The definition of critical psychiatry

I mentioned before my interview with Awais Aftab (see previous post), which has now been published as a chapter in his edited book Conversations in critical psychiatry. Awais has added an introductory chapter to the interviews he has collected in the book. In that chapter he quotes my comment that “critical psychiatry may be difficult to define precisely” and suggests that the most specific use of the term is merely to make reference to psychiatrists, such as myself, associated with the Critical Psychiatry Network (CPN) (see eg. previous post). This suggestion fails to take account of my further comment that CPN takes an ideological position that primary mental illness cannot be reduced to brain disease. There is a range of views within CPN, true, but it coalesces round a systematic collection of ideas (see eg. previous post) and seeks to move on from the reductionism and positivism of much of modern psychiatry. 

Awais tries to be open to critical perspectives in psychiatry (eg. see previous post), but he is not as explicitly ideological in his position as CPN. The trouble is that he is inclined to see what he calls the integrative tradition as continuous with the critical. He wants to see integrative and critical pluralism as a variant of critical psychiatry. I’m very much in favour of an integrative and pluralistic perspective in psychiatry but this is based on CPN’s ideological position about the nature of psychiatry and the uncertainty in the field, rather than wanting to hold on to the possibility of biomedical perspectives, as does Awais.

As Robin Murray says in his foreword to the book, Awais suggests critical and integrative pluralism as a corrective to what he calls the lack of self-criticism of critical psychiatry. I’m not so convinced that critical psychiatry is lacking in self-criticism. It's more Awais saying he can't accept at least part of its critique. True, there are those within the critical psychiatry movement that want to abolish psychiatry but actually, as Awais acknowledges, members of CPN are psychiatrists themselves. As he says, “They fundamentally see critical psychiatry as a form of psychiatry”. They are open to different perspectives and take a reflexive position in their critique.

Awais is correct that “The folk judgements of 'something has gone wrong’ [in mental illness] might or might not be indicative of failure of a psychological or neurobiological mechanism to perform its ‘natural’ function”. But Awais suggests critical psychiatry creates “various binaries that sort psychiatric conditions into diseases versus problems of living, biologically caused vs representing self-directed behaviours, and illnesses vs understandable reactions to circumstances”. I agree with him that there is a form of critical psychiatry that does that. But it need not, nor do I, as a member of the Critical Psychiatry Network, so therefore representing 'critical psychiatry', at least part of it, in his sense. Those that do, as Awais notes, can be called neo-Szaszian critical psychiatrists.  Critical psychiatry does not need to be neo-Szaszian. I have always emphasised how it needs to be integrated with the mainstream (see eg. previous post). Awais should take on board, as I say in my interview, that "most presentations to psychiatrists do not have an underlying physical cause, even if that is presumed still to be discovered". Psychiatry came out of its previous phase of brain mythology in the 19th century by recognising the structural/functional distinction of mental illness at the beginning of the 20th century (see eg. previous post). Over recent years this distinction has been fudged, if not obliterated (see eg. another previous post). The point is though that psychiatry must stop reducing people to their brains (see eg. yet another previous post).

Awais is clear that he thinks it is plausible that psychiatric medications “act on mechanisms that produce, sustain, and modify symptoms”. I agree with his emphasis on outcome-based prescribing (see eg. previous post). But he is not sufficiently critical of the notion of whether medication “works” (see eg. previous post). He speculates that it “is likely that psychiatric medications act on symptom mechanisms while also producing global psychoactive effects”. He doesn’t want to consider that any effect of psychiatric medication may be primarily due to the placebo effect (see eg. previous post). 

In the same way that Anthony Clare did for a previous generation by emphasising psychiatry's eclecticism against anti-psychiatry (see eg. previous post), mainstream psychiatry seems to be defending itself against the message of critical/relational psychiatry by promoting integrative and critical pluralism. The publication of Awais' book is welcome. The trouble is that although it engages with the critique of psychiatry, it does not properly take its message on board because psychiatry does not want to change. However difficult it may be to hear the critique of critical/relational psychiatry, it does need to be stated boldly in the interests of patients (see eg. another previous post). Otherwise, psychiatry will merely continue to defend and maintain its biologism.

The aetiology of mental disorder

I am grateful to Awais Aftab for his blog post, which follows our twitter conversation, I think after publication of my editorial. The same twitter conversation led to my last post.

