oxyhydro
Bluelighter
This is my second post on the subject of feeling the effects of nor-buprenorphine, buprenorphine's full agonist metabolite.
First a summary of the theory: nor-buprenorphine is a full opiate agonist which is the main metabolite of the partial agonist buprenorphine (suboxone). So in theory, if we could find a way to occupy our opiate receptors with nor-bupe, we would feel a full opiate effect, much stronger than bupe's effect. The problem is that bupe has a higher affinity for the opiate receptor, so when you take bupe normally it occupy's all the receptors and nor-bupe cannot attach, and is broken down into useless chemicals. This method, called "The Naltrexone Method" is a new theory I have developed, since I have been clean for a year I am unwilling to risk relapse by trying this myself so I will leave it up the the bluelight community.
Here are the facts: When you take buprenorphine, it goes strait to your brain and occupy's your opiate receptors. Since it is a partial agonist with a high affinity, it only stimulates the receptor slightly, causing little pleasure, and blocks all other opiates from attaching and having an effect. Because of this, by the time buprenorphine in your blood is converted into nor-buprenorphine, the full agonist metabolite of buprenorphine, there are not open opiate receptors to recieve the nor-bupe and it is wasted.
Here is my theory: By taking a small dose of naltrexone, a drug that blocks the opiate receptors, before taking the bupe, we allow the buprenorphine to be converted into nor-buprenorphine while the naltrexone prevents any buprenorphine from attaching to receptors. The challenge is timing, we need to take the naltrexone so that it blocks the receptors long enough to block the buprenorphine from attaching, but is gone by the time the nor-bupe is metabolized so that it can attach to the receptors.
You may be wondering why this doesnt happen normally because of the naloxone in suboxone, which is a shorter acting form of naltrexone. The reason is two-fold: absorption and bonding affinity. First abosption: when you take suboxone sublingually, the naloxone is barely absorbed and goes to your stomach, where the lover filters it out before it has a chance to get to the brain. The second reason is affinity: buprenorphine has a higher affinity for the opiate receptor than does naloxone, this means that even if you inject suboxone and get the full dose of naloxone, nothing will happen because the buprenorphine will attach and the naloxone cannot knock it off. This makes the naloxone pointless in suboxone, it is supposed to prevent users from injecting the drug, but it doesnt work, which is why people do inject suboxone. The only reason naloxone was added to suboxone was because the patent for subutex was still good, so in order to market a sublingual buprenorphine drug for opiate addiction, the manufacturer had to add naloxone and justify it so it didn't break the patent of subutex.
You may also be wondering how naltrexone can be used since it is supposed to last 24 hours, and the answer is low-dose naltrexone (LDN). Low dose naltrexone is when you take a very low dose of naltrexone, only a few mg compared to the 50mg in a normal pill. LDN is an alternative medicine treatment that has been reported to help cancer and manyt auto-immune disorders. It is believed to work by causing an increase in endorphines by blocking endorphine activity for a few hours, so the body makes more endorphines, and then when it wears off the increased amount of endorphines takes effect. This is basically what we are trying to do. We block opiate receptors for a few hours while the bupe is converted into nor-bupe, then the naltrexone wears off and we feel the effect of the nor-bupe.
HERE ARE THE CHALLENGES:
1. Finding out how long different doses of naltrexone have an effect.
2. How long does it take for most of the bupe to be converted to nor-bupe.
3. Using this information to find a dosing timetable for taking the naltrexone and bupe.
Now, we must use naltrexone because it is the only thing that can block the bupe, all other opiate receptor blockers are not strong enough to block bupe.
My theory is that we only need to block the receptors with naltrexone long enough to allow the buprenorphine to circulate through our liver, so no more than 10 minutes.
The danger is blocking the receptors too long, so both the bupe AND norbupe get filtered out by our liver. It seems like the best approach to take would be to take a low dose of about 3mg naltrexone, wait about 5 hours, and then take a dose of bupe (between 2-8mg). From there, in each trial we must reduce the amount of time between taking the naltrexone and taking the bupe, and recording the effects and finding where the effect is strongest. This will be hard because bupe has such a long half life, which is why i recommend 2mg doses and waiting a day in between trials.
Why do I think this will work?
I think this will work for a number of reasons.
The first is experience. Before I was clean, I had reduced my suboxone dose down to 2mg a day. I tried to go cold turkey after that and couldent, so I took a 1mg dose to try and ease the WD. What happened was I got a much stronger and shorter lived effect than I did from my 2mg doses, which I felt nothing from because I was so tolerant. This fit my "low dose bupe" theory, where we feel the nor-bupe because by taking a low dose of bupe, there isnt enough bupe to get ALL the receptors so some are left open for the nor-bupe, I explain more in another thread. After this, I started injecting 0.8mg doses and would get a good buzz every time like a normal opiate.
The second reason is more verifiable, and I got the idea from the form of buprenorphine used for pain. Buprenorphine is sold in sublingual tablet for in doses of 0.2mg for pain relief. I wondered why they didn't use suboxone liek doses of 8mg, since it would seem this would provide better and longer pain relief, but they only use 0.2 mg doses. I figured the reason is because of my low dose theory, that by taking a low dose such as 0.2mg, the metabolized nor-buprenorphine is allowed to attach to opiate receptors. This would explain a lot, if buprenorphine was responsible for the pain relief, then more buprenorphine would equal more pain relief but that is not the case, it must be that the pain relief comes from the nor-bupe, and that my low dose theory is correct!
So, sorry for the long post, but I had to include all the information I could if I expect anyone to do this experiment for me.
