Wednesday, February 12, 2025

Sticking to the argument about whether antidepressants work

I worry that the clash between Joanna Moncrieff and Awais Aftab about her new book Chemically imbalanced has become too personal (see eg. last post). For example, Awais’ recent blog post criticises Jo for her methods rather than necessarily actually what she says. In many ways, how Jo expresses her critique is irrelevant. What matters is the content of what she says.

Awais Aftab wants to see integrative and critical pluralism as a variant of critical psychiatry (see previous post). But he’s only semi-critical and does not follow through properly on his critique. And he believes antidepressants and other psychotropic medications work, whereas critical psychiatrists such as Jo, are more sceptical, if not convinced of their non-effectiveness, which Jo has been brave enough to say.

As we saw with the Simon Wessely debate with Jo on the This morning TV programme (see clip), mainstream psychiatry will not allow Jo to say that antidepressants do not work. I have always been cautious about making such a definitive statement, even if expressing to people, including my patients, my belief that it may well be true. I’m not sure how to prove the so-called placebo amplification hypothesis even if I agree with Jo that there is considerable evidence in its favour (see eg. previous post).

Tuesday, February 04, 2025

Indoctrinating people into taking antidepressants

People are being misled about the nature of mental illness. Of course brain abnormalities can cause organic mental illness, such as delirium or dementia. But most presentations of mental health problems are not caused by brain abnormalities. 

Using depression as an example, people have been encouraged to see depression as a chemical imbalance in the brain. Because SSRI antidepressants are said specifically to block reuptake of serotonin from the synaptic cleft between neurones, it has been suggested that they must be correcting a serotonin deficiency in the brain. Although doctors may have realised that such an explanation of the effect of antidepressants is at least an oversimplification, they have allowed the general public to go along with the idea. In fact people have often believed the chemical imbalance theory to be proven. They have accepted, even been told, this myth to provide a reason for needing to take their antidepressants. Hence the controversy created by Joanna Moncrieff’s recent book Chemically imbalanced: The making and unmaking of the serotonin myth (see eg. previous post and Jo’s response). 

More generally, depression tends to be seen as a brain disease. Of course people recognise that personal and social factors may also be important, but still the brain causation of depression tends to predominate as an aetiological factor. This is a fundamental misindoctrination of people that their brains determine what they think, feel and do. Of course the brain is needed for human functioning, as is the whole body, but people are more than their brains. It is a mistake to blame the brain for depression as much as it is for what we think, feel and do in general. We are not teaching our children a proper understanding of themselves (see eg. previous post). No wonder the demand for children’s mental health services, and mental health services in general, is out of control (see eg. another previous post). 

Thursday, January 30, 2025

Depression is real but not a concrete thing

Functional mental illness is an abstract not concrete concept. It differs from organic mental illness where there is brain dysfunction.

Illnesses tend to be seen as “things” which people “have” (see eg. previous post). Since the nineteenth century with the elucidation of pathological mechanisms, our positive understanding has become that the “thing” that people “have” is a diseased organ or bodily system. This model fits for organic mental illness such as dementia or delirium. For example, organic mental illness can be caused by a primary brain disorder or be secondary to a systemic illness. But functional mental illness, such as depression, is not primarily due to brain disease, although it can arise as a secondary consequence of illness. People are depressed, not their brains.

People of course are not separate from their bodies. They are alive, not machines, and embedded in their environment, which is social and cultural. Their bodies and environment afford various possibilities of action to them. Mechanistic dysfunctions of body parts may help to explain disease and why the person is ill. But the experience of illness is not necessarily due to diseased body parts. 

Depression, therefore, needs to be understood as a personal illness not a bodily disease caused by brain dysfunction. Its social implications can mean that various roles cannot be fulfilled, such as being able to go to work. It is not simply curable by willpower and motivation and, therefore, the person themselves should not be blamed for their illness. The expectation is that people will try to recover as quickly as possible with appropriate help and care if necessary. 

None of these social implications of illness necessarily require the presence of bodily disease to be entitled to the rights and obligations of the sick role (see eg. previous post). Such illness is not concrete in the sense of being caused by bodily mechanisms. But, functional mental illness, such as depression, even though abstract rather than concrete, is still real and valid. Regarding depression as a physical thing in the brain is a category error and does not make sense (see eg. previous post). 

Thursday, January 23, 2025

The disadvantages of antidepressants

As I’ve said before (see eg. previous post), I’m inclined to believe that antidepressants are no better than placebo. I can’t prove this but it is possible that the statistical difference between antidepressant and placebo in short-term clinical trials is an artefact because of methodological problems, such as unblinding (see eg. another previous post). Nor do antidepressants over the long-term necessarily produce good outcomes (see yet another previous post). Treating depression is not always as easy as we might hope. 

I just wanted to elaborate on what the consequences are if antidepressants are really no better than placebo. Of course the nature of placebo in this sense is that it is given inadvertently (see eg. my BMJ letter). Doctors do not knowingly prescribe antidepressants as placebos. In fact, as advocates of antidepressants they can react vehemently against suggestions that antidepressants do not work (see eg. previous post). Nor do patients assume that antidepressants are placebo, perhaps especially if the medication has a positive effect. They are more likely to ascribe any improvement to a true antidepressant effect of the medication. Faith in antidepressants is commonly reinforced by the belief that medication improves a brain problem causing depression such as a chemical imbalance (see eg. another previous post). 

I’m not wanting to undermine people’s faith in medication. It’s important we have a balanced view of the advantages and disadvantages of antidepressants (see eg. previous post). We have to live with the uncertainty of the ongoing debate about the efficacy of antidepressants (see eg. another previous post), however much some people may want to close that debate down and conclude that antidepressants are definitely effective.

