other times. Are you exercising and eating well? That could be part of what?s going on
 

Troglodyte

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Yeah you are lucky. What are your using habits the last month?
This past month has been; 2-4x/week good quality heroin, quite possibly cut with a little fent analog cuz im not sure if theres much that isn't these days, but if some does exist, it's probably what im getting about 70% of the time. only 1-2 bags/day(but each bag up here is worth at least 2 of the points i was getting down in Asheville, NC, and for half the price. sorry NC, im not boasting, merely contextualizing. I i.v. 3/4 of the time til about 2 1/2 weeks ago when i stopped and went back to insufflating.

The other 3-5 days i used suboxone. 2-4mgs, or on rare occasion, kratom. I was angry at myself because i couldnt maintain on 1mg like i used to. I felt like crap when i tried. which adds to the enigma. days ago i couldn't keep well a 1mg of sub. then i do 3 bags and im cured. That dont compute.

the funny thing is that my wife and i had literally said that those were our last bags!... we were both steeled and focused to quit, finally at the same time. and i really believe we were ready, not that it was going to be easy in any way, but it was time. But i was expecting a long drawn out sub taper for a month, most likely kratom and a dizzying variety of other drugs to cushion when we finally jump from the sub... but no, those were literally my last bags and its over? I say "funny thing" but i feel really bad because it's not fair. Not to my wife, not to anyone else enduring the usual route. im overjoyed, but i feel guilty
 

Troglodyte

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And it's probably not relevant, but i also took 2/5 of a mg of sub a couple hours before the dope.
 
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Troglodyte

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I don?t get high from Gabbies either, but god are they a life saver during WD?s. So really you?re just curious why you only have very minor withdrawals this time in comparison to other times. Are you exercising and eating well? That could be part of what?s going on
up until last night i had literally zero w/d's. And tiny bit that developed i wouldn't even consider minor, i wouldn't consider half of minor. and they completely went away with low dose(for me) phenibut and gabbies.

I usually get so sick that i vomit so intensely that i can't get breath in and i get to the point of blackout and i get scared sh*tless that im gonna drop and aspirate and i cant yell for help.

i don't even have goosebumps

Something happened. this isn't unusual. This is completely unheard of as far as i can find


And no, i definitely dont excercise or eat well the last few months
 

DoctorMolecule

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Maybe because you switched back to snorting. I?m at a loss dude

Yeah just to reinforce what you?ve already said mixing soma and opiates is a no-no. So my hats off to you for staying some good harm reduction
 
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Troglodyte

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Could it be this:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701363/Low dose naltrexone administration in morphine dependent rats attenuates withdrawal-induced norepinephrine efflux in forebrain

Elisabeth J. Van Bockstaele,* Yaping Qian, Robert C. Sterling, and Michelle E. Page

Author information Copyright and License information Disclaimer

The publisher's final edited version of this article is available at Prog Neuropsychopharmacol Biol Psychiatry
See other articles in PMC that cite the published article.


