Friday, March 27, 2020

The importance of the existential dimension in understanding psychiatric disorder

Sanneke de Haan makes a case for incorporating the existential dimension into the understanding of psychiatric disorders. As she says, the "existential stance of relating to oneself, to others, and to one’s situation is crucial for understanding psychiatric disorders." We can suffer from alienation when we do not coincide with ourselves and with our present situation, and this alienation may go on to develop into psychiatric disorders. How patients relate to their experiences and their disorder is likely to co-determine the course of their illness, and of their lives in general.

I'm not sure that I agree that Engel's biopsychosocial model does not do justice to patients' subjective experience. Nonetheless, I do like the idea of enactivism as a way of moving on from cognitive science (eg. see my book review). Cognition is a fundamentally embodied and embedded form of action and needs to incorporate the sense-making activity of a person in context. To understand psychiatric disorders, we should look at persons in interaction with their worlds. The evaluative interactions of a person with their world go astray in psychiatric disorders. When a person's sense-making goes astray, it is not appropriate to, or insufficiently grounded in, their situation and the person may well find it difficult to adjust their sense-making. In physical illness, sense-making may be secondarily affected as an effect of the illness but in psychiatric disorders these relations are directly implicated.

The term 'existentialism' was explicitly adopted as a self-description by Jean-Paul Sartre. There is a direct link with the work of R.D. Laing in that Laing & Cooper (1964) wrote an exposition together in english of Sartrean terms related to dialectical rationality. Laing (1964) said in New Society, that he thought there was a revolution happening at the time that was changing the clinical point of view in psychiatry to one that is both existential and social. It's taken a while to happen, maybe because Laing eventually became more interested in personal liberation and spiritual growth, including, for example, developing 'birthing' as a component of his practice following the technique of Elizabeth Fehr. There is an existentialist tradition in psychotherapy but enactive psychiatry seems wider than psychotherapy, and I look forward to finding out more about it.

Thursday, March 26, 2020

The nature of factors in the causation of mental illness

Thomas Fuchs (2011) makes the argument that reduction of mental illnesses to diseases of the brain is not possible in principle. As he says, "The use of 'brain language' is increasingly permeating our self-conception". For example, neuroimaging studies that literally 'light up the brain' are taken seriously (see eg. previous post). As another example, psychiatrists' compulsion to believe the evidence for a strong genetic component in conditions such as schizophrenia, has been reinforced by modern molecular studies building on family, twin and adoption studies (see guest previous post), despite the genetic case having been used for the sterilisation and extermination of the mentally ill in the past (see eg. Patrick Hahn's lecture and his book Hahn, 2019)

The reality is that altered subjective experience and disturbed reactions to others are essential elements of mental illness and not mere epiphenomena of a causal organic process. Subjective modes of experience and behaviour of course are enabled by neuronal processes. But neuronal processes are not meaning making and lack intentionality. As Fuchs puts it, "If neuronal processes function as 'carriers' of intentional acts, they can do so only as part of an overarching life process that includes the organism as a whole and its environment". People cannot be investigated as machines in the same way that their brains may be when they are considered in isolation or as part-functions (see another previous post). As Kant said some time ago, the link between mental and physical is an enigma that can never be solved (see eg. another previous post). Mental processes are enabled or realised by neuronal processes, but are not localisable in the brain. We should give up trying to explain mental illness in physico-chemical terms (see eg. previous post). It needs to be understood in interpersonal context.

In this situation, Fuchs argues for a circular causality of living systems. Circular causal processes are tied to mediation by the brain, but cannot exclusively be located within it. The whole organism is the condition of its parts, but is in turn realised by them. Cause and effect cannot, therefore, be assigned to separate agents acting externally on each other. We can only hope for formative causal influences, not efficient causality. Efficient causes at the level of physics and chemistry require formative causes at higher levels.

I still like Adolf Meyer's such understanding of science (see my book chapter):-
Lower or simpler categories are pertinent to but not explanatory for higher or more complex categories. Chemistry and physics are relevant to biology but the 'lower' sciences do not provide an adequate explanation for biological phenomena, which require a different explanation. The different levels are relatively discontinuous because of qualitative differences in their subject matter and limitations in the methods of study. Individuation first appears in biology beyond physics and chemistry. Within biology are the divisions of botany and zoology. Human beings emerge as a special and a higher biological product. The unitary organism is mentally integrated through symbolisation, which is the meaningful representation of time-bound experience, and through consciousness, which is the awareness of personal activities. There is a matter of degree rather than absolute separation of conscious from 'not-conscious'. Meyer failed to make his system explicit, but I think psychiatry would have done far better to build on his heritage rather than keep repeating its mantra that it's got loads of data demonstrating biological and genetic abnormalities in major mental illness (see previous post).

