Okay, before we start, here’s an extract from my lead mcmanweb article on antidepressants:
The strongest scientific evidence we have is not how well antidepressants work, but how badly they perform and how harmful they may be to certain individuals. Here's the low-down:
Two meta-analyses of the FDA clinical trials conducted by Irving Kirsch of the University of Connecticut in the late 1990s-early 2000s of Pharma-sponsored clinical trials - including ones not published - in the FDA database found that antidepressants worked only marginally better against depression than placebos. There have been a number of expert rebuttals to these findings, but no actual study to contradict Kirsch.
The article reports on the most authoritative real-world study on antidepressants, the NIMH-underwritten STAR*D from the mid-2000s. We continue from my article:
Commenting on STAR*D, in a 2009 blog, Nassir Ghaemi MD of Tufts University noted that: “Even if antidepressants worked in the short term (2 months, which is also what the meta-analysis assessed), one-half of patients who stayed on them relapsed into depression within one year. At the one year outcome, only about 25% of patients actually had remained well on and tolerated an antidepressant, much below the levels most clinicians seem to feel occurs in their clinical experience.”
One in four! According to the best data we have, just one in four individuals treated with an antidepressant get well and stay well. And this was in the best possible care setting. Is your clinician aware of this? Probably not.
Neither is Peter Kramer of Brown University. Dr Kramer is the author of the 1993 “Listening to Prozac,” which is largely a product of the time, back when we all trusted Pharma a lot more than we do now. We have learned a lot since then, including the fact that these drugs can be highly destabilizing to individuals with bipolar and with depressions that cycle like bipolar.
But Dr Kramer in his NY Times article mentions neither STAR*D nor the obvious risks of taking an antidepressant. Huh?
Dr Kramer’s defense of antidepressants is specious and drearily unoriginal, one based on a speculative nitpicking of Kirsh. Back in a newsletter piece I did nine years ago, I referred to this as the “Van Meegeren Defense.”
Prior to World War II, Han Van Meegeren earned a nice living for himself selling bad forgeries of Vermeers. When World War II came along, one of Van Meegeren’s customers turned out to Reichsmarshall Hermann Goring. After the War, Van Meegeren was arrested for collaborating with the Nazis and charged with treason.
Here’s the part of the story I love: Van Meegeren’s defense to selling cultural treasures to the Nazis was that they were not real Vermeers, but his own forgeries. In other words, he had to convince the court that he had cheated.
Okay, now that you “get” the Van Meegeren Defense, here is what Dr Kramer has to say in his NY Times article:
Consequently, companies rushing to get medications to market have had an incentive to run quick, sloppy trials.
In other words, to cheat. What Dr Kramer is saying is that clinical antidepressants trials sponsored by drug companies might have yielded better results had they stuck to protocol and included only patients most likely to respond to antidepressants, namely those with severe depression. In effect, the drug companies, in their haste to recruit patients, probably included a substantial number of likely non-responders, namely those with milder forms of depression or those who plain lied to get into a trial. Thus, according to Kramer:
Often subjects who don’t really have depression are included — and (no surprise) weeks down the road they are not depressed. People may exaggerate their symptoms to get free care or incentive payments offered in trials. Other, perfectly honest subjects participate when they are at their worst and then spontaneously return to their usual, lower, level of depression.
As I stated earlier, this is not a new explanation. I first came across it soon after Kirsch’s second meta-analysis was published in 2002. Basically, academic critics acknowledged that Kirsch had made a bullet-proof case based on the evidence. So, then, how to explain the evidence?
Ah, the Van Meegeren Defense. In other words, if the drug companies had not cheated to begin with, maybe, just maybe, the results might - just might - have come out more in their favor.
It’s all speculation, of course. The only real way to counter Kirsh’s bullet-proof evidence is with bullet-proof evidence of one’s own. And while we're at it, to come up with an authoritative real-world study to counter the STAR*D real-world study.
There are many nuances to the antidepressant debate, and in all likelihood these meds work for a certain subpopulation of depressed patients (if we only knew who they were), but - again - this is speculation, not science.
The bottom line is the most convincing evidence we have on the (non)efficacy of antidepressants comes from Kirsch and STAR*D. The only counter-evidence is recycled speculation, Kramer-style.
