A big reason the doctors are putting people on this crazy high doses is to basically sign them up for life on that shit.
There is actually clinical utility to larger doses - because of the half-life, when the drug is taken daily it accumulates considerably. A single 4mg dose will typically block the effects of someone's usual dose of an opioid for around 24 hours. This can vary where some people will not get as complete a blockade effect from that dose or the blockade's duration may be longer or shorter.
The main reason doctors are urged to push doses that are considerably above the threshold for maximum agonism (2-4mg) is because it drastically strengthens and prolongs the blockade effect. I can't count how many people I've known who used 1-2mg of suboxone on days where they couldn't cop or who would maintain on that most days so that when they wanted to/were able to get high, they easily could 12-36 hours later.
If someone is taking 8, 16 or 32mg/day, the amount of time they'd have to wait for the receptor saturation to clear is substantially longer. If someone has seriously struggled with an opioid habit, tried to quit and kept going back ensuring that every time they are tempted or even decide 'fuck it, I'm getting high', they have to wait 3, 4, 5 days, it seriously cuts down on the ability for a person to have a momentary lapse and slip up. If someone is genuinely trying to get clean, working a program or just serious about not going back to that life, that waiting period can make a huge difference.
With that said, there are a lot of doctors who are seriously mis- or under- informed, a lot of junkies who get extra to stash or sell and plenty of addicts who have no idea about the ceiling effect of agonism being as low as it is and think taking more and more will have a linear effect like full agonists. There are many factors that lead to widespread misunderstanding on this subject.
"It takes 24-32mgs of suboxone to completely saturate all the opioid receptors", they supposedly figured this out by using a brain-scan or something like that, a doctor told me how they arrived at this conclusion once, but it's clearly complete bullshit. Well, it does completely saturate your receptors, but it'[s way beyond any amount that someone actually needs to maintain an opiate habit!
I went to a state conference and attended a workshop with a Reckitt-Benckiser representative and discussed this with him. It's well-established that the ceiling effect to the opioid *agonist* effects is quite low but as discussed above, that is only part of the reason this medication is used. The reason this drug has become so widespread is because for a substantial amount of opioid users it can produce enough agonism to curb that craving that leads so many back time and again but it also helps to prevent using other opioids while on it (especially higher doses).
Methadone users can go out and shoot up on top of the methadone and while they might have some of the effects diminished through high-dose methadone increasing their tolerance, they can still feel the effects and they can still overdose quite easily.
Naltrexone users (whether via oral or implant) basically have their opioid receptors completely locked down so they can try to shoot up all they want and feel nothing but for so many, they are left with that lasting, nagging craving as well as the side effects of having their natural endorphins blocked as well.
Buprenorphine is intended to strike a balance and deal with both the craving and make it more difficult for users to get high via the blockade. The reported 32mg ceiling they found was the dose where there ceased to be any additional gains in the strength or duration of that blockade (again, according to the R-B representative).
