Difficulty inducting on subutex; a novel method to induct...

[bdomihizayka]

My sister has been on an on and off again opiate splurge for the past month. She’s been snorting 3-5 “nick” bags of “dope” 3-4 times a week.

I put “dope” in quotes; some of it may be heroin, but it’s definitely some unknown, long acting opioid or analogue in there as well.

She tried 3 times to get onto subutex, all unsuccessful. The withdrawal comes on slow, and she’s good the first 24 hours.

The first time, she made it to 36 hours, took 2mgs of subutex, and precipitated badly. Second time- 48 hours- sane deal. Third time- somewhere in the 60 maybe 70 hour range, and, well, same deal.

She pissed negative for methadone after the second precip misadventure- so her “dope” definitely isn’t cut with that. Positive for opioids. She’s using the same stamp. She’s probably inducted dozens of times and never precipitated for longer than ten-thirty minutes before the bupe would kick in- this is not the case here.... each time she’d twist around in the shower in agony for a couple hours before I’d agree to give her a ride and know she’s not bullshitting me.

Also, I don’t think she’s lying. She’s not a good actress, and the signs are there that the bupe isn’t working (hyperhydrosis, projectile vomiting etc).

On another drug forum, there are dozens of threads recently about people having the exact same problem. Waiting a couple/ few days to induct, and going right into precipitated withdrawals.

I’m am an addict myself and know for a fact she’s hasn’t been using longer, as we live together, and I see the quantity she uses to get her out of precip- so I have a gauge at where her tolerance is at, and it’s not making any sense-nor does it for all the other people on the other forum who are complaining.

I came about this article- a novel way of inducting patients onto bupe Buprenorphine Rescue from Naltrexone-Induced Opioid Withdrawal During Relatively Rapid Detoxification from High-Dose Methadone .

Any thoughts?

I’ve also come across a post here on bluelight where OP would take a sub, precip on purpose, use heroin to stabilize, then immediately take another sub, and swore that it worked. They never specified how much sub they took, but the theory/method seems similar enough.

Anyways, any and all input/ advice/ discussion would be nice. Now that I’m off the shit, I’d love my sister to join me.

Have a lovely day and thank you!

 

[sekio]

methadone or SR oral morphine are probably better, after all buprenorphine is only a partial agonist, if you are accustomed to strong full agonists like fentanyl doubly so

2mg is a pretty solid dose so your options are really either toughing it out and continuing taking bupe until she (eventually) feels better, maybe in inpatient setting with iv fluids and zofran/cesamet or smth., or switching to a full agonist therapy

this kind of makes me think the dope she is using has something like carfentanil in it... very strong agonist that overrides the bupes effects, so you feel fine until you have none left in your system (say 24-48h) then the bupe starts to bind and acts as a partial agonist -> sickness and w/d. Especially if taking more dope makes the bupe sickness go away - normally you can take heroin on bupe and it has very little if any effect, but fentanyl/carfent not so.

 

[rave23]

I've had an experience with a botched induction of suboxone last year.

I had 2 years of sobriety before I relapsed. I bought fent of the darknet, and used for like three months. What I got, I'm not sure, but it was extremely potent and short acting, which made me think fentanyl or it's analogues. It also had the typical rapidly increasing tolerance from a point every two days to a gram a day in a little less than 2 weeks. I knew I was fucked. Anyways, I went to the clinic and got myself an at-home induction kit for suboxone (2 mg every hour up to 16 mg for the first day, then up to 16 mg until the next appointment a few days later), where I took a piss test and tested hot for fent and oxycodone (never took oxycodone in my life so that was weird), and went home to do this.

I waited as long as I could take, which turned out to be 16 hours (with withdrawal starting at the 6 hour mark), took the first 2 mg and just crossed my fingers. Fat mistake. Less than thirty minutes later the bowel movements came in three distinct stages (I spare you the details, but think the three states of matter for that one), and another half hour later I nearly passed out puking. Oh well, I must have had a case of precipitated withdrawals right, nothing out of the ordinary and I was prepared for it, or so I thought.

What I wasn't prepared for was three days of catatonic misery and the worst withdrawal I've ever been through. It did not get better going up to 16 mg of suboxone, and it did not resolve in 24 hours with another 16 mg on top of it.

No idea what the hell I was on, but back when I ran into precipitated withdrawals with Heroin, it lasted a little less than a day and by day 2 I could walk again. This was not the case with whatever shit I ordered off the web, and I was floored for three solid days and a relatively large dose of suboxone In me. I don't think that was fentanyl. I kept testing positive for fentanyl for three more weeks after that, which also struck me as odd. I honestly don't think waiting 24+ hours until switching to suboxone would have mattered in this case.