Awais asks what is meant by 'functional mental disorder', even though he doesn't like the term because, he says, it is "too conceptually muddled". Nonetheless, he does seem to accept the validity of the term because he agrees some mental disorders will not "turn out to be the result of a cerebral disease". In fact, he says the majority will not.

Awais quotes a phrase that I commonly use: "mental disorders show through the brain but not necessarily in the brain". To be clear, it was not me that originated this phrase; it was Adolf Meyer. I do not think he used the phrase in any of his publications, but I came across it in his papers some years ago (see my book chapter). The actual phrase Meyer used was "All person disorders must show through the brain but not always in the brain [his emphasis]". As far as I am aware, there are no other references to this phrase in the literature. Meyer's use of the term 'person disorder' rather than 'mental disorder' in the phrase may give a clue as to how this debate about the meaning of 'functional mental illness' could be taken forward. The reason there is no independently diagnosable cerebral or systemic disease is because the disorder needs to be understood by focusing on the person. Several modern critics of psychiatry, perhaps particularly clinical psychologists (see previous post), argue that it's been a mistake to see personal problems as illness. I don't always agree with them, but the point is that the reason they are objecting to seeing mental disorder as illness is because they want to focus on the person. The critics generally do not even want to pathologise personal problems.

For me, Awais focuses too much on the causes, as such, of mental health problems. In my examinations when I trained in psychiatry, I was asked for my formulation or assessment of a patient that I had interviewed. This formulation was discussed in terms of differential diagnosis and aetiology. Note the use of the term differential diagnosis. Those who criticise one-word psychiatric diagnosis need to realise that the inherent uncertainty about psychiatric diagnosis is generally accommodated by discussing the options for diagnosis, rather than a specific diagnosis. I do realise this is not always the case and psychiatrists often jump too quickly to a single-word diagnosis, reifying complex personal issues (see eg. previous post). But this is not how they are, or should be, taught (see eg. another previous post).

For the purpose of this post, though, what I want to concentrate on is the way I used the term 'aetiology'. This has a wider meaning than simply causal. For organic problems the causes are cerebral disease, which can be primary or secondary to a systemic illness, or resulting from an exogenous toxic agent, or due to physical withdrawal of an addictive substance. But for functional disorders, we can't talk about a physical cause in the same way. We can't prove, in the sense of natural scientific proof, what causes functional mental health problems. That doesn't mean that we shouldn't make an attempt to understand them. We should! When I was asked for my formulation, what the examiner was looking for was some sort of assessment of the origins of the person's mental health difficulties in the context of their life history and personal and social situation. But that's very different from blaming causal factors.

I agree with Awais that there is inevitable uncertainty about whether a presentation is organic or functional. I have seen a few cases, but not many, in my working life where an organic disorder has unfortunately been missed. In fact the tendency of doctors is more to be biased in the opposite direction and make errors in favour of a physical diagnosis (see my book chapter). And, even one of the most psychosocial of psychiatrists, Harry Stack Sullivan, believed that a particular form of deteriorated schizophrenia must be neurobiological in origin. In retrospect, he may have underestimated the effects of institutionalisation in such cases, but because such patients' behaviour and presentation may be so difficult to understand, the temptation is to think that the cause must be biological. I can see why this happens, and for example, I think explains why Kendler thinks that schizophrenia has more risk factors in the biological arena than major depression or alcohol dependence (see previous post). But, paraphrasing Meyer, we need to guard against supposing a disease behind the functional presentation merely as a self-protective measure because of an insufficient knowledge of causal factors (see previous post). I can't prove a negative in the way Awais wants me to. Trouble is that he has the advantage because his view holds out the possibility of certainty (see my book chapter). My view can be just labelled as vague and woolly and dismissed for that reason, even though it may well be correct.

Awais seems to want to have it both ways by not saying whether depression is a functional or organic illness. This whole blog has been written against the misleading bias of biological psychiatry (of which Awais seems to be a part, even if at the more eclectic rather than radically reductionist end of that spectrum). In what sense can Awais really be said to be promoting the understanding of mental health problems? Knowledge of the brain may give no understanding of the person (see eg. BMJ letter).

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).

Critical thinking in psychiatry

I've been struggling trying to understand why Awais Aftab hasn't interviewed many critical psychiatrists in his 'Conversations in Critical Psychiatry' series for Psychiatric Times (see post on his blog). I think the title of the series should really be 'Critical Conversations in Psychiatry'.

