NAC, Magnesium, Carnosine, Carnitine, Memantine, Tadalafil are better options. Or you can increase the effect, mucuna prurriens, nicotine, caffeine, herbal maoi and liothyronine.. be ready for some important nerotoxic events. Ketamine is just.. i mean.. ketamine is for spiritual travels.. not tolerance reduction.
I'm not sure why everyone has these very strange opinions about "this drug is only meant for this one, single purpose and it's stupid or
wrong to use it for any other purpose." It's absurd to suggest that a drug has a "purpose," let alone a single one and only. This is a very narrow view of drugs and is really presumptuous to suggest that you know the only purpose, that any other is wrong or bad, and that a person who would do it is silly or stupid. Honestly, that's a really naive approach to drugs. I hear the same thing ALLLL the time about amphetamine/adderall and buprenorphine/suboxone: "I hate when people try to take suboxone (or amphetamine) to get high, that's not what it's meant for. It's whole purpose is to get you off drugs (to help you function normal for amphetamine), that's what it was made for. It doesn't make any sense to try to get a high off it, which isn't even possible." No. Drugs are made for many purposes or just out of curiosity, and they are very rarely designed with a highly specific purpose, though that does occur, and even when they are, they usually have different effects than expected or wanted. Buprenorphine is a drug with many effects which are different in different people and it can be used for a variety of reasons, none of which is it's "purpose," etc. Sorry for going off-topic a little, but it's relevant and I think important.
Ketamine is too short-acting of a NMDA antagonist to provide appreciable benfits for tolerance reduction.
In addition it has a shitload of other f/x including dopamine reuptake inhibition. It's like using cocaine to stop the crash of amphetamine... bit silly really.
You're right that it is rather short acting and that it has a lot of other effects other than NMDA antagonism, including some that would be rather contraindicated with amphetamine, like DAT inhibition. But that's absurd to suggest it's similar to cocaine in its DAT blocking capacity or in the contribution of that mechanism to its effect at any reasonable dose, or that it's as problematic, or anything else. Anyway, it doesn't seem like he's talking about alleviating "crash" symptoms, but just decreasing tolerance. But I strongly disagree, as does the literature, that it is too short acting to have appreciable benefits for tolerance reduction. Now, when I say the literature agrees with me, I mean at least for opioid tolerance, the efficacy of ketamine for which has been amply demonstrated (I wrote a grant on it). I'm only reasonably familiar with the amphetamine tolerance story, but from all the other NMDA antagonists shown to be efficacious (or at least anecdotally), I would imagine it would be just fine. But of course the lifespan of the drug matters and since it's so short, it's not quite as easy to achieve the effect you want; all you have to do is take it more often or in a different way. Now I'm not arguing that ketamine is the single best drug to use for this goal, but if it's what you have access to and you react well to it and it has other benefits, while being efficacious, I say go for it!
To increase the likelihood of it working, I would spread the dose out throughout the day, possibly even in a continuous fashion (from my reading that seems most likely to work). It seems to me that 100 mg is more than one needs to take all at once; 30 mg is probably a better dose. With that dose, you could insufflate 30 mg every 1 1/2 or 2 hours, then the last 10 an hour later or something. That would give you about 5-8 hours of consistent, moderate NMDA inhibition, which would likely produce some reduction in tolerance (hell, i notice a decrease in buprenorphine tolerance from a single 30-50 mg bump, nodding off and having trouble peeing later that day and the next). Or, if you can inject subcutaneously or intramuscularly, that would be even better and you could reduce the dose to 20 mg each time every 1.5 hours, achieving ~9 hours of inhibition. Of course, like I said, the issue here is feasibility and the annoyance of doing this. Another option, which is a pretty good one, but with some significant drawbacks, is to ingest (swallow) the ketamine. This has fairly low bioavailability, so it's definitely wasteful compared to the other methods, but if you have a consistent source of quality, affordable ketamine, then it could be a very good option since it lasts soooo much longer (~3-4 hours from a single good dose) and would permit a looser dosing schedule.
You should watch out for side effects, especially as relates to high blood pressure or other side effects of stimulants as ketamine is known to increase blood pressure and enhance the increased blood pressure caused by amphetamines. It's also a mild mu-opioid agonist and overall is known to be fairly addictive, so be careful of that. But it is reasonable and feasible to do.
The best studies I've read used a 24-48 hour long constant slow IV drip of ketamine at a dose of 0.1-1 mg/kg/hour. What's common is to infuse IV about 80-100 mg over the course of a whole day. The amazing thing is the reduced tolerance lasts for weeks to months! And the procedure can be repeated to decrease tolerance further. I'll give a few citations in a little bit, but in one paper, a woman on a very high dose of daily methadone for chronic pain was given 100 mg a day for two days and reduced her dose by 25% (from 80 mg, 3 times a day to 60 mg 3 times a day) with equivalent analgesia for the whole next month. She came back after the month and went through the same procedure, and reduced her dose by 33%, down to 40 mg 3 times a day, for another month with equivalent analgesia. They did it again and got her down to 40 mg twice a day. Amazing. Procedures like these, sometimes IM or SC, from ~80 mg/day to ~500 mg/day, are effective in about 40-60% of patients with chronic pain refractory to high doses of opioids, decreasing the necessary opioid dose or making the same dose effective when it previously wasn't.