If we have to accept the uncertainty about the advantages of antidepressants, perhaps looking at the potential disadvantages will help us better assess their value. Doctors have always underestimated the difficulties in withdrawing from antidepressants (see eg. previous post) and the extent to which doctors are making people dependent on antidepressants (see eg. another previous post). Patients are not always warned about the risks of stopping antidepressants when they first start them, which they should be. Even if doctors routinely provided this warning, people can still naturally become fearful that discontinuing medication may upset the mental equilibrium they have managed to achieve with antidepressants after being depressed (see yet another previous post). Patients may believe the antidepressant is maintaining that equilibrium, whether it has been the cause of the improvement or whether changes have happened for other reasons. In other words, people can form attachments to their medication more because of what they mean to them than what they actually do (see my article). Any change threatens an apparent stability related to the meanings that the medications have acquired over time. It may, therefore, be easier to stay on medication than stop it. Considering also the difficulties people can have when they do try to stop, it is not surprising that people can stay on medication for long periods of time. They can be left in a vicious cycle of wanting to discontinue medication but feeling compelled to continue. 

Furthermore, people can often be left with the sense that antidepressants have masked the real problem or altered their experience of themselves and relationships with others (see previous post). This is to be expected if antidepressants act as placebos. The experience is commonly expressed by patients as a flattening of emotional responses or emotional numbing (see eg. another previous post). 

Withdrawal problems and not feeling one has made a proper recovery are high prices to pay for taking antidepressants. It’s understandable people are attracted to the offer of antidepressant medication relief from what may well have been a desperate situation when depressed. However, if we can’t necessarily say that antidepressants are any better than placebo, and the medication can leave people with these drawbacks, which are caused because antidepressants are placebos, then have they really helped? More people seem to be deciding the harms caused are not worth starting antidepressants.

Tuesday, January 21, 2025

The sorry state of modern academic psychiatry

I’m not sure who advised the king about the appointment of Ed Bullmore as Regius Professor of Psychiatry at the Institute of Psychiatry, Psychology and Neuroscience (IoPPN) at King’s College London (see announcement). I wrote a satirical, even rude, review of Bullmore’s book The inflamed mind a few years ago (see previous post). As I’ve always said, psychiatry has been too dominated by biomedical psychiatrists, like Bullmore (see eg. previous post). . I haven’t always been totally complimentary either about Simon Wessely, the first incumbent of the Regius post (see eg. previous post). Nor do I think he’s made as much of reforming the Mental Health Act (see another previous post) as he had the opportunity to do (see yet another previous post). 

As I said in another previous post, modern academic psychiatry started in this country with the appointment in 1948 of Aubrey Lewis as Professor of Psychiatry at the Maudsley Hospital medical school, which changed its name to the Institute of Psychiatry, now IoPPN. Lewis had a much more sceptical scientific approach to psychiatry than Bullmore. Academic psychiatry’s emphasis has changed to be more biomedical since the start of the psychopharmacology era in the 1950s (see eg. another previous post). The limits of biomedical research do need to be recognised (see eg. yet another previous post), but I’m afraid Ed Bullmore will not lead the necessary changes.

Emotional blunting more a reflection that antidepressants don’t work than how they do

I’ve mentioned before my concerns about the notion that antidepressants work through being emotional suppressants (see eg. previous post). In fact, I’m more inclined to think antidepressants don’t work any better than placebo (see eg. last post), so there’s no need to explain how antidepressants ‘work’, as such. Although the emotional numbness theory has been promoted by Joanna Moncrieff, in her recent book she does qualify this hypothesis by saying she thinks “we should be cautious about assuming emotional numbing can be useful”. 

I’m more inclined to see emotional numbing as a reflection of the fact that antidepressants don’t work, than as an explanation for how they do. Many people are left feeling emotionally numb after being on antidepressants, particularly long-term (see eg. previous post). There is a sense in which taking antidepressants masks the real problem, particularly if depression is understood as physical caused, for example by a chemical imbalance, rather than having psychosocial origins. One’s view of oneself can be at stake in taking antidepressants (see eg. previous post). Undermining of emotional authenticity is not necessarily beneficial. Believing antidepressants are helpful may seem to produce apparent improvement, for example by counteracting demoralisation, but over the longer term such a perception may also leave people feeling dulled, numbed, flattened, blocked, blank, flat or apathetic, affecting their relationships with others and how they see themselves. Many people do initially feel released from these constrictions when they first stop antidepressants, but are then left with the difficulties of managing without them, which may well not be easy.

Saturday, January 18, 2025

Confusing brain and placebo effects of antidepressants

Jo Moncrieff in her new book Chemically imbalanced (see eg. previous post) discusses Peter Kramer’s 1993 book Listening to Prozac (see Wikipedia entry), which I mentioned in a previous post. As the New York Times said at the time (see article) Kramer’s best seller described “how Prozac … transformed his patients, making them calm, confident, cheerful and somehow better than well”. Jo admits that the miraculous transformations reported could have been “largely a function of the hype accompanying the introduction of a new medication” in the same way “as those described by Roland Kuhn in relation to imipramine” (see previous post). But she also uses Kramer’s book to support her speculation that antidepressants reduce people’s emotional sensitivity.

I have expressed concern before about how Jo talks about SSRIs causing emotional numbing or reduced emotional sensitivity (see eg. previous post). I agree there is a sense in which the placebo effect does not really deal with people’s underlying emotional problems. But Jo wants to argue that antidepressants work through their brain effects as well as their placebo effects. This is because she wants to build on her distinction between the disease-centred and drug-centred models of psychotropic drug action. I think it is possible to have an outcome-based understanding of antidepressant drug action without necessarily postulating that antidepressants work through their brain effects (drug-centred model in Jo’s terms) (see previous post). Antidepressants can be powerful placebos because of their effects caused through how people understand them (see eg. previous post).

Tuesday, January 14, 2025

Psychiatry misleading the public about chemical imbalance in depression

Awais Aftab has responded (see his blog post) to the Sunday Times magazine article about Joanna Moncrieff (see eg. previous post). He raises various useful questions about Jo's position but tends to be very critical of her perspective. It's possible some of the questions he raises may be answered in Jo's new book, due to be published this week. Nonetheless, Awais accepts that the "chemical imbalance story as it existed in the public imagination has little scientific legitimacy".