The last chapter of my edited Critical Psychiatry book (see previous post) had a section on the relationship between critical psychiatry and critical thinking (see extract). Critical psychiatry, of course, wants to promote critical reflection on practice and research in psychiatry. Psychiatrists need to be conceptually competent (see previous post).

Critical psychiatry is also based on critical theory, which is quite a loose term. When the Critical Psychiatry Network was first formed, probably the best known version of critical psychiatry was postpsychiatry (see previous post). I always had my doubts about basing critical psychiatry on postmodernism, and over recent years, perhaps particularly since reading John Iliopoulos's book (see eg. previous post), I think I have gained a better understanding of Foucault. David Ingelby (see another previous post) probably originated the term 'critical psychiatry' and, in the American context, where Awais is based, Manschrek and Kleinman (1977) decried the deficiency of critical rationality in psychiatry in their edited book Renewal in psychiatry (see yet another previous post).

Furthermore, critical psychiatry is a social and professional activity. The Critical Psychiatry Network provides a forum to develop a critique of the contemporary psychiatric system. It is a challenge to the biomedical dominance of psychiatry. More specifically critical psychiatry's challenge to reductionism and positivism, including mechanistic psychological approaches, creates a framework which focuses on the person and has ethical, therapeutic and political implications for clinical practice (see eg. my editorial).

I'm very happy for psychiatrists to identify themselves as critical thinkers. I don't want to undermine the series Awais is doing for Psychiatric Times. On the other hand, the number of psychiatrists prepared to adopt the theory and role of critical psychiatry may well be a different matter. As far as I can see, critical psychiatry is still marginal to mainstream practice. In fact, psychiatrists saying they are "all critical now" is a way of marginalising critical psychiatry further (see previous post).

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).

Schizophrenia genetic research: Still running on empty

I'm very grateful to Jay Joseph for agreeing to do this guest blog to respond to a post by Awais Aftab written in response to my previous post.

Awais Aftab’s arguments in his 3/21/2020 post 'Defending aggregate genetic effects in psychiatric disorders' are based largely on his claim that the “high genetic heritability of schizophrenia” and other major psychiatric disorders “has been pretty consistently reported in [the] literature.” Indeed it has, but the “literature” could still be wrong, especially when it is based on the acceptance of false assumptions, and on textbook and other authoritative authors’ frequent failure to critically analyze (or even read closely) the original “landmark” studies they cite. Not to mention that, as a pair of critics wrote, “The term ‘heritability,’ as it is used today in human behavioral genetics, is one of the most misleading in the history of science.” (See my description of the “heritability fallacy”.)

Aftab then asked, in relation to Duncan Double’s 3/20/2020 commentary 'The causes of psychiatric illness,” whether Double can “cite even one good study which demonstrates that schizophrenia does not have a high genetic heritability?” A better way of posing this question is to ask whether the body of research that psychiatry currently cites as showing that schizophrenia has an important genetic component holds up under critical examination. As I have attempted to show since the late 1990s, it does not.

Psychiatric genetic arguments that important genetic factors underlie schizophrenia are based on twin studies that require the acceptance of obviously false assumptions, and on massively flawed and biased adoption studies. (Although most psychiatrists claim that “schizophrenia” is a valid medical disorder which they and others can reliably identify/diagnose, there is plenty of evidence that it isn’t. Many critically minded authors now use the term “psychosis.”)

In my 2017 e-book Schizophrenia and genetics: The end of an illusion, I examined in great detail the evidence that psychiatry puts forward in support of its “high genetic heritability of schizophrenia” position. I showed that the famous 1960s-1990s Danish-American schizophrenia adoption studies, performed by American psychiatric genetic researchers Seymour Kety, David Rosenthal, Paul Wender and their Danish colleagues, were flawed and biased to an extreme degree. It is only necessary to carefully read their original publications with a critical eye to see that these researchers manipulated diagnoses, data, and group comparisons in order to obtain the desired genetic findings. As Stephen Jay Gould showed in The mismeasure of man, human genetic research has a long history of investigators “shifting criteria to work through good data toward desired conclusions,” and creating conditions in which “data” is not allowed to “overthrow … assumptions.” The Danish-American adoption researchers continued this scandalous tradition — simply refusing to permit their data to overthrow psychiatry’s need to establish “schizophrenia” as a valid genetic/biological medical disorder. The broad term now used to describe this practice is p-hacking, which includes various forms of scientific manipulation, misconduct, or fraud. (For an excellent description of these practices, see Chris Chambers’ (2017) The seven deadly sins of psychology.)