Please share your thoughts and ask questions!
First a summary of the theory: nor-buprenorphine is a full opiate agonist which is the main metabolite of the partial agonist buprenorphine (suboxone). So in theory, if we could find a way to occupy our opiate receptors with nor-bupe, we would feel a full opiate effect, much stronger than bupe's effect. The problem is that bupe has a higher affinity for the opiate receptor, so when you take bupe normally it occupy's all the receptors and nor-bupe cannot attach, and is broken down into useless chemicals. This method, called "The Naltrexone Method" is a new theory I have developed, since I have been clean for a year I am unwilling to risk relapse by trying this myself so I will leave it up the the bluelight community.
Here are the facts: When you take buprenorphine, it goes strait to your brain and occupy's your opiate receptors. Since it is a partial agonist with a high affinity, it only stimulates the receptor slightly, causing little pleasure, and blocks all other opiates from attaching and having an effect. Because of this, by the time buprenorphine in your blood is converted into nor-buprenorphine, the full agonist metabolite of buprenorphine, there are not open opiate receptors to recieve the nor-bupe and it is wasted.
Here is my theory: By taking a small dose of naltrexone, a drug that blocks the opiate receptors, before taking the bupe, we allow the buprenorphine to be converted into nor-buprenorphine while the naltrexone prevents any buprenorphine from attaching to receptors. The challenge is timing, we need to take the naltrexone so that it blocks the receptors long enough to block the buprenorphine from attaching, but is gone by the time the nor-bupe is metabolized so that it can attach to the receptors.
You may be wondering why this doesnt happen normally because of the naloxone in suboxone, which is a shorter acting form of naltrexone. The reason is two-fold: absorption and bonding affinity. First abosption: when you take suboxone sublingually, the naloxone is barely absorbed and goes to your stomach, where the lover filters it out before it has a chance to get to the brain. The second reason is affinity: buprenorphine has a higher affinity for the opiate receptor than does naloxone, this means that even if you inject suboxone and get the full dose of naloxone, nothing will happen because the buprenorphine will attach and the naloxone cannot knock it off. This makes the naloxone pointless in suboxone, it is supposed to prevent users from injecting the drug, but it doesnt work, which is why people do inject suboxone. The only reason naloxone was added to suboxone was because the patent for subutex was still good, so in order to market a sublingual buprenorphine drug for opiate addiction, the manufacturer had to add naloxone and justify it so it didn't break the patent of subutex.
You may also be wondering how naltrexone can be used since it is supposed to last 24 hours, and the answer is low-dose naltrexone (LDN). Low dose naltrexone is when you take a very low dose of naltrexone, only a few mg compared to the 50mg in a normal pill. LDN is an alternative medicine treatment that has been reported to help cancer and manyt auto-immune disorders. It is believed to work by causing an increase in endorphines by blocking endorphine activity for a few hours, so the body makes more endorphines, and then when it wears off the increased amount of endorphines takes effect. This is basically what we are trying to do. We block opiate receptors for a few hours while the bupe is converted into nor-bupe, then the naltrexone wears off and we feel the effect of the nor-bupe.
HERE ARE THE CHALLENGES:
1. Finding out how long different doses of naltrexone have an effect.
2. How long does it take for most of the bupe to be converted to nor-bupe.
3. Using this information to find a dosing timetable for taking the naltrexone and bupe.
Now, we must use naltrexone because it is the only thing that can block the bupe, all other opiate receptor blockers are not strong enough to block bupe.
My theory is that we only need to block the receptors with naltrexone long enough to allow the buprenorphine to circulate through our liver, so no more than 10 minutes.
The danger is blocking the receptors too long, so both the bupe AND norbupe get filtered out by our liver. It seems like the best approach to take would be to take a low dose of about 3mg naltrexone, wait about 5 hours, and then take a dose of bupe (between 2-8mg). From there, in each trial we must reduce the amount of time between taking the naltrexone and taking the bupe, and recording the effects and finding where the effect is strongest. This will be hard because bupe has such a long half life, which is why i recommend 2mg doses and waiting a day in between trials.
Why do I think this will work?
I think this will work for a number of reasons.
The first is experience. Before I was clean, I had reduced my suboxone dose down to 2mg a day. I tried to go cold turkey after that and couldent, so I took a 1mg dose to try and ease the WD. What happened was I got a much stronger and shorter lived effect than I did from my 2mg doses, which I felt nothing from because I was so tolerant. This fit my "low dose bupe" theory, where we feel the nor-bupe because by taking a low dose of bupe, there isnt enough bupe to get ALL the receptors so some are left open for the nor-bupe, I explain more in another thread. After this, I started injecting 0.8mg doses and would get a good buzz every time like a normal opiate.
The second reason is more verifiable, and I got the idea from the form of buprenorphine used for pain. Buprenorphine is sold in sublingual tablet for in doses of 0.2mg for pain relief. I wondered why they didn't use suboxone liek doses of 8mg, since it would seem this would provide better and longer pain relief, but they only use 0.2 mg doses. I figured the reason is because of my low dose theory, that by taking a low dose such as 0.2mg, the metabolized nor-buprenorphine is allowed to attach to opiate receptors. This would explain a lot, if buprenorphine was responsible for the pain relief, then more buprenorphine would equal more pain relief but that is not the case, it must be that the pain relief comes from the nor-bupe, and that my low dose theory is correct!
So, sorry for the long post, but I had to include all the information I could if I expect anyone to do this experiment for me.
Please share your thoughts and ask questions!
