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Bupe Suboxone/Buprenorphine FAQ & Megathread v3; 2010 - 2022

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K88ABY said:
Thing with bupe is that it should only be used as a SHORT TERM way of getting off whatever other opiate. Otherwise you will just swap one addiction for another. I have sucessfully detoxed more than once using just 5 8mg subs over a peroid of 10 days. It's very doable, and I am infact starting yet another cleanup tomorrow as I only have 1 bag of the other left.
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isnt the point to stay clean though..? detoxing is easy... staying clean is another story compared to that
 
FlyBoy81 said:
Hello fellow dopeheads,

I have had an over 10 year relationship with opiates. I've done most of them, and over the past 10-11 years I've been physically addicted for about 6 or 7 years with my longest addiction being to morphine for about 4 years straight. I've been addicted to Morphine, Oxycontin, Hydrocodone, and Tramadol. My longest clean streak in that period of time has been about a year. I've gone through 3 horrible withdrawals and multiple "minor" withdrawals during that time, but for some reason I keep going back. I get bad panic attacks and severe cravings along with some depression here and there although I don't really consider myself depressed.

I have heard that once you get on Methadone (don't want to do that) or Suboxone (my preferred option) that it is extremely hard to stop because the withdrawals are long and drawn out, so it's more of a safe maintenance rather than a detox tool.

Should I consider going to a doc and getting on Sub maintenance? I'm currently physically addicted to opiates at this time unfortunatily . Have anybody in a simlilar situation to mine gotten on subs and are happier? Any one regretted it? I'm seriously considering this as an option. Thanks for any help....
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So given my situation, is this as a 'maintenance' drug probably the best choice for me? I've detoxed only to relapse again and again. If I stayed on it a while, I could always do a really slow taper and try to jump off later. What do you guys think here?
 
Oh could I here from some long term Suboxone users? How are you? Depressed, or living okay? Is your life better than if say you had lots of money to buy whatever you wanted forever?
 
Interesting. Anyone care to explain why? Is it purely a case of methadone being the stronger opiate here and therefore the subutex wouldn't 'break through' to the receptors to get me high?

Much appreciated guys. :)
 
Interesting. Anyone care to explain why? Is it purely a case of methadone being the stronger opiate here and therefore the subutex wouldn't 'break through' to the receptors to get me high?

Much appreciated guys.
 
I enjoyed my time on bup. After every dose, I got a nice rush of energy and it had an antidepressant quality to it. Was fairly easy to taper off too.
I would recommend it over methadone. Although methadone makes for an easier transition, bup is alot easier to live with after induction.

Bup w/d can be bad if you jump off above 1mg/day, just keep going down till youre at 500mcg doses then taper down with some tramadol for a week . Most any doc will prescribe it cause it isnt scheduled.
 
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Alright I have an odd question.

I'm a regular user of snuff (Nasal Tobacco, Nose Chew) and am wondering how that will effect a nasal dose of suboxone? I know that people will add sodium carbonate to their snuff (I don't) to increase the pH to a more neutral level so as to increase bio-availability. That makes me question: Is my snuff making the mucous in my nose acidic enough that it will greatly effect the absorption of the bupe or break it down like the acidity of the stomach does?

further more would adding some alkaline ingredient to insufflated bupe increase the bio-availability? -sort of doubting this one but, who knows, a lot of people have overly acidic diets..
 
Buprenorphine Less Is More - or is it?

Is this any new information regarding bupe, norbupe, and the whole "less is more" theory?

http://derekwmeyer.blogspot.com/2011/07/followup-to-less-is-more-buprenorphine.html

"...Buprenorphine has NOT been proven in humans to have a bell-shaped dose response curve; also, this bell-shaped response shown in lab-studies was shown for only certain effects. Even assuming that bupe indeed does produce an actual DECREASE in intrinsic activity at higher doses, this pattern would take place beyond the 0 to 8mg level, more likely in doses well in excess of the clinically observed (many times over, in hundreds of subjects) ceiling range of buprenorphine's intrinsic ceiling (roughly the 24 to 32mg range) for tolerant/dependent maintenance users.