Psychiatric twin studies are based on the utterly false assumption that reared-together MZ (identical) and DZ (fraternal) twin pairs grow up experiencing similar or “equal” environments, and it is likely that twin studies of schizophrenia and psychosis have recorded nothing more than research bias, MZ pairs’ more similar environments and treatment, MZ pairs’ higher levels of identity confusion and attachment to each other, and MZ pairs’ greater tendency to experience “folie à deux” (shared psychotic disorder) compared with DZ pairs.

Awais wrote in relation to molecular genetic research that although “there is no evidence of single genes of large effect sizes for schizophrenia or other major psychiatric disorders … the evidence … suggests [the existence of] multiple genes of very small individual effect sizes but a large aggregate effect.” Psychiatric molecular genetic research dates back to the 1960s. Countless gene discovery claims have been published since then, especially since the late 1980s, only to be subsequently relegated to the ever-expanding psychiatric genetics “graveyard” of false-positive results. The most recent claims of “multiple genes of small effect” are based on associations, not causes, and like previous claims it is extremely unlikely that they will hold up. Although we have seen many reports that various genetic variants are “associated” (correlated) with schizophrenia, decades of molecular genetic studies have failed to produce variants shown to cause it.

The evidence in favor of environmental causes, coupled with the lack of evidence in favor of biological and genetic causes, supports a psychological/sociological/political/environmental understanding of “schizophrenia” and psychosis. In support of this position, I highly recommend the book Models of madness: Psychological, social, and biological approaches to psychosis (second ed.), edited by John Read and Jacqui Dillon. (See also Schizophrenia: A Scientific Delusion?, second ed., by Mary Boyle.)

Please see the following links to books and articles where I show that, based on a close examination of the original research publications, and building on the work of earlier pioneering critics (referenced therein), there indeed exists a literature “which demonstrates that schizophrenia does not have a high genetic heritability.”

Schizophrenia and genetics
The gene illusion: Genetic research in psychiatry and sychology under the microscope (2004)
Quotations frhom the genetics “graveyard”: Nearly half a century of false positive gene discovery claims in psychiatry (2015)
Schizophrenia and genetics: A closer look at the evidence (2016)
Schizophrenia and genetics: The end of an illusion (2017)
Schizophrenia genetic research — Running on empty (2017)

Twin Studies
The trouble with twin studies: A reassessment of twin research in the social and behavioral sciences (2015)
What do twin studies prove about genetic influences on psychiatric disorders? Absolutely nothing (2018)
Bad-science warning: The “Minnesota study of twins reared apart” (2018)

Jay Joseph, Psy.D. is a clinical psychologist practicing in the San Francisco Bay Area. He is the author of four books, most recently The trouble with twin studies: A reassessment of twin research in the social and behavioral sciences (2015), and Schizophrenia and genetics: The end of an illusion (2017). His blog 'The gene illusion' can be found at the Mad in America website. A complete list of his publications can be found at his website. 

Factors in the causation of mental illness

Twitter discussion with Awais Aftab led to a previous post about the aetiology of mental disorder. We may have got a bit bogged down with our different views about the biological, psychological and social foundations of mental health problems. But possibly there might be more agreement about dividing factors in the causation of mental disorder into predisposing, precipitating and perpetuating factors. Still, Kenneth Kendler's article on the causes of mental illness didn't really do this (see another previous post). Perhaps Awais can write a better paper than Kendler on the factors in the causation of mental illness.

Conceptual competence in psychiatry

Awais Aftab and Scott Waterman have an interesting article on conceptual competence in psychiatry. As they say:-

The considerable challenges facing our discipline [psychiatry] will not be met without rethinking our approach to educating and training the next generation of psychiatrists, specifically attending to the implicit—and thus rarely confronted, examined, and questioned—conceptual foundations of the field.

The four elements of conceptual competence are: assumptions and questions; tools;  discourse; and humility. Training can improve conceptual competence.

I asked Awais Aftab in a tweet what the implications for practice are and he gave an interesting and important initial response (see conversation). I don’t think all practitioners need to be philosophers of psychiatry but they do need to understand there is a mind/body problem. I also think it may be worthwhile emphasising how cultural competence overlaps with conceptual competence.

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. 