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Abstract

The administration of low dose opioid antagonists has been explored as a potential means of detoxification in opiate dependence. Previous results from our laboratory have shown that concurrent administration of low dose naltrexone in the drinking water of rats implanted with subcutaneous morphine pellets attenuates behavioral and biochemical signs of withdrawal in brainstem noradrenergic nuclei. Noradrenergic projections originating from the nucleus tractus solitarius (NTS) and the locus coeruleus (LC) have previously been shown to be important neural substrates involved in the somatic expression of opiate withdrawal. The hypothesis that low dose naltrexone treatment attenuates noradrenergic hyperactivity typically associated with opiate withdrawal was examined in the present study by assessing norepinephrine tissue content and norepinephrine efflux using in vivo microdialysis coupled to high performance liquid chromatography (HPLC) with electrochemical detection (ED). The frontal cortex (FC), amygdala, bed nucleus of the stria terminalis (BNST) and cerebellum were analyzed for tissue content of norepinephrine following withdrawal in morphine dependent rats. Naltrexone precipitated withdrawal elicited a significant decrease in tissue content of norepinephrine in the BNST and amygdala. This decrease was significantly attenuated in the BNST of rats that received low dose naltrexone pretreatment compared to controls. No significant difference was observed in the other brain regions examined. In a separate group of rats, norepinephrine efflux was assessed with in vivo microdialysis in the BNST or the FC of morphine dependent rats or placebo treated rats subjected to naltrexone-precipitated withdrawal that received either naltrexone in their drinking water (5 mg/L) or unadulterated water. Following baseline dialysate collection, withdrawal was precipitated by injection of naltrexone and sample collection continued for an additional four hours. At the end of the experiment, animals were transcardially perfused and the brains were removed for verification of probe placement. Low dose naltrexone pre-treatment significantly attenuated withdrawal-induced increases of extracellular norepinephrine in the BNST, with a smaller effect in the FC. These findings suggest that alterations in norepinephrine release associated with withdrawal may be attenuated in forebrain targets of noradrenergic brainstem neurons that may underlie reduced behavioral signs of withdrawal following low dose naltrexone administration.

Keywords: HPLC, microdialysis, morphine, naltrexone, norepinephrine, withdrawal

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INTRODUCTION

Since their first use in opiate detoxification over 30 years ago, the administration of opiate antagonists (e.g. naloxone and naltrexone) during detoxification has varied either by differences in interval of administration between agonist and antagonist, or by quantity of antagonist administered (Kurland and McCabe, 1976; Mannelli et al., 2004). The closer the antagonist is administered to opiate agonist exposure, the more acute the withdrawal syndrome. Interestingly, the administration of small quantities of naltrexone or naloxone during opiate exposure induces “anti-withdrawal” effects (Shen and Crain, 1997; Mannelli et al., 2004). A better knowledge of the effect of opiate antagonists and their potential role during the detoxification process may help improve the quality of existing treatments

Our previous studies have demonstrated that concurrent administration of low dose naltrexone in the drinking water of rats implanted with subcutaneous morphine pellets attenuates behavioral signs of withdrawal and decreases the expression of c-Fos (used as an index of cellular activation in autonomic brain areas (Sagar et al., 1988)) in the noradrenergic locus coeruleus (LC) and nucleus of the solitary tract (NTS) (Mannelli et al., 2004). The LC and the NTS, known to be hyperactive following withdrawal from opiates (Hayward et al., 1990; Stornetta et al., 1993; Beckmann et al., 1995; Chieng et al., 1995; Georges et al., 2000; Mannelli et al., 2004), have previously been shown to be important neural substrates involved in the somatic expression of opiate withdrawal (Nestler et al., 1994; Aston-Jones et al., 1999; Mannelli et al., 2004). In addition, immunoblot analysis of intracellular messengers, cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) and cAMP-response element-binding protein (CREB), demonstrated to be dramatically increased in noradrenergic nuclei following opiate withdrawal (Guitart et al., 1992; Lane-Ladd et al., 1997), showed a decrease in expression (primarily in the NTS) in rats that had received low doses of naltrexone in their drinking water and that were subjected to pharmacological precipitation of opiate withdrawal (Mannelli et al., 2004). Potential explanations of the efficacy of the naltrexone treatment include the possibility that low antagonist dosing may act to facilitate enkephalin release by blocking opioid presynaptic receptors (Ueda et al., 1994). Alternatively, low dose naltrexone may antagonize excitatory opiate receptor functions and unmask the inhibitory effects of opioids (Shen and Crain, 1997). We also reported increases in opioid receptor expression (specifically of the mu subtype) in the NTS following antagonist treatment that may contribute to the attenuation of behavioral expression of withdrawal following low dose naltrexone treatment (Van Bockstaele, 2006). Increased expression of mu-opioid receptors may result in increased tonic inhibition of noradrenergic neurons in the NTS that provide noradrenergic innervation to forebrain targets resulting in decreased release of norepinephrine in limbic and cortical targets (Van Bockstaele, 2006).
In the present study, the hypothesis that low dose naltrexone treatment in morphine dependent rats attenuates forebrain noradrenergic hyperactivity usually associated with pharmacological precipitation of withdrawal (Crawley et al., 1979; Swann et al., 1982; Grasing et al., 1997; Fuentealba et al., 2000) was tested. First, we measured (from morphine dependent rats that received low dose naltrexone or unadulterated water) tissue content of norepinephrine from two forebrain regions that are targeted by brainstem noradrenergic nuclei: the bed nucleus of the stria terminalis (BNST) that receives noradrenergic projections primarily from the NTS (Dunn and Williams, 1995; Delfs et al., 2000) and the frontal cortex (FC) that receives afferents primarily from the LC (Robbins, 1984; Aston-Jones, 1985). We also examined tissue samples from the amygdala, a region that receives noradrenergic innervation from both the LC and NTS (Robbins, 1984; Aston-Jones, 1985; Dunn and Williams, 1995; Delfs et al., 2000), and cerebellum, which receives noradrenergic afferents solely from the LC. Subsequently, norepinephrine efflux in the FC and BNST was assessed using high performance liquid chromatography (HPLC) with electrochemical detection (ED).

