Friday, April 07, 2017

An experiment in unstructured living for people with mental health problems

The film Mad to be normal was released yesterday. Almost my first post on this blog was about the plans for this film. As Bob Mullan explains (see iNews article), it has been a "long-gestating project". I first heard about it from him in 2006.

I haven't seen the film yet, but I thought it may be worth saying something about Kingsley Hall (see Guardian article), on which the film focuses. Kingsley Hall was the first of several therapeutic community households established by the Philadelphia Association, a charity founded in 1965 by R.D. Laing, David Cooper (although Cooper had nothing more to do with the project after it started) and others. (See extracts on Laing and Cooper from my book chapter 'Historical perspectives on anti-psychiatry'). Laing lived at Kingsley Hall for 18 months in 1965/6. It was an experiment in unstructured living and sought to allow psychotic people the space to explore their madness and internal chaos. It did not attempt to ‘cure’ but provided a place where "some may encounter selves long forgotten or distorted" (Morton Schatzman in Laing and anti-psychiatry).

The local community was mostly hostile to the project. Windows were regularly smashed, faeces pushed through the letter box and residents harassed at local shops. After five years, Kingsley Hall was largely trashed and uninhabitable. Even for Laing, Kingsley Hall was "not a roaring success" (Mullan, 1995). Laing’s dream of a place "without those features of psychiatric practice that seemed to belong to the sphere of social power and structure rather than to medical therapeutics" was only partially successful, even from his own perspective (Laing, 1985).

Kingsley Hall was designed to give people freedom from the social control of psychiatry. As I wrote in my chapter in Liberatory psychiatry, its association
with the counterculture of the 1960s and 1970s may have helped to propel anti-psychiatry into the limelight. It may also have contributed to its demise. Without this cultural support, anti-psychiatry seemed to lose its popular appeal. Also, some of its major proponents, such as Laing, were more obviously interested in personal authenticity than changing psychiatry practically. After Kingsley Hall, Laing went on retreat to Ceylon and India to pursue his interests in meditation, Buddhism and Hinduism. Later in life, Laing (1987) regarded his main achievement as being in the area of social phenomenology in philosophy, not psychiatry. Generally, anti-psychiatry is seen as having had no lasting influence on psychiatry and its practice (Tantam, 1991). For all its calls for liberation, these aspirations were largely sidelined into promoting personal and spiritual freedom with little interest in redeeming psychiatry itself. This diversion helped to allow mainstream psychiatry to marginalise anti-psychiatry’s influence.

I have always said that critical psychiatry has its origins in anti-psychiatry (see eg. my letter). The Philadelphia Association has survived over 50 years and still runs two community houses (see my book review of Testimony of experience). Critical psychiatry has sought to avoid the marginalisation that anti-psychiatry experienced and is looking for acceptance of its position from mainstream psychiatry. Even Laing probably ultimately sought the endorsement of the psychiatric profession as demonstrated by his wish to be professor of psychiatry in Glasgow towards the end of his life.

Thursday, March 30, 2017

Genuine interdisciplinarity in neuroscience research

I have been reading Neuro by Nik Rose and Joelle Abi-Rached. Like me (see previous post), they hope that neuroscience can become a genuinely human science. I like their notion of 'critical friendship' between social sciences and neuroscience. Some of the proper motivation for this friendship may be to share the money going into neuroscience research. It may also be important not to minimise the degree to which neuroscience funding is being wasted on the unattainable. However, there is a need for genuine interdisciplinarity to take the neuroscience research agenda forward. As they say:-
[W]e should not be surprised to find, in contemporary neurosciences, all the features of inflated expectations, exaggerated claims, hopeful anticipations, and unwise predictions that have been so well analyzed in other areas of contemporary biotechnologies.

Social sciences have nothing to fear about the 'neuro-turn' in modern culture (see previous post) and polarised attitudes in the debate are unhelpful (see another previous post). Pressures to translate research findings to clinical applications are also creating perverse effects. To quote again from Neuro:-
Neuroscientists might well be advised to be frank about the conceptual and empirical questions that translation entails, rather than suggesting that the outcome of a series of experiments with fruit flies or feral rats has something to tell us about human violence, or that brain scans of individuals when they are exposed to images of differently colored faces in an fMRI machine has something to tell us about the neurobiological basis of racism.

I also agree that the neuro-turn may be affecting how we view ourselves but that it "is too early to diagnose the emergence of a full-blown ‘neurobiological complex,’ or a radical shift from psy- to neuro-". Critical psychiatry has something to offer to the Neuroscience Project at the Royal College of Psychiatrists (see previous post).

Saturday, March 25, 2017

The faith of mainstream psychiatry

As I've said before (eg. see previous post), it seems obvious to most people that mental illness is due to brain disease. Critical psychiatry doesn't stand a chance! It must be wrong to question this assumption. But, of course, critical psychiatry isn't saying that mind and brain are separate (see previous post). What it is saying is that minds are enabled but not reducible to brains. It's got the weight of philosophy behind it.

