The Fake “War Between Neuroscience and Psychiatry”

By Neuroskeptic | April 26, 2017 9:15 am

Neuroscientists have launched an assault on the American Psychiatric Association headquarters and are engaged in bitter, boardroom-to-boardroom fighting. Psychiatrists have captured the leader of a militant pro-brain faction. A ceasefire, brokered by the American Association for the Advancement of Science, is due to come into effect at midnight.

Yes, indeed. A blog post by Daniel Barron in Scientific American yesterday claimed that there is a War between Neuroscience and Psychiatry


Here’s how the piece starts:

Earlier this month, JAMA Psychiatry published a land-breaking editorial. A group of psychiatrists led by David Ross described how and why post-traumatic stress disorder (PTSD) should be clinically evaluated from a neuroscience framework. The fact that this editorial was published in one of psychiatry’s leading journals is no small feat.

The appearance of pro-neuroscience paper in JAMA Psychiatry is, apparently, a notable achievement because psychiatry “houses a large and powerful contingency that argues neuroscience has little clinical relevance.”

But that’s not really true. Modern psychiatry is very closely integrated with neuroscience.

The the paper Barron linked to, by Ross et al. is far from being the first incursion of neuroscience into JAMA Psychiatry. A full 16% of all papers published in that journal mention ‘brain’ in their title or abstract, which is higher than the proportion that mention such typical psychiatry terms as “mental“, “diagnosis“, and “medication(s)“.

In fact if you Google JAMA Psychiatry, their tag-line is “The Science of Mental Health and The Brain”.

Meanwhile, a large proportion of neuroscience research is carried out by, or with, psychiatrists. Of all papers listed on PubMed with ‘brain’ in the title or abstract, nearly as many come from authors with “psychiatry” in their affiliation (e.g. Department of Psychiatry), as from authors with “neuroscience” in their affiliation.

brain_pubmedSo much for psychiatric research. What about clinical practice? Well, almost all psychiatrists prescribe medications, such as antipsychotics and antidepressants, which target the brain. So most psychiatrists are applying neuroscience in clinical practice, every day.

But when Barron complains about psychiatrists who think that “neuroscience has little clinical relevance”, I don’t think he’s talking about the small minority who reject the use of psychiatric drugs. Rather, I think he’s referring, rather unfairly, to psychiatrists who believe that mental illnesses are to some extent brain disorders, but who don’t think neuroscience has succeeded in allowing us to understand these disorders, yet.

Barron says that understanding is here. He takes the example of PTSD and talks approvingly about “key neuroscience themes” such as “fear conditioning, dysregulated circuits, memory reconsolidation, and epigenetic and genetic considerations.” Studying these themes, he says, and adopting “a mechanistic approach” allows psychiatrists to “trace the specific causes of PTSD to specific treatments that can target those causes.”

For example, “patients with PTSD have an overactive sympathetic nervous system [due to] overproduction of adrenaline” and this should “guides the clinician to prescribe propranolol and prazosin. These medications block aspects of the adrenergic system, thus targeting specific mechanisms that alleviate PTSD symptoms.”

Which is all lovely, neat and scientific. However, it’s naive to think that we understand the brain well enough for it to work.

The big discoveries in psychiatric medications were driven by serendipity, not through mechanism-based research. Someone noticed that an existing drug had effects that would be useful for psychiatry. The first antidepressant was invented as an antibiotic. The first antipsychotic was designed as a sedative, and so on.

It may be that propranolol and prazosin do help to treat PTSD, but the proof is in the pudding: we need randomized controlled trials to tell us how effective they are. We can’t assume that they will work, based on what we think we know about the mechanisms of PTSD. There might be a mechanism we’ve misunderstood, or one that we’ve missed.

We can’t put neuroscience theory above clinical reality. Down that road lies, well, madness.

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  • Uncle Al

    This is the shouted colloquy toward the end of The Wicker Man (1973).

  • CL

    But propranolol does not really work all that well in placebo controlled trials:
    And apparently, the war is now over, the blog title changed to “Why Psychiatry needs neuroscience”.

    • Neuroskeptic

      Lucky I took a screenshot of it!

      Unfortunately the headline was only one of the problems with the post.

    • rthorat

      That is embarrassing. “Duh, the obvious treatment is this one here. Wait, the only actual evidence seems to show that it doesn’t work at all? Oh.” It’s a cliche, but if I was as bad at my job as this example, I would be unemployed.

    • Bernard Carroll

      However, those trials of propranolol were designed as prevention trials not as treatment trials. As for prazosin there is good evidence of benefit in affected patients, especially against nightmares as well as more generally. There is also some suggestion that the benefit is linked to adrenergic arousal – see PMID: 27320368.

