Hey man, so since you read a book about Naltrexone and seem to understand some things about it I'd like to ask you some questions, but if you could refrain from using biochemical and scientific terms and explanations I'd appreciate it because I am bad with science and don't understand that kind of stuff. Like, you started talking about ''opioid-induced hyperalgesia'', but what exactly is that?
And when you wrote this 'the evidence seems pretty thin to me and hearing it always brought up as a reason to taper people off medications they are taking, sort of a deus ex machina Mac Guffin non sequitur rabbit in a hat...''
and this ''the fact that people mention opioid induced hyperalgesia in propaganda which also often denies there is such a thing a pseudo-addiction, where people with pain not being treated properly work very hard to get it treated properly, should raise suspicion too''....are you trying to say that you don't think that ultra low dose naltrexone can be used in combination with opioids to reduce tolerance and side effects and/or that you don't think ULDN can be taken safely alongside opioids''?
You have pretty good linguistic skills with your ''deus ex machina'' and ''non sequitur rabbit in a hat'' phrases LOL, but you just totally lost me...
My situation is that I am seeing a drug counselor and will also see a psycho-pharmacologist soon, and while Kratom is not a super bad drug to be dependent on, it has both helped me and hindered me in some ways, and that, along with some physical and psychological dependence on dexadrine and definitely being an alcoholic, are things I need some help with.
So I am interested in BOTH regular high dose Naltrexone to simply block me from using both Kratom and alcohol entirely for a while so i can just experience true sobriety for the first time in a long time and get myself clean, but then after that I am not 100 percent willing to commit to NEVER using Kratom or alcohol again, and both because I have heard cases of ULDN working as an antidressant and I have depression, and because I have heard reports that it CAN BE TAKEN WITH KRATOM safely to reduce tolerance and side effects and possibly even negate or even almost entirely eliminate withdrawal symptoms, makes me interested in that as well.
So my questions about ULDN as opposed to regular naltrexone are:
1) Do you think that these stories I've heard of people being able to take Kratom WITH ULDN (and in the study I read a guy actually used it with Morphine and was still able to safely ingest them simultaneously) have any merit to them, and do you think it would be possible for someone to take Kratom and ULDN at the same time without the ULDN putting them into precipitated withdrawal and actually lower tolerance, side effects and withdrawal effects like I have heard, or do you think that it wouldn't be possible since that's not how high dose naltrexone works?
2) If it were possible to do what I mentioned above, do you think you'd have to make sure to break your physical dependence to Kratom before trying it?
3) Do you know if ULDN completely blocks alcohol from getting you drunk or buzzed like high dose naltrexone does, or can one drink safely on ULDN?
4) If it is NOT safe or possible to take Kratom and ULDN simultaneously, but one were taking ULDN regularly and then stopped and started using Kratom again, how long do you think they'd have to then abstain from Kratom before safely going back to ULDN again?
5) Likewise, if using REGULAR naltrexone at higher doses, how long does one need to abstain from Kratom do you think before they can safely taken Naltrexone and then how long would they have to abstain from Naltrexone before they could again take Kratom without it blocking its' effects?
I've heard that for TYPICAL opioids like hydrocodone or heroin that one needs to abstain for at least 7-10 days before it is safe to take REGULAR naltrexone again, but I don't know if that also goes for Kratom, and I know that with alcohol one can just skip the Naltrexone the night before and drink again and get effects from it, but I don't know if it works the same way with Kratom, where you can just skip a dose and then the Kratom will effect you again the next day.
6) Have you heard anything about ULDN being used as an antidepressant by raising endorphins, and do you believe that it can work that way?
7) And in general, do you think there's anything else I should know about either ULDN or regular dose Naltrexone before using them, particularly considering that I am someone who, while he certainly wants a long break from both Kratom and drinking, will eventually use both those substances again?
Sorry for asking you so many questions, but I am going to see this psychopharmacologist for the first time next week and we only briefly talked on the phone, but she said that while she was aware of what Kratom is and how it works and has experience with Naltrexone that she is unaware if Kratom can be safely combined with ULDN and said that she'd ask her colleagues about it but that she'd be concerned about whether or not it's safe, and this is a question I'll eventually want answered.
Thanks.
1. People have been certainly able to do things such as that, with hydromorphone, smack, and morphine. The one hydromorphone case that comes to mind involved someone who took naltrexone two times a week on a dose I cannot remember exactly.