Wednesday, March 25, 2020

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.

Tuesday, March 24, 2020

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 √† 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

Saturday, March 21, 2020

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).

Friday, March 20, 2020

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 Dupr√©, 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.

Wednesday, March 18, 2020

Reification of psychiatric disorder

Peter Zachar & Kenneth Kendler (2012) discuss the parallels between removing Pluto from the list of planets (see eg. youtube video) and removing homosexuality from the list of mental disorders. Both decisions were made by a vote: on 24 August 2006 members of the International Astronomical Union voted to remove Pluto from the official list of planets; on 15 December 1973 the Board of Trustees of the American Psychiatric Association (APA) voted to remove homosexuality from the official list of mental disorders, and this decision was subsequently supported (by a narrow margin ie. 58%) in a vote of the whole APA membership (of which only 25% voted). One of the differences between the cases in astronomy and psychiatry was that the Pluto decision was not put out to a wider vote.

Zachar & Kendler do recognise that there are differences between the controversies. As they point out, the Pluto decision involved a new definition of 'planet'. They suggest in the case of homosexuality that the "compromise was also a definition, namely that a psychiatric disorder involves distress, social occupational dysfunction, or both". I'm not convinced, though, that the definition of mental disorder was changed as such. The argument about the definition of mental disorder as involving distress, social occupational dysfunction, or both was used, but I don't think there was a fundamental redefinition of 'mental disorder'. It was more about whether homosexuality should be seen as a mental disorder. Homosexuality, in fact, should never have been regarded as a morbid condition. As Zachar and Kendler note,
What homosexuality is like psychologically in an environment where it is considered a disorder will meaningfully differ from what it is like in an environment where it is considered a normal variation in sexual orientation.
Zachar & Kendler do say that a "compelling argument can be made that Pluto never should have been classified as a planet", but I can't see that it could have been foreseen that the definition of 'planet' would change.

There is an argument that the definition of mental disorder was wrongly changed in DSM-IV, in that the functional/organic distinction was abolished (see previous post). Robert Spitzer (2001), who chaired the task force for DSM-III, that removed homosexuality from the manual, always maintained that DSM-III took a neutral approach to causation and that it is not covertly committed to a biological approach to explaining mental illness. There is truth in this observation. DSM-III's primary motivation was to introduce operational criteria to replace what it considered to be vague and imprecise definitions of mental disorder. True, it was associated with reaffirmation of an implicit “medical model” with a focus on brain mechanisms and a positivistic approach to science, but the link between DSM-III and biological aetiology is merely associative, not necessarily logically causal. A classificatory system in itself is not necessarily biomedical. This is illustrated by the fact that DSM-I was influenced by the reaction types proposed by Adolf Meyer, despite Meyer's concern about the general over-emphasis on psychiatric diagnosis (see my book chapter). In fact, Meyer had "no use for the essentially ‘one person, one disease’ view”  and regarded the “…statistics published…[as] a dead loss…and an annual ceremony misdirecting the interests of staff”. DSM-5 did set out to change the definition of mental disorder but failed (see eg. previous post).

Of course, as Zachar & Kendler say, competition for “scientific authority” among competing groups is a normal part of scientific progress. Psychiatry has been challenged as unscientific for putting the decision about homosexuality out to a vote. Zachar & Kendler make clear that they are not reifying scientific authority but, by making the comparison with the Pluto case, do seem to be wanting to defend the scientific nature of psychiatry.

The real problem, though, is the reification of psychiatric disorder. Apart from organic disorders, mental disorders are not concrete entities, like Pluto. There will inevitably be limitations in the application of psychiatric diagnosis, whatever way symptoms and signs are grouped and conceptualised. Psychiatric practice needs to acknowledge this state of uncertainty. The concepts of psychiatric disorder do not need to be abandoned for this reason. They merely need to be recognised for what they are, as attempts to describe prototypical or ideal types of psychological states. They are merely idealised descriptions of those aspects of reality that interest us. As unobservable hypothetical constructs they are not capable of description in a natural scientific sense (see eg. my article).