However, Awais seems to want to exclude psychiatry from any responsibility for people believing the chemical imbalance theory of depression. This seems difficult to justify (see eg. previous post). Awais admits that the chemical imbalance theory has been so vague that it has been left "up to patients and the public to make of it what they want". Why has psychiatry allowed this situation to continue? It must have suited its interests. I have always argued that psychiatry allows, even perpetuates the myth, because it wants people to take their medication (see eg. my BMJ eletter). Psychiatry is so wedded to the notion of antidepressant effectiveness that it allows people to be misled by how antidepressants work (if they do).

Of course psychiatry will say that even though the chemical imbalance theory is too simplistic, then antidepressants still work through their effects on the brain. Even this claim needs to be challenged (see last post).

Monday, January 13, 2025

Daring to argue that depression is not a physical disease

I mentioned the Sunday Times magazine article about Joanna Moncrieff in my last post, where I focused on the issue of whether antidepressants work. I also wanted to pick up what the article says in its introductory rubric about Jo daring to argue that depression is not a physical disease.

At face value, saying that depression is not a physical disease may not appear to be so much of a challenge to psychiatry. After all, depression is a mental not a physical illness, isn’t it? Why should psychiatry find such a view so threatening?

Jo emphasises in the article that making appropriate changes in one’s life is a way of tackling depression. Mainstream psychiatry does not always promote such social treatment of depression. Instead it encourages antidepressant medication, which tends to rely on regarding depression as a physical illness. Antidepressants tend to be seen as having physical effects on the brain, correcting, or at least helping to correct, the brain problem causing depression. Even if no brain abnormality is hypothesised in depression, antidepressants are still regarded as affecting or improving brain functioning. 

The chemical imbalance theory is therefore a way of promoting the idea that antidepressants counteract the brain problem causing depression. Most psychiatrists, if pressed, will admit this theory is too simplistic (see eg. previous post). But nonetheless they continue to look for brain abnormalities in depression, even being unprepared to give up implicating serotonin in the mechanism (see eg. another previous post). 

Psychiatry has always been caught in the philosophical mind-body problem. There has always been a fundamental conflict between psychic and somatic approaches to mental illness. It’s just that mainstream psychiatry has become too dependent on physical approaches, particularly over recent years with the development of psychopharmacology. This is why it finds it such a challenge that psychotropic medication may be no better than placebo, as I discussed in my last post.

I have always argued that psychiatry should not find such a challenge so threatening (see eg. my edited Critical psychiatry book). Before the psychopharmacology era, psychiatry did have a broadly conceived view of mental illness as being psychosocially caused. Of course this did not mean that physical factors were ignored. But most presentations to psychiatrists were accepted as having functional rather than organic causes. Over recent years this differentiation has become fudged (see eg. previous post). In fact, DSM-IV wrongly abolished the distinction (see eg. another previous post). Psychiatry is too keen to avoid metaphysical questions about how the mind relates to the brain.

The trouble is that this means that people can be reduced to their brains. The truth is that primary mental illness cannot be reduced to brain disease (see eg. previous post). Brain language has wrongly permeated our conception of ourselves over recent years (see eg. another previous post). But altered subjective experiences and disturbed reactions to others are essential elements of functional mental illness and not merely epiphenomena of a causal organic process. As I keep saying, psychiatry must stop reducing people to their brains. Restricting its interventions to psychopharmacology inevitably does so.

Sunday, January 12, 2025

The legitimacy of asking whether antidepressants work

The Sunday Times magazine has an article about Joanna Moncrieff promoting the publication this week of her new book, Chemically imbalanced: The making and unmaking of the serotonin myth. This follows the 2022 umbrella review, of which she was the first author, which concluded that there is no consistent evidence of an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations (see previous post). This conclusion has caused controversy within mainstream psychiatry that wants to hold on to the idea that serotonin is implicated in depression (see eg. another previous post). This is because it believes that antidepressants work and wants to suggest that their effect on the serotonin system must be something to do with the mechanism.

The efficacy of antidepressants is a legitimate scientific question and my reading of the evidence is that the issue is still open, despite mainstream psychiatry’s insistence the issue is closed. Jo is not convinced antidepressants have any use. There is little doubt that short-term trials of antidepressants on average show a small significant difference above placebo. But because of methodological problems with the clinical trials this apparent benefit may be an artefact (see eg. previous post).

The placebo effect is powerful. Doctors have always exploited the placebo effect. Their beliefs and hopes about treatment, combined with patients’ suggestibility, can have an apparent therapeutic effect. Participants’ subjective beliefs about receiving active or placebo treatment in a clinical trial can significantly influence the assessment of the outcome of treatment. Whether antidepressants are mere placebo treatment is, therefore, a legitimate open scientific question (see eg. previous post). It should be possible to have this debate in public without having to label Jo as notorious. 

Wednesday, December 18, 2024

Discovering what psychiatry’s really like

I talked about Jan Foudraine in the first chapter of my edited Critical Psychiatry book. As I said, he became the ‘personal ambassador' in Holland of Bhagwan Shree Rajneesh or Osho, as he later came to be called. Osho was an Indian spiritual leader who preached an eclectic doctrine of Eastern mysticism, individual devotion, and sexual freedom while amassing vast personal wealth (see Foudraine’s obituary on the Osho website). My original idea was that the presentation Foudraine gave at a 2001 Critical Psychiatry Network conference, which I organised, would be included as a chapter in my book. However, I never received his consent, so it did not appear in the the published version.

As I also say in my chapter, Foudraine wrote the best selling book Not made of wood (1974). To his surprise, this book became an immediate bestseller. More than 200,000 copies were sold and later the book appeared in seven translations. I have been re-reading a manuscript that Jan sent me - ‘The man who dropped out of his mind: Pointers from a rebellious mystic’.

It’s interesting looking back how popular anti-psychiatry, represented by Foudraine amongst others, was at the time (see eg. previous post). As Jan said in the presentation and manuscript, becoming a mega-seller made him into “some sort of Jesus Christ of psychiatry”. The same happened to R.D. Laing (see eg. previous post) after his books were republished by Penguin. Laing was taken up by the 1960s counterculture and always hankered to return and be accepted by mainstream psychiatry, but once he had become infamous this was not possible.