Again, there is no solid evidence in humans that buprenorphine's intrinsic activity actually DECREASES at higher doses , rather than simply level off with no further increase.

Also; I think some folks are misinterpreting the context in which the term "mixed agonist-antagonist" is used in reference to buprenorphine; this refers to its ability to produce positive analgesic & reinforcing agonist acvtivity in post-detox opioid users or opioid naiive individuals while at the same time, playing the role of an antagonist with its tighly bound blocking of full agonists from associating with mu-receptors (this indeed is an antagonizing property) - additional properties earning it the antagonist reference include its tendency to precipitate withdrawal via its competitive binding in place of full agonists in dependent individuals, leading to a net-decrease in intrinsic activity, thus, acute opioid withdrawal (a property similar to naloxone).

It may also be taken in part to reference the kappa antagonist effect of buprenorphine. Considering the aforementioned properties along with its limited agonist properties, bupe can be referred to as an agonist/antagonist, or an opioid partial agonist with individual antagonist traits under certain conditions.

This is not at all to say that I am refuting the possibility of a bell shaped dose response curve in humans, particularly in the maintenance context, but to try and explain what I believe is misunderstood by some; it doesn't help with people all over the web perpetuating the phrase "less is more" as if it's really so simple.. Indeed many have actually listened to this type of anecdote and end up either sick, or "craving" (i.e. inadequately medicated)

Yes, with low doses of bupe, if one's tolerance permits, one will experience pronounced euphoric/anxiolytic and opiate-type effects and actually FEEL each dose, as opposed to feeling no lift, no glow, and no increase in effect as with higher maintenance range doses (4 to 16mg) and I believe this is leading some to believe that the higher (plateau-level doses) are in fact providing a LESSER intrinsic agonist effect than these fun little micro-doses.
Believe it or not - though a higher dose (8 to 12mg for instance) may not produce the obvious glow you feel at .5 to 1mg, you are in fact MORE stimulated than you are with the micro-dose (which is indeed why you feel so little). That's right, an 8mg dose will keep withdrawal at bay longer, and more effectively than a 1mg dose.

There's much more to it than "less is more", and this statement is almost senseless in a way, and comes riddled with assumptions which have never been proven clinically in the human-maintenance setting; and even if it were, this particular myth still would not apply. as this mythological NET-DECREASE in mu-stimulation would take place in double digit doses well beyond the typical maintenance range.. (opposed to a 0 to 2mg range)

So, micro dosers; by all means continue low dose bupe, I am happy you are able to keep yourself in that low range and am not surprised you "feel" more, but what alot of these folks suggest to someone such as this OP who in fact do not find these low doses effective (and won't unless they taper themselves to this level of tolerance), is a bit misleading, very misleading actually. I say that with all due respect.

I'm just weary of hearing this already somewhat strangely chosen -and more methaphorical than factual - phrase taken far out of context in a way that simplifies and distorts the true understanding of bupe's pharmacological properties
 
jojoodd said:
Interesting. Anyone care to explain why? Is it purely a case of methadone being the stronger opiate here and therefore the subutex wouldn't 'break through' to the receptors to get me high?
Click to expand...

I would expect that you would experience precipitated withdrawals.

An associate of mine took 8mg sub while taking 40-60mg/day of methadone and was almost immediately thrown into what he described as, 'the most excrutiating, unbearable experience of my life.' He ultimately resorted to using a rather large amount of black tar to get back to 'normal.'
 
Hey yall, I'm currently on 1.75mg. When I was on 8mg it merely kept me well. 6mg and then 4mg same. When I began 2mg I actually began feeling the very subtle antidepressant and stimulant effect - or it's a helluva placebo.

I've picked up the pieces of my life and am chugging along very well, but I am wondering if I can get away with a bit of euphoria from my rx'ed script.

I used to take the bigger dosages SL exclusively, but now as I get to lower <2mg doses, I occasionally insufflate it.

My question is this, when I gradually go down to 1mg and lower, is there a chance I will experience more full agonist effects?
 
scruples said:
I would expect that you would experience precipitated withdrawals.