Furthermore, it is also saying that the assumption that mental illness is due to brain disease is not based on logic, but rather on faith, desire and wish fulfilment. As I've also said before (see previous post), psychiatry is more like a religion than a science. It's much simpler to believe that brain pathology is the basis for mental illness and that its nature and cause will eventually be discovered. Believing this can be a way of justifying psychiatric treatment.

Actually, there's no need to justify treatment in this way. Mental health problems exist and professional expertise may be beneficial in treatment. The problem is that objectifying people through reducing their problems to brain disease make make psychiatry part of the problem rather than necessarily the solution to these problems.

Tuesday, March 14, 2017

The contested nature of psychiatry

Charles E. Rosenberg has an interesting paper on how psychiatry expanded in the last third of the 19th century to "include an ever-broader variety of emotional pain, idiosyncrasy, and culturally unsettling behaviors". Our modern somatic understanding of illness had to accommodate older "[h]umoral explanations of temperamental peculiarity", such as hypochondriasis, hysteria and melancholy. It began to do this at the beginning of the 19th century, by, for example, Benjamin Rush seeing hypochondria as having a corporeal cause. These "reductionist, mechanism-oriented, and antivitalist" ways of viewing illness created hypothetical disease entities, such as neurasthenia, regarded by George Beard in 1869 as a somatic condition which would eventually be confirmed by postmortem pathology.

As Rosenberg says:-
The dominance of reductionist styles ... has an extraordinarily salient place today. We have never been more infatuated with visions of molecular and neurochemical — ultimately genetic — truth.
As he also says, "yet at the same time we are reflexive [and] critical ... in our approach", even if this is a minority perspective. As discussed in my previous post, psychiatry is polarised about the nature of mental illness. Psychotropic medication has helped legitimate the specific disease entity model of mental illness. This is a "phenomenon that is always in process, always contested, and never completed". With the expansion of the "range of human dilemmas that we ask medicine to address", to quote from Rosenberg:-
[I]t is ... inevitable that the powerful concept of disease specificity has been — and will continue to be — employed as a tool for the ideological management of problematic emotions and behaviors.


(With thanks to a tweet from Richard Hassall)

Monday, March 13, 2017

Polarisation in the debate about mental illness

I have mentioned Mike Owen in a previous post. In a recent blog, he argues for less polarisation in the debate about the nature of mental illness. I couldn't agree more.

However, Mike does need to represent his opponents correctly if there is going to be a rapprochement. He says, "They assume, implausibly, that mind and brain are separate entities rather than different aspects of the same thing". This isn't true. The argument being made is not Cartesian. As Steven Rose says, "That brains enable minds is uncontroversial. That they 'are' the mind is a reductionism too far" (see Lancet article).

Similarly, Mike also says "They also fly in the face of a large body of evidence indicating the importance of genes and altered brain states in contributing to disorders of mental health". Again, not true. The critiques are evidenced-based. Genes, of course, set the boundaries of the possible but environments define the actual. More caution is needed in interpreting so-called altered brain states.

It is important that Mike understands what people are saying who are critical of his view. As Steven Rose says, people like Mike should not "dismiss without a backward glance not only millennia of philosophical debate but also a huge current literature on mind/brain relationships". There is a "conceptual innocence" about his position, although he is, of course, trying to dismiss any criticism. Despite what he may think, modern psychiatry has not solved the mind-brain problem.

Thursday, February 23, 2017

What does it mean to say that antidepressants don't work?

Like Carmine Pariante, I have treated thousands of patients since I started as a trainee psychiatrist in 1985 and became a consultant over 25 years ago (see post on my personal blog). He is convinced that antidepressants work (see article), whereas I am more sceptical. He's correct that I'm in a minority. The trouble with relying on personal experience is that we can delude ourselves.

Pariante does recognise that "about one in three patients with serious clinical depression who takes them doesn't get better". Actually what he means is that about a third of patients do not seem to be helped in clinical trials. These trials are only short-term and people on antidepressants are compared with those taking placebo. About a half of patients in the clinical trials taking placebo also seem to improve. It's, therefore, misleading to imply that two-thirds of patients are getting better because of antidepressants (see post summarising evidence of outcomes with antidepressants). The difference between active and placebo treatment in clinical trials is much smaller than most people realise. In fact it's so small it could be an artefact (see previous post). 

