Monday, January 16, 2017

Is schizophrenia associated with brain volume changes independently of medication?

Further to my previous post, I have been looking at the 2010 study by Jo Moncrieff & Jonathan Leo on the effects of antipsychotic drugs on brain volume. I had not looked at this study before my previous post and perhaps I was being unfair concluding there needed to be more systematic review of brain scan studies of patients with psychosis or schizophrenia prior to them receiving antipsychotic drugs, because Jo and Jonathan have already done it. In her book, The Bitterest Pills, Jo mentioned this joint paper, which was published by Robin Murray, as editor of Psychological Medicine, "despite opposition from most of the five referees" (p.157).

The authors managed to find 21 "drug-naive" studies published between 1995 and April 2009 of patients who had had no more than 4 weeks of antipsychotic treatment. They conclude:-
Most studies of drug-naive patients examined here did not report or detect differences in total brain volume, global grey-matter volume or CSF volumes between patients and controls, including three studies of untreated patients with long-term illness. These results are particularly remarkable, given the difficulty of selecting a comparable control group in these studies. The results suggest that the brain changes found in some first-episode studies may also be attributable to drug treatment, especially because some studies suggest that structural changes may occur after only short periods of treatment.
They reinforced this conclusion in response to correspondence:-
As we showed in our systematic review, a large majority of studies with drug-naive patients with psychosis or schizophrenia have not found any differences in global brain or grey-matter volumes, or in total CSF or ventricular volumes between patients and controls (Moncrieff & Leo, 2010). Although some of these studies reported differences in the volumes of specific structures, such as the thalamus and the caudate nuclei, others found no differences and multiple testing suggests some of the results may be false positives.
I'm left wondering exactly what the evidence is for Robin Murray's view, mentioned in my previous post, that "subtle brain changes [are] present at onset of schizophrenia".

Modern resurgence of biomedical psychiatry may be totally based on an artefact

As Robin Murray mentioned in his article discussed in a previous post, a 1976 paper by Eve Johnstone, Tim Crow et al showing cerebral ventricular enlargement in chronic schizophrenia "kickstarted the huge and ongoing endeavour of neuroimaging in psychosis". This finding was seen as validating the "view that schizophrenia was a neurodegenerative disorder".

As I've mentioned before (see previous post), it was this paper that also produced the remarkable change in the position of E. Fuller Torrey from being Szaszian to a biomedical advocate of forced psychiatric treatment. From his point of view, psychiatry stopped "groping in the dark" from this 1976 point in time (see my book extract). This meant he no longer doubted that schizophrenia is a brain disease.

However, the general acceptance over recent years that antipsychotic medication can reduce brain volume (eg. see previous post) has led to a rethink, exemplified by Robin Murray's article. The cerebral atrophy demonstrated by Johnstone et al (1976) was almost certainly due to antipsychotic medication, at least mainly, and was not an indication that schizophrenia is a brain disease. Johnstone et al were wanting to make out that schizophrenia led to a dementing illness, as they found a significant association of increased ventricular size with measures of cognitive impairment. But any cognitive impairment in schizophrenia is functional not organic, so the whole basis of the paper was flawed. And, its misinterpretation has misled a whole generation of psychiatric researchers.

I've always argued that any difference in ventricular volume may be non-specific rather than due to schizophrenia (see my article). As with any statistical association, a causal connection is not necessarily implied. The brain is a dynamic, not static, organ and ventricular enlargement can change over time affected by confounding variables, such as nutrition and hydration. In fact, ventricular enlargement can also be found in other psychiatric conditions, such as bipolar disorder.

Furthermore, like Robin Murray, maybe I have underestimated the effects of antipsychotic medication. As I said in my book review of The Bitterest Pills, Jo Moncrieff "makes a stronger case than even I was aware of for ventricular enlargement in schizophrenia being a drug-induced phenomenon". Robin, even though he accepts that "high-dose antipsychotics contribute ... to the subsequent 'progressive' changes", still believes there are "subtle brain changes present at onset of schizophrenia". But Jo shows (p. 158) that the interpretation of the results of studies of antipsychotic-naive patients are not clear cut, with inconsistency about the area of the brain identified. Some studies have not reported any difference in global brain volumes in patients prior to them receiving antipsychotic drugs, even though they may have been unwell for many years.

There does, at least, seem to be a need for a proper review of studies of brain scans of patients with psychosis or schizophrenia prior to them receiving antipsychotic drugs. If the Johnstone et al (1976) study is really the reason for the modern resurgence of biomedical psychiatry, its conclusion that cerebral ventricles are enlarged in schizophrenia may be totally based on an artefact.

Monday, January 09, 2017

Constructing a psychiatric future

I'm not sure if Nassir Ghaemi's letter to a medical student about choosing psychiatry as a speciality (see Medscape article) is another acknowledgement of mistakes in his career, like that of Robin Murray (see previous post). He says that DSM is "inherently unscientific" and psychiatric diagnoses are social constructions. From his point of view, psychiatry has pretended diagnoses are scientific facts. As he says, "This has been proven a lie, but we are unwilling to admit our self-deception". He seems to be saying it took him two decades to realise this.

I have several times mentioned the spat I had with Ghaemi when I reviewed one of his books (eg. see previous post). As I said in my review, he was one of the psychiatrists at the forefront of promoting bipolar depression, which I guess he now realises he helped to construct.

Actually, I don't think he needs to be quite so disillusioned about the prospects for psychiatry. It just needs to accept its inherent uncertainty (eg. see previous post).

Sunday, January 01, 2017

Rethinking antipsychotic medication

In a comment on my previous post about his article, Robin Murray has highlighted what he calls critical psychiatry's "scepticism about the unthinking advocacy of prophylactic antipsychotics". I think he has in mind a BJPsych article, which discuses the lack of evidence for long-term effectiveness of antipsychotic medication and expresses concern about antipsychotics causing a decrease in cortical volume and dopamine receptor supersensitivity, besides having side effects on physical health. I suspect this article was written in response to Jo Moncrieff's questioning of the need to rethink antipsychotic maintenance treatment (see her article).

Critical psychiatry has always emphasised discontinuation effects from psychotropic medication. Personally I have always pointed to the importance of psychological aspects in discontinuation. Many of the posts on this blog have been about antidepressant discontinuation (eg. see previous post) but the same principles apply to antipsychotic discontinuation. Removing a drug which is thought to have been beneficial is likely to produce a nocebo response.