Psychiatric diagnoses are simply categories justified by clinical utility. They are working concepts for clinicians. The value-laden nature of psychiatric diagnosis is not a sign of scientific deficiency but of its meaningful nature. We must stop too easily assuming a functional mental disorder is an entity of some kind and thereby using such an association as a justification for treatment. To quote from Adolf Meyer (see my paper):
Very often the supposed disease back of it all is a myth and merely a self-protective term for an insufficient knowledge of the conditions of reaction

Tuesday, March 17, 2020

Can clinical psychology be an antidote to biological reductionism in psychiatry?

The Medical Section of the British Psychological Society (BPS) formed in 1919 and included doctors (see previous post). Clinical psychology developed as a separate profession after the Second World War. In-service training in clinical psychology started at the Tavistock Clinic and Crichton Royal Institution in Dumfries, and the first University-based course was at the Maudsley hospital. Interestingly, Eysenck (1949) thought clinical psychology should develop separately from psychotherapy. The initial focus in training courses was on psychological assessment, with the Tavistock course being predominantly psychoanalytic, therefore including projective testing, and the Crichton course being more eclectic, but, again, not emphasising treatment. The Maudsley course eventually led the push by clinical psychologists to colonise behaviour therapy.

Voluntary admission to psychiatric hospital was only possible after the Mental Treatment Act 1930. Even then, application needed to be made in writing to the person in charge of the hospital. The Mental Heath Act 1959 set the foundations for modern psychiatric treatment and made informal admission the usual method of admission. As the doors of the asylums were opened in the 1950s and efforts were made to make asylums more therapeutic, the mental health population peaked. As the numbers of people reduced, the traditional asylum became increasingly irrelevant to the bulk of mental health problems. Clinical psychologists worked in inpatient settings and the increasing emphasis on therapy and opportunities for outpatient and community work gave impetus to the development of their profession.

In this context, psychology became more professionalised through the BPS (see BPS history timeline). The Committee of Professional Psychologists (Mental Health) was concerned with professional conduct and was formed in 1943 and became the Division of Professional Psychologists, with the Division of Clinical Psychology (DCP) forming in 1966, separating from Educational and Child Psychology. Alongside this professionalisation of clinical psychology itself, a proposal for a Division of Therapeutic Psychology was made in 1972 . The Counselling Psychology Section was formed in 1982, which merged with the Special Group in Counselling Psychology set up in 1989 and the Special Group in Counselling Psychology was redesignated as the Division of Counselling Psychology in 1994. The NHS has been slow to offer opportunities for counselling psychologists, although some did work part-time in primary care and over recent years some have found jobs as high intensity therapists within Improving Access to Psychological Therapies (IAPT).

The professional dominance of psychiatrists has caused tension with clinical psychology. The Standing Joint Committee of the Royal College of Psychiatrists and British Psychological Society was set up in 1975 and held its first meeting on 7 January 1977. Medical arrogance can make claims which go beyond the evidence. Clinical psychology may be more free to appreciate the uncertainties of psychiatric practice. There is a critical tradition within clinical psychology building on the work of people like Lucy Johnstone (see my review of her second edition of Users and Abusers of Psychiatry), Mary Boyle and Richard Bentall (mentioned in previous post) (see my article).

Although, of course, I agree with the critical psychology critics about the overemphasis on biomedical psychiatry, I have always expressed concerns, for example, about completely abandoning psychiatric diagnosis (see my article), maybe because I am more aware of the psychosomatic aspects of medicine itself as I am trained as a doctor. Over more recent years, critical clinical psychologists, such as Peter Kinderman and Lucy Johnstone have become more specific about their claim that mental health practice should be non-medical, which, again, has caused me concern (eg. see previous post and links from it).

I do appreciate their arguments and I'm writing this post to encourage further debate. Peter, maybe in particular, is suggesting that a non-medical profession needs to be recognised as having expertise in psychological health issues, so that for example these clinicians can sign certificates to be off work if necessary and to obtain benefits. He is not suggesting abolishing the Mental Health Act, but as far as he is concerned this should not be based on illness. Clinical psychologists can currently in theory, although not much in practice, be Responsible Clinicians for patients in hospital, but cannot at present make recommendations for detention.

There does need to be more discussion about these issues within the mental health professions, including academic journals (see previous post).

Saturday, March 14, 2020

All mental disorders involve cerebral processes

The ICD-10 Classification of Mental and Behavioural Disorders made clear that:
Use of the term "organic" does not imply that conditions elsewhere in this classification are "nonorganic" in the sense of having no cerebral substrate. In the present context, the term "organic" means simply that the syndrome so classified can be attributed to an independently diagnosable cerebral or systemic disease or disorder.
Nonetheless, DSM-IV wrongly abolished the distinction between functional and organic mental disorder (see eg. previous post) because it suggested the term 'organic' perpetuated a false dichotomy and implied that the remaining categories included in the diagnostic manual represented nonorganic conditions. Organic disorders are in fact distinguished on the basis of their aetiology as psychopathological manifestations of cerebral disease or disorder. Functional disorders lack such an aetiological basis.

