Drink_Tea_Love_Cat
Bluelighter
- Joined
- Dec 25, 2016
- Messages
- 167
I think this should probably go in neuroscience but I'm not sure as it's also about harm reduction (please mods help me here) - But I'm tired of reading opinions or theories stated as fact when it comes to potentiating opiates, but I would really appreciate a little bit of an objective analysis of exactly how strong an effect Clonidine and/or Quinine tablets will have on an opiate, and also clarification of the debate over codeine potentiation.
the opiates in question are Opium/morphine, DHC, codeine, and kratom. I intend to experiment with these following products for potentiation and also tolerance reduction during a taper. Essentially using less or the same amount and getting the same or higher buzz so I can reduce dosages without crying like a baby. It's also for science.
I have just acquired:
Arkamin (Clonidine) - 100mcg (30 Tablets) X 1
Quinin (Quinine Sulphate) - 300mg (10 Tablets) X 2
I also have DLPA, Agmatine Sulphate, Promethazine, Diphenhydramine, Rhodiola, Benzos, loperamide and magnesium and calcium. I'm more experienced with these, but I want to paint the full picture that these may be used in conjunction at some point or another.
So I have read people using Quinine from tonic water to potentiate their high. But from my understanding a full bottle of tonic is only about 80mg Quinine, and also administration would be slower than a tablet. How much impact would a quinine tablet have on an opiate? should I be extra cautious and half my dosage, or even more cautious? I know there is a debate about codeine and or DHC, and I will come back to that. Let's talk about morphine and Kratom primarily.
I also have read about Clonidine helping with WDS. I haven't read so much about it being used to potentiate but I have heard it cited. I would be interested to try it, alone first, and then to potentiate, and then later with detoxing. Again, how cautious should I be exactly? half dosage? more? less? I don't want to be super paranoid I just want to be realistic. Any harm done will be my responsibility alone, so please just be frank and discuss this from the point of view of a drug addict, not from the point of view of a straight edge mother figure wagging her finger.
Then what about co-administration?
SCIENCE BIT
Lastly, this codeine debate, maybe DHC, I haven't got the grips with DHC metabolism yet tbh. Perhaps I need a new thread about this. But if things like quinine, grapefruit and more inhibit the enzyme needed to convert codeine to morphine, shouldn't that be a good thing? I mean, if there is less enzyme then the rate of conversion is slower so it has the potential to be more efficient. e.g. the high might be more sustained and longer? There is so many conflicting opinions about this I don't know who to believe. Further to my theory, if it inhibits that enzyme, those enzymes are also needed to metabolise morphine out of the system - so once we have morphine in our blood, again, it should sustain the high and potentiate it because the morphine is more slowly metabolised. Obviously it depends on your definition of "potentiation" - whether that means "efficient" or "rush" or "sustained" or what. To further the analogy or description, I will quote wiki:
"Taken orally, 20 mg of immediate release oxycodone is equivalent to 30 mg of morphine.[57][58] Extended release oxycodone is considered to be twice as potent as oral morphine.[59]"
So if we are inhibiting enzymes that metabolise the drug, shouldn't that make it more of a sustained release, therefore more efficient, therefore more potent overall? (even if it's not quite a "rush" as some would prefer)
the opiates in question are Opium/morphine, DHC, codeine, and kratom. I intend to experiment with these following products for potentiation and also tolerance reduction during a taper. Essentially using less or the same amount and getting the same or higher buzz so I can reduce dosages without crying like a baby. It's also for science.
I have just acquired:
Arkamin (Clonidine) - 100mcg (30 Tablets) X 1
Quinin (Quinine Sulphate) - 300mg (10 Tablets) X 2
I also have DLPA, Agmatine Sulphate, Promethazine, Diphenhydramine, Rhodiola, Benzos, loperamide and magnesium and calcium. I'm more experienced with these, but I want to paint the full picture that these may be used in conjunction at some point or another.
So I have read people using Quinine from tonic water to potentiate their high. But from my understanding a full bottle of tonic is only about 80mg Quinine, and also administration would be slower than a tablet. How much impact would a quinine tablet have on an opiate? should I be extra cautious and half my dosage, or even more cautious? I know there is a debate about codeine and or DHC, and I will come back to that. Let's talk about morphine and Kratom primarily.
I also have read about Clonidine helping with WDS. I haven't read so much about it being used to potentiate but I have heard it cited. I would be interested to try it, alone first, and then to potentiate, and then later with detoxing. Again, how cautious should I be exactly? half dosage? more? less? I don't want to be super paranoid I just want to be realistic. Any harm done will be my responsibility alone, so please just be frank and discuss this from the point of view of a drug addict, not from the point of view of a straight edge mother figure wagging her finger.
Then what about co-administration?
SCIENCE BIT
Lastly, this codeine debate, maybe DHC, I haven't got the grips with DHC metabolism yet tbh. Perhaps I need a new thread about this. But if things like quinine, grapefruit and more inhibit the enzyme needed to convert codeine to morphine, shouldn't that be a good thing? I mean, if there is less enzyme then the rate of conversion is slower so it has the potential to be more efficient. e.g. the high might be more sustained and longer? There is so many conflicting opinions about this I don't know who to believe. Further to my theory, if it inhibits that enzyme, those enzymes are also needed to metabolise morphine out of the system - so once we have morphine in our blood, again, it should sustain the high and potentiate it because the morphine is more slowly metabolised. Obviously it depends on your definition of "potentiation" - whether that means "efficient" or "rush" or "sustained" or what. To further the analogy or description, I will quote wiki:
"Taken orally, 20 mg of immediate release oxycodone is equivalent to 30 mg of morphine.[57][58] Extended release oxycodone is considered to be twice as potent as oral morphine.[59]"
So if we are inhibiting enzymes that metabolise the drug, shouldn't that make it more of a sustained release, therefore more efficient, therefore more potent overall? (even if it's not quite a "rush" as some would prefer)