These posts examine modern psychiatry from a critical point of view. Unfortunately, mainstream psychiatrists usually react badly to any sort of critical analysis of their activities, labelling critics as “anti-psychiatry,” whatever that is. Regardless, criticism is an integral part of any scientific field and psychiatry is no different. As it emerges, there is a lot to be critical about.
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At glacial speed, mainstream psychiatry is reluctantly turning to confront the unimaginable: that its treatments don’t actually work. It may reach the point where psychiatry trainees and medical students in general are taught, not just how to put more people on more drugs for longer and to blame them for not liking the experience, but how to actually take people off them. Before that day dawns, however, there is ample scope for psychiatry’s bold and adventurous thinkers to push into new therapeutic territories. Mostly, this is driven by failure, the fact that many people do not show any benefit from their treatment or may even be worse off, and not just financially. In most fields, if you try something and it doesn’t work, you ask what you’ve done wrong. Maybe you misunderstood the task or your model doesn’t apply to that case, that has to be sorted out, but psychiatry is different. The psychiatrist is never wrong, and what is needed is more of the same but never a bit of soul-searching.
The clearest example of this is the fairly recent notion of “treatment-resistant depression” (TRD) where a person doesn’t respond to standard antidepressants. This is about one third of all people given the drugs and is much the same whether they’re given active chemicals or placebos, i.e. antidepressant drugs are hardly an improvement over inert chemicals. This has led to a whole new field, “treatment of TRD,” where ever-more heroic treatments are thrust on the miserable sufferers. ECT has been around forever, of course, and has been joined by TCMS, magnetic stimulation of the brain and its variants; by dosage with a range of hallucinogenic drugs; and a newer one called vagal stimulation, which applies electrical pulses to the vagus nerve that controls our innards. There are probably others floating around but the principle is that the cause of treatment failure is always located in the patient, never in the treatment. One reviewer noted that there are something like 155 definitions of TRD and described a trend to rename it as “... the broader, more clinically honest construct of difficult-to-treat depression.” Does this mean TRD was dishonest? Unlikely they would admit that but he gives a case example to illustrate his point:
“Ellen,” a woman in her early 60s, is referred to you with “treatment-resistant depression.” Her chart lists 4 antidepressants across 2 classes over 18 months, 2 of them stopped early for adverse effects and one abandoned without explanation. What dominates the picture is not sadness but a flat, effortful anhedonia: she moves slowly, tires within an hour of waking, and complains that her memory “isn’t there anymore.”
This article is trying to make the case that this type of depression is due to excessive inflammatory chemicals floating around in the blood stream. In this view, depression is a case of “neuroinflammation acting on reward circuitry” of the brain, which means more blood tests and scans and more specific drugs. Just on the skimpy history, we can diagnose the problem in psychiatry. It’s highly likely that she is obese, that the obesity causes the high levels of inflammatory chemicals, and that she needs to be checked for Type II diabetes, thyroid problems and possible early cognitive decline. However, more telling is the peculiar comment in the next sentence:
Buried in her intake and easy to skim past is a history of early-life trauma, a childhood of chronic adversity and fear, that no prior note has connected to the adult in front of you.
Hang on, what do you mean nobody has taken notice of her early life experiences? That’s like saying “I didn’t notice that the patient had to be wheeled into my office a ventilator.” But this is the point: they’re not interested in her early life experiences, they don’t want to know about it. In fact, they’re so disinterested that the psychiatrist doesn’t even take a history. That’s left to a busy nurse somewhere in the process who quickly goes through a proforma and ticks boxes – or just leaves them blank. The psychiatrist then flicks through it, asks one or two questions more, writes a prescription and leaves. And, surprise surprise, the patient doesn’t get better, but that’s because she’s got “difficult to treat depression,” DTD, not because there’s anything wrong with their system.
A video in Psychiatric Times expands on this while talking about a new field called “interventional psychiatry.” It seems that prescribing drugs no longer counts as an intervention in a patient’s life, that’s reserved for more active treatments, mainly those listed above (ECT, TCMS etc). The rationale remains the same: the patient didn’t respond to treatment so let’s bring out the big guns. The video is long (about 45mins) and says precisely nothing but is revealing in what it doesn’t say: the complete absence of anything like a formal justification of what psychiatrists do to patients. Remember that this is a video of two senior psychiatrists talking for the benefit of other psychiatrists, this is the actual inner workings of the trade, not their propaganda:
I still find it tough to explain to patients how ECT works (at 7.33) ... TCMS is FDA approved for treatment resistant depression and the target is the dorsalateral prefrontal cortex. This is where we think is sort of like the traffic light that sort of like directs the signals around where where where the brain is (at 28.35; that’s how they talk).
(Interviewer speaking, at 43.40): I think artificial intelligence is the future because we are not diagnosticians, we do a very poor job of diagnosing patients and until we can get the correct diagnosis, we throw spaghetti at the wall and see what sticks because that’s how we cycle through medications. We don’t have precision medicine. Is neuromodulation better spaghetti than pharmarmacology? (Psychiatrist): I don’t know. I don’t know ... but I do believe that it’s AI that is going to help us become better diagnosticians (44.35) ... (Interviewer): Okay. What a good note to end on. We’ve covered so much. I hope we talked about interventional psychiatry in the midst of this lofty conversation about what are the targets of treatment and really what are we doing inside the brain that we hope is going to make things better and how do we decide about persisting with the treatment versus backing away ... (fades out).
