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.