Jan admits in the manuscript that Not made of wood was “almost naive”. He said, “The experience of being a so-called famous ‘anti-psychiatrist’ led to much loneliness and despair”. This made him realise “the undeniable fact that this whole planet looked … very much like one big insane asylum”. He went into a personal crisis over several years with a sense of utter emptiness that the follow-up to his success had created. He was rescued from this mental state by his lightening-like realisation of the Truth. He read books and listened to audiotapes giving a discourse on Zen by Osho, as he became known, and went to Poona to “land right at the blessed feet” of his Guru. Foudraine published a book in 1979 entitled Original face, a journey home, although it was never translated from the Dutch, declaring his love for Osho, of whom he became his disciple. He described his mystical communion with Osho, who he thought was genuinely wise in his belief that “humanity is committing a collective suicide”. 

Laing too went on retreat to Ceylon and India in 1971. As I wrote in my book chapter 'Historical perspectives on anti-psychiatry', this retreat could be said to have symbolised a lack of commitment to changing psychiatry. The difficulty in changing psychiatry is real and I have often commented in this blog about how hard it is to get the message of critical/relational psychiatry accepted (see eg. previous post). Overcoming the power of the prevailing biomedical structure in psychiatry, and medicine in general, is not easy. I have always argued that any critique of psychiatry needs to accept that there will not be a paradigm shift away from biomedical psychiatry, however much it may hope for one. Still, psychiatry can become, and needs to be, more open and therapeutic in its practice. But I think it is likely to remain a conflictual area of clinical practice. 

So, rather that being deflected from the conflict involved in trying to change psychiatry to promoting personal authenticity, as were both Foudraine and Laing, the differences within mental health practice do need to be acknowledged and accepted. Foundraine's mystical solution to the dilemma of psychiatry does need to be respected, even if I don't personally accept it.

Friday, December 13, 2024

What does it mean to be diagnosed with ADHD?

Owen Jones is a succesful Guardian journalist. He was central to the Jeremy Corbyn movement. He feels as though he has been held back by his ADHD, and obtained this diagnosis over a year ago (see his YouTube video). The charity ADHD UK was founded in 2020. It aims to help people like Owen Jones navigate their life with ADHD, and wants to reduce the stigma that some people attach to those with ADHD, build awareness, and undertake or fund research that will have a meaningful positive impact on those with ADHD. 

I’ve never sought a psychiatric diagnosis to explain my inadequacies or failures, or medication to treat them, although I did have twice-weekly psychotherapy for 3 years until my therapist retired. I do think psychiatry can be beneficial, although it can also cause harms. It worries me that people are being misled about the nature of ADHD (see eg. previous post). 

I’m not sure what Jones now thinks of his ADHD diagnosis and treatment after a year. Psychiatry has moved on from its modern origins in diagnosing madness (see eg. previous post). Incorporating neurodivergence over recent years has broadened its remit. Whether this has always been beneficial is at least an open question.

Saturday, November 23, 2024

Psychiatry needs to be more thoughtful

Linda Gask, who I have mentioned before (see eg. previous post), has reviewed Conversations in critical psychiatry (2024) edited by Awais Aftab (see her review and eg. my comment about the book in a previous post). As she says, reading the book reminds her of when she first tried to make sense of psychiatry in her training. Such an experience of trying to make sense of psychiatry in the wake of the so-called anti-psychiatry of the time was common for our generation of psychiatrists (see eg. my MIA radio interview). For example, I've mentioned before (see eg. previous post and my article) Simon Wessely's description of how he went through this process  and was rescued by the book Psychiatry in dissent (1976) by Anthony Clare. As I said in my comment about Awais's edited book, there is a sense in which his book is trying to rescue psychiatry from the more recent critical psychiatry movement, in the same way as Clare did with anti-psychiatry.

As Linda says, she has "never identified with the British version of ‘critical psychiatry’, finding it rather like having to adopt a complete ideology that will only consider hypotheses that are self-confirmatory". I'm not exactly sure what she means by this. If critical psychiatry's ideology is so self-confirmatory, why don't more psychiatrists and people in general go along with it? As I've said several times (eg. see previous post), critical psychiatry has found it very difficult to get its message across. Nonetheless I agree with Linda's conclusion to her review that:-

We need to encourage those training to be psychiatrists to not only be more thoughtful but listen to as many patients’ stories as they can and read widely, even the work of those they are convinced they will disagree with. 

Wednesday, November 13, 2024

Is psychiatric diagnosis of any value?

I responded (follow my Twitter thread) to a tweet by Justin Garson (mentioned in previous post). What he said was:-

I can’t fathom how a psychiatric diagnosis would ever be useful to anyone except as a tool to get accommodations or drugs. As far as understanding myself – who I am, why I act and think as I do – it contributes nothing.

I do understand what he means (see eg. previous post). As I said in response, I agree there is no value in the ‘one person, one disease’ view of psychiatric diagnosis. However, I worry that his critique goes too far and can only polarise debate and alienate mainstream psychiatry which does need to change its views about psychiatric diagnosis.

What needs to happen is that psychiatry should recognise psychiatric diagnosis for what it is rather than completely abandon it, as Justin would like. Diagnosis is justified as a means of communication. It is a way of trying to manage clinical complexity. But the boundaries of any diagnosis are fuzzy and there is no point of rarity between different syndromes. These are not absolute terms. Most psychiatric presentations are not natural kinds with an identifiable brain abnormality. 

The problem is that it is too easy to assume a diagnostic concept is an entity of some kind, which then acts as a justification for treatment. In fact a psychiatric diagnosis is an unobservable, hypothetical construct. It is more an idealised description of those aspects of psychiatric presentation that are of interest. Diagnostic concepts are therefore justified by their clinical utility. Diagnosis is not only about identifying disease but also about the reasons for mental health problems.