A difference between antipsychotic and antidepressant discontinuation is the clear evidence for the development of dopamine receptor supersensitivity. Physical effects may therefore be important but it is not clear to me that dopamine supersensitivity is responsible for antipsychotic discontinuation problems. Certainly tardive dyskinesia can be made worse by antipsychotic discontinuation, which is a physical effect, but dopamine supersensitivity may merely be significant for motor rather than psychological symptoms.

I have also always been cautious about the argument that 'antipsychotics should not be used because they cause brain damage' (see previous post). Actually this effect has always been clear, at least for traditional neuroleptics, because of the potential irreversibility of tardive dyskinesia.

Anyway, I'm glad Robin is now recognising the much neglected research question about whether people who manage to deal with their problems without medication may actually do better in the long-term.

Reassessing sociopsychobiological psychiatry


In a BJPsych article, Will Davies & Rebecca Roache (2017) identify a philosophical research programme for reconceptualising George Engel's biopsychosocial paradigm. I have always argued that Engel's biopsychosocial model and, before that, Adolf Meyer's psychobiology are the historical bases for critical psychiatry (eg. see previous post and my article).

Like me, Davies & Roache recognise the value of the biopsychosocial model and disagree with Nassir Ghaemi, who rejects it. I do not totally agree with them, though, that Engel did not try and provide details about how his model should work but this was primarily in relation to psychosomatic disorders. Yet, they are right, as is Ghaemi, about the eclectic way in which the model is used in current practice which is why I prefer the term 'sociopsychobiological' (see previous post). There have also been other recent attempts to reconsider the biopsychosocial model (see another previous post).

Still, their philosophical perspective is welcome. Critical psychiatry, as does the biopsychosocial model, has ontological, epistemological and moral implications for psychiatric diagnosis and treatment. These are practical implications, for example for the Reseach Domain Criteria (RDoC) project mentioned by Davies & Roache (see eg. previous post). These philosophical issues require more rigorous scrutiny.

Friday, December 23, 2016

Schizophrenia is not a neurodevelopmental disease

Professor Sir Robin Murray confesses to mistakes in an end of research career mea culpa (see article). He questions whether schizophrenia is a neurodegenerative disease and accuses psychiatrists of refusing to accept the evidence, clinging to the "nihilistic view that there exists an intrinsically progressive schizophrenic process". This is what he believed once! He makes much of the fact that he did not sufficiently take into account the effects of medication. He even admits that he was surprised the neurodevelopmental theory of schizophrenia achieved such widespread acceptance. As far as he is concerned, saying that schizophrenia is a neurodevelopmental disease is at least overstatement, with the evidence against it.

Murray also admits that he ignored social factors in the aetiology of schizophrenia for 20 years. Like me (eg. see previous post), he points out that even social psychiatrists, such as Paul Bebbington and Julian Leff, tend not to regard social factors as causal.

Don't think, though, that this means Murray is saying critical psychiatry was right all along. He still believes the "final common pathway underlying psychosis is excess synthesis of presynaptic dopamine". His recommendation to newly qualified psychiatric researchers is to throw themselves into "examining gene x environment interactions and epigenetics", or if they are not clever enough, to go instead into neurochemical imaging, because "at least the pictures of the brain are pretty". The silly chump also still promotes ideas such as tobacco use causing psychosis (see eg. previous post).

Monday, December 12, 2016

Psychedelic drugs and psychiatry

The Philosophy Special Interest Group of the Royal College of Psychiatrists has asked for submissions for its conference next year on Philosophical issues in psychedelic drug use (see call for papers). It's interesting to look at what motivates this focus.

As I said in my book chapter in Liberatory Psychiatry, Tom Wolfe's book The electric kool-aid acid test acknowledged the expansion of the limits of immanent experience through psychedelic drugs. Ken Kesey who, with his Merry Pranksters drove across America in a brightly painted bus, was the author of One flew over the cuckoo’s nest. This accomplished novel depicts Randle McMurphy’s attempt, apparently on behalf of the counterculture, to overthrow the bureaucratic control of Nurse Ratched in the psychiatric institution. It was made into a successful film starring Jack Nicolson.

The blurb for the conference states that "Neuroimaging studies are revealing how changes in brain function can lead to the particular changes in emotional and cognitive experiences produced by psychedelic drugs. These findings may be relevant to our understanding of psychoses and other abnormal mental states." I'm not sure what neuroimaging studies it is referencing, but I agree that the overlap with psychosis is what makes the topic interesting. The blurb goes on that psilocybin and LSD "have been used on a trial basis in a range of psychiatric disorders including depression, PTSD and ‘existential anxiety’ in people with terminal illnesses". R.D. Laing, perhaps the most famous of the anti-psychiatrists (see eg. previous post), used LSD in treatment.

It is interesting how the strands of anti-psychiatry were interwoven with the 1960’s counterculture. Laing's perspective that civilisation represses transcendence and so-called ‘normality’ too often abdicates our true potentialities cannot be completely divorced from the use of psychedelic drugs.

The interest in psychedelic drugs came not only from anti-psychiatry but also from mainstream psychiatry, such as William Sargant. He reviewed The doors of perception by Aldous Huxley for the British Medical Journal. It seems likely he was involved with trials of LSD as a truth serum at Porton Down between 1953-5 (see BBC News story).

These historical aspects are of interest and require further elucidation. I'm not quite sure what the relevance of psychedelic drugs are to current psychiatry.

The value of anti-psychiatry

RSM videos have recently uploaded a lecture by Tom Burns (see previous post) given earlier in the year on anti-psychiatry (see video). However simplistically, he at least thinks anti-psychiatry matters, or at least the work of Michel Foucault, Erving Goffman and R.D. Laing (see my book chapter). Despite what he says, there is even value in the work of Thomas Szasz (see previous post).

Friday, December 09, 2016

Bias against critical psychiatry in peer-reviewed publications

I used Kam Bhui's photo to accompany my previous post. Kam is editor of the British Journal of Psychiatry (BJPsych). In the past, he was chair of the Transcultural Special Interest Group of the Royal College of Psychiatrists, and, I thought, sympathetic to critical psychiatry.