Implications of critical psychiatry for practice

Daniel Cohrs & Awais Aftab (2025) provide a useful overview of the heterogeneity and debate within critical psychiatry and adjacent movements. Although the article proposes a reorientation of psychiatric practice, I have criticised Awais before (see eg. previous post) for not going far enough in his critique. When commenting on another article about critical psychiatry by Samei Huda (see previous post), I tried to simplify this issue. Essentially, it is that people tend to understand from psychiatry that mental illness is due to brain disease. Psychiatry needs to be far more explicit that most mental illness is not due to brain disease. It wants to hold on too much to speculative hopes that a biological understanding of functional mental illness will be found.

Conversation about critical/relational psychiatry

I've posted a summary (see link) of my views about critical/relational psychiatry, which is to be published in a forthcoming Oxford University Press book adaptation (late 2023) of  'Conversations in Critical Psychiatry' edited by Awais Aftab. The essential message of critical/relational psychiatry is that primary mental illness cannot be reduced to brain disease. Such a view tends to be dismissed or marginalised as it may be difficult to believe and accept. Of course mental illness has something to do with the brain, people say. Is critical/relational psychiatry really suggesting otherwise?

Of course it isn’t! The brain mediates our thoughts, emotions and actions, including mental illness. This statement is of course true. But biomedical psychiatry’s claim is that mental illness will be shown to be due to an abnormality in the brain, even that there is considerable evidence already to come to this conclusion. This hypothesis may seem to stand to reason, but it doesn’t. Let me explain.

Abnormalities of the brain can of course cause mental symptoms. Such is the case for example with a brain tumour. Definite neurological signs may also be present in cerebral disease. Fortunately such organic conditions tend to cause symptoms affecting cognitive functioning that usually allow them to be distinguished in clinical assessment from non-organic mental illnesses, like schizophrenia or depressive illness. Primary mental illness, not caused by brain disease, is functional and not structural. It shows through the brain but not in it.

Acknowledging this situation has advantages for psychiatric practice. It should mean that people are not reduced to their brains. They must not be treated as objects. Clinical work needs to be focussed on understanding patients’ histories and mental states and formulating their problems in those terms. Treatment needs to be about supporting them to deal with their problems.

This basic message needs reinforcing in the current mental health system which has become too dysfunctional and fragmented. Psychiatry needs to move on from an outdated belief in mental illness as brain disease.

Taking relational psychiatry forward

I completed two years in semi-retirement of a five year part-time PhD on ‘The foundations of critical psychiatry’ at the University Department of Psychology in Cambridge in 2017/9. My supervisor left after 4 terms and I couldn’t find a replacement! Still, I managed to write three articles in Royal College of Psychiatrists’ journals: (1) Twenty years of the Critical Psychiatry Network; (2) Critical psychiatry: An embarrassing hangover from the 1970s?; and (3) Toward a more relational psychiatry: A critical reflection. An interview with Awais Aftab expressing my views about critical/relational psychiatry is to be published in a forthcoming book. 

As I said in the interview, part of the reason I changed the name of my blog from critical psychiatry to relational psychiatry was to try to move on from debates about so-called anti-psychiatry and incorporate more recent perspectives from anti-cognitivist phenomenology and enactivism and the tradition from cultural psychiatry. Key contributions here would be: two books by Thomas Fuchs: Ecology of the brain: The phenomenology and biology of the embodied mind (2018) (see eg. previous post); and In defence of the human being: Foundational questions of an embodied anthropology (2021) (see eg. previous post); the book Enactive psychiatry by Sanneke de Haan (2020) (see eg. previous post); and the contributions over many years by Laurence Kirmayer (see eg. previous post) including the book Re-visioning psychiatry: Cultural phenomenology, critical neuroscience, and global mental health (2015), of which he was the first editor. 

Other initiatives include the Relational Practice Movement, which has developed out of the therapeutic community movement (see eg. previous post). It has produced a Relational Practice Manifesto. Russell Razzaque has also produced a Relational Psychiatry vlog. He is now the Presidential lead for compassionate and relational care at the Royal College of Psychiatrists. It would be nice to think that the College could help to bring all these strands together to make psychiatry more relational. 

Psychiatry must be clear that most mental illness is not due to brain abnormality

I reviewed Samei Huda’s book The medical model in mental health: An explanation and evaluation (2019) when it first came out (see review). Jo Moncrieff and I also responded to his Asylum article entitled ‘Critical psychiatry: Dead ends and avenues of opportunity’ (see both articles).