Where psychiatry went wrong over recent years was in response to the so-called anti-psychiatry critique. In a way, Justin could be said to be resurrecting aspects of that critique. But psychiatry needs to move on from the polarisation between pro-psychiatry and anti-psychiatry. For example, Thomas Szasz became famous for his view that mental illness is a myth. He was correct that psychiatry has misled too many people that their mental health problems are due to their brain. Of course the brain mediates what we think, feel and do, including when we are mentally ill. But that does not mean necessarily that there is an underlying brain abnormality causing the problems. Szasz was right that the supposed brain disease behind functional mental illness is a myth. But Szasz wanted to go further by abandoning psychiatric diagnosis altogether because he did not think psychiatric detention could ever be justified (see eg. previous post).

Mainstream psychiatry’s response to so-called anti-psychiatry has merely reinforced its belief that functional mental illness is due to brain disease. It tends not to take a hardline position on this issue by saying that functional mental illness is completely caused by brain abnormality. However, it wants to say that there must be brain abnormality as a factor in most psychiatric presentations. This is not necessarily the case. It’s wrong to reduce people to their brains. Personal and social explanations of why we do what we do can improve our understanding of the reasons for our actions but cannot provide a complete causal explanation, certainly not in biological terms.

As I keep saying, too many people are being misled by psychiatry that their mental health problems are due to their brain (see eg. previous post). This includes misleading children who are being given a neurodivergent diagnosis to justify their sense of difference from others. This blog is called “Thinking differently about mental health”. Being different does not necessarily need to be justified by a psychiatric diagnosis. I know the neurodivergence movement does not want to pathologise a neurodivergent diagnosis. But overvaluing the diagnosis, including implying that any personal difference is due to brain differences, is not really helping children, including people in general. Here Justin does have a point. Psychiatry needs to undo the way in which it is itself benefitting  from encouraging a psychiatric label as “the answer” to people’s mental health problems.

Saturday, November 09, 2024

Work needs to be undertaken now as part of the process towards complete reform of mental health legislation


I was hoping the new government would revisit the Parliamentary Scrutiny Committee’s report on the last government’s draft Mental Health Bill. This would have also given an opportunity to produce a new Bill taking into account the recent WHO/OHCHR guidance to countries on mental health legislation (see previous post). Instead the new government has produced a Bill not that dissimilar to the draft Mental Health Bill of the last government (see eg. blog post from DHSC Media Centre and version of amended Mental Health Act (MHA) 1983 as if amended by the Bill prepared by Alex Ruck Keane). 

Homicide by psychiatric patients is a political issue which still seems to be preventing proper human rights MHA reform (see eg. previous post about case of Valdo Calocane as an example). Such reform will now almost certainly need to take place over time, maybe in the context of the also necessary reform of the Mental Capacity Act (MCA). In my view, the last government should have been more ambitious looking to replace both the MHA and MCA. There also needs to be a cultural shift of attitude within mental health services to make them more person-centred. As Mind said in its initial reaction to the new Bill:-

[T]here is more to do and questions to ask about whether this [Bill] will go far enough to fix the broken system as we know it. The mental health emergency we are facing will need much more than a reformed Act.


Work needs to be undertaken now as part of the process towards complete reform of mental health legislation. Mere amendment of the 1983 Act as will be enacted by the new Bill is not sufficient. This work (see eg. previous post) should include: reform of the Mental Health Tribunal to make it more rights-based; improving mental health advocacy by creating an integrated service of Independent Mental Health Advocates (IMHAs), mental health lawyers and independent experts; and further reducing the commissioning of secure placements, leading to the prevention of all civil detentions to secure facilities, apart from to short-term Intensive Care Units. The latter development needs to be supported by a renewed focus on improving the quality of acute psychiatric inpatient and crisis resolution and home treatment services. Work could also be undertaken on creating a new Mental Health Commissioner for England. The mental health reviewer and Second Opinion Approved Doctor (SOAD) functions of the Care Quality Commission will also have a role in monitoring the implementation of the new S56 treatment provisions for Approved Clinicians to follow a clinical checklist and the introduction of statutory care and treatment plans.

Monday, November 04, 2024

Blaming the brain is out of control in psychiatry

I've said before it's been difficult to get the message of critical/relational psychiatry accepted (see eg. previous post). People are being encouraged to see themselves as their brains. It's almost become heretical to suggest otherwise. Of course the belief that what we think, feel and do are caused by our brains is plausible. This assumption must not be questioned, though.

After all there are brain scans that prove this, aren't there? We've probably all seen pretty coloured scans that show areas of the brain lighting up when they are said to show connections to various human activities. But we’ve forgotten what our forefathers learnt in the late 19th/ early 20th centuries that human activity is not as well localised in the brain as we might have expected or hoped. They appreciated that the brain, indeed the complete human body, generally acts as a whole. People are also alive and cannot be explained in mechanistic terms. 

Elliot Vallenstein's book Blaming the brain was first published in 1998. It described how theories of chemical imbalance in the brain had replaced previous ideas that early experience in the family were the cause of mental disorders. As the publishers website says (see webpage), the book sounded a “clarion call throughout our culture of quick-fix pharmacology and our increasing reliance on drugs as a cure-all for mental illness”. This situation has in fact in many ways only got worse since despite the warning. For example, over recent years, the neurodivergence movement has promoted the idea that our differences from each other are due to our brains. No wonder there is therefore a burgeoning demand for a neurodivergent diagnosis. If it’s believed that the reason why we’ve seen ourselves as different from each other all these years is because of our brain, then the sooner we get a diagnosis the better.

We need a serious rethink about the nature of mental disorder. It may have suited psychiatry to go along with the idea that mental illness is due to the brain. Of course brain abnormalities can cause mental symptoms. But most of the presentations to psychiatrists are not caused by a brain abnormality, however much psychiatrists may have misled people that they are.

Sunday, October 27, 2024

The untruths of psychiatry

I’ve said several times (see eg. previous post) that biomedical psychiatry wishfully thinks that primary mental illness will be shown to be caused by brain abnormality in some way. It even commonly acts as though that has already been proven. People are encouraged to think that there is something wrong with the brains of people who are mentally ill. That there must be something wrong may seem plausible but people are not just their brains. Of course what they think, feel and do is mediated by the brain. However, people are not completely driven by their brains. Their environment and circumstances, for example, have some influence. How people lead their life means that in a way people are also forming themselves. There may well be reasons why people become mentally ill but there is a sense in which we can never prove why they have.

