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.

How do I get confused with Digby Tantam?

Tom Szasz in his new book Antipsychiatry: Quackery squared quotes my critical psychiatry website page on 'What was antipsychiatry?' but attributes it to Digby Tantam, not me. What I wrote was, "A key understanding of 'anti-psychiatry' is that mental illness is a myth (Szasz 1972)." Szasz objects to this because he is not an anti-psychiatrist. However, unfortunately for him, it is true that he has been identified with anti-psychiatry, and the myth of mental illness is a key idea that is associated with it.

I don't feel too bad about Szasz's criticism as he calls RD Laing an anti-psychiatrist, and Laing disowned the term, like Szasz.

He also complains that I put the date of his The myth of mental illness book as 1972, because of course it was first published in 1961. I did this because I was referring to the Paladin edition, which was first published in 1972.

Antidepressants are placebos with side-effects

Irving Kirsch's new book The Emperor's new drugs: Exploding the antidepressant myth makes the strongest case yet for antidepressants being merely amplified placebos. Irving does not make reference to a paper by Thomson (1982), which I think was the first to suggest this specific hypothesis. There were also previous references to the importance of the breaking of the blind in clinical trials.

I have always been sceptical about the value of antidepressants and psychotropic medication in general (eg. Limitations of double-blind trials) and share this lack of evidence with patients in my clinical practice. However, I have always felt it has been very difficult to get away from the notion that, however small the difference is between active and placebo groups in clinical trials, there is still a statistically significant difference. If patients have wanted an antidepressant I have felt I have had no choice but to prescribe.

Irving is more confident in his presentation of the case than I have been that this statistical difference is an artefact. Perhaps he has been more definitive because he started from a belief in antidepressants, which he no longer has, whereas, having always been sceptical, I have tended to qualify my position eg. Why is the effect size so small?.

Irving's evidence is summarised on page 21 of his book:-

The final piece of evidence to which he makes reference ie. a paper by Barbui et al is still to appear in print entitled 'Is the paroxetine-placebo efficacy separation mediated by adverse events?' As Irving says, the evidence "may not be conclusive proof, but it is strong". It'll be interesting to see the impact of this more confident case.

Critical psychiatry is not neurophobic

An article by Bullmore et al entitled Why psychiatry can't afford to be neurophobic followed up Craddock et al's article mentioned in my last post. It suggested that "there seems to be a deep-seated reluctance to embrace the theoretical and therapeutic potential of neuroscience for psychiatry".

I don't think this reluctance comes from critical psychiatry as such. It has always emphasised the integration of mind and brain. It's a mistake to think that mental symptoms are not based on a neural substrate. Critical psychiatrists can understand the wish, as much as anyone else, that neuroscience could solve the theoretical and therapeutic problems of psychiatry.

The problem is that fulfilling that wish is "intellectually bold" in Bullmore et al's own words. They are fearful that psychiatry will be cast "adrift from the core principles of medicine". They can't understand why anyone would want to prescribe psychotropic medication without thinking that symptoms were "somehow related to abnormal synaptic signalling between nerve cells".

Correspondence in reply (eg. by Andrew Blewett) sees through this argument. Neurohawkishness seems to be on the defensive.

Is there a debate about the future of psychiatry?

All in the Mind broadcast a programme that included a debate between Nick Craddock and Pat Bracken. It suggested there was a fierce debate within psychiatry about the very future of the profession.

I think the origin of this so-called debate is supposed to be an article by Craddock et al entitled "A wake-up call for British psychiatry". It has been portrayed as a biomedical reaction to the policy of New Ways of Working.

I think the issues are more complex (see my e-letter). There has been a deprofessionalisation of services in the sense of an undermining of professional expertise. New Ways of Working encouraged a fragmentation of services and, in fact, Department of Health policy now seems to have moved on to focusing on the "creative, capable workforce" and not so much about the structure of services.

The question is whether there is really a debate about the conceptual basis of psychiatry. Pat has always tended to argue that postpsychiatry is not another model (eg. see Openmind article). I may have misunderstood the implication of Pat's point but I do think there should be a debate about whether psychiatry has a biomedical or truly biopsychosocial foundation. "Biopsychosocial" may not be the best term as it has been used to mean an eclectic, atheoretical position. But I think critical psychiatry is clear that psychiatry can be practiced without postulating brain pathology as the basis for mental illness. That is a debate worth having but I haven't seen much engagement in it.