I congratulated the previous BJPsych editor for publishing a special article a few years ago written from a critical perspective (see previous post). It is not always easy to get such articles published in mainstream journals. One advantage of the internet is that it allows free expression. However, it does mean that it can be difficult to distinguish quackery from mainstream science.

I have always argued for the mainstream presence of critical psychiatry. However, particularly over recent years, I have resorted to blogademia (see post on personal blog) to express my views. I don't think this makes my critical psychiatry blog any less scientific. But, we do need psychiatric journal editors to take a balanced perspective and be willing to publish critical articles. Considering my comments in my previous post, I'm not convinced that Kam is brave enough to do this. True, The Lancet Psychiatry editor published a letter of mine following a previous post. But, critical psychiatry needs to have more presence in mainstream psychiatry journals. Because of the bias against it, this process does need to be facilitated by journal editors. After all, having obtained the power of such influential positions, why not use it?

Tuesday, November 29, 2016

Definition of mental illness

I have been thinking about the definition of mental illness by Dinesh Bhugra, Antonio Ventriglio and Kam Bhui which I quoted in my previous post. Dinesh and Antonio Ventriglio would be seen as representatives of social psychiatry (eg. see their article). Kam would be seen as a representative of cultural psychiatry, being a Professor of Cultural Psychiatry and Epidemiology. It concerns me than modern social and cultural psychiatry are apparently diluted versions of biomedical psychiatry.

Mental illness is not merely a "socially elaborated" state. Proper social and cultural psychiatrists would recognise the psychosocial origins of mental disorder.  They should not merely be talking about incorporating "sociocultural dimensions of individual experiences and distress as life story narratives" into diagnostic and management frameworks. Understanding these narratives can provide reasons for mental health problems. However helpful the perspective of McHugh & Slavney may be, there are problems with it (see previous post). Talking about getting "social psychiatry at the core of our clinical practice" (see article) won't happen if "neurophysiological or chemical alterations in body or brain functions" are seen as the cause of mental illness. I'm all for recognising the need to "reclaim professionalism and renew our contract with society", but we don't need genomics and epigenetics to tell us that psychiatric disorders are caused by psychosocial determinants. Transcultural psychiatry should not encourage a biomedical model of mental illness for all mental health systems worldwide (see previous post).

I've said before (eg. see previous post) that psychiatry needs to be more thoroughgoing in adopting a sociopsychobiological model of mental illness. In the last chapter of my Critical psychiatry book, I showed that Julian Leff, who represented social psychiatry for a previous generation, still upheld the biomedical model (see extract). It seems the present generation of social psychiatrists are no different. 

Friday, November 25, 2016

Problem with the term 'mental illness'?

As I have said before (eg. see previous post), I don't have a problem with the term 'mental illness'. In a recent comment in The Lancet Psychiatry, Dinesh Bhugra et al make a case for what they call reclaiming the term. They suggest that psychiatrists have given up using the concept. Part of their argument is that "A large number of psychiatric disorders ... are ... socially elaborated states of pathology or disease, with neurophysiological or chemical alterations in brain or body functions". But are they brain dysfunctions? No evidence is offered to support this conjecture and, as I keep saying in this blog, such a belief is mere conjecture.

Actually, perhaps I do have a problem with the term 'mental illness' if this is what it is supposed to imply, although I don't think it necessarily does. Better to stick to terms that Dinesh et al tend not to like, such as 'mental health problems', which don't have this ideological implication.

I think Dinesh et al are right that mental illness does imply a major or more serious rather than minor mental health problem. Before the 2007 revision, the Mental Health Act (MHA) used the term 'mental illness', although it was never defined. This has now been replaced by the more generic term 'mental disorder'. In principle, people should only be detained under the MHA for mental health problems of a nature or degree that warrant this intervention and psychiatrists would have generally understood the term mental illness to mean functional psychosis. And, as I've said several times before (eg. see previous post), there may be potential advantages in seeing mental health problems as illness as it integrates the medical perspective. Illness can be mental and not purely physical. The problem with Dinesh at al's view is that they may appear to regard mental illness as physical in origin.

Saturday, November 12, 2016

Artificial kinds of mental disorder

Tsou (2016) makes a case for natural kinds of mental disorders. This seems to be dependent on his claim that there is "good evidence that the symptoms of schizophrenia are underwritten by stable neurobiological mechanisms". By this he means the dopamine theory of schizophrenia. Similarly he says "multiple lines of research indicate that the core signs of depression are underwritten by stable neurobiological mechanisms". Again, by this he means the monoamine hypothesis of depression. I guess if the dopamine and monoamine hypotheses are incorrect, his whole argument fails.

He does acknowledge the article by Kendler and Schaffner (2011) that I have mentioned before (eg. see previous post). This apparently doesn't undermine his faith in the dopamine hypothesis. The monoamine hypothesis is similarly not tenable (eg. see previous post). Even psychiatrists have described the 'chemical imbalance theory' as a kind of urban myth (see previous post and book review). Psychopharmacologists stopped believing in it a long time ago.

Tsou wishfully hopes that "mental disorders should be classified at a level of generality such that the characteristic signs of disorders are associated with stable biological mechanisms". His lack of clinical and scientific experience does not provide a sound basis for his philosophical theorising. Psychiatric diagnosis is inevitably purely descriptive. Considering the motivation for the revision of DSM-5 (see eg. previous post), information about the biological causes of mental disorders would have been incorporated if there is any, which there isn't.

Friday, November 04, 2016

Improving psychiatric training

Mary-Ellen Lynall in a BMJ blog says she'll be "deeply concerned" if new and better mental health treatments don't grow out of a deeper understanding of brain function. I haven't written a piece potentially undermining a trainee for a while (eg. see previous post) and I don't want to dull Lynall's enthusiasm, but I worry it's misdirected. I don't know what she means about "improved understanding of the neuroscience behind psychiatric disease ... recently".

I'm sure there'll be different medications introduced in coming years but whether they'll be any better than placebo is open to question. She worries that she won't be able to "explain the complex neurobiology of conditions such as depression, addiction, and psychosis to patients in an understandable way" and I agree this might not make sense. I hope she learns how to do the fundamentals of a history, mental state and formulation of people's problems (see previous post).