People generally find this conclusion too difficult to accept. If they did there would be too much uncertainty in life and psychiatry in particular (see eg. previous post). They therefore embark on pseudoscientific speculations about the biological nature of mental illness believing them to be true (see eg. last post). These speculations can be repeated in the media misleading the public about the evidence. 

Peter Gøtzsche, who I've mentioned before (see eg. previous post), writes on Mad in America (see blog post) about the claim on Danish national TV that patients with an ADHD diagnosis die 5 years earlier if they are not treated with drugs. Peter managed to obtain a correction from Danish TV that there is no evidence for making such an unequivocal statement. The trouble is that such statements about ADHD (see eg. previous post) and neurodiversity in general (see eg. another previous post) are widely propagated in the media. Peter talks about the “pervasive lies of psychiatry” and there is a legitimate question about how much people are being misled about the role of the brain in mental illness and life in general. Mistakes and wishful thinking can become outright falsehoods in psychiatry that it should make more effort to avoid.

Friday, October 25, 2024

Biomedical psychiatry is a pseudoscience

Scientific knowledge is seen as the most respectable form of knowledge (see eg. last post). It is based on the scientific method of reasoning about observations to develop hypotheses which can be tested. Biomedical psychiatry claims primary mental illness is brain disease, or at least that brain abnormalities are a factor in its cause. Mental illness of course shows through the brain. That’s mere tautology. But biomedical psychiatry wants to claim that primary mental illness will be demonstrated to be located in the brain in some way.

Even eminently plausible and widely held beliefs, such as psychiatry’s mainstream belief that something is wrong in the brain in primary mental illness, can be pseudoscience. The value of scientific theories depends on their objective support. Psychiatrists as scientists want their theories to be respectable and provide genuine knowledge. Like all scientists, their aim is to prove their scientific theory beyond doubt, even though that may be an impossibly ideal dream. However, there still isn’t any proof that primary mental illness is brain disease, despite the vast research programme directed towards fulfilling that aim (see eg. previous post). When evidence accumulates against or fails to confirm the latest hypothesis, then attention is turned to another line of inquiry or some adaptation is made to the theory to accommodate the lack of evidence to rescue the original hypothesis. The underlying fundamental belief that progress is being made in discovering the cause of mental illness is therefore maintained. How psychiatry will change from its fundamental belief that brain pathology is at least an element in the causation of mental illness is unclear (see eg. previous post).

Tuesday, October 22, 2024

Psychiatry stuck in Newtonian physics

As I’ve said before, psychiatry tends to treat people as machines (see eg. previous post). Newtonian physics sees existence in terms of cause and effect rather than meaning. Modern science is based on experiment and has a comprehensive, mechanical, rational approach to nature. External observation is seen as the basis of worthwhile, definite knowledge. However, since Einstein, even our understanding of the physical world needs to be supplemented by quantum mechanics and the theory of relativity. Moreover, some kinds of knowledge are unknowable to us in terms of Newtonian physics, as we have beliefs and opinions which are not directly observable (see eg. another previous post). Our reality is social constructed by active shifting of moving and multiple points of view reinforced by social perspective-taking (see eg. yet another previous post). This does not mean that anything we think is true but that we need to think carefully about the way in which the external world impinges on our sense of reality. 

Psychiatry does not seem to realise that the mechanistic ambition of Newton’s laws has failed, at least beyond the physical world. The way in which the so-called human machine is constructed as viewed by natural science does not completely control and constrain human behaviour. Human beings have some freedom within those limitations. Human nature and life in general cannot be completely accounted for within the same laws and principles as the natural world. The body is both alive and lived. Biology cannot be a sufficient explanation of mental illness or human life in general. The brain mediates mental illness but cannot be its locus (see eg. previous post).

Wednesday, October 16, 2024

Expectancy effects in antidepressant withdrawal studies

Zhang et al (2024) have published a systematic review and meta-analysis of the incidence of antidepressant withdrawal symptoms. More than 40% experienced such effects. This figure is higher than the 15% estimate from another recent systematic review (see previous post). As I pointed out in that previous post, so-called withdrawal symptoms also occur in the continuation arm of randomised controlled trials (RCTs), when such withdrawal symptoms wouldn't necessarily be expected in this group as participants are still taking their antidepressant. This could be said to demonstrate how expectation can influence the experience of antidepressant withdrawal, as participants may have expected adverse reactions on withdrawal, thinking they were being withdrawn from antidepressant even though they were in the blinded control group. Zhang et al report that the incidence in the discontinuation group is significantly higher than the continuation group. What I want to challenge is their claim that this significant difference therefore necessarily excludes such expectancy, or nocebo, effects as an at least partial, if not complete, explanation of antidepressant withdrawal symptoms.

I want to emphasise that I'm not saying such nocebo effects are not real. They are felt and experienced as true medication effects. It may well be difficult for people who experience withdrawal effects to understand that they could be nocebo effects. However, in my experience, people do generally appreciate that people may become dependent on antidepressant medication. It was the basis for me writing my BMJ letter that led to my special interest in antidepressant withdrawal (see eg. my book chapter). A drug that is thought to improve mood may well be expected to be difficult to give up because of, for example, a fear of relapse. Psychological dependence with antidepressant medication is not surprising (see eg. previous post). What people find difficult to accept is that such nocebo effects can be so powerful that they can cause the severe and longlasting effects that they do. But, again for example, if the taking of antidepressants is associated with the belief that the medication is correcting a brain problem, even though this is the wrong way of understanding how mental health problems are corrected, then it's not surprising that it may take some time to come to terms with managing without the drug because of the complex set of meanings that the medication has acquired. Undoing these beliefs is not easy, particularly perhaps if the experience of taking antidepressants initially seemed to help.