2. Given that people have used it as I mention in (1) would point to it being possible to also do so on kratom, though there is less knowledge about kratom so far as there is about morphine
3. The effect in the cases of alcoholism make me think that the theory that naltrexone prompts the body to make more endorphins has something to it. So I am inclined to conclude that there is not an actual literal alcohol blocking effect taking place. The two other drugs used for alcoholism are disulfram, which changes the metabolism of alcohol, and ketamine, which has an anaesthetic effect, so ketamine also does not literally block alcohol. The prn drugs for anxiety and insomnia in recovering alcoholics are clomethiazole, diazepam, and phenobarbitone, and at one point there were scientists proposing looking at methaqualone again for this purpose as well as sodium oxybate (Georgia Home Boy, Grievous Bodily Harm) - all of those impact the Gaba system but I don't think there is a literal blocking of alcohol in the CNS going on, there is dopamine reuptake inhibition or release, and various Gaba effects. Meprobamate, carisoprodol, and tripelennamine, to mention just three, can also help folks out at night.
As far a drinking on naltrexone, so many things are caused or prevented by metabolism of alcohol that it is not possible to say with certainty, also with oral dosing of naltrexone it will modify the Liberation, Absorption, Distribution, Metabolism & Elimination profile which could be good or not. Like the kind of dose dumping that got extended-release hydromorphone withdrawn from the market in the United States is one possibility, and getting more naltrexone than was intended is not the best idea.
4. Avoiding precipitated withdrawal is going to be on the order of days, up to a week it sounds like and . . .
5. The washout period for naltrexone in such a case could be 6-14 days depending on a number of things like other drugs being taken, individual metabolism, and narcotic use history
6. I know that naltrexone is being investigated for this purpose and I tend to think it is the endorphin effects . . . the buprenorphine-samidorphan mixture researched for anti-depressant efficacy probably works the same way.
7. Naltrexone will lower or more or less eliminate any opioid tolerance you may have, which is very important to keep in mind when going back to Kratom or narcotic analgesics.
Opioid-induced hyperalgesia is, according to the theory being batted around, that after some point opioids make people more sensitive to pain and may cause some sort of pain, especially in the muscles. I hear of a lot of people being told they may have it when they report that their dose of narcotics is not working like it used to -- so the patient may have better results with little or no narcotics. We all know about tolerance and it can be demonstrated, so tapering someone down or off narcotics -- how on God's Green Earth will
that make a positive difference? Cases like that usually call for opioid
rotation not cessation, such as replacing morphine with ketobemidone, piritramide, methadone, or another chemically dissimilar medication, and/or the introduction or changing of adjuncts and atypical analgesics like hydroxyzine, nefopam, and dozens of others. So opioid-induced hyperalgesia is a political tool for doctors who are being threatened by regulators or are just ignorant.
I have also heard the theory that chronic pain may be caused or exacerbated by a Vitamin D deficiency and that was a regular test I would get every so often in the States, sort of CYA in the case of my general practitioner back there who didn't believe in that, or opioid induced hyperalgesia for that matter. So after the patient has tried everything, opioid-stingy doctors or those under pressure from management or regulators will propose that one, the other, or both is what is happening. Often these two things are brought up when tolerance is the real issue, and it comes up
Pseudo-addiction is very sensible "drug seeking behaviour" when a patient is in pain and knows or have at least a vague idea of what will help them.
I have known people who do slow down or even slightly reverse tolerance to narcotics with low doses of naltrexone on a fixed schedule, including people with physical dependence on things like hydromorphone, smack, morphine and so on. So it definitely seems to work, and I am inclined to support the endorphin theory for this and other things involving the nervous system -- perhaps metabolism of naltrexone leads to formation of metabolites with some agonist activity, especially one which may hit some of the opioid receptors which have been suspected to exist and are still the subject of research (after all, there are the Opioid-Like Receptor and a fourth official opioid receptor, the ζ opioid receptor, found more recently, and there are effects on opioids from NMDA, nociception and others aside from the official opioid receptors). It could also be that, like nalorphine (Nalline) an antagonist and antidote which used to be used in the same fashion naloxone is now (nalorphine is to morphine as naloxone is to oxymorphone) naltrexone actually could have agonist effects as well . . . nalorphine used to be used for analgesia on patients for acute pain in cases where it will not be necessary to maintain a patient on strong analgesics, and it was listed under controlled substances laws various places.
