Opioids How often can I dose Bupinorphine 2mg and under for maximum Norbupe potential?

[SirSalty]

So if you didn't know doses of 2mg or less turn into the full opioid agonist Norbupenorphine whereas higher doses don't and traditional Bupinorphine is only a partial opioid agonist.

I've heard people describe it as "less is more"..

My thoughts are:
1. What is the half life of Norbupe?
2. How often can you dose 2mg and under for maximum effect?
3. Does this mean that 'jumping off' would actually be harder at LOWER doses of 2mg and under compared to the 4mg a day I'm currently on.

I am not so good at using my own experience for reference as I'm on so many drugs for my bipolar and anxiety disorder that I don't even know but to me 2mg does actually feel stronger than 4mg and a lot of other people will attest to that.

I'm just curious how long it takes to 'reset' where you can take another 2mg and it act the same way.

I'm hopeful that some interesting theories will stem from this thread at the very least if not a scientific concrete answer.

Many thanks

 

[DeathIndustrial88]

I don't believe norbupe is even active in the CNS when using bupe.

The reason bupe feels more like a full agonist in lower dosages, I think has more to do with blood levels.

Let's say you have 100 opioid receptors & you take 4mg of bupe. Let's say that 4mg covers 80 of those receptors & sticks around for 24+ hours.
So when you go to take 4mg again the next day, it only has 20 receptors it can attach to & now you're at 100% of your receptors covered. So taking more the next day isn't going to do a whole lot.

Now let's say 2mg only covers 30 receptors. When you go to take 2mg again the next day, you still have 70 receptors open that can be activated.

Once that half-life of the 2mg drops, you'll have even less in your system as well, where was with 4mg, you'd still have 2mg in your system when it's half-life is over.

I made those numbers up, but it still gets my point across. The higher you dose, the more your receptors become saturated & don't allow for anymore agonism with subsequent dosing.

Saturating your receptors that fast not only stops more agonism but also increases your tolerance exponentially.
This is why lower doses have more an effect than higher doses, but it's because you're leaving receptors open for your next dose rather than norbupe being active.

In order to keep that 2mg working well, you'd probably have to go at least 24-48hrs in between dosing. Buprenorephine has a ridiculously long half life, so each dose stacks up on top of one another. Essentially you'd want to keep your doses low, like 0.4mcg every couple of hours or something. That's how it gets used for pain, in micrograms every 4-6hrs. Because that 0.4mcg will wear off much faster & leave your system a bit faster than taking 1mg & up.


Buprenorphine was a great help for stabilizing my mood, so you should have some luck in that department at least.


I found the "less is more" theory a bit faulty & risky, because years ago I would only stick to low doses too & my cravings started coming back with insane vengeance. It wasn't until I raised my dose that it went away either, which tells me that "less is more" might not be for everybody. Especially people who struggle with hardcore cravings every day. Keeping yourself at 2mg a day is gonna cause you to start craving again eventually & then you'll just need to up your dose again anyway.

 

[SirSalty]

I don't believe norbupe is even active in the CNS when using bupe.

The reason bupe feels more like a full agonist in lower dosages, I think has more to do with blood levels.

Let's say you have 100 opioid receptors & you take 4mg of bupe. Let's say that 4mg covers 80 of those receptors & sticks around for 24+ hours.
So when you go to take 4mg again the next day, it only has 20 receptors it can attach to & now you're at 100% of your receptors covered. So taking more the next day isn't going to do a whole lot.

Now let's say 2mg only covers 30 receptors. When you go to take 2mg again the next day, you still have 70 receptors open that can be activated.

Once that half-life of the 2mg drops, you'll have even less in your system as well, where was with 4mg, you'd still have 2mg in your system when it's half-life is over.

I made those numbers up, but it still gets my point across. The higher you dose, the more your receptors become saturated & don't allow for anymore agonism with subsequent dosing.

Saturating your receptors that fast not only stops more agonism but also increases your tolerance exponentially.
This is why lower doses have more an effect than higher doses, but it's because you're leaving receptors open for your next dose rather than norbupe being active.

In order to keep that 2mg working well, you'd probably have to go at least 24-48hrs in between dosing. Buprenorephine has a ridiculously long half life, so each dose stacks up on top of one another. Essentially you'd want to keep your doses low, like 0.4mcg every couple of hours or something. That's how it gets used for pain, in micrograms every 4-6hrs. Because that 0.4mcg will wear off much faster & leave your system a bit faster than taking 1mg & up.


Buprenorphine was a great help for stabilizing my mood, so you should have some luck in that department at least.


I found the "less is more" theory a bit faulty & risky, because years ago I would only stick to low doses too & my cravings started coming back with insane vengeance. It wasn't until I raised my dose that it went away either, which tells me that "less is more" might not be for everybody. Especially people who struggle with hardcore cravings every day. Keeping yourself at 2mg a day is gonna cause you to start craving again eventually & then you'll just need to up your dose again anyway.

Thank you SO much for your response. It makes sense how you laid it out and I really appreciate you taking the time to help out.

I'm currently on 2mg bupe (gonna take the other 2mg later) and I plugged 21 30mg codeine phosphate tablets so should be feeling quite nice soon.

How would the two interact in my body, would they be competing for receptors?

I always assumed that because you can OD on fentanyl that the receptors can get overwhelmed way more than just with codeine or bupe?

I really don't understand how any of this works and I'm terrible at maths.

I understand if you don't respond because this post is all over the place and I really appreciate your initial response you helped me understand a lot more about what's going on.

 

[DeathIndustrial88]

Thank you SO much for your response. It makes sense how you laid it out and I really appreciate you taking the time to help out.

I'm currently on 2mg bupe (gonna take the other 2mg later) and I plugged 21 30mg codeine phosphate tablets so should be feeling quite nice soon.

How would the two interact in my body, would they be competing for receptors?

I always assumed that because you can OD on fentanyl that the receptors can get overwhelmed way more than just with codeine or bupe?

I really don't understand how any of this works and I'm terrible at maths.

I understand if you don't respond because this post is all over the place and I really appreciate your initial response you helped me understand a lot more about what's going on.

Buprenorphine is a mixed agonist / antagonist. This means not only is it an opioid but it's also an opioid blocker.

So taking 2mg of bupe & then plugging all that codeine, it's variable. For most people, the buprenorphine would block any of the codeine/morphine from really working. But people can vary. For example, I can feel 10-20mg of hydrocodone on about 1-2mg of buprenorphine. It's incredibly blunted, but it's there. But the general consensus is that taking bupe before a full agonist, will block it. And taking bupe while you actively have a full agonist in your system will cause precipitated withdrawals.

Most full agonists (morphine, heroin, fentanyl, etc..) only ever occupy a small percentage of your receptors at a time. If you were to saturate all of your receptors with a full agonist, it would kill you. Actually you'd probably die long before you could saturate all your receptors with a full agonist. The reason it doesn't kill you with buprenorphine is because buprenorphine is only a partial agonist & it also has a ceiling limit on respiratory depression, where as full agonists have no ceiling limit (meaning the more full agonist you take, the more it's going to depress your breathing).

People tend to OD on fent because it's super potent & they aren't able to accurately dose it. So they end up accidentally taking more than their tolerance allows & it depresses their breathing to the point of being unconscious.


No worries! I'm glad I could help! Feel free to ask anything on here! It's good that people learn about the drugs they're using, it keeps people safer than trying to do it all alone in the dark.