It is indeed difficult to explain what ECT does because, even after 90 years, nobody knows. I say it doesn’t actually work [1] but it’s very lucrative so we’re probably stuck with it for a while. And traffic lights in the brain? The model of brain function that these people are using is more like one of those fancy model train sets where the trains whizz around through tunnels and over bridges. But the revealing line is this: “We do a very poor job of diagnosing patients.” That’s pretty scary, it says: “We can’t diagnose them but we know what the treatment is.” The notion that depression is due to inflammation of the brain’s reward (“pleasure”) centres is simply fanciful. Now that the serotonin notion has gone to a well-deserved grave [2], they need something so paralysis of the pleasure centres sounds like it will do the job (the job being psychiatrists fooling themselves that they know what’s going on so they can fool everybody else).
Two problems arise, the first physiological. The inflammatory chemical they’re talking about, C-Reactive Protein (CRP), is found in the blood during a variety of inflammatory processes. It’s secreted by the liver on instructions (interleukins) released by the inflammatory cells known as macrophages (science-speak for ‘big eaters’) which gobble up damaged cells and foreign bacteria. They instruct the liver to release CRP which prowls around and fixes itself on damaged cells or bacteria, which then attracts the local macrophages. Inflammation and immunity are fascinating but incredibly complicated processes in the body, the more is discovered, it seems the more there is to know. The immune process can and does go wrong in a variety of ways but the idea that, for no reason, one specific part of the brain suddenly becomes inflamed and switches off, to be cured by antidepressants, ECT and magic mushrooms, cannot be taken seriously. Obesity is a far more important cause of high CRP because that chemical is also released by healthy fat cells. Oh dear, didn’t think of that. High levels then lead to coronary artery disease and insulin resistance, which helps explain why obesity causes heart trouble and diabetes in a self-reinforcing loop.
The second reason why they shouldn’t talk of “paralysis of the pleasure centres” is because that’s already been claimed, by a psychological theory of depression, in fact. Oh dear again. As we discussed last week, the biocognitive model says that anxiety must be seen as the normal response to the perception of a threat [3]. A threat triggers a mixed psychological and physical response, which becomes a problem when the physical component is subsequently seen as a separate threat, i.e. the person is stuck in a vicious circle. Using the same model, depression is to be seen as the response to the perception of a loss. The awareness of a loss triggers a mixed psychological and physical response, mediated by paralysis of the putative “pleasure centres” in the brain. That’s all. Every time the person thinks of the loss, it sends another barrage of signals to the emotional centres of the brain, forcing them to shut down for a while, meaning nothing pleasurable can be experienced. With a severe loss, the signals are more or less continuous and the person is unable to experience any joy in life, i.e. what the paper called “not sadness but a flat, effortful anhedonia.”
With long term problems, the two most common being chronic anxiety and chronic pain, people sit daily on the edge of despair, sometimes slipping over for a while before they slowly manage to drag themselves out. One day, however, they get pushed a bit too far and decide: “This is how it’s always been, it’ll never be any different, I wish I could just die.” We call that depression but it is not an illness in any meaningful sense of the word. It is a realistic response to a life of more or less permanent suffering. It is definitely not caused by inflammation of the brain. The brain is perfectly healthy and is responding correctly to the signals it is getting, it’s just getting too many bad signals for any one person to bear. But what a damning thing to say for senior psychiatrists to say about themselves:
I think artificial intelligence is the future because we are not diagnosticians, we do a very poor job of diagnosing patients and until we can get the correct diagnosis, we throw spaghetti at the wall and see what sticks.
In any other field but psychiatry, that would prompt a very serious bout of self-criticism, such as “Hey, why don’t we try taking a proper history? Then we won’t overlook the terrible events in her childhood.” No, as fast as they lose one skyhook, they find another: Serotonin is dead, AI to the rescue. Wow, let’s see how long we can string this one out.
References:
1. McLaren N (2017). Electroconvulsive Therapy: A Critical Perspective. Ethical Human Psychology and Psychiatry 19: 91-104.
2. Moncrieff J et al (2022). The serotonin theory of depression: a systematic umbrella review of the evidence. Molecular Psychiatry (2023) 28:3243–3256; https://doi.org/10.1038/s41380-022-01661-0
3. McLaren N (2021): Natural Dualism and Mental Disorder:
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My critical works are best approached in this order:
The case against mainstream psychiatry:
McLaren N (2024). Theories in Psychiatry: building a post-positivist psychiatry. Ann Arbor, MI: Future Psychiatry Press. Amazon (this also covers a range of modern philosophers, showing that their work cannot be extended to account for mental disorder).
Development and justification of the biocognitive model:
McLaren N (2021): Natural Dualism and Mental Disorder: The biocognitive model for psychiatry. London, Routledge. At Amazon.
Clinical application of the biocognitive model:
McLaren N (2018). Anxiety: The Inside Story. Ann Arbor, MI: Future Psychiatry Press. At Amazon.
Testing the biocognitive model in an unrelated field:
McLaren N (2023): Narcisso-Fascism: The psychopathology of right wing extremism. Ann Arbor, MI: Future Psychiatry Press. At Amazon.
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