Attracting people into psychiatry

Thomas Insel, in his NIMH Director's blog, views clinical neuroscience as the answer to psychiatry's recruitment problem. The dean of the Royal College of Psychiatrists, Rob Howard, has also said that recruitment into psychiatry is at a crisis point (see his May 2009 newsletter). Solutions were discussed at a London division academic day (see Frontier Psychiatrist blog).

The problem with Insel's remedy  is that too many young psychiatrists, if they believe him, will become disillusioned. He makes reference to an NIMH Neuroscience and Psychiatry module Translating neural circuits into novel therapeutics, which suggests that impaired GABA neurotransmission in chandelier neurons in the dorsolateral prefrontal cortex contributes to cognitive impairments in schizophrenia, which may be corrected by an agonist for GABA_A alpha 2 subunit receptors. The module mentions a small RCT using such a drug, MK-0777, which seemed to find evidence of improved performance on memory tasks, but doesn't mention a larger scale study which failed to show any improvement in cognition.

Putting on one side that cognitive impairment in schizophrenia may well be functional, the complexity of speculation is supposed to excite people into understanding the pathological basis of psychiatry so that they can develop so-called rational treatments that then undergo rigorous testing. But are hypothetical, wishfulling phantasies really going to attract a new batch of recruits?

Personally, I suspect we need to remind ourselves of the interest in psychiatry which Aubrey Lewis stimulated at the Maudsley Hospital Medical School after he was appointed Professor of Psychiatry in 1948. For him, postgraduate psychiatry should be for "ardent, critical, lively, disputatious and reflective, eager minds" (Lewis, 1947). He encouraged a sceptical approach to psychiatry. He had little patience for imprecision or poorly thought-out ideas.

As Michael Shepherd pointed out in a BJPsych article, "Throughout his professional life Sir Aubrey was at all times an educator who was much concerned with the problems of recruitment into psychiatry, more especially with quality rather than quantity." Doctors with open minds, who are sceptical of psychiatric quackery, need to be attracted into psychiatry.

Whistling in the wind

Edward Shorter, in his response to an article by Thomas Szasz, says there are solid biological findings in psychiatry. Shorter, who I've mentioned in a previous post, is the Hannah Professor of the History of Medicine at the University of Toronto. In 1996 he was cross-appointed to a professorship in psychiatry. As a non-clinician, has this professional association gone to his head?

The examples he gives of "obvious evidence" are the role of panicogens in triggering panic disorder; the response of catatonia to barbiturates and benzodiazepines; and what he calls the reliable accompanying of melancholic depression by hypothalamic-pituitary-adrenal dysregulation, as reflected in high levels of serum cortisol, a positive dexametasone suppression test (DST) and a shortened rapid eye movement sleep latency.

The reference Shorter gives for the importance of panicogens is from the proceedings of the 32nd annual meeting of the American Society of Clinical Investigation held in Atlantic City on 6 May 1940. In this study, patients with anxiety neurosis were found to increase sighing respiration more than controls when exposed to carbon dioxide and rebreathing. The feelings that they had during this rebreathing tended to resemble or be identical to their panic attacks. Shorter suggests that studies such as this were marginalised because of the influence of psychoanalysis. He doesn't make any mention of the controversy in the literature about the mechanism of action of lactate, which has been seen as the common pathway for the mechanism of action of carbon dioxide and several other panicogens.

The reference he gives for the evidence of the organicity of catatonia was a study of 4 cases, which were actually thought to be neuroleptic-induced, which responded to intravenous lorazepam. Shorter also mentions the response of catatonia to barbiturates. William Bleckwenn's use of intravenous amobarbital to produce lucid intervals in catatonic patients quickly led to the development of the so-called "truth serum".  How's this proved the organic basis of catatonia?

The reference Shorter gives for the biological basis of melancholic depression is his own recent book, written with Max Fink, entitled Endocrine Psychiatry. Fink has been an advocate of ECT over the years. I need to read the book. The DST was rejected as a biological marker because it was insufficiently sensitive and specific. I know that Fink thinks it shouldn't have been rejected, but this does seem to be a very idiosyncratic view. I'll come back to this when I've read the book.

Shorter seems to be using his historical expertise to suggest that modern psychiatry has overlooked evidence of its biological basis. As I have repeatedly said, please do not misunderstand me. Of course mental illness has a biological basis, as does our "normal" behaviour. But to be suggesting that biological markers have been established, or even overlooked in history, is whistling in the wind. This is what Shorter accuses Szasz of doing by claiming the opposite. As Szasz makes clear in his article, what he is stating is what he calls an "analytic truth", not dependent on scientific research.

Furthermore, Shorter suggests views such as those of Szsaz (he actually says the makers of the movie One flew over the cuckoo's nest) have led to many people committing suicide because they've avoided treatment. Not surprisingly, he doesn't give any reference for this opinion. As I've commented in a previous post, it's a pity debates such as this get so polarised.

And I'm not saying this because I totally agree with Szasz (eg. see my book review). But on the point on which Shorter has attacked him, he's correct. Shorter may be right that mainstream psychiatry now acknowledges a neurological basis for much psychiatric illness, whereas when Szasz was first writing psychoanalysis was more influential (see my article). But it's just as wrong to take a biomedical view now as it was then.

Where should first meeting of International Critical Mental Health Movement be held?

In a previous post I mentioned the idea of setting up an International Critical Mental Health Movement. Is there any momentum for this? I'm happy to help organise the first conference. Where should it be held?

Why did the balance between the genders for psychiatric detention switch?

Kate Millett, the feminist and survivor of mental health services, at a seminar organised by Anthony Stadlen that I attended last Sunday, said that more women than men are detained in psychiatric hospital. My thought, although I did not have the figures, was that in fact more men, particularly young men, are detained because of their violence.