Of course using placebos in clinical trials of efficacy is designed to exclude placebo effects. In the same way in discontinuation trials, having a control group which continues antidepressant is designed to control for nocebo effects. How effective these control methods are in preventing placebo/nocebo effects depends on how well blinded the participants are from knowing to which group they have been allocated. There is considerable evidence that people are not completely blinded in antidepressant efficacy trials (see eg. previous post). As far as I know, there has been no attempt to measure unblinding in an antidepressant withdrawal study. If unblinding occurs in antidepressant efficacy studies, I think it is also likely to occur in antidepressant withdrawal studies. As the blind can be broken in antidepressant efficacy trials, it cannot be said that expectancy effects have been eliminated.  So my case is that it cannot be said that expectancy effects have been eliminated from antidepressant discontinuation RCTs, because I think there is also likely to be significant unblinding in these withdrawal studies as well.

Habituation to antidepressants is to be expected (see eg. previous post). It helps to explain why people take them for such long periods of time. Psychological mechanisms causing antidepressant withdrawal symptoms should not be dismissed. I have considerable doubts about antidepressants being more than placebo in their antidepressant effect (see eg. previous post). Those that argue that antidepressants cause organic physical dependence tend to say that the sense that antidepressants have stopped working, which can occur, sometimes colloquially called the "poop-out" effect, is evidence that there is tolerance with antidepressants. As I don't think antidepressants are "effective" in the sense of being more than placebo, this explanation doesn't make sense to me. I am at least consistent in my scepticism about the effects of antidepressants, which for their apparent benefit I put down to placebo, and for their withdrawal effects I am inclined to think could be due to nocebo. To emphasise again, this does not mean I am saying any experienced benefit for antidepressants is not real. Nor am I saying that the experience of antidepressant withdrawal is unreal. What brought me into the area of antidepressant withdrawal years ago was my critique of mainstream psychiatry for denying the reality of such symptoms. I just don't think that there's necessarily been much progress since in understanding the mechanisms of such withdrawal effects, and it worries me that psychological mechanisms seem to be being ignored, even within the Critical Psychiatry Network (see previous post). 

Tuesday, October 08, 2024

Thinking differently about mental health

I’ve changed the name of this blog before (see eg. previous post). I’m not convinced it’s really made much impact in terms of attracting more readers (see eg. another previous post). I’m making another attempt to see if expressing what this blog is about in more everyday langauage, avoiding the use of the term ‘psychiatry’, makes a difference. As mentioned in another previous post, ‘mental health’ has come to mean the conditions and practices that maintain mental health. There is general acceptance that mental health needs to be rethought (see eg. yet another previous post).

Psychiatry struggles to cope with its inherent uncertainty


Terry Lynch, who wrote a chapter for my Critical Psychiatry edited book, has posted a video asking why doctors pay so little attention to trauma in the lives of people with psychiatric diagnosis. As Terry says, Robert Spitzer, Chair of the DSM-III taskforce (see eg. previous post), when asked in an interview whether psychiatric diagnosis shouldn't always take into account a person's life circumstances replied "If we did that then the whole system falls apart".

As I've said before (eg. see previous post), psychiatry is a cultural system. The belief that primary mental illness is brain disease clothes psychiatry with an aura of factuality, even though that belief is incorrect. As I also keep saying, biomedical psychiatry is more like a faith than a science (see eg. previous post). That includes what's often called the biopsychosocial approach to psychiatry, which can be more of an eclectic mix of biological, psychological and social in psychiatric assessment, regarding these aspects as more or less equally relevant in all cases and at all times. This understanding of ‘biopsychosocial’ makes psychiatry merely a weakened, ill-defined form of the biomedical model (see eg. another previous post), rather than truly anti-reductionistic in the way originated by George Engel (see eg. yet another previous post).

Psychiatry is sustained by its professional institutions, such as the American Psychiatric Association (see eg. previous post) and the Royal College of Psychiatrists (see eg. previous post). These professional bodies can’t always be relied on for information (see eg. another previous post). In fact, they are biased and do not take a pluralistic and integrated position to psychiatry, despite claims that they do (see eg. previous post). They tend to think that primary mental illness is brain disease or at least is caused by biological factors to some extent, whereas it is not a structural brain but functional personal problem. The American Psychiatric Association is responsible for the Diagnostic and Statistical Manual (DSM) which has resulted in a dead-end in its 5th version (see eg. previous post), building on the direction started by Spitzer.

The biomedical model gives a sense of direction and purpose to psychiatry. The trouble is it induces certain dispositions and ways of understanding in psychiatrists that can lead to them treating patients more as objects than people. It provides a worldview that, if psychiatrists did not accept and believe in it, would make their practice too uncertain for most. I think that’s what Spitzer meant. He was so panicked that psychiatric diagnosis may be unreliable that he initiated the process of taking psychiatry, particularly American psychiatry down the DSM route to its dead end in DSM-5 (see eg. previous post and my 2002 article). 

Thursday, October 03, 2024

Mad studies and critical/relational psychiatry

I’ve mentioned before the chapter written by key members involved in the foundation of the Critical Psychiatry Network (see previous post). The book for which it was written has now been published: Mad Studies Reader, edited by Brad Lewis (who has written a guest post for this blog) et al. My chapter with Ameil Joseph in Mat Savelli et al’s edited book highlights how mad studies, critical psychiatry, anti-psychiatry, and decolonizing activism contribute to mental health education and transformation.

Wednesday, October 02, 2024

Do antidepressants cause emotional numbing?

George Dawson (mentioned eg. in a previous post) and Ronald Pies (also mentioned eg. in another previous post) argue in a Psychiatric Times article that antidepressants do not work by numbing emotions. They wrote the article to counter the claim by Joanna Moncrieff and Mark Horowitz, members of the Critical Psychiatry Network (CPN), that one of the pharmacological actions of antidepressants is emotional numbness and that is how they “work”. This hypothesis builds on Jo’s differentiation of a disease-centred and drug-centred understanding of the mechanism of drug action (see previous post). Psychiatric drugs do not necessarily work because they are correcting a disease process (disease-centred model) but because they have drug effects that may be useful in managing the illness (drug-centred model). Emotional numbing is hypothesised to be of benefit when using antidepressants for depression. 

