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Re: Picky, picky

Posted by Adam on April 16, 2000, at 22:38:06

In reply to Re: Selegiline without the Patch, posted by Elizabeth on April 15, 2000, at 16:03:34

> How long did you take 15 for before upping it?

I took it for about a month. For the first couple of weeks, I thought things were going OK, and I was kind of psyched, but then I really started to notice, especially by the end of the third week, a worsening in mood. It was slow to come, but it's like by the middle of the third week I found myself feeling really withdrawn, pessimistic, uninterested in being with anyone but my girlfriend, etc.

When I took the extra 15mgs, I felt an improvement in mood in about two to three days. This seems to fast, but now, having taken 30 mg. for about 8 days, I feel pretty good. Maybe I should monitor myself with an online HAM-D or something.

> > No, but I may get some. Heard anything about Sonata?
> Too short-acting, but it might be okay for you if you don't have trouble staying asleep.

Hmm. Well, I'll give it a try, I think, before going to the Ambien.

> > Well, everybody's got OCD these days.
> ????? !!!

Sorry! This is a bit sarcastic, though the irony isn't directed at you. I read an article someplace a while ago that OCD diagnoses were on the rise, and that some suspected people without OCD were getting misdiagnoses with greater frequency.

> > I find it interesting that neuroleptics, which block DA receptors, cause restlessness, while stimulants, which antagonize DA receptors somehow (among other things), cause restlessness. Does akathisia come only later, after DA signalling has readjusted to dysregulation by DA receptor antagonism?
> I don't know about akathisia, but some of the extrapyramidal effects of neuroleptics are supposedly caused by down-regulation, notably tardive dyskinesias & dystonias.
> As for your question, I guess anxious people just can't win when it comes to meds!

Rats. Above, I meant to say stimulants "agonize" DA receptors (saying stimulants stimulate sounds kind of funny), the implication being the DA system might become desensitized somehow following increased DA, maybe in a similar fashion to somatodentritic autoreceptor-mediated downregulation of other neurotransmitter systems.

> I think you'd be the one to answer that, since you know what OCD feels like. Does this feel the same?

Kind of, yeah. There's other stuff, too, but I don't feel like going into it now.

>But, FWIW, I do know lots of people who've taken Risperdal who have nonpsychotic depression or manic-depression.

Did any of them mention side effects? I would think that Risperidal might be helpful to manic-depressives because of its effects not only on the dopamine but serotonin systems. I hope to take it, if I do, in doses that only effect the DA system. My concern is that, while the DA effects are a pain for anxiety, they're part of this great antidepressant response I get from selegiline.

Man, this sucks sometimes.

> Apples & oranges.


> It really is too bad you couldn't stay on the patch.

I never realised how much nicer selegiline would be on the patch than off. I don't know if it will get approved or not, but it seems to me that it should. People are using the selegiline transdermal system (STS) for a number of indications now, and all reports show it's easier to take that way, for reasons you already know. My only fear is that if they can't show it's a gangbusters antidepressant for a significant number of people, even if they approve the STS, it will be for doses far smaller than what I need, and I would have to plaster myself with patches to get the right amount. This is probably a silly concern, but it nags at me all the same.

>Do you think that transdermal administration might make other drugs more tolerable too?

I think that so long as one does not have a bad skin reaction either to the drug or the adhesive, and diffusion throught the skin to the bloodstream is efficient, such an approach should help with many drugs. I actually asked about other MOAIs, and was told that Parnate was "too toxic" for this approach. I don't know why. Also, while Dr. Bodkin was taking some blood from me (after an RA totally impaled me, but failed to hit the vein), I asked him: "Why the heck can I get an MAO-A and B inhibitory dose of selegiline and still eat cheese? What's going on in the gut, anyway?" His answer was that no one really knows. He also pointed out that higher doses than what I was taking on the patch necessitated dietary restrictions. There is partial inhibition of MAO-A in the gut at 20mg/day (what I was taking), but not enough to fully potentiate the tyramine pressor response. I don't know if this would be true for other MAOIs.

But even if there's no benefit to the patient in the area of dietary restrictions, the tolerability issues avoided by STS delivery must be significant indeed. Other drugs, so long as first-pass metabolism rapidly degrades the parent compound and produces troublesome metabolites, should, I think, be as transformed by transdermal delivery as selegiline: lower dose needed to reach efficacious levels in the blood; fewer issues with short half-life, as it is lengthened, and also drug administration is spread out evenly over the day; fewer annoying side effects from metabolites, not only because first-pass metabolism is avoided, but also because actual dose is far smaller than is needed for oral delivery.

I wonder if you might even do well on transdermal selegiline. If what the literature says is true, I was getting an effective dose of the parent compound well in excess of the equivalent of a 100mg oral dose, and felt better than I do now on a 30mg oral dose. And, at least for me, the response was fast as hell. Hands down the most amazing thing I ever tried for mental health.

> Not sure how helpful I was, but you're welcome.

Quite helpful, as always.

Take it easy.




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