It seems we were both right in a way. Up to 1994-5, when Kate Millett was surviving mental health services, more women than men were formally admitted under civil procedures using the Mental Health Act in the UK. After that time more men were detained (Audini and Lelliott, 2002). And it is particularly younger men where there is the imbalance (see figure). And once admitted they tend to stay in hospital longer, as the ratio of men to women resident in hospital at any one time is even higher (see table).

There does not seem to have been much comment about this switch. Women's disadvantaged social status is commonly seen as a factor generating mental health problems, but this doesn't explain the rise in men being detained. Maybe the emphasis over recent years on risk management and accountability is responsible. Ideas please and I'd also be interested in any references in the literature as I can't easily find them.

There should be concern if children are being prescribed medication as a quick fix.

As I mentioned in a previous post, reviewers have been critical of Richard Bentall's book Doctoring the mind for taking aim at child psychiatrists. They also suggest that he characterises psychologists as better educated and trained than psychiatrists to "understand people and the human experience and to provide healing therapy".

I'm not sure if this is the case, but I do know that psychiatrists are more likely to take a biomedical rather than biopsychological approach. I'm a member of both the Royal College of Psychiatrists and the British Psychological Society (see my talk Psychiatrists can have understanding too).

And, it's the British Psychological Society that has supported a call for a national review of the use of medication to treat children’s behavioural issues (see Treating children's behaviour). Peter Kinderman, Chair of the Division of Clinical Psychology, seems confident that psychiatry colleagues would be equally concerned if there is evidence of inappropriate use of drugs or medication.

I don't know how much these sort of reviews achieve. A previous technical report for MPs is a bit out of date now. Still Richard Bentall is concerned that there is inappropriate use of medication, whereas it seems Peter Kinderman would only be concerned if there was. Perhaps we do need an authorative view to let us know. And the reviewers criticised Richard for not providing a reference to back up his view, so he would at least then have one.

Facts about NAMI funding

In my previous post, I noted that reviewers of Richard Bentall's book Doctoring the mind, which I recommend on my Critical Psychiatry website book recommendations page, criticised him, amongst other reasons, for indicating that the National Alliance on Mental Illness (NAMI) is funded primarily by Big Pharma. According to an article in the NewYork Times, "drug makers from 2006 to 2008 contributed nearly $23 million to the alliance, about three-quarters of its donations".

NAMI now lists on a quarterly basis in its website registry all major corporate and foundation grants and contributions above $5,000. What NAMI emphasises is that, as a matter of policy, it does not endorse any specific treatment or service.

NAMI-Vermont has recently decided to diverge from national policy and no longer accept direct corporate contributions from pharmaceutical companies (see message to the membership). On their website, NAMI-Vermont Board President Ellen Vaut of South Burlington explains: “Though NAMI-Vermont has only received between three and seven percent of its total revenues from pharmaceutical companies in each of the past six years and none during the past fiscal year, we voted to dispel any concerns or public perception that our programs and/or organizational practices are influenced by pharmaceutical company money.”

I guess that the national organsiation will find it difficult to follow this lead because of the higher proportion of pharmaceutical funding. Still, quite why the reviewers of Richard's book criticise him for stating the truth is not clear. Perhaps the truth is "incendiary and divisive".

More heat in the debate about psychiatry

A review in Psychiatric Services is reluctant to recommend Richard Bentall's book Doctoring the Mind because it is said to be "incendiary and devisive". The reviewers are frightened that the book exaggerates issues for service users.

I'm not sure who's doing the exaggerating. Richard is said to suggest that there is a long-standing battle for supremacy between psychologists, "who are educated and trained to understand people and the human experience and to provide healing therapy", and psychiatrists, who are "indoctrinated with the medical model, have unwittingly carried Nazi-era notions of the genetic origins of psychosis into the present and are intent on pumping people full of as much useless, dangerous medicine as possible while simultaneously avoiding any conversation".

Richard is also criticised for saying that as many as 50% of psychotic patients would be better off without taking drugs, for claiming that the term "schizophrenia spectrum disorder" was introduced to get the results wanted in genetic research and for indicating that the National Alliance on Mental Illness is funded primarily by Big Pharma. Furthermore, he is said to provide no reference for his suggestion that child psychiatrists do not seem to be troubled by the as yet unknown long-term impact of psychotropic drugs on the developing brain and for his impression that medications are often prescribed by child psychiatrists without any serious attempt to understand or remedy the awful social circumstances in which psychologically disturbed children often live.

It's unfortunate that Richard's argument noted by the reviewers that "the case for a genetic cause of mental illness has been overstated by psychiatrists and that symptoms are much more the result of psychosocial stressors" including behaviour by families, gets lost in this polarisation of the debate. As I've indicated in a previous post, there seems to be some difficulty in having a calm discussion of these matters.

There were even some flames about my own Critical Psychiatry book (see another previous post), although I never managed to get a review in a mainstream psychiatric journal. Still there was a reasonably generous BMJ review. So maybe we should be grateful that books such as Richard's are at least being considered, even if dismissed, by mainstream psychiatry..

Is deep brain stimulation promising?

Deep brain stimulation (DBS) involves placing one or two thin wires into specific locations deep within the brain and then connecting the wires to a battery situated just beneath the skin. A recent article in the American Journal of Psychiatry reports on the  follow-up of 20 patients who received DBS for treatment-resistant depression.

Unfortunately two of these 20 patients died from suicide and one died from colonic cancer. As I said in my psychiatric update for Openmind, there is no clinical trial data about the effectiveness of DBS. I'm sure case reports, such as the latest article, will be used to justify continuing experimentation with it, however limited. I just wish that psychiatry could focus its efforts on providing more hope and effective treatment than DBS.

What should alternative to biomedical model be called?

Tim Thornton has posted a chapter on his In the Space of Reasons blog entitled "The recovery model, values and narrative understanding ". He points to the confusion about the meaning of recovery, and even more so about what a recovery model might be.

As I wrote in my paper "Redressing the chemical imbalance", the concept of recovery is inherently critical of the biomedical model, and Tim Thornton seems to agree with me. I think the problem is its acceptance into official policy and nullification of its impact by interpretation within the biomedical context.