I don't understand why the Royal College of Psychiatrists is only reviewing its teaching of neuroscience and not its whole training. I guess it's easier to get funding just to look at neuroscience. Simon Wesseley denies that this initiative reflects a biomedical bias but it would be nice to see a more balanced response from the College to improve training. I've said before we need to train open-minded psychiatrists (eg. see previous post). We need to return to modern psychiatry's educational roots in Adolf Meyer and Aubrey Lewis.

Tuesday, November 01, 2016

Mind-twist or brain-spot hypothesis of mental illness

I have always taken the view that modern psychiatry has been split between two conceptual understandings of mental illness. At the Triennial Medical Congress at Washington in 1910, Ernest Southard called these "two great groups of friendly opponents in the field of psychiatric theory" the 'mind twist men' and the 'brain spot men'.(1) He thought it was important to distinguish between those that looked for a psychogenic cause of mental illness and those that emphasised brain aetiology.

Southard was more of a brain-spot man himself. The main mind-twist man at the time in US psychiatry was Adolf Meyer. I have several times pointed out the link between the theory of Adolf Meyer and critical psychiatry (eg. see previous post).

I think modern psychiatry needs to make more of the differentiation that Southard described. The way was lost when psychiatry thought there was a "twisted molecule behind every twisted thought", which is clearly wrong.

(1) Southard, E.E. (1914) The Mind Twist and the Brain Spot Hypotheses in Psychopathology and NeuropathologyPsychological Bulletin 11: 117-130

Thursday, October 27, 2016

Flawed pioneer of biological psychiatry

I have been reading Richard Noll's book American Madness, which is well worth a read. He includes information about Bayard Taylor Holmes (1852-1924), a Chicago physician and surgeon, whose son was diagnosed with dementia praecox aged 17. Holmes was devastated by his son's illness and vowed to use his scientific expertise to find a cause and cure for dementia praecox (the precursor name for schizophrenia).

He came to believe that caecal stasis led to the production of ergot-like toxic amines that poisoned many organs in the body, including the brain leading to dementia praecox. The solution was appendicostomy or caecostomy and daily irrigations of the caecum. This theory was congruent with popular theories of autointoxication at the time. For example, Emil Kraepelin, the originator of the concept of dementia praecox, speculated that the sex glands were the source of toxins that poisoned the brain in dementia praecox. In fact, Kraepelin was unusual in blaming the sex glands rather than the intestines for autointoxication.

The first patient Holmes operated on was his son, but unfortunately he died 4 days later. This didn't stop him and colleagues operating on a further 21 patients. Only one other patient died from complications of his surgery. This story needs to be set in the context of Andrew Scull's book, Madhouse (see my review), about Henry Cotton, who operated on 645 patients by removing what he considered to be hidden infections in various parts of the body, particularly teeth and tonsils. 25-30% of Cotton's patients died, particularly from colectomy.

As I said in my book review, I think we can learn from our sense of outrage about these misguided attempts to produce biological cures for mental illness. Psychiatric practice needs to have a strong ethical foundation.

Wednesday, October 26, 2016

Functional psychosis without brain disease

Allen Frances in a blog on Huffpost suggested that psychosis is at least partially caused by neurological (brain) malfunction. Of course brain dysfunction in medical disease can cause an organic psychosis (see previous post). But Frances means more than this. He talks about "misfiring nerve cells" playing a central role in schizophrenia and delusional disorder. I don't know what he means by this unless it's pure speculation.

Like Frances, I have expressed some concerns about the BPS report on psychosis (eg. see previous post). But its psychosocial emphasis is its strength. It was Allen Francis, who as Chair of the DSM-IV Task Force, abolished the distinction between functional and organic psychosis (see eg. previous post). It needs to be reinstated.

Tuesday, October 18, 2016

Psychiatrists are still needed

Frank Blankenship comments on Mad in America about my previous post on "Psychiatry as a cultural system". He suggests there's a simpler explanation for why psychiatrists are resistant to giving up the biomedical model than because it's like a religion - they'd be out of a job!

I do understand his view. I too was schooled in the biomedical perspective that mental illness is brain disease. It's such an ingrained perception in society that people don't think to challenge it. Medical training reinforces this indoctrination (eg. see previous post and my Lancet Psychiatry letter).

I also agree that psychiatrists are worried that non-medical professionals are taking over their job (eg. see previous post). This fear encourages them to adopt a biomedical model by focusing on "what doctors do best".

However, where I disagree is that it is important to remember that medicine is psychosocial as well as biological, if only to ensure that practice is patient-centred. It's not purely a bodily exercise. Even more so, patients go to doctors with physical symptoms which have a psychological origin. Medicine has to adopt a sociopsychobiological approach to provide an integrated perspective in practice (see previous post).

I've also mentioned before my disagreement with Peter Kinderman, who has argued that mental health care should actually be non-medical, as it is not treating 'illness' as we understand it (see
previous post). From his point of view, doctors should concentrate on the biological aspects of mental health care and this should be seen as a minority activity within the field as most psychiatric presentations are psychosocial, not biomedical, in origin. By contrast, Peter Sedgwick, in the same way as I have been saying, would have regarded Peter's position as ‘psycho-medical dualism’, because psychosocial approaches should not be separated too much from medicine. Sedgwick adopted a unitary concept of illness, beneath which is subsumed both physical and mental aspects (Cresswell & Spandler, 2009).

Conceptual conflict exists about the nature of mental illness and this is as much of an issue for psychiatrists as it is for specialists from other mental health disciplines. Merely putting psychiatrists out of a job won't solve this dilemma. And, medicine needs the specialty of psychiatry.

Sunday, October 16, 2016

Too much neuroscience

NIMH has a new director, Dr Joshua Gordon. An article in The New York Times criticises the previous director, Thomas Insel, for shifting the focus of the NIMH research budget too much away from clinical research to neuroscience. Although the article could have been more sceptical of the possibilities of neuroscientific research, there is an important question about whether biomedical research funding is good value for money. Powerful vested interests don't necessarily produce the most neutral scientific progress.

I would like to see more investment in social psychiatry (see previous post) and critical neuroscience (see another previous post).


(With thanks to Facebook post by Christian Perring)

Friday, October 14, 2016

Is psychiatry currently undergoing a crisis?

Richard Bentall (mentioned in eg. previous post) and Simon Wessely (again, mentioned in eg. previous post) go head-to-head in a conference next year, as to whether psychiatry is currently undergoing a crisis. I suppose I can see both sides. Psychiatry ought to be in crisis but it isn't.