The only thing I could think of I perhaps some analogue that occupies receptors that takes ages to clear. Usually suboxone should displace whatever is in you over some time, but it felt like whatever was in me was fighting with the suboxone for three solid days for binding. I'd like to know more about this. I still have some of this devil dope for academic purposes, as I'd like to get it conclusively tested one of these days. Any clue of there's services that can test this perhaps?

 

[Coffeeshroom]

This clearly differs from person to person, as i can take 2mg subutex roughly 18 hrs after last use and not get precipitated withdrawals. and this is also after a binge on H. But like i said that's just me.

 

[dopamimetic]

Why is a partial agonist worse than none? Shouldnt precipitated wd only happen while a stronger agonist with weaker affinity is active?

 

[dopamimetic]

Push (sorry). Guess there must be kappa opioid effects in the OP ... ? As bupe is a kappa antagonist.

 

[sekio]

Why is a partial agonist worse than none? Shouldnt precipitated wd only happen while a stronger agonist with weaker affinity is active?

Precipitated withdrawl only occurs when you have a high-efficacy (full-agonist), low-affinity opioid suddenly being displaced by a lower-efficacy (i.e. partial agonist, neutral antagonist, or inverse agonist), high-affinity opioid. This leads to an overall decrease in opioid receptor activation, which leads to withdrawal symptoms.

You can compare this to the effects produced by Narcan (naloxone) on someone who is high on opioids (for the sake of argument let's say morphine). The naloxone has a higher affinity, but does not activate the opioid receptors. Therefore, the morphine is displaced from the receptors, opioid receptor activation ceases, and more often than not some unpleasant effects develop - nausea, panic, generalized malaise, gastric hypermotility, excessive sweating, hyperreflexia, etc - until the naloxone has been metabolized/excreted, generally after 30-60 minutes.

Some people find that making the transition from a strong full agonist like fentanyl to a partial agonist is a rougher experience than substitution with a full agonist like methadone, or even just letting the fentanyl slowly leave the body (I would imagine that with chronic, high dose fentanyl usage, there could be blood levels high enough to provide at least the theoretical possibility that there could still be mu-opioid activation at some level. Also, I'd think your natural endorphin peptides would have their acitivty reduced by buprenorphine as well. This all means some people find buprenorphine overall doesn't work for them. Then again, some people prefer it!

Further reading: comparative binding affinities of many opioids, efficacy vs affinity vs potency, extensive review on mu opioid receptor

 

[copium7777]

I wonder if taking ultra low dose naltrexone with the fentadope and gradually upping the dose of naltrexone before inducing on subs could help. With ultra LDN there is usually a p low risk of precipitating withdrawals and maybe could start the mechanisms of reversing tolerance r enough to make for a softer fall when you jump onto subs. Maybe ita a dumb idea. Just something to ponder

 

[AlphaMethylPhenyl]

Precipitated withdrawl only occurs when you have a high-efficacy (full-agonist), low-affinity opioid suddenly being displaced by a lower-efficacy (i.e. partial agonist, neutral antagonist, or inverse agonist), high-affinity opioid. This leads to an overall decrease in opioid receptor activation, which leads to withdrawal symptoms.

You can compare this to the effects produced by Narcan (naloxone) on someone who is high on opioids (for the sake of argument let's say morphine). The naloxone has a higher affinity, but does not activate the opioid receptors. Therefore, the morphine is displaced from the receptors, opioid receptor activation ceases, and more often than not some unpleasant effects develop - nausea, panic, generalized malaise, gastric hypermotility, excessive sweating, hyperreflexia, etc - until the naloxone has been metabolized/excreted, generally after 30-60 minutes.

Some people find that making the transition from a strong full agonist like fentanyl to a partial agonist is a rougher experience than substitution with a full agonist like methadone, or even just letting the fentanyl slowly leave the body (I would imagine that with chronic, high dose fentanyl usage, there could be blood levels high enough to provide at least the theoretical possibility that there could still be mu-opioid activation at some level. Also, I'd think your natural endorphin peptides would have their acitivty reduced by buprenorphine as well. This all means some people find buprenorphine overall doesn't work for them. Then again, some people prefer it!

Further reading: comparative binding affinities of many opioids, efficacy vs affinity vs potency, extensive review on mu opioid receptor

Well I don know that peptides are way big and go a long way in the brain comapred to smaller chemicals, but...

I know that abilify is a partial. At higher doses, it seems, it has low efficacy, so a low ceiling basically. But it's still an antipsychotic and a D2 partial.

Bupe is getting a name for itself in treatment-resistent depression. Other opioids don't work well without constantly raising the dose. I've even heard that, over a longer period of time, opioid dependence can cause depression itself, and can even lead to more physical pain. I believe it was on this forum. But you'll probably know the latest.