The use of the term 'recovery model' is unlikely to help fully define an alternative psychosocial paradigm. Nor, despite its merits, do I think the notion of 'narrative' will either. I've always said that the origin of the psychosocial approach was with Ernst von Feuchtersleben's The principles of medical psychology, first published in german in 1845 (see my article).

An optimisitic moralism, such as an emphasis on recovery, has always had its moments, perhaps particularly identified in the progressive outlook before the First World war. This can be contrasted with the materialism of an emphasis on structural pathology, producing a therapeutic pessimism, minimising the potential of people to change. It is important to give people hope in mental health services. This strand is one of the sources for a psychosocial alternative to the biomedical model, but I think it's unlikely to define the whole paradigm.

Has the concept of bipolar spectrum been broadened too far?

Catherine Zeta-Jones booked herself into a clinic for 5 days for treatment of her bipolar II disorder (see Guardian story). I don't want to underestimate the emotional impact of dealing with her husband's throat cancer. She has been praised for raising the profile of mental health issues.

One issue that might be worth commenting on further is the way in which the concept of bipolar disorder has been expanded since it became the new name for manic-depressive illness (see my book review for some background). I'm not saying that Catherine Zeta-Jones doesn't have bipolar II disorder, but it might be worth understanding what this diagnosis means.

The expansion in the concept of bipolar spectrum is not dissimilar to what happened to schizophrenia in the 1960s and 70s, particularly in USA, leading to the American Diagnostic and Statistical Manual in its third revision tightening up the definition, so that it was more reliably applied. People may find it helpful to put a label to their mental health problems, but I do have concerns that the diagnosis of bipolar spectrum has become so variable that its validity must be in question.

I've been dismissed as "postmodern" for this sort of questioning of the nosological basis of bipolar depression (see comments following another book review, also previous blog entry). What I am clear about is the need to avoid reification of psychiatric diagnosis. There's always a danger that we tend to assume that a diagnostic concept implies an entity of some kind. But a diagnosis is not a "thing". It's merely an abstract device which is useful for thinking about mental health issues.

I just have concerns that bipolar depression is not as useful as some people make out. And I don't think the argument can be dismissed that one of the reasons people have found the new concept useful is because of the development of so-called mood stabilising medication. There's even been a marketing ploy to develop medication specifically for bipolar depression (see previous blog entry).

Don't get too heated in the debate about psychiatry

Two reviews in Psychiatric Services recommend reading Robert Whitaker's book Anatomy of an Epidemic even if it makes you angry and you want to dismiss him as an anti-psychiatric activist. It's apparently good to read biased, flawed books like this to be able to marshall a response to defend psychiatry. Let's please have this debate. It's not really dealing with the issues by just expressing disappointment that Whitaker blames biomedical psychiatry and suggesting he's illogical to connect the taking of medication with poor outcomes.

Actually, I think all he's asking for is a debate about how drugs increase the risk that people will become chronically ill (see previous post).

Challenging myths about psychiatry

Nada Stotland was the 2008-9 President of the American Psychiatric Association. She writes on Huffpost Health challenging "myths about psychiatry". The trouble is she has promoted just such a myth. She writes, "Using brain scans ... we now can distinguish between the brain of a person with depression and a person who is not depressed". Evidence please. And perhaps she could explain what the "many, many other such observations" are.

Political nature of psychiatry

Interesting seminar last week, which I attended, organised by Tony Stadlen, invited Vladimir Bukovsky, the anti-communist, to talk about his experiences of being detained in psychiatric hospital in the Soviet Union. Luckily for him, he was never given psychiatric medication and there was a dispute amongst psychiatrists about his diagnosis.

His case nonetheless highlights, which Bukovsky himself did, the political nature of psychiatric diagnosis and its potential for misuse. In Soviet psychiatry, the particular problem was the development of diagnoses such as sluggish or creeping schizophrenia and paranoid development of the personality, and the Soviets withdrew from the World Psychiatric Association for a while because of criticisms of their political abuse of psychiatry. People who do not fit into society are at risk of being regarded as mentally ill and such a mechanism can be exploited by the state.

Many factors affect the number of antidepressant prescriptions dispensed in particular areas

The Guardian has published a map of GP antidepressant prescribing. Its article based on the data makes a lot of the finding that it tends to be Northern parts of England with higher numbers of prescriptions.

However, as the care services minister commented, "There are many factors that affect the number of antidepressant prescriptions dispensed in one particular area". For a start the Guardian data is not age standardised. There are significant differences between GP practices in the same area, which can be greater than the average differences between areas. The article doesn't mention the high rates in Norfolk and Waveney where I work.

Deprivation is likely to be a factor in prescribing as mental health need is correlated with deprivation. Pharmaceutical company marketing influences cannot be ignored.

Rank order of antipsychotics for producing weight gain

A review in the Archives of General Psychiatry looks at the evidence for weight gain and changes in other cardiovascular risk factors caused by antipsychotic treatment. It has produced a rank order of the different drugs with olanzapine noted to cause more weight gain than all other second-generation antipsychotics except clozapine. Clozapine causes more weight gain than risperidone, risperidone more than amisulpride, and sertindole more than risperidone. The average weight gain after 6 to 8 weeks taking olanzapine was found to be 5 to 6 kg, which was significantly higher than the average weight gained while taking risperidone (4 kg) or haloperidol (3 kg).

Antipsychotic medication does seem to reduce brain volume

I have mentioned a study in a previous blog entry that seemed to show that antipsychotic medication reduces brain volume. This study was referred to in an interview with Nancy Andreasen. The point I was making in the previous entry was that the research had been "sat on" for fear it may lead to people stopping their medication.

The study has now been published in the Archives of General Psychiatry. The authors mention, as I did in my previous blog entry, that an association does not necessarily mean a causal connection. However, the evidence is quite strong considering that illness severity and substance misuse had minimal or no effects and data from animal studies also suggests brain tissue loss.