(continued in link up top)


So it might be that low dose antagonist administered with a full agonist might encourage enkephelin release, the dampenining of excitory opiate receptor functions thereby "unmasking" the inhibitory effects(on noradrenergic neurons presumably?), upregulation of mu receptors thereby inhibiting noradrenaline and norepinipherine, or any combination of these.

I have been using suboxone, a partial agonist/antagonist with naloxone as antagonist, in relatively small doses and alternating with heroin for a while, then i took a microdose, took my last heroin, and stopped. It could conceivably be a similar protocol. What do you think? it's the only thing i've come up with yet, and it sounds feasible. i just dont know why no one else has stumbled into it if it is this. perhaps because of the expectation of using again and the automated behaviour of self administration?
 
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Troglodyte

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Would anyone else like to try microdosing suboxone along(actually prior to) with thier self administration of a full agonist for a couple weeks, then stop and see if withdrawals start and if they are nearly as bad as expected? it might not work, but this journal article and possibly my experience say it might. i'd think maybe like my last sub dose of 2/5's of a mg, or even lower. it's not enough to precipitate any withdrawal, and likely wont even effect the high from the DOC.

I was taking larger doses of sub, but not taking the full agonist until the next day when the levels of the sub had diminished significantly. so if someone is using everyday, taking a daily microdose a couple hours before might lead to somewhat equivalent blood and brain concentrations of the partial agonist and antagonist as i had at the time of agonist use, thereby creating what might be an equivalent situation.

any takers?

actually my wife is going to be my guinea pig i think. i sure hope this works
 
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fairnymph

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I thought I replied to this? I really think it's the nalaxone. You took enough for long enough to get rid of most of your tolerance/dependence. Continuing your sub use & occasional h would confirm this.

I don't have suboxone & I really hate how bupe makes me feel, but I do have nalaxone. Not very much though - probably not enough to use for more than a week. I'll check though. The bigger issue is that it's in pill form, 2 big doses, so dividing it into accurate micro doses will be problematic. I'd have to grind it into a fine powder, mix it well, then weight it out on my mg scale. But it might not mix well. If I have enough for 3wks I'll consider it. I'd definitely like to get my tolerance down.
 
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Troglodyte

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Whats the mg of the pill you have? I actually just read a study about someone they were detoxing, but the only naloxone they could source in switzerland was a 50mg pill, so they just shaved some off. not terribly scientific for a published study, i have to say. your method seems far smarter. That study was about something different and doesn't fit the situation at hand. But i do wish they published the mg/kg used in the study i posted above, woulda been pretty damn helpful... sheesh.