Samei has taken forward his commentary on critical psychiatry in a recent BJPsych Bulletin article ‘Critical psychiatry in the UK: Potentially useful but in need of regeneration’. As he recognises, critical psychiatry aims to improve practice. This acknowledgement may indicate that critical psychiatry has at least moved on from anti-psychiatry, which Martin Roth (1973) condemned as  “anti-medical, anti-therapeutic, anti-institutional and anti-scientific” (see eg. previous post).

Samei accuses critical psychiatry of not fully taking on board the evidence against some of its views. His critique is not dissimilar to Anthony Clare's critique of anti-psychiatry (see eg. previous post) or Awais Aftab's promotion of integrative and critical pluralism as a variant of critical psychiatry (see eg. another previous post). The claim being made by Clare, Aftab and Huda is that mainstream psychiatry is not really as damned as critical psychiatry makes out.

As I've often said, critical psychiatry seeks to move on from the reductionism and positivism of much of modern psychiatry. Similarly, I've often said psychiatry needs to move on from a system based on a ‘disease’ model of primary mental illness. Despite Samei, I do think mainstream psychiatry is as damned as critical psychiatry makes out. Quite simply, most mental illness is not due to brain abnormality. This is not what most people hear from psychiatry and has consequences for their understanding and treatment of their mental health problems (see eg. recent post).

The implications of enactivism for psychiatry

I don’t think I fully appreciate all the nuances in the recent debate in Philosophy, Psychiatry and Psychology (PPP) about the implications of enactivism for psychiatry. I’ve mentioned before (eg. see previous post), the book by Sanneke de Haan entitled Enactive Psychiatry. It was published before Kristopher Nielsen had completed his PhD thesis, in which he had independently developed his own ideas about the psychiatric implications of enactivism. There are differences in their views and they disagree about the significance of these differences. In the PPP journal, Nielsen (2021a) compares the two perspectives, followed by comments by de Haan (2021) and Richard Gipps (2021) (see his previous guest blog post), and a rejoinder from Nielson (2021b). 

As I said in a recent previous post, I think enactivism can be a way of revitalising Engel's biopsychosocial model. Mental processes need to be understood in a dynamic, integrated and enactive way, as they are embodied in the brain and the body more generally, and embedded in the environment, which is social and cultural, affording various possibilities of action to the organism (see eg. my article). Mental illness cannot be isolated in material processes in the brain, excluded from people's relationship with their environment. 

In some ways, such an anti-reductionist position is not new (eg. see another article of mine). I do think, though, that enactivism can be seen as a more thoroughgoing basis for anti-reductionism. Like Sanneke, I worry that Kristopher's position is not explicitly anti-reductionist enough. There is evidence for this in his interview with Awais Aftab. Kristopher still wants to understand mental disorders in an "entitative and more mechanistic way". He may well make too much of the biological functionality of human values, although I think there is merit in seeing mental illness as failed adaptations, as did Adolf Meyer (see eg. previous post). I summarised, in another previous post, how Sanneke demarcates 'abnormality' from 'normality'. I'm also not sure what Kristopher means by somatic and mental disorders being "probably continuous with each other". As I've highlighted before (eg. see previous post), the organic/functional distinction of mental disorders, which was abolished by DSM-IV, needs to be reinstated. 

I also have questions about the implications of Sanneke's views. For example, how do they relate to American pragmatism (eg. see previous post)? For all her emphasis on the existential dimension in mental disorders, how does her perspective relate to existentialism as a philosophy (see eg. another previous post)? 

As I've also been emphasising in this blog, there are links with other phenomenological perspectives, such as that of Thomas Fuchs (see eg. previous post); cultural perspectives, such as that of Laurence Kirmayer (see eg. another previous post); and other critical perspectives in psychiatry, not least Foucault (see eg. last post). I have been trying to bring them together under an umbrella term of relational psychiatry. 

This is not some grandiose project, but an attempt to encourage psychiatry to move on from its misguided belief that primary mental illness will be found to be a physical disease. Relational psychiatry also has practical implications, and is not merely an out of touch academic dispute about the implications of enactivism for psychiatry. There is some urgency about the need to improve the treatment of people with mental health problems. A recent focus of this blog, for example, has been on the current reform of the Mental Health Act (see eg. previous post), as the rights of people with mental illness can be abused.

The causes of psychiatric illness

Awais Aftab in a twitter conversation accused me of not engaging with the substance of an article by Kenneth Kendler that I've mentioned in a previous post. My original post was based on a cursory reading but I've now re-read the article.