***
Robert Whitaker on his Mad in America blog picks Kramer apart in far greater detail, concluding with:
On Sunday, in this essay "In Defense of Antidepressants," the American public has been treated to yet another dose of misinformation.
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8 comments:
The reason the results for the trials are so bad is that the drug companies included people who weren't really that sick -- I wonder how that defense will play in the class action suit. And where is that class action suit so I can sign up?
Meanwhile, NIMH did its own study, STAR*D, which I notice Kramer didn't mention. Still scientifically flawed and stacked in favor of the drug companies. Yet that is the study today most frequently published to demonstrate the piss poor results of these meds for the vast majority of those who take them.
Hey, Willa. Kramer's dissembling is startling. In effect, he is the reverse Thomas Szasz, who refused to even slightly modify his antipsychiatry rhetoric in the face of overwhelming brain science evidence.
Kramer displays the same obdurate refusal to look at the facts. Instead, he is saying, in effect, "Antidepressants work because I say so." And he is hiding behind his MD and reputation.
Maybe he thinks if he says the same thing often and loud enough, antidepressants will suddenly start working.
There is room for legitimate debate on the various pros and cons. But we need to be hearing from the people who know what they're talking about.
I haven't read any of Kramer's books, but I have read a number of his articles. He understands nothing about depression, either.
I actually thought I may have found an informed blogger, until I read your comment in reply to Willa.
"in the face of overwhelming brain science evidence."
pray tell, what evidence is this, overwhelming or otherwise???
Sorry, Anonymous. I don't have to prove brain science exists.
Well, my household is split 50-50, after ten years on assorted antidepressants my diagnosis was switched to BP2 and I went thru almost every AD then available before the dx switch. I am not sure if I was misdiagnosed in the first place or if the ADs had something to do with it.
My husband, on the other hand is a textbook case for ADs, he was put on celexa for his second bout with depression (talk therapy alone worked for the first) had excellent results and is still on it with only one dose change about 10 years later. And I can tell and so can he if he misses a dose. Crotchedy, cranky and crabby, thats him if he forgets his pill.
Just goes to show that even with the brain, perhaps especially with the brain, there is no such thing as standard anatomy. And itmust be really hard to do a truly scientific study when the particpants reporting of results is so subjective.
Once again we auffer from lack of objective measuring tool. Maybe someone needs to do a study with before and after MRIs. Of course that would cost real money. OK, I'll shut up now.
Hey, Lizabeth. You nailed it. For psychiatry to be credible in the future (and it has largely lost its credibility in the present) it has to move the way you suggested. Namely, with reliable biological readings - brain scans, DNA, blood tests, EEG, you name it.
I attended a session that addressed these points at the NAMI convention last week, and I will be blogging on it fairly soon.
So, imagine (as you have), someone like your husband gets a reading that determines he is a likely responder to an SSRI. Someone like you gets a reading that you are a likely nonresponder.
Wouldn't that save countless millions years of heartache and frustration.
The diagnosis - depression - is a smokescreen. Kramer is stuck in the depression-ergo-antidepressant mindset which is totally out of tune with our clinical reality and what we are learning about the brain.
The reality you are describing is the reality we all face - matching the right person to the right treatment. There is nothing wrong with any drug per se - only when it is used on the wrong person. Our docs, however, don't seem to recognize this. They are engaged in a pharmaceutical crapshoot rather than the actual practice of medicine.
Thanks for this. Your real-life example says it better than anyone, and should be regarded as the final word.
"Crotchedy, cranky and crabby, thats him if he forgets his pill."
that was me too and it proved to be the beginning of withdrawal, not therapeutic interruption.
some people have horrendous withdrawal syndromes from ADs...and yes, that does mean one is dependent on the drug.
For some getting off ADs takes years if it can be done at all. That includes folks who at first like their AD but at some point it goes south on them.
I've been out of the loop for a while on your blog but reading back your posts has been a delight. It is quite funny how many people can pass off any 'fact' which at first seems to address the question but in fact addresses nothing. Politicians too are quite the splitting image of this (and how we trust them!?).
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