Friday, February 17, 2017

Buying into idea of chemical imbalance causes psychotropic medication discontinuation problems

As mentioned in my previous post, I have been reading The sedated society: The causes and harms of our psychiatric drug epidemic edited by James Davies (2017). The chapter by Luke Montagu, entitled "Desperate for a fix: My story of pharmacetical misadventure", describes the problems he had discontinuing psychotropic medication after "having bought into the idea of a chemical imbalance" when he was taking medication. Luke's father is the Earl of Sandwich, and one of the co-chairs of the All Parliamentary Group for Prescribed Drug Dependence (see previous post). As Luke says:-
[P]sychiatry, in league with the pharmaceutical industry, chooses to perpetuate two fundamental hoaxes. The first ... is that the suffering we call mental illness has a biological basis, like cancer or diabetes, caused by an imbalance of chemicals in the brain ... The second hoax follows on from the first, namely, that today’s drug treatments target and correct this chemical imbalance, just like antibiotics fight infection or insulin treats diabetes.
He goes on:-
One day these beliefs and treatments will seem as misguided as the theory of the four humours, when bloodletting, blistering and purging were believed to restore the correct balance of blood, phlegm and bile
As I said in my previous post, historically it helps to see the chemical imbalance theory as a myth, as it's wrong like humoral theory. I hope Luke's right that it will be found to be misguided, but there are powerful reasons why people do believe it (see eg. previous post). Maybe one of the major reasons for getting rid of it is to prevent people developing discontinuation problems.

Wednesday, February 15, 2017

Social construction of childhood depression

Sami Timimi, in his chapter "Starting young: Children cultured into becoming psycho-pharmaceutical consumers - The example of childood depression" in The sedated society (2017), describes how SSRI antidepressant prescribing for young people has increased, apart from a hiatus around 2004 because of concerns at the time about lack of efficacy and increased suicidality. Despite these concerns, prescribing has continued to increase by arguing in a biased way that the benefits of antidepressants outweigh the risks.

As Sami says:-
It was only relatively recently (in the late 1980s) that our understanding of childhood depression began a far-reaching transformation. Prior to this childhood depression was viewed as a very rare disorder, different to adult depression and not amenable to treatment with antidepressants ...  A shift in theory and consequently practice then took place as influential academics claimed that childhood depression was more common than previously thought (quoting figures such as 8–20% of children and adolescents), resembled adult depression, and was amenable to treatment with antidepressants.

Sami tries to relate this construction of childhood depression to child-rearing practices. I tend to prefer the simpler explanation that it reflects our belief in the chemical cure. I suppose the view in which I was schooled that childhood depression is uncommon and different to adult depression was also socially constructed (see previous post). However, as I said in my BMJ letter, I don't want to get too hung up about whether childhood depression exists. The problem is when it is seen as a biological entity for which antidepressants are indicated.

Monday, January 30, 2017

Meyerian history and examination in psychiatry

I mentioned the article about One hundred years of psychiatry at Johns Hopkins in my previous post. The article focuses on how Adolf Meyer developed an organised approach for history taking and mental state examination in psychiatry, which became standard in the US. It was taken over by the Maudsley Hospital in the UK, again becoming standard (see previous post and my review of most recent edition of The Maudsley handbook of practical psychiatry). However, as the article points out, the "meyerian history and examination ... is little used in the United States today as it is often judged to be too time-consuming".

The clinican comes to a formulation at the end of the history and examination, of which a differential psychiatric diagnosis is merely one element. Some may see formulation as more opposed to psychiatric diagnosis (see previous post), but formulation should, as the article says, summarise "the story focusing on the salience of the problems and context - how has the problem developed, interrupted, and/or distorted the patient's life trajectory".

The article discusses why psychiatry does not focus on the meyerian history and examination in a comprehensive and systematic way, and is, therefore, not as patient-centred as it should be (see previous post). One reason is that too many influential psychiatrists are research-based, rather than being involved in routine clinical care settings. Today's medicine doesn't teach a broad enough basis "for knowing our patients and partnering with them in patient care". Meyer made these methods explicit. This is a "truly personalized medicine, distinct from the ongoing extension of the disease model at a molecular level, which is commonly referred to as individualised or precision medicine" (see eg. previous posts The gap between neural circuits and understanding people and Psychiatric research folly).

Critiquing the neuro-turn

Roger Cooter has an article on why the neuro-turn in popular and academic culture needs to be taken seriously. I tend to regard it as 'neo-phrenological phantasy' (eg. see  previous post), but Roger cautions against being "so lightly dismissive". The neuro-turn may be affecting how we view ourselves. Furthermore, it seems to be beyond criticism, or, as Roger puts it, "the neuro-turn stymies ... its own critique".

As an example, another recent paper I have read is about One hundred years of psychiatry at Johns Hopkins. Whilst discussing the heritage of Adolf Meyer and Paul McHugh for current american psychiatry, it suggests that, "One happy byproduct of current research is that ... the competitive jousting between the 'biological' and psychological' ...[has] dissipated". It goes on:-
It has proven difficult to maintain such debates when research now shows the human brain responding robustly to all manner of psychological, pharmacological, and stimulatory interventions.
So, I've been wasting my time trying to encourage this debate! Studies that literally 'light up the brain' have shut down the argument.

Roger describes the attractions of an ahistorical, posthumanist worldview, which may help to mediate neoliberal politics. At least he concludes that critique is even more "vital and urgent". So, maybe I need to keep going.

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.