Of course we have known for some time from clinical evidence that antipsychotics cause brain damage in that tardive dyskinesia is not necessarily reversible when antipsychotic medication is discontinued. This is reflected in the finding of a specific increase in size in the putamen in the present study. We don't know that brain changes are necessarily "bad" for patients, but, as the study itself concludes, we have to entertain the possibility that antipsychotics may have potentially undesirable effects of brain tissue volume reduction.

Understanding psychosis

This post has the same title as the latest post from the Healthy Minds. Health Lives blog, my favourite for commenting on because it is published under the auspices of the American Psychiatric Association (APA) (see previous post). The APA blogger suggests that it helps to understand psychosis by recognising its connection with the brain. Does it really? It's merely tautologous. Of course it's something to do with the brain. So what? Knowledge of the brain doesn't give any understanding about personal and social factors.

Actually understanding the irrational may require more than being logical. What makes us think that someone is mentally ill may be that what they are saying is difficult to follow and understand. It makes us think there is something wrong mentally. It doesn't help to wishfully speculate about brain processes when what is required is considerable effort to understand why someone may have crazy experiences and express themselves in a mad way. We don't live in the real world for all sorts of reasons, including our own convenience about understanding the world. And it suits the APA blogger to have her biomedical belief about psychosis.

Menacing cloud hovering near prospective patients

Seroquel is the best-selling psychiatric medication in the US and, as pointed out in a feature in Medical Marketing and Media (MM&M), its patent is due to expire in 2012. Its manufacturers, AstraZeneca, last year reached an agreement to settle US product liability litigation over Seroquel for about $198 million (see Wall Street Journal article). Earlier in the year it also paid $520 million to resolve allegations that it marketed regular Seroquel for off-label uses between 2001 and 2006.

However, this doesn't seem to matter to Astrazeneca financially with global Seroquel sales of $4.9 billion in 2009. And it is MM&M's Large Pharma Marketing Team of the Year. It has approval for an XR formulation which extends the use of the drug under patent. This formulation has been approved as an add-on to antidepressants for the treatment of major depressive disorder. 

There's a full page advert for it on the back of this week's BMA News, which does not use the cloud as in the US campaign. The image of the depressed woman curled up in her kitchen unable to do her washing, which is used to advertise seroquel XL (it's called XL, not XR, in the UK) to UK doctors, for some reason seems to be different from that used for direct-to-consumer US advertising.

Off-label use of atypical antipsychotics

A Reuters report based on an article in Pharmacoepidemiology and Drug Safety suggests atypical antipsychotics are overused. The article looked at trends in outpatient prescribing in the US. Antipsychotic use for indications without FDA approval increased between 1995 and 2008 with an estimated cost associated with off-label use in 2008 of US$6.0 billion. Atypical use has grown far beyond substitution for the now infrequently used typical agents.

(With thanks to Vince Boehm)

Opportunities and threats for psychiatry

In an e-interview in The Psychiatrist, John G. Csernansky was asked what he saw as the most promising opportunity facing the psychiatric profession and what he saw as the greatest threat. He said the most promising opportunity was the introduction of new knowledge about neuroscience into the practice of psychiatry. The greatest threat was that the public has become impatient with the lack of progress of biomedical research and may begin to withdraw its support for it.

Psychiatry has seen itself on the verge of neuroscientific breakthrough ever since its modern origins over 150 years ago. We are no nearer being "finally on the threshold of knowing enough to develop reasonable models of the pathophysiology of neuropsychiatric diseases and how to treat them", as Csernansky believes, than we were then. It's not so much that the public has become impatient with the lack of progress but that there needs to be a conceptual shift in understanding. The reason progress hasn't been made in biomedical research is that it is "barking up the wrong tree". The sorts of neurobiological processes underlying mental disorder may be no different from the basis of our "normal" thinking, feelings and behaviour.

By the way, when Csernansky was asked what single change would substantially improve quality of care, he said simplification of how we pay for mental healthcare. This is just at the time when the UK government is reforming health care (eg. see my personal blog entry), which will lead to the introduction of a mental health tariff based on clusters of patients which people don't, at least currently, understand. Still, it will be possible to undercut the national tariff, so maybe the new clustering system will never get off the ground. Anyway, the introduction of a tariff complicates block contract arrangements which we have got used to in the NHS and there is a lack of evidence that this change will lead to an improvement in services.

A cute little video about a visit to a psychiatrist

(With thanks to Adinah's post on ICSPP Discussion Group giving the link. See also her comment on another blog.)

Does it really take several weeks for antidepressants to work?

In my previous post, I have gone on about the errors about the treatment of depression in the latest blog entry on the APA's Healthy Minds. Health Lives. There's another mistake about how long it takes for antidepressants to work. Patients are commonly told, as they are in the blog entry, that antidepressants can take up to 4 to 6 weeks to have an effect.

What the blogger should have said is that it commonly takes 4-6 weeks for a statistically significant difference between active and placebo treatment to be detected in clinical trials. But this is an artefact of the way in which statistical significance is measured. Larger size clinical trials will detect a statistical difference earlier than trials with smaller numbers of subjects.

Actually, the largest improvement per unit time produced by antidepressants occurs within the first 2 weeks of treatment (Mitchell, 2006). Recovery from depression fits an exponential model (Priest et al, 1996). The false 'delay' hypothesis has been used to call for research into better antidepressants that act more quickly. Maybe it would be better just to be honest and accurate with patients about the limitations of antidepressants.

How easy is it to treat depression?

The latest blog entry from APA's Healthy. Healthy Lives., besides making the misleading statement that antidepressants work by increasing the amount of serotonin between nerve cells, also gives the wrong impression that depression can be readily treated. The blog makes out that there are lots of options to try, so if you just keep making changes of medication everything will be alright.

