The anti-psychiatry, anti-Big Pharma blog post that reads like a science blog post

I’ve long been a fan of Io9.com, a blog about science fiction and other things to do with science. The writers of that blog have been, for the most part, very reasonable in their approaches to things having to do with science. They’ve come out against antivaxxers and all their nonsense. But I guess the streak had to end at one point.

In a blog post titled “The Most Popular Antidepressants Are Based On A Theory We Know Is Wrong“, blogger Levi Gadye, a neuroscience graduate student, postulates that the theory that depression is the end result of neurotransmitter function deficits or defects is wrong. Further, he seems to imply that Big Pharma had something to do with hooking “one in ten Americans” on antidepressants.

But let’s not get ahead of ourselves. Let’s take his blog post one piece at a time.

First, Mr. Gadye tells us that one tenth of Americans is on antidepressants. In a country with 320 million, this means that 32 million of us are on antidepressants. Is that true? Like all statistics, these numbers need to be seen in context. Yes, a lot of people are on antidepressants, but that number was derived from the NHANES study, a periodical survey of Americans’ health. Here’s what CDC had to say about these numbers:

“This data brief discusses all antidepressants taken, regardless of the reason for use. While the majority of antidepressants are taken to treat depression, antidepressants also can be taken to treat anxiety disorders, for example. The report describes antidepressant use among Americans aged 12 and over, including prevalence of use by age, sex, race and ethnicity, income, depression severity, and length of use.”

Also,

“Less than one-third of persons taking a single antidepressant have seen a mental health professional in the past year.”

What does that tell you? It tells you that the problem isn’t so much that everyone is being treated for depression. The problem is that antidepressants are being over-prescribed and that people who should not be on them are on them. It is clear that there is a disconnect between who is prescribing the medication. It’s not mental health professionals, for the most part.

Let’s move on.

Mr. Gadye acknowledges that the problem is not mental health professionals. It’s Big Pharma, dammit:

“What’s less clear is why these medications work, but decades of research on the subject suggest that an explanation parroted in ad campaigns and physicians’ offices alike – that depression boils down to a “chemical imbalance” – is wrong.”

Well, not just Big Pharma. It was Big Pharma and psychiatrists:

“This is the story of how pharmaceutical companies and psychiatrists convinced the public that depression was the result of a simple chemical imbalance – and how scientists, patients, and psychiatrists are working to piece together the more complicated truth.”

Who will save us? Psychiatrists, of course! Wait. What? Yeah, he mentioned psychiatrists as both the problem and the solution. My guess is that psychiatrists in league with Big Pharma are the problem, and psychiatrists who are not in league with Big Pharma are our saviors. Where have I heard that before?

Anyway, Mr. Gadye takes us through some history of psychiatry in the mid-20th century and summarizes it thus:

“Psychiatry had lagged behind other medical fields for decades, in large part because it lacked treatments tailored to treat specific conditions. Thorazine helped accelerate the acceptance of biological psychiatry, which focused on the biological basis of mental disorders. Biological psychiatry also provided a welcome opportunity for psychiatrists to work directly with pharmaceutical companies to develop targeted, drug-based treatments for mental disorders. Change was in the air.”

Indeed. That change was that case reports, animal models, and incidental discoveries showed that neurotransmitters like serotonin were associated with psychiatric disorders, like depression. Who would take that research and run with it? Let Mr. Gadye tell you:

“Pharmaceutical companies saw a major (and, potentially, majorly lucrative) opportunity: A drug that could increase serotonin levels without causing severe side effects could revolutionize the treatment of depression.”

If you’re noticing a theme in Mr. Gadye’s blog post, you might be onto something. In the comments section, he refers to drugs to treat ADHD as “pharmacrack.” But I digress.

Mr. Gadye then tells us that modern serotonin reuptake inhibitors (SSRIs) took 20 years to go from lab to market, but, once they did, Big Pharma was more than happy to shove commercials for them down out throat. He mentions psychiatrists over and over again, though, as the CDC report shows, most people on SSRIs didn’t go to psychiatrists for their prescriptions. The problem is physicians who were undertrained — or not trained at all — on how to deal with mental health problems being suddenly presented with evidence that SSRIs worked in most cases.

