Posted by Zeke on December 15, 1999, at 10:26:36
In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Adam on December 14, 1999, at 22:06:45
> >
> > I'm not talking about people taking ecstasy every weekend at the local rave -- though that's the reason it's schedule 1. I'm talking about limited clinical use to augment therapy just as pindolol augments Prozac. When I say morality, I mean the government passing along research that supports its view and withholding research that doesn't, or even preventing research in the first place. I get upset when they rant that 'MDMA destroys serotonin neurons," but never mention that administration of an SSRI four hours later will block the uptake and damage. I'm sorry, I just get upset when moral prejudice strongarms block scientific discovery. And remember that many of these folks would like to cast all psych meds in to the sea -- ' and by God, you should just pull yourself up by your bootstraps!'
> >
> I had the opportunity to take MDMA not too long ago which I thankfully declined. Anyway, what I read lead me to believe that it takes very high doses of MDMA or chronic use to kill
> brain cells. However, axonal damage might still be a problem at lower doses, and even though axons can grow back, it's tough to know how they will grow back, and in the mean time
> the cell is out of comission.I don't want to beat this subject to death but one more ecstatic respone!
I am referring to limited, controlled use of entactogens (eg, MDMA) in psychotherapy, in persons where fear and anxiety are roadblocks to insight and expression. I think two factors must be considered:
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.
2. Lack of effective treatment (often) allows for high levels of glucocorticoids (eg, cortisol) which also have documented neurotoxicity. This toxicity however, has been more clearly linked with behavioral deficits and abnormalities.
> MDMA also stimulates excessive dopamine release, and reactive oxygen species produced during metabolism of dopamine by MAO have been implicated in
> neurotoxicity.(And you're taking deprenyl right?!!!)
Yet I think you'd agree that the significant toxicity is to 5HT processes, and this seems to occur when MDMA is carried inside the neuron, and thus the protective effect of an SSRI. I susbect that MDMA competes with 5HT for entry so initially there is very little MDMA uptake and damage.
As for free radical damage, there are MAOis but also other central antioxidants.
> Addition of an SSRI might offer some protection, but its difficult to know how much and what neurons.
I agree it is complex and damage may occur at different times. But documentation of the damage (immediate vs. delayed) suggests that testing SSRI interactions whould be one of the next steps.
> This may all be really nitpicky, though. I've become very casually aquainted with a couple fairly regular users, and it's hard to tell if "Adam" (gotta love _that_ nickname) is doing
> them any real harm or not.Not nitpicky at all, and this observation is typical. Correlation between reported damage and obvious behavioral changes have been the exception, to my knowledge.
>
> > > > IMHO Parnate is also mainly for refractory depression:
> > > >
> > > > "Tranylcypromine in high doses (20 to 30 mg po bid) is often effective for depression refractory to sequential trials of other antidepressants; it should be administered by physicians experienced in the use of MAOIs."
> > > > --The Merck Manual
> > >
> > > True, that's what I use MAOIs for (haven't given tricyclics an adequate trial due to side effects, though).
>
> I wonder what it takes before some people decide you are "refractory" enough and insist you consider an MAOI. I had one doctor keep me on Serzone for more than two months even though
> I knew it wasn't working and started rapidly spiraling the drain while on it. I guess a quivering, weeping, suicidal state of frenzy is "refractory."
>But who knows what else may have worked in you.
> >
> > Despite all the bliss, I think the side effects of SSRIs cause many to drop those too. I can't deal with higher doses of Luvox but use a lower dose and pindolol.
> > >
>
> I never got anywhere near bliss on an SSRI, but had a couple fun side effects for my troubles: a spare tire around the waist, anorgasmia, and loss of libido. Perhaps if I had
> tried Prozac I could have been thin, asexual, and depressed. Will MAOIs never be a first or even second-line treatment again?I meant the bliss ABOUT them, not from them! But I hear you. A spare tire from an SSRI --- really?
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?
poster:Zeke
thread:9748
URL: http://www.dr-bob.org/babble/19991212/msgs/16953.html