Hello, I have been taking cucurmin with bioperine (piperine) with my Topamax and Zubsolv prescriptions ever since I got out of a horrible inpatient hospital setting that I got trapped in. I was supposed to get tapered off of massive doses of gotu kola that I was taking with my gabapentin at doses that escalated to 1lb of c/s herb every 3-4 days, I know, absurd doses.
If you don't know, gotu kola is a gabab-ergic herb that is (probably) basically pharmacologically identical to Lyrica minus the calcium channel inhibition. I was going to get tapered off of it and phenibut that I was taking as well with the help of phenobarbital, but at the last second my mom took control because I was very deep in withdrawal and sent me to a behavioral health hospital instead where they didn't know anything about this sort of thing, and the insane 50s-style psychiatrist gave me absolutely nothing for withdrawal, took away my gabapentin entirely, LOWERED my Topamax dose, and basically did everything possible to maximize neurotoxicity while holding me against my will for 48 hours. There was an alcoholic there going through DTs with NO benzos at all given, he told me i wasn't going to have much luck. The end result was a lot of brain fog and memory problems and extra nerve damage in my arm and basically becoming a recluse in the weeks following, after some acute hyper-glutamatergic mania, which I should have taken more for, but I only took NAC, magnesium, and fish oil.
Besides asking for help in how to repair myself following this disaster, I have a more pressing question: I have been taking cucurmin with piperine, 5mg of piperine a day, to help with the neuroinflammation. But I failed a drug test for suboxone and so now I have another one coming up soon, and they gave me diazepam in the hospital. I have been taking the cucurmin/piperine the whole time since, and I have realized that I need to stop, since it inhibits cyp3a4 and it will make it look like I have been taking more diazepam and more suboxone due to its effects on the metabolism of desmethyldiazepam that is still floating around and its blocking of the demethylation of the buprenorphine.
However, I have been worried about stopping, because if it is inhibiting the metabolism of the Topamax as well, I will damage myself by stopping, or I will need to taper. I cannot find any info on if Topamax is degraded by cyp3a4. Some papers say it is degraded by a cyp enzyme, but that they do not know which one. http://www.ncbi.nlm.nih.gov/pubmed/16250251
It apparently induces cyp3a4 as well. What I want to know is: does this make it more likely to be degraded by cyp3a4? If it is degraded by cyp3a4, I will have to taper the piperine to stop taking it, or I risk excitotoxicity. Missing my Topamax even an hour after this horrible withdrawal nightmare gives me a bad hangover-like headache and makes me feel really stupid, so even though these papers all say "primarily excreted unchanged, hardly any of it is metabolized hepatically," I can't really risk just stopping taking the piperine if it is increasing the amount of Topamax in my body.
When I look it up on simple interaction checkers with other cyp3a4 inhibitors like erythromycin, it shows that it would actually DECREASE the amount of Topamax in systemic circulation, but I just don't understand how that's possible. If it is, that would be a good thing, because I could just stop taking it immediately, go through the slight opioid withdrawal from the drop in buprenorphine dose, and know that I'd have more Topamax in my system.
Anybody have any input or can find any info on its metabolism or know if a drug inducing an enzyme means that it is more likely to be a substrate for that enzyme? I'm also trying to get my psychiatrist to prescribe me memantine to help with the post-acute withdrawal, but she is really hesitant. Do you guys think that will help? Anything else I should be taking?
If you don't know, gotu kola is a gabab-ergic herb that is (probably) basically pharmacologically identical to Lyrica minus the calcium channel inhibition. I was going to get tapered off of it and phenibut that I was taking as well with the help of phenobarbital, but at the last second my mom took control because I was very deep in withdrawal and sent me to a behavioral health hospital instead where they didn't know anything about this sort of thing, and the insane 50s-style psychiatrist gave me absolutely nothing for withdrawal, took away my gabapentin entirely, LOWERED my Topamax dose, and basically did everything possible to maximize neurotoxicity while holding me against my will for 48 hours. There was an alcoholic there going through DTs with NO benzos at all given, he told me i wasn't going to have much luck. The end result was a lot of brain fog and memory problems and extra nerve damage in my arm and basically becoming a recluse in the weeks following, after some acute hyper-glutamatergic mania, which I should have taken more for, but I only took NAC, magnesium, and fish oil.
Besides asking for help in how to repair myself following this disaster, I have a more pressing question: I have been taking cucurmin with piperine, 5mg of piperine a day, to help with the neuroinflammation. But I failed a drug test for suboxone and so now I have another one coming up soon, and they gave me diazepam in the hospital. I have been taking the cucurmin/piperine the whole time since, and I have realized that I need to stop, since it inhibits cyp3a4 and it will make it look like I have been taking more diazepam and more suboxone due to its effects on the metabolism of desmethyldiazepam that is still floating around and its blocking of the demethylation of the buprenorphine.
However, I have been worried about stopping, because if it is inhibiting the metabolism of the Topamax as well, I will damage myself by stopping, or I will need to taper. I cannot find any info on if Topamax is degraded by cyp3a4. Some papers say it is degraded by a cyp enzyme, but that they do not know which one. http://www.ncbi.nlm.nih.gov/pubmed/16250251
It apparently induces cyp3a4 as well. What I want to know is: does this make it more likely to be degraded by cyp3a4? If it is degraded by cyp3a4, I will have to taper the piperine to stop taking it, or I risk excitotoxicity. Missing my Topamax even an hour after this horrible withdrawal nightmare gives me a bad hangover-like headache and makes me feel really stupid, so even though these papers all say "primarily excreted unchanged, hardly any of it is metabolized hepatically," I can't really risk just stopping taking the piperine if it is increasing the amount of Topamax in my body.
When I look it up on simple interaction checkers with other cyp3a4 inhibitors like erythromycin, it shows that it would actually DECREASE the amount of Topamax in systemic circulation, but I just don't understand how that's possible. If it is, that would be a good thing, because I could just stop taking it immediately, go through the slight opioid withdrawal from the drop in buprenorphine dose, and know that I'd have more Topamax in my system.
Anybody have any input or can find any info on its metabolism or know if a drug inducing an enzyme means that it is more likely to be a substrate for that enzyme? I'm also trying to get my psychiatrist to prescribe me memantine to help with the post-acute withdrawal, but she is really hesitant. Do you guys think that will help? Anything else I should be taking?