The next section is about the “chemical imbalance” myth, which is not a myth in the full definition of the word. It’s not a myth even in the way that Mr. Gadye describes it. His logic seems to be that we cannot directly measure what is happening with serotonin in the human brain, so we can’t say that a chemical imbalance is what causes depression. Even if SSRIs deal with the problem, it can’t possibly be the serotonin, can it?

The rest of the blog post calls upon two scientists who agree with Mr. Gadye’s thesis. He then summarizes his post thus:

“Psychiatry has been slow to actively correct the myth of the chemical imbalance theory of depression, and SSRIs remain the therapy of choice for millions of patients, but scientists and psychiatrists seem eager to improve our understanding of depression and its treatment. Big Pharma may have led the public to believe that drugs alone could cure a singular cause of depression, but evidence-based reasoning and experimentation stand to put us back on track.”

What puzzles me the most about this blog post is that Mr. Gadye (in it and in the comments) agrees that the human brain is very complex, so finding the one true cause of depression and many other psychiatric disorders is going to be hard. But to say that the theory that it’s a neurotransmitter (chemical) imbalance or defect is outright wrong? Well, it doesn’t really explain why SSRIs work for so many people.

All that the blog post did for me was to bark at me that Big Pharma and psychiatrists are out to make a buck. Yet, again, SSRIs work on a lot of people. And if it isn’t Big Pharma who brings these products to market, then who is? I mean, I know it’s not the perfect setup, but no one really offers much in the way of alternatives when ranting and raving about Big Pharma.

Judging by the comments in Mr. Gadye’s blog post, my comments included, he managed to come off as somewhat of a conspiracy nut in continuously asserting a collaborative effort between psychiatrists and Big Pharma to get everyone on SSRIs even when they don’t need them, going as far as to assert that it’s all just a placebo effect that patients on SSRIs are exhibiting.

I expected better from a blog I’ve followed for so long.

Finally, in the interest of full disclosure: My wife is a physician assistant with two master’s degrees. One is a master’s in physician assistant studies. The other is a master’s in mental health. She is teaching a college-level course this coming summer on psychopharmacology and the intersection of medicine, psychiatry, and psychology. I myself do not receive any money from her endeavors, or from Big Pharma.

I'm a fourth-year doctoral candidate in the Doctor of Public Health program at the Johns Hopkins University Bloomberg School of Public Health. All opinions posted here are my own, of course, and they do not necessarily reflect the opinions of my school, employers, friends, family, etc. Feel free to follow me on Twitter: @EpiRen

5 thoughts on “The anti-psychiatry, anti-Big Pharma blog post that reads like a science blog post

  1. It’s interesting that he only goes on about SSRI’s and ignores TCA’s, SNRI’s and NRI’s.
    I was taking TCA’s, as they’re quite effective against neurological pain. Regrettably, after going into anaphalaxis after taking Amitriptyline.
    But then, that’s “Big Pharma” too. Making pain disappear, how terrible of them!

    But, I’ll consider looking at his page and asking him a few questions. For one, asking how many receptors are on a synapse. If he says few or only one, we now have the source of his flawed views, as there are many receptors on each synapse. Indeed, the more that neruron fires, the more receptors are produced and migrate to the synapse. Such improves performance, as not all receptors will be activated, so that before the activated receptors have to be cleared, the nerve can fire again when needed. Clearance being accomplished either via absorbtion, termination (typically hydrolyzed), neutralized by an antagonist, etc.
    Add in neuromodulators, yep, it gets *really* complicated.

    But, we *can* track these actions by tagged chemicals. So, we can indeed see what acts in what way and where it acts. We can study groups of neurons in a culture and stimulate the neurons chemically or electrically.

    So, perhaps he needs to go back to biology class and take introductory neurology.

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  2. Well, maybe I am a conspiracy nut. One who has read a LOT of peer-reviewed science about anti-depressants and depression. That placebo effect claim? It’s far from fringe – though it is controversial, even within psychiatry. Irvin Kirsch is the expert who has driven the research on this claim. Here’s one of his articles. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2582668/

    Looking back, I omitted the primary source of anti-depressant prescriptions (doctors not trained in psychiatry), and I regret that.