I agree with Kendler that
"[p]sychiatry has been confused long enough by Descartes’ error" (see eg. previous post). I also agree with Kendler that there are problems with the computer functionalist view of the solution to the mind/brain problem. Nonetheless, information processing has usefully emphasised that there are top-down as well as bottom-up aspects of psychological processes (see Psychology concepts webpage and eg. my previous post).

Kendler suggests that the brain/mind and hardware/software dichotomies are mutually reinforcing. However, I don't think the organic/functional distinction of mental disorders (see eg. previous post) equates to the hardware/software dichotomy. For a start, brain biological processes are not like mechanical computer programmes (see eg. previous post). Life is characterised by a continuous dynamic preservation of its internal environment. Comparing brains to computers is not a satisfactory metaphor (see eg. Psychology Today article). And, it's mistaken to think of 'functional' as meaning non-organic (see eg. another previous post). Functional disorders are distinguished from organic disorders on the basis that their aetiology is lacking psychopathological manifestations of cerebral disease or disorder.

I agree with what Kendler goes on to say that:-

most modern psychiatrists and neuroscientists when pressed will deny being dualists, insisting that they are ‘eclectic’ and/or fully recognize that psychiatric disorders are ‘multi-factorial.’ Yet, their actions belie their words. In the ways that we think about patients and their treatments, and the etiology of our disorders a strong tendency remains for us to emphasize either a mentalistic mind-based or a biological brain-based view of illness.

Kendler references this quote from his article to Tanya Luhrmann's (2000) book Of two minds, which studied American psychiatry by participant observation. The book highlighted the divided consciousness between the practices of drug therapy and psychotherapy. I have gone on at length in this blog about the eclecticism in modern psychiatry and how it is really just a weaker form of the biomedical model (see eg. previous post).

Kendler gives two examples of what he suggests are "the ‘either/or’ ness of the organic functional divide within our field". He mentions Gary Greenberg's book Manufacturing depression. Kendler questions, what seems to me, the quite reasonable assumption of Greenberg's therapist that depression is functional and not due to "little bugs swimming in your blood or something, making you feel dread". His reason for questioning that depression is functional is because of "much data available then and now", but then does not say what this data is, at least at this stage of his argument (see below). The other example is from his own training, when his supervisor "assumed a priori that all SZ [schizophrenic] symptoms were brain based and, therefore, trying to improve them by cognitive therapy was a waste of time". I agree such polarisation between drug therapy and psychotherapy may be unhelpful, although I'm not suggesting combining drug treatment and psychotherapy unsystematically.

I also agree with Kendler that "many causal processes impact and intertwine in their influences" on psychiatric disturbances. Risk factors increase the probability of illness but may not be necessary or sufficient. Again, I agree with Kendler that we do not live in a universe where psychiatric disorders are like dysfunctional computers where problems arise either from the hardware or the software. Psychosocial factors contribute to risk factors for psychiatric disorder. However, Kendler believes that genetic risk factors have been shown to be aetiologically important in all major psychiatric and substance abuse disorders, a claim which is at least open to question. This genetic case is often overstated. The real situation is that genes set the boundaries of the possible; environments define the actual (Eisenberg, 2004).

The trouble is that because of this combination of genetic and psychosocial factors, Kendler goes on to say:-

Therefore, with little fuss, we can conclude that for most psychiatric disorders, risk of the illness-related dysfunction of the HMBS [human mind/brain sytem] results from processes at both psychological and neurobiological levels.

However obvious this state-of-affairs may seem to Kendler, he hasn't really made enough of an argument for this conclusion, although he does accept his argument is "a bit facile". He, therefore, goes on to look in more detail at the risk factors for schizophrenia, major depression and alcohol dependence based on what he calls empirically based pluralism.

Kendler divides genetic effects into aggregate genetic effects and those due to molecular variants. I'm not sure how much this division really stands up. Nonetheless, from his point of view, genetic effects, particularly aggregate genetic effects, are the factors that contribute most to the variance in liability for all three conditions under consideration. There has been over half a century of false positive gene discovery claims in psychiatry (see eg. Mad in America blog post by Jay Joseph), and Kendler does not seem to have learnt from them. In fact, the complexity of the genetics of common disorders, such as schizophrenia, makes accurate prediction unlikely and, if there is any genetic influence in mental disorders, it does not seem specific. Kendler should be far more sceptical about his overenthusiasm for genetic explanations.