Zbigniew Lipowski was the member of the DSM-III task force responsible for the revision of the organic category (Lipowski, 1990a). He recognised that affective, personality or delusional symptoms could be due to somatic disease or a toxic factor. The organic category was not abolished in DSM-III.

Lipowski (1990b) expressed concern about the "far reaching changes" proposed to organic mental disorders in DSM-IV. As he said, abolition of the organic category was a radical step which should not have been undertaken lightly. There were no new findings to support such a change, instead "idiosyncratic views".

There was further correspondence between Spitzer et al and Lipowski (1991). As Lipowski pointed out, DSM-IV was at variance with ICD-10. But Spitzer et al's (1992) proposal to retire the term "organic mental disorders" held sway. Lipowski suffered for several years from frontotemporal dementia and amyotrophic lateral sclerosis before he died in 1997 (see Wikipedia entry) and I wonder whether his dementia explains why there doesn't seem to have been a response from him.

Spitzer et al (1992) wrongly relate the distinction between organic and functional to Cartesianism. As Lipowski (1990a) pointed out, Georg Stahl was the first to distinguish mental conditions that are psychological from those that are organic (see previous post). In a way, Spitzer et al (1992) were more interested in avoiding the vitalism of Stahl, rather than adopting a more integrative position in psychiatry (see another previous post). Spitzer el al (1992) did acknowledge the importance of attention to underlying physical disorder or toxic factors. But they did not realise that functional/structural and psychological/biological distinctions are not the same as mind/body dualism.

Instead Spitzer et al (1992) proposed seeing functional disorders as primary mental disorders and organic disorders as secondary mental disorders. I'm not sure how much this distinction has really been taken up. To be clear, I'm not against the more widespread use of the term 'primary mental disorder'. As Spitzer et al (1992) pointed out, Lipowski's definition of organic is in agreement with their definition of secondary. However, there may well be potential misunderstandings with the term 'secondary mental disorder', because, for example, a functional depression may be said to be secondary to a physical illness, in the sense that it follows becoming physically ill because of the nature of being ill. What worries me is that a mistaken fear of dualism seems to have driven the abolition of the term 'organic' (see eg. previous post). At least Spitzer et al (1992) realised that their proposal was not solving the mind-body problem.

The trouble is that the fudging of the distinction between organic/functional has suited biomedical psychiatry which claims that neuroscience is moving us towards having a biological and genetic understanding of primary mental disorders, when, in fact, there are no such clear established biological causes (see eg. previous post). This is why I have argued that critical psychiatry's essential message is that functional mental illness should not be reduced to brain disease (see previous post). In the interests of clarity, I am happy to say that the essential message of critical psychiatry is that primary mental illness should not be reduced to brain disease. I don't want to get caught up in semantic arguments to divert attention from the fact that psychiatry can be practised without the justification of postulating brain pathology as the basis for primary/functional mental illness.

Thursday, March 05, 2020

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).

Wednesday, March 04, 2020

Meta-analysis of inflammatory markers in depression shows depression is related to stress

If you've been attracted to this post because of its title, you may well be wondering why I'm stating the obvious (see tweet). Of course depression is related to stress. But a recent meta-analysis of inflammatory markers in depression didn't make this point clear. Instead, it indicated (as I've said in a previous post) that the motivation for studying the role of inflammation in depression is to identify a novel therapeutic target. It concluded that depression is a pro-inflammatory state (without being very precise about what that means).

Actually, the meta-analysis is useful as it provides evidence that the inflammatory marker elevations are not due to an inflamed sub-group as such. Nonetheless, if we ever get as far as anti-inflammatory agents being marketed for depression (see previous post), I suspect this will, at least initially, be focused on those with raised markers or those with physical illness as well as depression (see another previous post).

Despite attempts to eliminate confounders, such as smoking and obesity, there are questions about how effective these strategies are. More importantly, any increases in inflammatory markers in depression are generally not of the same order as in autoimmune or inflammatory diseases (see another previous post). Psychosocial stress itself raises inflammatory markers. So, why don't we just stick with the obvious explanation that the increase in inflammatory markers in depression is due to psychosocial stress?