    These drugs do increase serotonin, and help about a quarter to half of the depressed patients who try them out. The impact of this on the human brain is still, largely, a mystery, though some interesting hypotheses of how elevated serotonin treats depression include increased neurogenesis, and rewiring of particular circuits (namely the various networks linking the frontal cortex with the amygdala). However – the link from synapse to our mental health is still unknown. Here’s a good article about that mysterious link. http://www.scientificamerican.com/article/new-theory-of-antidepressants-could-help-predict-patients-response/

    I am one of many to have written on this topic. I’m glad my post blasted off – clearly there’s a lot of misunderstanding about depression out there. But in the early 2010s, a flurry of articles like this NPR piece (http://www.npr.org/blogs/health/2012/01/23/145525853/when-it-comes-to-depression-serotonin-isnt-the-whole-story) made claims similar to mine.

    If you read my article more closely, the last source – Poul Videbech – does not, in fact, simply back up my claims. He provides a broader view of what scientists suspect causes depression. I did not recruit people who agreed with me. He was the sole psychiatrist of four who replied to me, and his responses were sincere and well-rounded. If you’re fine with Google translations, I recommend you read his balanced views about depression and psychiatry on his personal website (videbech.com).

    I’m skeptical of institutions that profit enormously off of human health. That’s my bias. But my claims about depression, SSRIs, etc? That’s science. That’s why it reads like a science blog post. Maybe pharm companies and psychiatrists haven’t worked directly hand in hand, especially in the last decade (now there are more rules preventing docs from receiving kickbacks from big pharma). But it is undeniable that there are more people taking these drugs than there should be (http://well.blogs.nytimes.com/2013/08/12/a-glut-of-antidepressants/), and that’s a problem worthy of our skepticism.

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  3. Also I don’t need introductory neurology. Wzrd1’s speculation about plasticity resulting from SSRIs is certainly plausible, and indeed testable in isolated cultures of neurons (and animal models), but there is no conclusive evidence painting a thorough picture of how SSRIs change the human brain, either in the course of the 3 weeks it takes for them to begin treating depression, or when administered chronically.

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    • I’ll simply ask lgadye what an animal model is and how an animal model illuminates the effects of these drugs?
      Or does lgadye subscribe to human exceptionalism?
      For, with animal models, we can dissect the brain of an animal and measure receptors. We can invasively test the animal brain in ways unethical and unlawful to do in humans.

      Our ignorance on how the brain works fades each and every year, with major breakthroughs coming at irregular intervals, but those intervals seem to be becoming more frequent. As our knowledge becomes more mountainous, we now receive veritable avalanches of knowledge, crushing our ignorance on entire systems within the human brain.
      As our knowledge grows, newer drugs can be developed to target specific problems within those multiple systems within a brain.
      So, we now have drugs that are far more effective than anything we’ve had (or not had at all) in the past, improvement will come with efficacy as our knowledge builds. We’ve come from an era where mental illness was thought to be demonic possession, passed through an era of ignorance where mental illness was thought to be a character flaw and the mentally ill were warehoused, to an era where we do have effective treatments for some maladies. In the latter cases, improvement has been incremental from barely effective to highly effective in specific classes of mental illness. We can only improve upon that gradually, as out of a thousand potential drugs, very few will ever make to human trials and fewer will make it to license.

      I do find it interesting that lgadye entirely ignored norepinephrine receptor agonists, which are also used in treating depression. Also ignored, serotonin–norepinephrine reuptake inhibitors. Instead, we’re treated to serotonin exclusive theory, which ill meets the subject.

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      • Animal models illuminate the effects of these drugs in animals. Not humans. No good neuroscientist would argue that getting a mouse to swim around a water maze for an extra minute on Prozac is the same thing as treating depression in humans. We are certainly very different from mice. And in fact, as much as we understand many of the neurotransmitter systems in the brain, we are a long way from developing tailored treatments for every type of patient. The treatment of depression has not improved (in terms of efficacy) since MAOIs, TCAs, and SSRIs were first developed – we’ve merely invented drugs with more mild side effects. Efficacy still hovers around 50% on a good day.

        I don’t know what point you’re trying to make. “It’s wrong to criticize psychiatry, look how far we’ve come!” I acknowledged repeatedly how drugs help some people in my article. Constructive criticism of any field is necessary for progress, and my article provided measured evidence of how psychiatry is moving forward as we speak. Up to you whether you ignore that nuance and choose to argue strawmen like I don’t understand how animal models work 😉

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