I don't want to appear pessimistic about the outcome of treatment for depression. However, the reality is not as simple as the blogger makes out. Some people fail to respond to treatment and some relapse after responding. Over 6 months, maybe, about half of people do quite well, a third have a fluctuating course and 1 in 9 remain unwell (Mulder et al, 2006). Of those who are doing quite well at 6 months, maybe about half relapse in the following year (but a third of those depressed at 6 months recover) (Mulder et al, 2009).

Over the long-term, recurrence is high. Figures in studies vary from 40-85%. If about a quarter of people are improved by treatment, there's a quarter of people who do not have good outcomes (Hughes & Cohen, 2009).  Even if there's a clinical improvement, this does not necessarily  mean there's been a social recovery (Kennedy et al, 2007). Many patients still report residual symptoms despite apparently successful treatment (Fava et al, 2007).

Outcomes for non-drug treated samples are not necessarily any worse over the long-term (Hughes & Cohen, 2009). Doctors do not generally tell patients about the small effect size and substantial non-response rate of antidepressants for fear of undermining the effectiveness of medication. The serotonin imbalance theory is used as a means of encouraging patients to take their medication, which is why the Healthy Minds. Health Lives. blog mentions it.

The role of psychiatry is to give hope to depressed people. It is also to be honest with them about the cause of their problems and the appropriate treatment. Patients are able to understand that the 'chemical imbalance theory' is only a theory. What they find more difficult to appreciate is why they are told that this theory has been proven, when this is clearly not the case. They may also struggle when antidepressants may not give the simple and easy answer they have been led to expect.

Are pharmaceutical companies really moving away from psychiatric drug development?

In my previous post, I mentioned that Thomas Insel, Director of NIMH, had noted that pharmaceutical companies are moving away from psychiatric research. He elaborated on this further in a previous post on his blog, when he expressed concern about GlaxoSmithKline and AstraZeneca apparently terminating their psychiatric medication development programmes. Jeffrey Lieberman discussed this issue further in a Medscape broadcast.

However, PhRMA reported earlier in the year that a record 313 new medicines to treat patients suffering from mental health disorders are being developed by America’s pharmaceutical research and biotechnology companies (see press release with link to full report). Doesn't sound like a lack of investment to me, even if there are no drugs working by new mechanisms. As has always been the case, the motivation for research is to fulfill the wish for medication that will provide the cure we've been hoping for.

A report from NIMH takes the issue of cure  further to prevention and emphasises the importance of so-called personalization and preemption as the foundations for new treatments. As the report itself notes, psychiatric genetics has not yielded a single validated target for any mental disorder. The causes of mental disorders and their mechanisms are unknown making the development of so-called personalized psychiatry a risk for the pharmaceutical industry, which it understandably may not wish to take (see News and Notes from Psychiatric Services).

Mental health breakthroughs in 2010

Thomas Insel, Director of NIMH, who I have mentioned in a previous post, has listed his top 10 research events and advances of 2010 on his blog. I'm not quite as convinced as he is that these represent advances for psychiatry and I think we do need to question whether we are really getting value for money from NIMH (see previous post).

Insel concentrates on genetic research. I'm not saying this research doesn't need to be done, but would question its value for psychiatry. For example, whole genome sequencing has demonstrated the surprising number of variants in normals - as he says each child shows "50 – 100 new mutations not present in his or her parents". But it's speculation to correlate rare “structural” variations in the genome with autism, schizophrenia and other neurodevelopmental disorders. Parental imprinting is an interesting phenomenon and we need to understand it further, but it's unlikely to change the way we approach mental disorders. Epigenomics does need to be developed as a basic science but it's unlikely to provide us with a new way of understanding mental illness.

I don't think funding for genetic research should be obtained on the back of what is provided for psychiatry. Nor can I see induced pluripotent stem cells (iPSCs) cell technology, despite its interest and potential, contributing to psychiatry. Similarly, the Human Connectome Project may well produce basic scientific advances in the understanding of patterns of brain-function connections. It's the belief that this will uncover abnormal brain circuits that worries me. HIV/AIDS is also an important condition for research but so-called potential progress in its prevention isn't really going to help psychiatry. There was a thought that we could all take medication to prevent us developing mental illness, but this seems to have dropped off the horizon for the moment. I think we should also be sceptical about the value of expensive antiretroviral chemoprophylaxis for HIV/AIDS - shouldn't we be spending money more on prevention through condoms?

I'm not exactly sure why pharmaceutical companies have moved away from the development of psychiatric medication. Insel makes out that there are various basic science developments that they could pursue. In terms of the basic science hypotheses, I think the ones he mentions are just as likely to end up on the failed heap of neurobiological hypotheses of the basis of mental illness. Nor have we really made the advances this year in the understanding of the autistic brain that he implies. And surely it's scraping the barrel to screen for chemicals capable of enhancing neurone formation in the hippocampus of adult mice to develop them as antidepressants.

I hadn't realised that Nature had produced a whole issue on schizophrenia this year, which Insel classes as one of the events for psychiatry of 2010. I'll have to look at it further.

Is money well spent on mental health research?

A New York Times article suggests that an entire psychiatric textbook was ghostwritten by a writing company funded by a drug company. Perhaps we shouldn't be too surprised by this. As another New York Times article points out, ghostwriting has not been that uncommon in medical journal articles.

Doctors are not always neutral agents in the marketing of pharmaceutical drugs. Understandably, maybe, they want to find effective medications for their patients. Their promotion of these medications may well be biased. However, patients do look to their doctors to provide a balanced assessment of the effectiveness of medication, even if they may wish for a simple, quick and complete cure.

Academic psychiatrists may see their presentation of material in a textbook as scientific knowledge. From their point of view, it therefore doesn't matter too much who writes the chapters. After all, they sign off the final copy. They accept responsibility for what has been written. A press release from the American Psychiatric Association (APA) admits that editorial assistance from a writing company has not been that uncommon and insists this isn't ghostwriting by a drug company. From their point of view, it's merely compiling and checking facts. The problem is that "facts" in psychopharmacology are usually open to interpretation. I suppose it depends how much of the "compiling" has been done by the writing company as to whether it should be seen as "ghostwriting". Actually, perhaps what the APA is more objecting to is that technically it wasn't the drug company doing the ghostwriting - which is what it says the original NYT article implied (it's been amended since) - it was a writing company paid by the drug company.