  • rthorat

    The problem is that we now know just enough about neuroscience for people like Barron to be dangerous. For example, the assertion that “patients with PTSD have an overactive sympathetic nervous system [due to] overproduction of adrenaline”. How do we know that is the problem and not just an observed symptom? It’s like saying that someone who is vomiting should have their vomiting treated and the actual cause is irrelevant. Sure, if the symptom can be safely treated while we look for and/or treat the cause, that is fine. But that’s the rub, because it’s not at all clear that we can safely treat psychiatric symptoms. Put aside the very real problems with tolerance and dependency, and instead think about how complex the brain is yet people like Barron talk about it in such simplistic terms. There is an overproduction of adrenaline, so we should just slow down the production of adrenaline. Overproduction compared to what? How do you know it’s an overproduction? Maybe that “overproduction” is critical to functioning given the stress the person is under. How the hell does Barron know? He doesn’t. No one really does.

    And looking at other brain systems involved in psychiatric illnesses, the picture gets even scarier. The “serotonin hypothesis” and “dopamine hypothesis” have both been popular explanations for depression and schizophrenia, respectively. But both are pretty much in the garbage bin now, yet the treatments based on them are still used. But what exactly do these drugs do? What does it mean to decrease dopamine activity in the brain?

    The truth is the brain is a complex machine and you can’t just pull levers here and there and expect it to have only very targeted consequences. It doesn’t work that way. A better way to describe how all psychoactive substances work is that they cause dysfunction in the affected brain regions. But don’t let this stop people like Barron from thinking we can just go into the brain and dial things up and down like we know what we are doing.

    • CL

      Don´t throw out the baby with the bathwater. We don´t need to understand how a treatment works for it to work. But a treatment needs to be better than placebo.

      • OWilson

        Placebos and “reassurance” (a good bedside manner) will always have their successes with certain patients. :)

    • smut clyde

      the brain is a complex machine and you can’t just pull levers here and there and expect it to have only very targeted consequences

      Lessons earned from the SSRI debacle: Absolutely none.

  • smut clyde

    “patients with PTSD have an overactive sympathetic nervous system [due to] overproduction of adrenaline”

    I remember when patients with PTSD had aberrant glutamatergic-pathway functioning due to the neurotoxicity of too much glutamate activity. That theory was popular a few decades ago, and the reason I am unable to forget it is probably because I have aberrant glutamatergic-pathway functioning.

  • reasonsformoving

    Unless we figure out how the brain enables the mind, neuropsychiatry will be more promises than reality.

  • CL

    “Can you imagine this with any other treatment outside of the brain?”

    Sure, aspirin is a good one, we now have some ideas about the mechanisms, but it has worked wonders for many years.
    In general, I agree with you concerns about side effects and potential long-term effects, but being anti-pharmaceuticals without nuance is also reckless and dangerous. People have been told to flush their pills, and died as a consequence.

    • rthorat

      I will concede there are some examples outside the brain where we do not, or did not, understand the mechanisms, though they are rare. And in many cases they are cautionary tales. Aspirin is one of them. Many of the problems it causes were unknown for a long time and a lot of damage was done by its widespread use.

      I am not anti-pharmaceuticals without nuance. I simply believe in science. And much of modern pharmaceutical research is pseudoscience, particularly in the brain and psychiatry.

      “People have been told to flush their pills, and died as a consequence.” I hear this a lot. It seems to be a vague insult meant to label the other person as irresponsible. It’s the opposite of the truth. I don’t know anyone with any knowledge of the subject who would ever advocate just flushing your pills. Jesus, that is dangerous. Many psychoactive drugs cause dependency, and withdrawal from some of them can be quite dangerous. Withdrawal from SSRIs can cause suicidal thinking, just as starting them can do. Withdrawal from antipsychotics can cause a range of schizophrenia-like symptoms as a result of destabilizing the dopamine system. Withdrawal from benzodiazepines and similar drugs (alcohol) can cause seizures and death. But honestly, I think more blame lies with the people who start patients on these drugs without any credible evidence they work, or without understanding the long term consequences, than I do the people who simply point out that the science behind these drugs is lacking in credible evidence.

      For example, even if you believe antipsychotics are an effective treatment for schizophrenia and related illnesses (the evidence says they are not in the long term), how can you ethically prescribe them when all the available evidence says that most patients you give them to will stop taking them cold turkey at some point due to side effects? And when they do stop, they will be in great danger. That seems totally unethical to me, yet the topic is almost never discussed.

  • OWilson

    Still a conundrum.