An associate of mine took 8mg sub while taking 40-60mg/day of methadone and was almost immediately thrown into what he described as, 'the most excrutiating, unbearable experience of my life.' He ultimately resorted to using a rather large amount of black tar to get back to 'normal.'
Click to expand...

I will also attest to this. Luckily I had a bottle of morphone'
 
As someone with very low opiate tolerance, this explains a lot.

4mg of bupe was enough to pretty much disable my ability to walk.

Thanks for the info, I could never understand this substance fully.
 
Hmm so what you saying is im getting more of a effect at 12mg then the person at say 1mg just he feels his 1mg more then I feel my 12mg right? Do I got that right?

So to me who takes 12mg would a 2mg redose give me added effect? or 4mg? or would I be better of waiting for some of it to wear off before taking more?
 
cdigital said:
Is this any new information regarding bupe, norbupe, and the whole "less is more" theory?

http://derekwmeyer.blogspot.com/2011/07/followup-to-less-is-more-buprenorphine.html

"...Buprenorphine has NOT been proven in humans to have a bell-shaped dose response curve; also, this bell-shaped response shown in lab-studies was shown for only certain effects. Even assuming that bupe indeed does produce an actual DECREASE in intrinsic activity at higher doses, this pattern would take place beyond the 0 to 8mg level, more likely in doses well in excess of the clinically observed (many times over, in hundreds of subjects) ceiling range of buprenorphine's intrinsic ceiling (roughly the 24 to 32mg range) for tolerant/dependent maintenance users.

Again, there is no solid evidence in humans that buprenorphine's intrinsic activity actually DECREASES at higher doses , rather than simply level off with no further increase.

Also; I think some folks are misinterpreting the context in which the term "mixed agonist-antagonist" is used in reference to buprenorphine; this refers to its ability to produce positive analgesic & reinforcing agonist acvtivity in post-detox opioid users or opioid naiive individuals while at the same time, playing the role of an antagonist with its tighly bound blocking of full agonists from associating with mu-receptors (this indeed is an antagonizing property) - additional properties earning it the antagonist reference include its tendency to precipitate withdrawal via its competitive binding in place of full agonists in dependent individuals, leading to a net-decrease in intrinsic activity, thus, acute opioid withdrawal (a property similar to naloxone).

It may also be taken in part to reference the kappa antagonist effect of buprenorphine. Considering the aforementioned properties along with its limited agonist properties, bupe can be referred to as an agonist/antagonist, or an opioid partial agonist with individual antagonist traits under certain conditions.

This is not at all to say that I am refuting the possibility of a bell shaped dose response curve in humans, particularly in the maintenance context, but to try and explain what I believe is misunderstood by some; it doesn't help with people all over the web perpetuating the phrase "less is more" as if it's really so simple.. Indeed many have actually listened to this type of anecdote and end up either sick, or "craving" (i.e. inadequately medicated)

Yes, with low doses of bupe, if one's tolerance permits, one will experience pronounced euphoric/anxiolytic and opiate-type effects and actually FEEL each dose, as opposed to feeling no lift, no glow, and no increase in effect as with higher maintenance range doses (4 to 16mg) and I believe this is leading some to believe that the higher (plateau-level doses) are in fact providing a LESSER intrinsic agonist effect than these fun little micro-doses.
Believe it or not - though a higher dose (8 to 12mg for instance) may not produce the obvious glow you feel at .5 to 1mg, you are in fact MORE stimulated than you are with the micro-dose (which is indeed why you feel so little). That's right, an 8mg dose will keep withdrawal at bay longer, and more effectively than a 1mg dose.

There's much more to it than "less is more", and this statement is almost senseless in a way, and comes riddled with assumptions which have never been proven clinically in the human-maintenance setting; and even if it were, this particular myth still would not apply. as this mythological NET-DECREASE in mu-stimulation would take place in double digit doses well beyond the typical maintenance range.. (opposed to a 0 to 2mg range)

So, micro dosers; by all means continue low dose bupe, I am happy you are able to keep yourself in that low range and am not surprised you "feel" more, but what alot of these folks suggest to someone such as this OP who in fact do not find these low doses effective (and won't unless they taper themselves to this level of tolerance), is a bit misleading, very misleading actually. I say that with all due respect.