What the authors of the book don't mention is that they have been paid handsomely to put their name to such a book. The NYT article actually implies that they didn't tell their publisher about the writing company (but anyway, according to the APA press release, the publisher wouldn't have been too bothered if it had known). Nor is the book likely to have very high quality scientific content, in the sense of critically and independently examined and reviewed. It's these researchers that obtain large research grants, and have been shown up before for not disclosing their interests to their University (eg. see another NYT article).

The Project On Government Oversight (POGO) takes a keen interest in strengthening the integrity of federally funded science and has written to the National Institutes of Health (NIH)  I think NIH are the right target here. The funding they put into mental health research and medical research in general is very significant. Such vested interests do encourage a biomedical bias (eg see my article) within psychiatry. Challenging the myth that a biological basis of mental illness will be elucidated by further research undermines the basis for these large NIH grants. Losing research funding is what biomedical psychiatry finds difficult to accept. Academic standing to obtain research grants can be improved by writing a textbook, and it's even easier if a writing company does it for you, and money can be made out of it.


(With thanks to posting on Mad in America blog)

Why no amplified placebo effect for reboxetine?

A recent article in the BMJ has shown that the data on reboxetine has not proven its effectiveness. This evidence has at least partly been hidden because of publication bias.

However, the FDA never gave reboxetine a licence anyway. Intriguingly, in a rapid response to the BMJ article, the medical officer who reviewed the FDA application hints that we still haven't got all the relevant data. We still don't know why the FDA turned reboxetine down in 2001.

It's tempting to speculate, as GoozNews does, that somehow it was connected with David Healy's overinflated promotion of reboxetine at the time in terms of restoring social interaction. Reboxetine is a NARI rather than a SSRI, which means it is more specific for blocking the reuptake of noradrenaline, rather than serotonin. Serotonin specific reuptake inhibition (SSRI) was marketed as the mechanism of action of a whole new generation of antidepressants, such as fluoxetine. The competitor noradrenaline reuptake inhibition (NARI) hypothesis never really gained ground, not least because the FDA did not approve reboxetine.

So, it could be said there's always been a bias against reboxetine. I suppose this could explain why no amplified placebo effect has been found and therefore reboxetine is no better than placebo. If apparent antidepressant efficacy is due to an amplified placebo effect (see previous post) one might have expected the same to be found with reboxetine. As it hasn't, it is already being said (see post by Neuroskeptic) that the amplified placebo hypothesis must be wrong.

But there could be other explanations, such as the lower expectancy for reboxetine. In other words, the placebo effect was not amplified because there was a lack of belief in reboxetine. Also, in another rapid response to the BMJ article, it is pointed out that the BMJ meta-analysis may have been selective, certainly compared to the NICE analysis.

It'll be interesting to see what NICE make of the BMJ article. Hopefully, we can also find out what was behind the FDA decision in 2001.

How may antidepressants worsen the long-term outcome of depression?

Robert Whitaker in his latest posting on his Mad in America blog (to which I have referred before) elaborates on the work of Giovanna Fava about the vulnerability to relapse created by taking antidepressants. Fava has produced a recent review in which he builds on his hypothesis that the neurobiological mechanism underlying the increased vulnerability is due to oppositional tolerance. By this he means that the effects of the drug are opposed or counteracted by homeostatic changes in the brain, and when drug treatment ends, these processes may operate unopposed.

I am cautious about calling the effect 'tolerance'. Unlike, for example, alcohol, there is no evidence of the need to increase the dose or concentration of antidepressants to produce the desired effect. Maybe what Fava means is a tolerance-like effect.

More fundamentally, I'm not convinced that looking for an underlying neurobiological explanation is the real way to look at the issue. Surely the problem is psychological dependence. As I've said in a previous post, doctors concentrate too much on the physiological explanation of drug effects. People form attachments to their medication more because of what they mean to them than what they do. It's an identity-altering experience taking antidepressants. Discontinuing them is going to cause all sorts of problems which take time to make sense of.

The official view about mental illness

I was not intending to be personal about the bloggers on Healthy Minds. Heathy Lives. in two of my previous postings (see link to the first and to the second). The reason I've focussed on this blog is because it's published under the auspices of the American Psychiatric Association (APA). It therefore has the official backing of American psychiatry.

I've expressed concern before about the biomedical bias which has developed within the APA (see article). It's not so long ago that the APA was more pluralistic. Although I stand to be corrected, I think the Royal College of Psychiatrists in the UK would be more cautious about tying its ideological understanding of mental illness, at least in official statements, to a biomedical model.

Loren Mosher resigned from the APA in 1998 saying it had become the American Psychopharmacological Association rather than the American Psychiatric Association (see his resignation letter). Will the Healthy Minds. Healthy Lives. blog allow a debate about this situation? I doubt it, which I think is a cause for concern.

More on stigma of mental illness

The psychiatrist, Gariane Phillips Gunter's, MD, latest blog on Healthy Minds. Healthy Lives. has a video of her in which she argues that mental illnesses are "not your fault" because they are “biological illnesses, just like having high blood pressure, diabetes or cancer". She believes her crown as Mrs United States 2008 gave "her a greater opportunity to be a voice across this great nation for patients with mental illness and their families".

Reducing stigma is welcome but should not be based on a speculative biological theory of mental illness. As mentioned in the previous post, such a theory could actually increase stigma, as it doesn't really promote understanding of mental illness. As I keep saying, please do not misunderstand me. Of course, our thoughts, behaviour and emotions have their origins in the brain, but if that's all that Dr Gunter's saying, it's merely tautologous. However, she's making a statement about how we understand the world and it's not right.