Also being a member of CPN, I have some concerns about Jo and Mark’s claim. I accept that emotional numbing is a common side effect of antidepressants, particularly in long-term use. I don’t think it’s usually a very immediate consequence of taking antidepressants, for example within the short-term (often about 6 weeks) clinical trials that are used to make claims about the effectiveness of antidepressants. So, I don't quite see how emotional numbing can explain any significant difference between antidepressant and placebo demonstrated in these trials over the short-term. 

But over the longer-term, people often complain that antidepressants seem to have stopped them really dealing with their problems and complain of a flattening of emotional responses which includes feelings of being ‘dulled’, ‘numbed’, ‘flattened’ or completely ‘blocked’, as well as descriptions of feeling ‘blank’ and ‘flat’, affecting their relationships with others and how they see themselves (see previous post). If antidepressants have seemed to help, even if more because of a placebo effect than true antidepressant action, then it's not surprising that people may feel that a physical rather than psychosocial approach to their depression has not really helped. They may express that as emotional numbness and not being in touch with their feelings. They might even still have the same underlying personal and social reasons that led to their depression, which haven't really been dealt with, as such, by mere taking of an antidepressant.

The trouble is that there is only a limited literature about emotional numbing caused by antidepressants that does not allow proper assessment of its significance and mechanism. One study that is commonly quoted is Goodwin at al (2017). They found that emotional blunting is reported by about half of people on antidepressants and is correlated with their depression score ie. a poorer quality of remission is associated with more blunting. However, the screening method used a leading question ‘To what extent have you been experien­cing emotional effects of your antidepressant?’, and followed this up with an explanation that ‘emotional effects vary, but may include, for example, feeling emotionally "numbed" or "blunted" in some way; lacking positive emotions or negative emotions; feeling detached from the world around you; or "just not caring" about things that you used to care about’. Those that gave a positive response were asked to complete a fuller questionnaire about emotional blunting. 

As the paper admits, the data is very much affected by subjective factors. People were guided by the methods used in the study into essentially having a wide understanding of the meaning of emotional numbness or blunting. I tend to think what's meant by emotional numbing is more to do with people feeling antidepressants are masking the real problem and thereby preventing them having their full range of experiences, rather than a direct physiological effect of the drug. Jo and Mark disagree with me about this, but I'm not convinced they've got the evidence for their view. People commonly, at least initially and maybe over time if they can sustain having stopped the antidepressant despite withdrawal symptoms, say that they feel more alive and in touch with their feelings after stopping the drug. That may not be surprising, as there must be relief, at least, that they do not have to take the antidepressant. There must also be a sense that emotions are no longer being controlled by the antidepressant. Trouble is that it's not always very easy stopping antidepressants, perhaps particularly if they were started when there didn't seem to be much alternative and the person has been misled into thinking that there must have been something wrong with their brain. This means that they get stuck in a vicious cycle of wanting to stop antidepressants but fear relapse and withdrawal symptoms if they've previously experienced them. Withdrawal symptoms are very common (see eg. previous post).

It worries me how the notion that antidepressants work by emotional numbing seems to be catching on, perhaps particularly with patients. As I've said, I'm not convinced there's the evidence for the hypothesis. As I've commonly said, I tend to think antidepressants are no better than placebo (see eg. previous post). That doesn't mean that I think they're inert. In fact, the reason I think antidepressants are no better than placebo is because I think the significant difference between antidepressant and placebo found in short term trials may be a methodological artefact. This arises, for example, because trials are not as double-blind as is commonly assumed. Trial participants may well be able to break the blind in randomised controlled trials because of side effects, so I'm not saying antidepressants are inert.

But I do worry that critics of biomedical psychiatry may be creating another myth, like the serotonin hypothesis, that antidepressants work by emotional numbing. In fact, because I don't think antidepressants probably work any better than placebo, in a way I'm saying they don't "work". There's no need, therefore, to even have an explanation of how they "work"! That's not meant to undermine the people that feel that antidepressants have helped (see eg. another previous post) but the limitations of medication do need to be acknowledged. The trouble is that mainstream psychiatry is committed to supporting the use of antidepressants because they are seen as effective.

Thursday, September 26, 2024

Fearless speaking about psychiatry

John Heaton has been mentioned in this blog before (eg. in a guest post by Miles Clapham). John wrote a chapter in my edited Critical psychiatry book. He used the Greek notion of parrhesia from Foucault to help explain that critical psychiatry is a practice that states frankly what one thinks about the nature of persons and psychiatry. 

In the Fall Term of 1983, Foucault gave 6 lectures in English at the University of California in Berkeley as part of a seminar entitled ‘Discourse and Truth’ devoted to the study of parrhesia. These were taped recorded and edited by Joseph Pearson and published as Fearless Speech (2001). The general objective of the seminar was to construct a genealogy of the critical attitude in Western philosophy. 
The parrhesiates is someone who uses parrhesia and opens their heart and mind completely to other people through their discourse. The parrhestiastes makes clear they are expressing their own opinion by using the most direct words and expression they can find to express what they actually believe. In a positive sense, they are telling the truth because they know it is true. They are saying something dangerous because it is different from what the majority believe. They expose themselves to harm as the truth may cause hurt or anger but they prefer to be a truth-teller rather than being false to themselves. Parrhesia is therefore a form of criticism from a less powerful position than the one with whom the parrhestiastes speak. 

Parrhesia may become a problem of truth if it is seen as mere frankness in speaking when everyone is equally entitled to give their own opinion. It actually has a relation to knowledge and education. Bad, immoral or ignorant speakers may endanger democratic organisations. Saying what people want to hear avoids the necessity of being critical and the need to attempt to change people’s understanding and will. Parrhesia, in the positive sense, is, therefore, a virtuous personal attitude and quality to speak the truth boldly. 

I’ve commonly said that psychiatry is more like a faith than a science (eg. see previous post). That implies it is not true that primary mental illness is brain disease. Challenging the claim that primary mental illness is brain disease, as does critical/relational psychiatry, is not denying the reality of mental illness. It is a necessary challenge to the power of psychiatry speaking from the position of the parrhesiastes (see recent post ‘Truth-telling in psychiatry’ on my personal blog).