I'm just weary of hearing this already somewhat strangely chosen -and more methaphorical than factual - phrase taken far out of context in a way that simplifies and distorts the true understanding of bupe's pharmacological properties
Click to expand...


Yes, yes, and YES!... The "less is more" philosophy really has been taken too far. Don't get me wrong; there are situations in which this apply. But that is for people with LOW tolerances. If you have a considerable tolerance, then the "low dose bupe" regimen is not going to cut it. I mean the whole premise is flawed, really. Especially IV. Just to reiterate the situation, buprenorphine is metabolized by the CYP3A4 enzyme into norbuprenorphine. Now bupe itself is only a partial agonist; an extremely potent partial agonist, but a partial agonist nonetheless. Norbupe is a full agonist. Thus the belief is by doing small doses, the body will produce norbupe and, in turn, there will be open receptors for it to attach to. If we were talking about other MOA's, such as sublingual and especially oral(horrible BA notwithstanding) it would make more sense, as the body would be able to convert a higher portion of the dose to the full agonist, norbupe. But IV, the conversion happens AFTER bupe hits the blood brain-barrier. And even then, it happens slowly, and only a little bit at a time. Now bupe antagonizes it's own metabolite, so the way I see it, any norbupe will simply be blocked by bupe itself.

I am not denying the low-dose regimen works. I just belive it only works in very small doses. The obvious problem with that is that most people taking suboxone/subutex will already be addicted and therefore have a considerable tolerance. In this case, any full-agonist effects achieved will be all but irrelevant, because at such small doses they will not be held from they're initial addiction. I IV my suboxone, because I cannot afford to go to a doctor to buy the ridiculous $10 per pill, not to mention the dealers(ahem, doctors) fee. And as many times as I tried, microgram doses do nothing for me, because my tolerance is just to high. But there are other things that make me skeptical. I myself have tried using st. john's wort to achieve these mysterious full-agonist effects I hear so much about. At small doses, it had no effect, and at heroic doses, it actually LOWERED my euphoria, and caused me to need double my dose just to hold WD. ALso I have given friends with no opiate tolerance suboxone. IV, they seemed to get no effects until a 2nd dose was given, in which case the effects seemed the same. Low dose via the sublingual route seemed to fare better. It took a while for the "subject" to get noticable effects, but once they did, they much preferred it to the longer recreational doses.

ANyway, I am just blabbing on at this point, but I just wanted to state my opinion(and experience) with this matter, and give you props for bringing up an issue that has always seemed suspicious to me.

(One more interesting thing: I almost have to use CYP3A4 inhibitors(specifically Large doses of tagament/WGFJ) to get full effect from my bupe. I say this because logic say's that using enzyme inhibitors will actually reduce the effect of bupe, because it eliminates the body's ability to produce norbupe. Yet whn I take inhibitors with bupe, I am actually able to get euphoria which helps me too not crave other drugs as much, and the individual injections last much, much longer. Now without inhibotrs for more than a day or so, I literally have to double my dose, and then get no euphoria, just relief of WD, further leading me to believe that norbupe is rendered useless, because bupe itself antagonizes it.)

2 more things why I remember:
1. When you IV suboxone your getting a full dose of active Nalaxone. Buprenorphine has an even higher binding affinity then nalaxone, rendering nalaxone useless. But does norbupe, a full agonist, have this same binding affinity? Considering that bupe itself blocks norbupe from reaching mu receptors, I would say HELL NO, because bupe does NOT antagonize the mu receptor, yet norbupe is still not getting through, leading me to believe that it doesn't have the same binding affinity as bupe itself, meaning via the IV route, nalaxone would be beating it to any receptors that bupe isn't holding, at least rendering it even more useless for the first 60-90 minutes and
2. I have heard norbupe isn't as good as crossing the BBB, but haven't found any good evidence to this effect.
 
Sort of seems like the gabapentin phenomenon. Not saying it's anywhere near the same chemical reason for the bioavailability degeneration.
 
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