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Re: Effexor + Mirtazapine MORE effective than PARNATE! » SLS

Posted by Robert_Burton_1621 on February 13, 2015, at 6:50:52

In reply to Re: Effexor + Mirtazapine MORE effective than PARNATE! » vanvog, posted by SLS on March 12, 2013, at 8:36:26

> > I found this study of Parnate vs. a combo of Effexor and Mirtazapine which seems to indicate that the combo is twice as effective for MOST treatment resistant patients.> >


> This particular arm of the STAR*D study is meaningless.

"The mean daily dose at exit for tranylcypromine was 36.9"

The low dosage of Parnate used was woefully inadequate to treat depression. Most people don't respond to Parnate until a dosage of 40 - 80 mg/day is reached.>

- Scott

Scott, this is so well-said, well-spotted, and well-deserving of repeated emphasis.

Your observation is instructive because it prompts all of us who are "treatment-refactory" to pay very close attention to the protocols which are appplied in studies purporting to demonstrate the relative superiority of x strategy over y strategy.

Last year I was also, foolishly, excited by the discovery of this paper on ven + mirtaz v. tranyl. The excitement was aroused because I simply could not convince, at that time, any psychiatrist to prescribe parnate. (For one psychiatrist, I printed out and indexed a number recent research papers on the drug published since 2000, by eminent and rigorous psychopharmacologists, which supported its efficacy and corrected misconceptions as to its intrinsic "dangers", but to no avail). Rather, the efforts I went to in order to demonstrate the sincerity of my motivation, my desperation, to overcome my depressive illness were interpreted as evidence of a discreditable belief that there exists a "magic bullet" in the form of a mythical drug which will "cure" this illness once and for all. The particular psychiatrist who delivered this assessment (not the same one to whom I had given all the papers mentioned above), quite a senior and apparently reputable one, remarked that I had done more solid research into possible treatments than any patient he had seen before. It was clear that his remark was not intended as a compliment.

So my next strategy was to press the merits of the combination studied in this paper. And he was perfectly happy to prescribe the ven + mirtaz combo, though without any understanding of the mechanisms by which it was claimed to have such an effective, and extraordinarily positive, action in treatment-resistant cases. This same psychiatrist refused to consider an MAOI, on reasons which recent research, which should have been known to him if he were scientifically conscientious, has proven to be entirely erroneous.

The lesson I learnt from this experience is that, for psychiatrists, while all forms of ignorance may be equal, some are more equal than others.

The effect of this combination was (on me) negligble. The (posited) increase in noradrenergic neuro-transmission may have contributed to an acute, and very unpleasant, episode of troublesome anger I went through. Not wholly unsurprisingly given his deficient learning, the psychiatrist who prescribed this very combination refused to offer any constructive advice about this side-effect ("I don't treat side-effects"); I was simply advised to address my concerns to my GP.

The idea that this combo's appeal as an efficacious psychotropic with superb anti-depressant properties should be publicised popularly by the moniker "Californian rocket fuel" may well be some evidence for its source as a marketing ploy. I would, however, not wish to dismiss the positive experiences of people who have benefited from it.

Any "anti-depressant" benefit from Mirtazapine may in any case arise predominantly as a result of its extremely potent H1 antagonism. The supposition that it is "dual-action" has been pretty much exploded. But I don't possess sufficient learning to draw any conclusion.

Scott, you mention the Star*D trials. I agree that no competent psychopharmacologist could possibly assent to the proposition that their outcome has any clinical bearing on the relative efficacy of parnate. The only point I'd make in response is that the majority of psychiatrists, in my experience, are incompetent or barely competent psychopharmacologists; and the supposed definitiveness of the Star*D outcomes is routinely invoked in a knee-jerk and uncritical way whenever MAOIs are raised.

I was informed unequivocally by the same psychiatrist whose "advice" I was subject to for eight months last year that, given the trials of medication to which I had been non-responsive or only partially responsive in the past, there was (if I recall correctly) only a 6 - 10% chance (i.e., a pretty negligible chance) that I'd be responsive to anything else. This ex cathedra declaration was made in full awarenesss of, and must therefore have been taken to have incorporated due consideration of, my desire to trial an MAOI. But the idea that Star*D (or any trial using a similar a protocol as regards MAOIs) has anything at all to say about tranylcypromine is unsupportable; indeed, risible.



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