|>> || 1582932566268.jpg -(31391B / 30.66KB, 600x412) Thumbnail displayed, click image for full size. >>613895 |
The naloxone isn't even relevant in your case. Naloxone only matters when it comes to switching from a full agonist to bupe+naloxone, and even then it ONLY really matters if you're inducing micro/low doses, like ~1-2mg in particular, or I guess possibly up to 4mg bupe, and ONLY if you use it via IV, I guess IM/SubC, and to about half the extent if you snort or boof it. EVEN THEN, its impact is debatable, not experienced by everyone, and even if it is noticeable, it's relatively marginal.
Bupe displaces full agonists, which causes precip WD if you're dependent. If you induce say 0.5mg of bupe via IV (~1.5mg or so sublingual equivalent), you also IV 125ug of naloxone. That means that (making up a fake number to show my point) if say 0.5mg IVed bupe alone would normally displace say 33% of receptor sites, if basically all your receptor sites were occupied by say oxycodone, it would cause (at least on "paper," experience isn't linear) 33% of the max precip WD causable by a full bupe replacement on your receptors.
By since only 33% of receptor sites would be displaced, that means the additional 125ug naloxone would have access to additional undisputed oxycodone-activated receptor sites, allowing the naloxone to in theory cause additional precip WD. And on paper, something like naloxone/naltrexone should cause worse precip WD symptoms than bupe, assuming they occupy exactly the same quantity of receptors.
Now it gets more complicated because it's not entirely clear if naloxone truly has a subjective threshold "requirement," or if such threshold is different when combined with bupe and a full agonist in a vacuum compared to just oxy and naloxone. Either way, according to at least one source I read, just ~0.2mg naloxone IVed is capable of causing precip WD, at least without bupe around.
Supposedly something like ~8mg bupe via SL use (or in theory ~24mg if taken orally via intact tablet/film without dissolving/being kept in the mouth), ~5-5.33mg snorted/boofed, or ~2.5-2.67mg IVed occupies ~80-90%+ of one's receptors, and that's assuming no previous bioaccumulation from previous doses. The more receptors are replaced with bupe instead of say oxy, the fewer receptor sites are conveniently available for naloxone. Once you reach ~90%+ bupe receptor saturation, pretty much all the conveniently available receptor sites that were either entirely empty of exogenous opioids or occupied by oxycodone have been replaced.
So just about any receptor sites that might have had oxycodone ripped off and replaced by naloxone, would in turn be ripped off and replaced by the bupe.
>tl;drnaloxone in suboxone only really is even possible of making a difference if you're already physically dependent on a full agonist and therefore at risk of precip WD, only if your bupe doses are below 4mg sublingual equivalent (possibly below 6-8mg to a much lesser degree), and ONLY if you snort, boof, or inject suboxone. Snorting or boofing the naloxone portion of suboxone is only capable of causing roughly half the potential marginal WD as IVing it mg for mg, and even then it's less sudden.
Even then, we're talking such marginal effects. I personally didn't notice any difference between suboxone and subutex when dependent on PST in the past, whether subbed, snorted, or boofed.