Genetic theory not cure for stigma of ADHD

Ben Goldacre, in an article in his Guardian Bad Science column, comments on the Lancet ADHD study (as have I in a previous post). What he emphasises is that in fact a genetic theory of ADHD may actually potentially increase, not decrease, the stigma of the condition by encouraging a social distance from people identified as genetically damaged.

Can there be an open debate about biomedical psychiatry?

Robert Whitaker, in a posting on his Mad in America blog, writes about how he sometimes loses the hope that "our society will ever be able to have a thoughtful, honest discussion about what is truly known about mental disorders, and about the merits of psychiatric medications". I understand the sentiment. However, we do need to remind ourselves that biomedical psychiatry is a cultural system. Like a religion, it expresses a view about the nature of the world that provides what Clifford Geertz called an 'aura of factuality'. This feeling of realness is not easy to upset. People don't want to have their worldview turned upside down.

Whitaker's books The Anatomy of an Epidemic and Mad in America are well worth reading. One of their main themes is the vulnerability created by taking psychotropic medication. Relapse rates when people stop medication are very high. There is also evidence of a loss of benefit emerging with long-term treatment and also on retreatment after discontinuation of treatment. People may actually do better over the long-term if they work through their problems without medication. This is a legitimate scientific hypothesis (eg. Can long-term treatment with antidepressant drugs worsen the course of depression?).

(with thanks to News and Alerts from Mind Freedom International)

Psychosocial theory of ADHD does not blame parents

Sarah Boseley's report in the Guardian about the Lancet genetic study of ADHD, which concludes in the paper that ADHD is not purely a social construct, quotes Professor Anita Thapar, the senior author of the study, as saying that she hopes "that these findings will help overcome the stigma associated with ADHD". She's confident that ADHD is a genetic condition, which, to her mind, shows she was right that ADHD should not be dismissed as being due to bad parenting or poor diet.

Avoiding blaming the parents is commonly used as an argument for a biomedical view of ADHD and other mental disorders, such as schizophrenia. However, it's a misunderstanding of the psychosocial perspective to take this as its implication. Trying to understand why a child becomes hyperactive is several steps away from blaming anyone. There's no suggestion that there's any conscious intention to cause harm and there is no one-to-one causal connection. Understanding reasons is not the same as causal connections.

Oh no, not another neurobiological theory of depression

When I initially read Scicurious' posting on the Guardian Science blog, I wondered whether it was a spoof. But no, there are some references in the literature to antidepressants increasing neurogenesis in animals. Scicurious wonders whether this may be the mechanism of action of antidepressants, as she's given up on the low serotonin theory of depression.

Scicurious blogs at Neurotic Physiology. She makes clear her view on her About Scicurious page that "we have [now] discovered that all “neuroses” and psychiatric disorders have a physiological basis". I don't want to undermine her faith, but she should make it clear she's just promoting her belief and not call it science.

She notes that "antidepressants do work in some patients". As I've said in a previous post, the way in which they work may be merely as amplified placebos.

Adult executive brain dysfunction

Felicia Wong, in a posting on the Healthy Minds. Healthy Lives. blog (the American Psychiatric Association’s online resource for mental health issues), refers favourably to a Wall Street Journal article on adult ADHD. As the article says, ADHD is "thought to be an imbalance in neurotransmitters, the chemical messengers that relay signals in the brain, particularly in the frontal cortex that governs planning and impulse control." Ivan K. Goldberg, a psychiatrist in New York City, who co-developed a commonly used screening test, is quoted as saying "What it really is is a disturbance of the executive functions of the brain".

Dr Wong recommends that those who suspect they have ADHD should have a thorough evaluation with a psychologist or psychiatrist. How do psychologists or psychiatrists know if there is an executive brain dysfunction? It's an hypothesis but how do we know whether it's true? Using the screening test co-developed by Dr Goldberg is not a diagnostic test, although there are rating scales used for diagnosing ADHD. But they're not measuring executive brain dysfunction. So what is being diagnosed when a diagnosis of adult ADHD is made and why link it to speculation about executive brain dysfunction? It's just a convenient way of viewing the world, isn't it?.

Does it matter whether biomedical psychiatry is true or not?

Lesson 5 of the NIMH course curriculum on mental illness, mentioned in a previous post, looks at the problem from the diagnosed children's perspective. Like any other kid is a video in three parts.

Regarding their problem as caused by a brain disorder has helped to make sense of their situation for these young people. Biomedical psychiatry can provide a genuine order to the world. Does it matter whether it's true or not?

Mental illness as faulty circuits in the brain

Research in mental health has moved on from chemical imbalances as the cause of mental illness to circuitry dysfunction in the prefrontal cortex, at least according to Thomas Insel, Director of NIMH. For example, in his article Disruptive insights in psychiatry: Transforming a clinical discipline, he says aspects of schizophrenia can be mapped onto dysfunction of dorsolateral prefrontal circuits that mediate executive function; depression appears to involve dysfunction in a region of the midline infragenual prefrontal cortex important for regulation of mood; OCD (obsessive-compulsive disorder) involves dysfunction in the orbitofrontal prefrontal cortex via its role in perseverative behaviours; and posttraumatic stress disorder (PTSD) can now be mapped to dysfunction in prefrontal circuits required for the extinction of fear.

There is of course some localisation of function in the brain but dynamic interactions between multiple regions produce thought, emotion and behaviour. It's a long step to mapping specific mental illnesses to dysfunction of brain circuits. Insel himself concedes that more research is needed.

Moreover, Insel clearly juxtaposes his concept of mental illness as brain disorder with psychological disorders caused by psychic trauma or conflict. He says we need to rethink our approaches to diagnosis, treatment, and professional training. So he's happy for his approach to encourage psychosurgery and intracranial brain stimulation.

He got an airing of his views in an article, Faulty circuits, for the popular Scientic American. His claim that neuroscience will revolutionise psychiatry is no different from the one made by modern psychiatry since its origins with the asylums. How many more blind alleys will psychiatric research lead us down? Faulty brain circuits in mental illness are as much of a myth as biochemical imbalances.