As Richard says, the biomedical model is "on the edge". Its wishful thinking about finding a biological basis for mental illness has failed to come to fruition (eg. see previous post) but that doesn't seem to matter. As Simon says, "psychiatry is in good health". It can plough ahead with its ecelectic view that it is not narrowly biomedical even though it does not really take a psychosocial perspective. I'm not sure how this impasse can be broken.

Nonetheless, I think we do need to move forward. We need to accept that psychiatrists find it difficult to give up the biomedical model (see previous post). But more of them need to abandon the faith that mental illness is due to brain disease.

Tuesday, October 11, 2016

Is critical psychiatry merely anti-psychiatry?

I have been looking at a presentation I gave on whether critical psychiatry is the same as "anti-psychiatry" (see powerpoint slides). I have always tended to emphasise critical psychiatry's links with mainstream psychiatry.

For example, I have mentioned Adolf Meyer several times in previous posts (see example). He was the foremost US psychiatrist in the first half of the twentieth century. His approach, which was called Psychobiology, has the same integrated understanding of mind and brain as critical psychiatry. The problem with Meyer was that he did not follow through on his challenge to biomedicine. He had a tendency to compromise. The full impact of his objection to the biomedical model in psychiatry tended to get lost. In a personal note in his papers a few years before he died, he himself admitted that he should have made clear his "outspoken opposition, instead of a mild semblance of harmony" [his emphasis].

Similarly, George Engel promoted the biopsychosocial model, which forms the basis for patient-centred medicine and psychiatry, as does critical psychiatry. As I pointed out in another talk, Engel was specifically responding to a paper by Arnold Ludwig when he published his 1997 paper in Science arguing for a new medical model. He was explicit that he was challenging biomedical dogmaticism. However, what has happened over recent years is that the biopsychosocial model has been interpreted in an eclectic way evading its full ideological impact. Nassir Ghaemi agrees with me on this point (see my review of his book The rise and fall of the biopsychosocial model). Where we disagree is that I don't think he has fully appreciated the validity of Engel's biopsychosocial model in its original form. I have even suggested using the term "sociopsychobiological" to make clear that I am not using biopsychosocial in an eclectic way (see previous post).

The point I'm making is that critical psychiatry does have roots in mainstream psychiatry. It is not "anti-psychiatry" in that sense.

Sunday, October 02, 2016

Psychiatry as a cultural system

Gary Sidley expresses his frustration in a blog recently reposted on Mad in America that it "seems unrealistic – even naïve – to expect that radical change away from bio-medical approaches to human suffering can be achieved organically". Nonetheless, he remains "optimistic that, in the next decade or so, we will witness a radical change in the way we as a society respond to human suffering" (see recent post on Tales from the Madhouse).

I do understand his frustration and I think we may need to understand better why there is such reluctance for psychiatry to change. To do this, it may be helpful to look at the work of Clifford Geertz, who I have mentioned before (see previous post). Geertz saw religion as a cultural system (see his paper). In the same way, psychiatry can also be understood as a cultural system. 

The biomedical model that mental illness is brain disease is both a model of "reality" and for "reality", to use Geertz's terms. Note the use or the word "reality" in inverted commas. A model does not necessarily describe the real world, which is what critical psychiatry would say about the biomedical model, that it does not. The biomedical model is a model for "reality" because it justifies treatments such as physical interventions, including medication.

The biomedical model gives a sense of direction to psychiatry. It induces certain dispositions in psychiatrists to treat people in a particular way. It provides a worldview, which if psychiatrists did not believe it would make their practice uncertain, too uncertain for most. To quote from Geertz, "Man depends upon symbols and symbol systems with a dependence so great as to be decisive for his creatural viability and, as a result, his sensitivity to even the remotest indication that they may prove unable to cope with one or another aspect of experience raises within him the gravest sort of anxiety". The biomedical assumption is clothed with an aura of factuality by people having faith in it. It is sustained by professional institutions. 

Viewed in this way, it's not surprising that people don't want to give up the biomedical model. To do so is like giving up one's religion.

Thursday, September 01, 2016

Neuroscience can be critical

I've said before that neuroscience needs to be more critical (see previous post). If it wants to include psychology, it is essential that it is seen as more than a physical science. Psychology inevitably includes human aspects which cannot be described in physical causal terms. Human knowledge includes meaningful understanding of action.

For example, Andrew Huxley wrote the website introduction to Cambridge Neuroscience. As he said:-
Perhaps the most difficult, and at the same time the most interesting problem in neuroscience, is the nature of consciousness and its relationship to physical events in the brain.
He suggested that:-
[T]his is the biggest problem facing neuroscience at the present time. Whoever solves it will have earned a place in the history of science comparable to that of Newton and Darwin.

This objective has always been the wishful hope of neuroscience. But maybe it needs to take a more pragmatic approach and realise that the mind-brain problem won't be solved, as it is a philosophical not neuroscientific problem. As far as psychiatry is concerned, this means that trying to understand the reasons for mental health problems and helping people deal with them is what is central for practice. Understanding their problems in terms of brain abnormalities is missing the point.

Saturday, August 13, 2016

Changing mental health services

An article in The New York Times says that alternatives such as the Hearing Voices Network (HVN) and Open Dialogue are starting to take hold in the USA. As the article says, these approaches may be better integrated with mainstream services in the UK. Gail Hornstein, whose books To redeem one person is to redeem the world and Agnes's jacket, are well worth reading, is quoted as saying that it is important "these groups do not become medicalized in any way". I understand what she means but the main problem, as I keep saying throughout this blog, is the biomedical assumption of psychiatry. The article also quotes from Caroline White, who has heard voices since she was in grade school and is involved with HVN:-
I was told by one psychiatrist at age 13 or 14 that if I didn’t take the meds, my brain would become more and more damaged ... Of course I believed it. And I became hopeless, because the drugs just made me feel worse.
Both mainstream and alternative mental health services need to stop making such claims and demeaning people in this way.

Sunday, July 03, 2016

Denial of the functional nature of schizophrenia

An article in The Lancet Psychiatry accuses those who refuse to accept the evidence for schizophrenia being an organic condition as being in denial. It does at least admit that the evidence for organicity in schizophenia may be "questionable". But it then goes on to say, "We can no longer divide [mental] illness into organic and inorganic".