He also needs to be more sceptical of his claims for neurobiological influences, which he divides into molecular and systems neuroscience. Again, I'm not sure how much this division really holds up. What he seems to be talking about is more to do with whether the neuroscientific explanation is neurochemical or brain structural. As far as neurochemical explanations are concerned, this blog has repeatedly complained about the promotion of chemical imbalance theories, such as the serotonin theory of depression (eg. see previous post). Kendler doesn't point out that he himself doesn't believe in the dopamine theory of schizophrenia (see another previous post). As far as brain abnormalities are concerned, he needs to be far more cautious of his assessment of brain scan evidence, which is plagued by inconsistencies and confounders (eg. see previous post).

Kendler also includes other biological factors, such as the neurodevelopmental hypothesis of schizophrenia, which even its originator no longer believes in (see previous post). Even other examples he gives, such as cannabis causing functional psychosis do not stand up (see previous post). Kendler didn't include the idea that tobacco might be a cause of psychosis, but however crazily, articles are published in eminent journals examining just this hypothesis (see previous post). As Gardner and Kleinman (2019) said, academic psychiatry needs to be rebuilt recognising the limits of the evidence for the biological basis of mental illness (see another previous post).

I'm not sure how well Kendler divides up the more psychosocial factors. He lists neuropsychological; personality and cognitive/attitudinal patterns; trauma exposure; social; political; and cultural. Trauma exposure is clearly an important stressor for mental illness, but not the only related stress. Although mental health problems are psychological, they occur in context, which brings a social dimension to the understanding of such problems. People may have a predisposition to mental health problems. This vulnerability need not necessarily be biological as such, but for example may be caused by upbringing. The way individuals react to the environment is important. People are not just potentially vulnerable showing poor adaptation to stressors and inappropriate responses that may become persistent, but also potentially resilient and able to perceive stressful events in less threatening ways, promoting adaptive coping strategies. Adolf Meyer regarded functional mental illness as failed adaptations. Whatever has happened to this idea in psychiatry, supposedly overtaken by the so-called "data" of recent psychiatric research?

Furthermore, what Kendler doesn’t really talk about is the question of whether psychosocial factors can be really understood as causal as such, in the same sense as physical factors. Psychosocial factors may well help us to gain an understanding of the reasons for mental health problems but any one-to-one connection cannot be proven. The difference between understanding and causes is fundamental within philosophy and is totally inadequately dealt with by Kendler in a paper said to be about the nature of causes of psychiatric illness.

Kendler produces three causal signature charts for each of the three conditions: schizophrenia, major depression and alcohol dependence. These are essentially arbitrary, even phantasy, or as he admits, “necessarily subjective”. But I guess the pseudoscientific nature of their presentation may seem to give them apparent authority. If this is really what empirically based pluralism is all about, I want nothing to do with it. It is not empirical and lumping together unthinkingly potential risk factors does not really tell us anything about the reasons for mental health problems. The specific patterns suggest schizophrenia has more risk factors in the biological arena, major depression in the psychological arena and alcohol dependence in the higher-order social domains. What does this mean?  I suppose it’s surprising that alcohol dependence is even considered to have biological causes (see previous post).

Kendler does admit that the three specific patterns are “tidy pictures” and imply that each level of risk factor is independent of each other even though any relationship is obviously more complex. But instead of following this implication to concluding that the patterns are meaningless, instead he suggests this just confirms how pluralistic the causes of psychiatric disorder are.

Kendler thinks empirically based pluralism is better than Engel’s biopsychosocial model. But he is mistaken to think that Engel’s model starts from pluralism or eclecticism (see eg. previous post). He quotes favourably from McHugh and Slaveney (see my comments on one of their articles in previous post), who from my point of view tarnish Engel himself with the eclectic way in which his biopsychological model is used in current psychiatry. Kendler wrongly thinks this eclecticism is justified by the research.

In fact, psychiatry moved away from Descartes some time ago with Georg Stahl (see eg. previous post). True, Stahl sent us down another mistaken route of vitalism but at least he created an integrated position in psychiatry, which was built on by people like Ernst von Feuchtersleben, Adolf Meyer and George Engel (see my editorial). I do understand Kendler’s wish to avoid a radical reductionism (see previous post). I agree with him that the original aims of DSM-5 were mistaken (see eg. another previous post). But his eclectic position is still reductionist. I don’t think Kendler really understands the work of John Dupré, whom he references (see previous post).

I hope I haven’t been overinclusive in my response to Kendler’s paper. In many ways the more brief dismissal of it in my previous post was very understandable. I can’t see that the paper deserves the attention it currently gets from many thinking psychiatrists.