Also, i found a follow up study to the original one. i can't access the full text, im not in college anymore, but i did find this:

"To examine further the cellular mechanisms in noradrenergic nuclei that could underlie attenuated withdrawal behaviors following low dose naltrexone administration, the nucleus of the solitary tract (NTS) and locus coeruleus (LC) were examined for opioid receptor (OR) protein expression. Results showed a significant increase in muOR expression in the NTS of morphine-dependent rats that received low doses of naltrexone in their drinking water, and increases in muOR expression were also found to be dose dependent. Protein expression of muOR in the LC and deltaOR in either brain region remained unchanged. In conclusion, our previously reported decreases in c-Fos and PKA expression in the NTS following pretreatment with low doses of naltrexone may be partially explained by a greater inhibition of NTS neurons resulting from increased muOR expression in this region."
 

Troglodyte

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so i did the math and it was generally about 0.1mg of naloxone i was taking shortly before my doses of full agonists. that's gonna be a very small portion of a 50mg pill... guess thats why they were shaving a pill...

And i think naltrexone would be even more effective for this purpose tbh. in fact the short halflife of naloxone is actually making me rethink whether that couldv'e been the deciding factor at all... hmmm. it could, and i have to look back at my dosing the best i can. and i wonder how much buprenorphine itself might have a similar effect.
 
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fairnymph

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I would probably try 5mg to start, so I have plenty for a test run. You dosed 1x daily with the sub? I use continously, so there is no way for me to pre dose, though I could take it first thing when I wake up. But I couldn't wait long before using more h due to how bad my pain is on waking. I have to try to nip it in the bud ASAP. Maybe I should dose midday?
 

Troglodyte

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That sounds kinda high. be careful. i can't find a real equivalency chart anywhere and i don't know much about naltrexone dosage. But i found a reference in a study that suggests that 0.5mg/kg of naloxone is equivalent to 2mg/kg of naltrexone. If thats accurate, maybe you should try 1mg. you don't want to accidentally precipitate withdrawal. Or maybe your a masochist and into that sort of thing. what do i know. But i would advice starting low, and finding some concrete equivalency info.

And to answer your other question, i was taking sub 1-2 or maybe 3x a day, but it was only because i was trying to take the smallest amount i could, so i'd take a mg or 2, then an hour or 2 later i'd have to add to it to find the smallest comfortable dose, which was about 3-4mgs usually. sometimes i would do dope later that day, but often it was the next day, so i guess the naloxone would be gone, but can bupe antagonize enough to make an effect? I emailed one of the authors of the study i posted and i'm hoping to hear back. meanwhile i have my wife microdosing sub and continuing to do her H, which im very surprised to find, isn't effecting me too much in terms of cravings. In fact i drove her to pick up earlier, the same route to the same place i've been a million times before to score, and i was fine, in a good mood, chipper if you will. This gift is really focusing me and lifting my mind out of the reflexive urges ive been slave to for so many years. i couldn't believe i could drive there and be fine. I wasn't going to do it, but then i rallied my strength an did it without any problem. We're going to try 2 weeks for her, continuing to use but taking microdoses before. your naltrexone will last all day, but we're going to have to time this well with naloxone, and hope it has some effect. it might well not. But the possibility of it working makes the experiment worth it either way.

Hopefully i'll get clarification on a few things, like the dose of the naltrexone used in the study, and the duration of the co-administration from the author of the study. Maybe she'll even express interest in my case, who knows. I desperately want to figure this out so it can help others. This is too big to just happen to me and end there. So many others have suffered gravely as i have, and we all deserve a road out of that hell. Many lives can be saved. That's all i want, and thats why i made this thread and the one i made in ADD, originally to try to find a referal to a researcher that might be interested so that we could maybe get to the bottom of this.
 

Troglodyte

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I also noticed today that i had a paradoxical reaction to adderall for the first time in my life. That might elucidate some of the goings on here. But, tho i'm pretty well versed in this field, i regret that i don't have the requisite knowledge to tie that in. i just emailed another author of the study. i hope i hear back
 
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