I don't think I've ever heard schizophrenia called 'inorganic' before. Rather, the difference is made between organic and functional psychosis. The idea of psychosis was originally a functional concept following Ernst von Feuchtersleben (eg. see previous post). The anatomoclinical method of understanding illness developed in the 19th century, and despite all the wishful speculation since, it has not established a physical basis for functional mental illness. As I said in my previous post, "more caution needs to be made about drawing any conclusions about biological abnormalities in schizophrenia".

The article is worried about the implications of seeing schizophrenia as functional (or, in its terms, non-organic). But functional illness is as much illness as organic illness. There's no need to deny the reality of functional mental illness by calling it organic.

Inferences about the biology of schizophrenia

A seminar on schizophrenia in The Lancet says the syndrome "seems to originate from disruption of brain development caused by genetic or environmental factors, or both". Note the use of the word 'seems'. The article is not saying that schizophrenia does originate from disruption of brain development. In fact, as the sentence stands, it's not absolutely clear that the article is saying any more than the tautologous statement that mental illness is due to the brain. Of course it is. And so is our "normal" behaviour.

More specifically, the article makes out that "advances in genomics, epidemiology, and neuroscience have led to great progress in understanding the disorder". The problem is that it does not make any firm inferences about the biology of schizophrenia. The studies it discusses are plagued by so many inconsistencies and confounders that more caution needs to be made about drawing any conclusions about biological abnormalities in schizophrenia. The findings may well be artefacts or of dubious value as far as establishing the aetiology of schizophrenia. The article is misinforming people in this respect.

The authors imply there is less controversy about the issue of the biological origins of schizophrenia now because of these studies over recent years. They do need to recognise the critical challenge to their position.

Tuesday, June 21, 2016

Stop psychiatric abuse

Peter Breggin has a blog on Mad in America entitled "Forced 'treatment' is torture". His blog follows that by Peter Gøtzsche entitled "Abolishing forced treatment in psychiatry is an ethical imperative". I agree psychiatric abuse must be prevented.

For both Peters, as it did for Thomas Ssasz, psychiatric abuse includes detention in hospital. They want to abolish all forced intervention in psychiatry. Here I do not agree. Society does expect psychiatry to manage madness on its behalf. However much informal and voluntary interventions, including psychotherapy, may have developed since the origins of psychiatry with the asylums in the 19th century, they have not completely replaced the need for compulsory detention. From a position in private practice, Peter Breggin may well have never detained anyone against their will. As he says, "Someone in an out-of-control manic episode or someone threatening to do harm in a psychotic episode presents difficult problems to civil libertarians and to those of us who wish to help people in distress while protecting others from them." However, he can't use these situations to justify mental health legislation, whereas I think I can.

Where I do agree is about the need to improve safeguards for forced medication. In England, apart from the right of appeal to the Mental Health Tribunal and hospital managers, this is primarily about having access to a Second Opinion Approved Doctor (SOAD) but only after 3 months of receiving medication. Patients on a community treatment order (CTO) with the threat of recall to hospital may take medication and be considered to be consenting to medication and therefore not be referred to a SOAD. The Alaska Supreme Court case ruling, referred to by Peter Gøtzsche, needs to be enforced so that someone should not be given medication against their will without "first proving by clear and convincing evidence that it is in their best interests and there is no less intrusive alternative available". We do need to have much more of an open debate about whether there is any justification for the forcible injection of medication, and, therefore, I welcome the two Peters contribution to this debate. Coercion in psychiatry needs to be reduced.

Wednesday, June 15, 2016

Philosophical perspectives on critical psychiatry

Next May's meeting of the Association for Advancement of Philosophy and Psychiatry in San Diego is on "Philosophical Perspectives on Critical Psychiatry: Challenges and Opportunities" (see call for abstracts). It should be an interesting meeting.

I just wanted to comment on the blurb saying that critical psychiatry  is primarily about taking the "profession to task for being a source of oppression". There is no doubt that psychiatry can be oppressive. There is also no doubt about the role of psychiatry in social coercion, as it is expected to manage mental illness on behalf of society. Critical psychiatry does focus on the rights of psychiatric patients.

However, I have always argued that critical psychiatry is primarily about the conceptual nature of mental illness (see my attempt to summarise critical psychiatry in previous post). Reducing people's problems to something the matter with their brain is unhelpful, even oppressive at times. The reference to the Frankfurt school in the blurb may come from one of my references (eg. see chapter 12 of my Critical psychiatry book). I have also always been sceptical whether critical psychiatry is really based on Foucault's thinking, however much Foucault was concerned that the reason of the Enlightenment was oppressive.

Still, the suggested topics for the conference do merit further examination and I encourage you to contribute by submitting an abstract.

Wednesday, May 11, 2016

Antidepressants can cause psychological dependence

Robert Whitaker (who I have mentioned previously eg. see previous post) has posted on the Mad in America blog about the All party parliamentary group for prescribed drug dependence. He includes a link to his slides for his presentation to the group on "Causation, not just correlation: Increased disability in the age of Prozac". The meeting to which he gave this presentation today is a product of the book Cracked: Why psychiatry is doing more harm than good (see my review), which led to the Council for evidenced-based psychiatry (CEP).

There is no doubt that psychotropic medication can lead to psychological dependence. Since my BMJ letter, I have emphasised psychological aspects of antidepressant discontinuation problems (see eg. my Antidepressant discontinuation problems webpage and my book chapter "Why were doctors so slow to recognise antidepressant discontinuation problems?).

As I have also said previously (eg. see post), Robert Whitaker, in his original books Anatomy of an epidemic and Mad in america, has emphasised the vulnerability created by taking psychotropic medication. He may have implied this is more of a physical problem than I think is the case. In his current presentation he mentions the idea of drug-induced oppositional tolerance which comes from Giovanna Fava, which I am not convinced is valid (see previous post). But the correlations Whitaker points to still stand without postulating a biological explanation for why psychiatric drugs may have harmful long-term effects. I think CEP would do better to emphasise the psychological aspects of prescribed drug dependence.

In fact, the problem is not necessarily specific to medication at all. Medicine has always tended to create dependency. This critique of medicine is not new and was famously expounded by Ivan Illich in Limits to medicine (see Jo Moncrieff's recent blog on this classic book). I wouldn't want to go as far as Illich in suggesting there is no need for professional services and that "do it yourself" care is preferable. But there is an onus on doctors to provide proper expert advice and as a society we may well need less medicine not more (see eg. post on my personal blog). 