    The brain responds to chemistry, but it’s the the soul that responds to therapy and counseling. placebos, and a good bedside manner! :)

    • OlegMR

      Well, as an atheist, I quibble with “soul”, but I’d agree it is our conscious (and subconscious, too, I suppose) states that respond to these things. They respond to drugs, too. It would be really nice if psychiatrists admitted what philosophers (and neuroscientists) have admitted for millenia; to wit, that we know next to nothing about how one generates the other. Neuroscientists are working on this, psychiatrists won’t admit they have a problem. That’s a problem.

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  • OlegMR

    “What about clinical practice? Well, almost all psychiatrists prescribe medications, such as antipsychotics and antidepressants, which target the brain. So most psychiatrists are applying neuroscience in clinical practice, every day.”

    The logic of the conclusion escapes me (this is the kindest way I can put what I’m actually thinking).

  • Julie Katz

    You’ve aligned against medical intervention in favor of psychological interventions even though there is as little evidence of efficacy or mechanism of effect in psychological approaches as in medications, and in many cases there is even less evidence of the efficacy of psychological approaches than medication. Psychology has basically concluded about itself that the magic of relieving psychological distress (mental illness) is in ineffable qualitative dynamics and personality characteristics in the *relationship* between patient and psychological practioners. Even psychological interventions that were designed with the sole intention to be “measurable” (e.g., DBT), fail to outperform interpersonal/psychosocial counseling where the practioner and patient hold each other in positive regard.

    You’ve also asserted a causal relationship between psychological states (stress) and changes in brain structure which haven’t been validated, nor has demonstrated your assertion that psychological interventions cause changes in brain structure that can overcome previous negative changes, nor the implied assertion that these (supposed) changes in brain structure cause improved psychological health.

    You’ve failed to take into account genetic variants that may predispose one to less stress resilience, you’ve made no distinction between types of stress or exposure levels, nor have you given any thought to potential epigenetic changes from chronic (and/or extreme) stress that may cause permanent dysfunction in the HPA Axis and neurochemical systems, though increasing evidence suggest these changes are pervasive and permanent in cases of adverse childhood experiences and lead to lifetime immunologic morbidity and early mortality.

    Despite the lack of evidence of a causal relationship (in either direction) between negative psychological states and brain structure, and despite your claim that the more efficacious treatment for negative psychological states is “hope” and psychological treatments, you also assert that the diagnosis of psychological disorders is damaging to people because of the stigma attached to such a diagnosis.

    It seems you are presuming that being diagnosed with a mental illness causes stress that is psychologically damaging, though there’s no evidence that being diagnosed by a psychiatrist or psychologist causes pathological stress. One could hypothesize that it’s not the diagnosis that causes stress, but rather the diagnosed’s beliefs about mental illness and/or the reaction of their social circle to the diagnosis that causes stress (having nothing to do with DSM), if pathological stress were to be shown as a result of diagnosis. Given your assertion that stress causes changes in the brain which causes negative psychological states, the logical extension of your beliefs is that being diagnosed with a mental illness causes negative changes in brain structure, for which there is no evidence nor even heuristic logic.

    You make no distinction between types and duration of stress in terms of its ability to cause changes in brain structure, though nascent research on changes to brain structures point to *prolonged* patterns of mind (decades) to be a critical factor (e.g., Buddhist monks spending a life time meditating), so it seems quite unlikely that simply being told a diagnosis would be sufficient to to create a prolonged stress reaction sufficient to change the brain. Besides that, in your causal model of psychological stresses, these people who are being brain-damaged by being diagnosed by psychologists and psychiatrists, should then have this brain-damaging stress response treated with hope and psychology?

    You make no sense. The only way to find cohesiveness in your theories is to place you in the center as a person who has an irrational negative opinion about the DSM and an irrational and internally inconsistent faith in the power of psychological interventions and hope.

    • Sys Best

      “also asserted a causal relationship between psychological states (stress) and changes in brain structure which haven’t been validated”
      what do you mean by “brain structure”? we don’t understand yet how the brain activity patterns are generated in response to external and internal cues, we can measure it to some extent but we have a long way to go to understand it. and yes, anxiety/stress will change your brain activity, right away, there are EEG studies on it. and if anxiety persists for prolonged periods of time, then sleep disturbances can appear, and epigenetic changes will follow, for example. the system (brain) will adapt and its subsystems (e.g. neurotransmitter systems) as well.
      ID9192 posted a pertinent opinion, food for thought in your psycho-philosophical lingo, not a lengthy review about how stress can change the brain function … and you really went off the rails in the last paragraph of your answer



No brain. No gain.

About Neuroskeptic

Neuroskeptic is a British neuroscientist who takes a skeptical look at his own field, and beyond. His blog offers a look at the latest developments in neuroscience, psychiatry and psychology through a critical lens.


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