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Elizabeth: MAOI threads

Posted by Zeke on December 16, 1999, at 2:03:22

In reply to Re: Parnate: weight gain, & the literature - Zeke, posted by Elizabeth on December 15, 1999, at 21:10:30

> > 1. A protocol of giving the entactogen and several hours later giving an SSRI (and perhaps deprenyl) would aloow for the beneficial effects but minimize possible neurotoxicity. Use of the levo isomer of MDMA appears safer as it excludes delayed damage -- loss of uptake sites. SSRIs may offer no protection from this toxicity, but again is is stereospicific.
> Even excluding the slight problem of illegality of MDMA (yes I am opposed to this, but it is a difficulty nevertheless!)

IMHO the illegality issue is relative. Amphetamine and methylpheniate are illegal substances -- schedule II controlled substances -- but they are used legally in ADHD and narcolepsy and to a lesser degree in affective disorders. Research of methampletamine(Desoxyn) demonstrates somewhat lesser but very similar neurotoxic effects as MDMA by virtue of acting on 5-HT neurons. But it is an amphetamine and is used in the previously mentioned disorders. It often provides relief when the others fail.

Or a better example is ibogaine -- a schedule I controlled substance like MDMA -- that is being actively considered here in the US for treatment of addiction (opiate dependence). On Nov. 5 & 6 a conference was held at the New York University School of Medicine, to discuss and plan applications and possible trials. The audience was not hippies or or new age pot heads, but physicians, neuroscientists, NIDA officials and social scientists. 'A single oral dose on the order of 20mg./kg. is given Individuals undergoing ibogaine treatment for the objective of "addiction interruption" ' So illegal status need not be an absolute barrier to a therapeutic application.

see also: ibogaine in the treatment of chemical dependence disorders: clinical perspectives

> I think you would have a nigh-impossible time convincing most pdocs to do this, between the speculative uses of SSRI and selegiline, and the mixing of the three. Indeed, I believe more research needs to be done before this is done clinically, and the patient would have to be very well monitored.

I totally agree Elizabeth. It won't be available to the average psychiatrist at this point. And like the limited licenses to despense methadone for heroin addict, ibogaine isn't likely to be a among the psychopharmacy of the average psychiatrist in the future.

Note that ibogaine would not be an ongoing medication but would be administered once (or perhaps twice) early in treatment. This is the same protocol as MDMA. And BTW, MDMA was in the 60s and 70s already used by therapists. I'm not just making a novel proposal!

Re coadministration consider the treatment of Parkinson's syndrome: L-Dopa is frequently given with carbidopa, a peripheral decarboxylase inhibitor, to lessen periferal dopamine side effects. And drugs such as tolcapone -- Catechol O-methyltransferase (COMT) inhibitors -- and deprenyl -- the selective MAO inhibitor -- as likewise coadministered with L-Dopa to increase central dopamine and thus allow lower doses of L-Dopa. This in turn decreases tolerance to L-Dopa which is a common problem as the disease progresses. So the protocol is not novel inestablished medicine. see:

> That said, though, interesting idea. Can you explain (on a psychological level) the mechanisms whereby MDMA might aid with this kind of "blocking?" Never experienced the stuff myself.

Let me quote from Alexander Shulgin:

"Here is a drug that has the unusual property of, more often than not, freeing a patient in psychotherapy from the anxiety and lack of trust that often prevents the emotionally fragile person from expressing his feelings to another. And, as has been attested to by many therapists and patients, MDMA allows a personal perspective, which is called "insight," with a minimum amount of fear and self-censoring. All of this without any loss of self-control or rationality... I am completely convinced that this is the type of tool that must be developed and explored as a possible adjunct to psychotherapy."

But he also says:

"However, since it came to administrative attention at the same time that the Fentanyl analogs became notorious, it was labeled a designer drug, and condemned as an abuse drug that had no virtue. The DEA holds that it is a hallucinogen, which is simply untrue. MDMA is not a hallucinogen."

see: Barriers to Research, Alexander & Ann Shulgin, Yearbook for Ethnomedicine and the Study of Consciousness,, Issue 2, 1993, pp9-20.

> > As for free radical damage, there are MAOis but also other central antioxidants.
> I hope you just mean selegiline (you *do* know what happens when you take a nonselective MAOI with MDMA, right?

The would be a great danger of the serotonin syndrome IMHO.

> do we actually know this won't happen with selegiline? especially with an SSRI too?).

Well that's what the research says. Deprenyl(selegiline) is specific for MAO-B which effects dopamine. MAO-A effects serotonin and tyramine, and deprenyl doesn't inhibit MAO-A. This is why deprenyl is free of the so called 'cheese effect' (at clinical doses).
> > I think selective MAO inhibitors will be their resurrection. Side effects and interactions are few(er) and rare, and efficacy in depression is being demonstrated. What do you think?
> Not that you asked :), but I thought selegiline was much more difficult to tolerate than the nonselective MAOIs (I took it at high (nonselective) doses, though). It also did not work - doh.

I believe just the opposite is true -- by not inhibiting MAO-A it is free of the side effects of MAO-A inhibition so is better tolerated that nonselectives like Nardil or Parnate. At higher does however, deprenyl may begin to inhibit MAO-A and share the side effect profile of the older nonselective MAOIs.

> As for moclobemide, it has a rep in countries where it's used for not being particularly effective in the people who would be trying the irreversible MAOIs (those who've already tried a lot of other stuff). I also don't think, based on the stories I've heard from patients who've tried it, that it's really all that much more tolerable than the irreversible MAOIs.

I admit present ignorance about this.

> Does anyone know what happened to clorgyline, though? Was it ever marketed for clinical use?
Clorgyline is irreversibe has been supplanted by moclobemide and toloxatone, which are reversible, and theoretically safer re the serotonin syndrome and tyramine crises. All are effective antidepressants, but the latter are safer re hypertensive crises.

BTW deprenyl is an IRREVERSIBLE inhibitor of MAO-B.

> But anyway, I think it's more likely that the nonselective MAOIs will be resurrected as the "stigma" surrounding them (re the dietary restrictions, which it turns out have been overblown) vanishes.

Perhaps overblown -- but they're real; I wouldn't chuck down a chunk of aged cheese if I were you! The selective and reversible MAOIs are indeed safer. This is similar to the preference of lorazepam over diazepam, where lorazepam(Ativan) lacks active metabolites but diazepam(Valium) doesn't.

I want you to know that I do respect your thoughts about this and enjoy the dialog.

BTW, you are lucky to be in Boston because of the avant guard medical community there. You have so many more options than those of us out here in the sticks!

Is your doc associated with one of the Harvard clinics/hospitals there?




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