Saturday, April 23, 2016

Patient safety measures will be associated with suicide reduction when rates are falling

The latest paper from the National Confidential Inquiry into Suicide and Homicide (NCISH) published in The Lancet Psychiatry starts from the hypothesis that implementation of service changes associated with improvements in patient safety have led to a reduction in the rate of suicide. It manages to show an association of about 20-30% reduction in suicide between 1997-2012 with 16 policies and procedures that relate to ward safety (eg. removing non-collapsible curtain rails), availability of community services (eg. implementing a Crisis Resolution and Home Treatment team within community health services), staff training (eg. training clinical staff in suicide risk management), adoption of specific policies (eg. policy regarding response to inpatients who abscond), and adoption of The National Institute for Health and Care Excellence (NICE) guidelines (eg. NICE depression guidelines). An accompanying comment paper hails this finding as a success for clinical governance.

But what if this 20-30% reduction in suicides in the clinical population happened for other reasons rather than anything to do with these 16 service changes? The fact that the incidence rate ratio was very similar for all 16 policies could be said to support this inference of lack of causal effect. The article notes that the incidence rate ratios were higher for the general population than for the patient population in the study, but the patient population in mental health services has also changed over recent years, with probably more minor cases being referred.

Although the paper does acknowledge that this "study was observational therefore we cannot make causal inferences", I can't find any specific mention of the fact that suicide rates were falling during the period under study. If the same study had been done during a period of rising suicide rates, the service changes would have been associated with an increase rather than decrease in suicide. And by writing that "service delivery variables are associated with suicide rates", the paper, as does the comment paper, leads people to think that a causal connection is being inferred, which is what the original hypotheses was. But the study isn't a hypothesis testing paradigm, as the paper notes, because the use of "randomised controlled designs for this research would be extremely challenging".

NCISH seems to have a habit of using data to justify its own prejudices (see previous post). Whatever happened to the principle of scientific scepticism? And how does a paper like this get through The Lancet Psychiatry peer review process?

The gap between neural circuits and understanding people

A new Personal View in The Lancet Psychiatry goes overboard trying to create a taxonomy of brain circuit dysfunctions in depression and anxiety. It suggests 6 neural circuits have been implicated, viz. default mode, salience, negative affect, positive affect, attention and cognitive control:-
Accepting such circuits have been established, eight biotypes of circuit dysfunction in depression and anxiety are then suggested, viz. rumination, anxious avoidance, negative bias, threat dysregulation, anhedonia, context insensitivity, inattention and cognitive dyscontrol:-
It's even suggested how neural circuits might relate to treatments:-

I think what's being proposed is that the precision psychiatry of the future will identify apparent brain circuitry dysfunction and treat on this basis. I guess it won't need to interview patients. The article is certainly a tour de force of imagination, but does it relate to the real world?

As I keep saying, mental function is not well localised in the brain and I'm not sure we've really identified any more localisation of function through identifying the so-called brain circuits mentioned in the article, even if they are valid. As I said in a previous post, "It's a long step to mapping specific mental illnesses to dysfunction of brain circuits". The article suggests that people like me that believe that mental disorders are not brain disorders, which the article concedes is the typical view, have a "limited understanding of real-time coordination in the brain”. I don't think this is the case and the article at least recognises that a lot of money has been spent through the RDoC project (see previous post), the White House's Brain Initiative and DSM-5 (see eg. previous post) to prove me wrong without success. 

The language about brain circuits cannot be incorporated into clinically meaningful taxonomies because, although mental phenomena have a biological substrate, that substrate cannot tell us the meaning of mental phenomena. The psychiatry of the future will still have to interview patients to get them to tell their story. We can't see that in a brain circuit.

Monday, April 18, 2016

Does cannabis cause psychosis?

An article in Biological Psychiatry reviews evidence about the association between cannabis use and psychotic outcomes. Despite the consistent association, the article highlights how difficult it is to infer a causal link because of confounding and bias in the data.

As I said in my BMJ letter, the use of cannabis can cause emotional problems and people may use it to deal with their emotional problems. Cannabis use is likely to be a proxy measure for poor premorbid adjustment associated with psychosis. As the article says, "few studies have adjusted for measures of early life attachment, abuse, and trauma".

Bias may also be introduced as heavy users of cannabis may be rarely unintoxicated, leading to misdiagnosis of the induced psychotic-like experiences, which are usually transient in less heavy users. There is some evidence of a dose-response relationship between cannabis and psychotic diagnosis.

There is also an association between other drugs and psychosis and mixed data about whether the association with cannabis is more specific. Despite the increase in the use of cannabis since the 1960s there is no clear evidence of a corresponding increase in the incidence of psychosis. Cannabis exposure among adolescents and young people is common and psychosis remains rare.

Despite highlighting the methodological difficulties of making causal inferences from observational studies, the article suddenly jumps to the conclusion that, "There is no doubt that a public health message that cannabis use is harmful is appropriate". This leads to today's Guardian editorial saying that what it calls the "small risk of a dreadful outcome", ie. psychotic breakdowns that "smash up lives and can lead to full-blown schizophrenia", is something "well worth a proper public health campaign".

Of course cannabis can cause harm, as can alcohol. But, as the article points out, it is important to have the facts right for any public health campaign to be effective. The causal link between cannabis and psychosis has not been proven.

Saturday, April 09, 2016

Psychosis can be organic in origin

I have been struggling with a post by Vaughan Bell @vaughanbell on the Mind Hacks blog. He suggests that critical mental health writings implicitly demean people with brain disorders, but I don't think they do.

He gives four quotes to support his argument. However, they don't seem to support it. In fact, the first two aren't about brain disorders. The other two mention organic brain problems but are not demeaning of people with these problems. If you don't believe me, look for more detail about these quotes in the appendix to this post.

Essentially, Vaughan Bell does not want to make too sharp a distinction between mental health problems and brain diseases. He thinks critical mental health supporters do this because having a brain disease is demeaning. This is totally missing the point. This isn't the reason for the argument that functional mental illness is not brain disease. In fact, Bell himself acknowledges that there is "no evidence for consistent causal factors". But he goes on to speculate that these factors will be found in the same way as they have for organic brain disease.