Psychiatrists rarely think about the impact of medication on anything other than brain chemicals

David Karp in his book Is it me or my meds?: Living with antidepressants talks about how one's view of oneself is at stake in taking antidepressants. In an earlier paper, he described the initial resistance to drug taking; negotiating the terms of treatment; adopting new rhetorics about the cause of depression, such as "chemical imbalance"; experiencing a conversion to medical realities; and becoming disenchanted with the value of medication for solving personal problems. Adopting the view that one suffers from a biochemically based emotional illness can be an identity-altering view of reality.

The obvious effects of antidepressants

Edward Shorter, in his book, Before Prozac, rues the fact that there has been no progress in the pharmacological treatment of mood disorders, since imipramine was introduced in the 1950s. He quotes from Roland Kuhn, who discovered imipramine, and who "never used 'controlled double-blind studies' with 'placebo', 'standardised rating scales' or the statistical treatment of large numbers of patients". Instead, what Kuhn noticed was an "obvious effect" in improving vital depression in psychiatric patients that he tried it on. To use a quote, again from Kuhn in Shorter (2009), "The patients become generally livelier, their depressive whisper voices become louder, the patients appear more social, the yammering and crying come to an end."

As I pointed out in a previous post, how do we know that antidepressants aren't just placebos with side effects? What Kuhn may have "discovered" was merely the placebo effect.

Shorter thinks we may have "lost something" because today "Kuhn would be kicked out of the door at the FDA", by which he means imipramine would never have come onto the market without controlled trials to support it. As he says, what we've got at the moment is a "mesh of patent-protected remedies". I agree this isn't progress, but Kuhn may have merely sent us down the route of the wish-fullfilling phantasy of the chemical cure of depression.

Academic freedom for critical psychiatry

As a follow-up to my post on Why haven't professors of psychiatry used their tenure to go up against the system that we’re in?, I suppose Thomas Szasz is the exception that makes the rule. There's a tweet that agrees with me. I guess Szasz has been lucky to have tenure.

The best article that explained what happened to Szasz when his tenure was threatened is by Ronald Leifer. Perhaps I'm just jealous that I've had to carry on in the real world of psychiatric practice and not had the freedom of tenure like Szasz, still going aged 90.

Am I a bromide?

Now Nassir Ghaemi has called me a "bromidic anti-biological critic". I have reviewed his book The rise and fall of the biopsychosocial model, which I mentioned in a previous post. He has replied to my review and I have responded to his comments. I can understand him being upset about my views about his book. But I have gone on at length about the misunderstanding of saying that critical psychiatry is anti-biological (eg. see another previous post).

By the way, bromides were used as sedatives in psychiatric hospitals in the past. And I don't think critical psychiatry is bromidic in the sense of being conformist to majority opinion. Maybe I should be happy to be bromidic in the adapted words of the song from South Pacific:-

Wonderful critical psychiatry 

I expect everyone of my crowd to make fun of my proud protestations for critical psychiatry. 

And they'll say I'm naive as a babe to believe that the fables of psychiatry will be exposed. 

Fearlessly, I'll face them and argue their doubts away. 

Loudly, I'll sing about flowers in spring. 

Flatly, I'll stand on my little flat feet and say.... Critical psychiatry... is a grand and a beautiful thing. 

I'm not ashamed to reveal, the world famous feeling I feel. 

I'm as corny as Kansas in August, 

I'm as normal as blueberry pie, 

no more a smart little guy with no heart, I have found me a wonderful cause. 

I am in a conventional dither, with a conventional star in my eye. 

And you will note there's a lump in my throat, when I speak of that wonderful cause. 

I'm as trite and as gay as a daisy in May a cliché coming true, 

I'm bromidic and bright as a moon happy night pouring light on the dew. 

I'm as corny as Kansas in August, high as the flag on the 4th of July. 

If you'll excuse an expression I use... 

I'm committed, I'm committed, I'm committed, I'm committed, I'm committed, I'm committed to a wonderful cause! 

(interlude) 

I'm as trite and gay as a daisy in May a cliche' coming true. 

I'm bromidic and bright as a moon happy night pouring light on the dew. 

I'm as corny as Kansas in August, high as the flag on the 4th of July. 

If you'll excuse an expression I use... I'm committed (13x) to a wonderful cause! 

 (To the music of "A wonderful guy" from South Pacific)

Why haven't professors of psychiatry used their tenure to go up against the system that we’re in?

Profile of Leon Eisenberg who died last year. I've always found some of his articles seminal eg. The social construction of the human brain.

Arthur Kleinman's obituary comments are pertinent. Eisenberg "follows in the great footsteps of ... William James, because James argued powerfully for the broad range of normal experience, for our tolerance of multiple ways of being human." (WPA obituary). “He was a major voice in American medicine." (Boston Globe obituary)

Why have I been called a postmodernist?

Nassir Ghaemi in his book The rise and fall of the biopsychosocial model says I am an "explicit proponent of applying postmodernism to psychiatry". His evidence for this is said to be my 2002 BMJ article.

In the article, I say that "Psychiatry needs to return to a biopsychological view to limit its excesses". True, I do go on to say that "Such an approach conforms to the new direction that has been called "postpsychiatry" and there is a box summarising the central tenets of postpsychiatry.

What I meant by this is that postpsychiatry is one form of critical psychiatry, which, as far as I am concerned is about 'returning to a biopsychological view'. Ghaemi has got it right that I am trying to rehabilitate the ideas of Adolf Meyer (whose perspective was called Psychobiology) (eg. see my article Adolf Meyer's psychobiology and the challenge for biomedicine).

I see postpsychiatry as one form of critical psychiatry (see my letter to Psychiatric Bulletin). Personally I take a more pragmatic view than postmodernism. In fact some would juxtapose critical psychiatry and postpsychiatry even more than I would eg. see entry for Critical Psychiatry on Wikipedia.