Where Bell might have a point is that supporters of the critical mental health approach do not always explicitly state that psychosis can be organic in origin. He uses the example of the BPS report Understanding psychosis, which he says doesn't discuss organic psychosis, although I have already pointed out that, despite its strengths, there are deficiencies with this report (see previous post). To be clear, people can have psychotic symptoms in a toxic confusional state (delirium) and with dementia, such as Alzheimer's disease.

But not being explicit that psychosis can have an organic cause is not the same as being demeaning about people with brain disease. Functional mental health problems are fundamentally social and psychological. It's as important to combat the stigma of organic brain disease as mental health problems.

Attempts have been made to undermine the critical mental health argument by accusations of attacking a 'straw man' (see Guardian article and my response). It seems opponents of critical mental health are not immune to using this form of argument.

Appendix to above

This post has been made as an appendix to the above post. I'm looking in more detail at the quotes Vaughan Bell used to try and justify his argument that critical mental health demeans people with organic brain disease.

The first quote is from Kinderman et al:-
such approaches, by introducing the language of ‘disorder’, undermine a humane response by implying that these experiences indicate an underlying defect
Here the authors of the quote are arguing that mental health problems should not be seen as disorders or pathologised, as they are better seen as understandable responses to difficult circumstances. I do understand what the authors are saying but I have commented before that such a way of viewing mental health problems may be potentially misleading (eg. see previous post). Generally the implication of identifying a mental health problem is that the person's reaction has been maladaptive. This is why the person has gone for help.

Although there is this debate about whether mental health problems should be seen as illness or disorder within the critical mental health movement, I don't see how this quote supports Bell's argument that people with brain disorders are being demeaned by a critical mental health approach. The quote is not talking about people with brain disorders - in fact, it's saying that mental health problems are not brain disorders.

The second quote that Vaughan Bell gives is from Mary Boyle:-
The idea of schizophrenia as a brain disorder might offer further comfort by distancing ‘normal’ from disturbing people. It may do this by placing disturbing people in a separate category and by suggesting uncommon process to account for their behaviour…
Bell seems to have problems with the idea of "distancing". What Mary means is that reducing mental health problems to brain disease may be a way of protecting others from the pain the person is experiencing. Surely this is correct. Again, this quote isn't about people with brain disease.

The third quote is from Lucy Johnstone:-
The fifth category… consists people suffering from conditions of definitely physical origin… where psychiatric symptoms turn out to be indications of an underlying organic disease… medical science has very little to offer most victims of head injury or dementia, since there is no known cure…
Here, Lucy is talking about people with brain disorders. What she is saying is correct that medicine in the literal sense can't cure organic disease. What she goes on to say, which isn't quoted, is that behavioural and social interventions are what is needed. Again, this is correct and isn't being demeaning of people with organic brain disorders.

The final quote is from Doing psychiatry wrong:-
To be sure, these brain diseases significantly affect mental status, causing depression, psychosis, and dementia, particularly in the latter stages of the illness. But Andreasen asks us to believe that these neurological disorders are “mental illnesses” in the same way that anxiety, depression, bipolar disorder, and schizophrenia­ are mental illnesses. This kind of thinking starts us sliding down a slippery slope, blurring distinctions that must be maintained if we are to learn more about why people are anxious, depressed, have severe mood swings, and lose contact with reality.
This quote is saying there is a difference between organic psychosis and functional mental illness, which is correct (eg. see previous post). Again, this isn't demeaning of people with organic brain disorders.

Friday, April 01, 2016

What does it mean to say that psychotherapy is a biological treatment?

BJPsych editorial this month argues that the target of psychotherapy, like pharmacotherapy, is diseased neural functioning. It does recognise that the method of delivery of these said neurobiological changes is different, with pharmacotherapy seemingly working through chemical changes and psychotherapy through the patient-therapist relationship. It starts from the assumption that the brain disease model of mental illness is valid and therefore tries to justify psychotherapy as a treatment by viewing it as biological like pharmacotherapy.

I've commented before on such neuromania (see previous post). Raymond Tallis uses this term 'neuromania', which he critiques, in his book Aping mankind. People do seem to be taken in by such nonsense which is neo-phrenological phantasy (see another previous post).

The problem is that the disease model of mental illness is not valid. Mental phenomena are meaningful. Of course this doesn't mean that mental phenomena don't have a biological substrate. But neuroscience can't tell us anything about the meaning of that biological substrate. If there has been any advance in neurobiology over recent years, it is in recognising the dynamic nature of the brain. Brain cytoarchitecture is fashioned by the social environment but this should lead to an integrated understanding of mind and brain, not promotion of the brain disease model of mental illness.

To suggest that psychotherapy might correct neural functioning presumes that we know what the abnormality was in the first place. However, we don't know the neurobiological basis of mental illness because the abnormality is functional rather than structural. Mental function is not well localised in the brain. In the nineteenth century phrenology attempted to map mental functions onto the outside of the head. This may seem ridiculous now but neuroimaging provides no better explanations. We knew about the limbic system, prefrontal cortex and reticular activating system, for example, before neuroimaging. To suggest that psychotherapy is a biological treatment is counterintuitively stupid not clever. The mind-body problem can't be solved by calling it a myth.

Tuesday, March 29, 2016

Psychiatry is still biomedical, even if not "narrowly biomedical"

Simon Wessely in a Guardian article says that psychiatry does not recognise the narrow biomedical way in which it is sometimes portrayed. Despite what he says, some psychiatrists are narrowly biomedical (see extract from my book chapter). However, I do agree that most psychiatrists are generally more pragmatic.

It's interesting that Simon is an acolyte of Anthony Clare, whose book Psychiatry in dissent was written to create a consensus after the anti-psychiatry debate of the 1960-70s. Clare wanted to avoid psychiatrists having to adopt a model of mental illness (eg. see previous post). This led to the common claim, which I suspect Simon would support, that psychiatrists adopt a biopsychosocial approach to practice (eg. see another previous post).

The problem is that even though most psychiatrists are not narrowly biomedical, they are still biomedical (see my edited book Critical psychiatry). They generally believe that mental illness, at least major mental illness, such as schizophrenia and bipolar I disorder, is due to brain abnormalities, even though the evidence is against this conjecture. It's about time a president of the Royal College of Psychiatrists addressed this issue rather than avoiding and deflecting it, but I don't think Simon will.