Professor John Read, back in the UK after a long period away, is struck by some important changes in the way we view mental health problems.

It’s good to be back in the UK after twenty years in New Zealand – well, apart from the weather, the political, economic and spiritual state of England, and the endless phone calls to India to get someone from up the road to install a phone. Amid it all I’m writing my first ever blog! What an antiquated old prof.

As regards mental health research, the difference I notice most is how far people’s thinking has moved on from the old, simplistic, ‘blame-the-brain-for- everything-and-medicate’ idea.

Two papers I’ve published since returning will both, I hope, contribute to this on-going development. The first was published with colleagues from Scandinavia and the USA in the journal Neuropsychiatry. With the snappy title ‘The Traumagenic Neurodevelopmental Model of Psychosis Revisited’  it reports on 125 papers that support a model we first put forward in 2001 outlining how psychosis can be related to  trauma. This model is a challenge to those I call ‘contextless brain researchers’: people who when they find a difference in the brains of two groups of people, assume that they have found the cause of the difference. It rarely seems to occur to them to ask a vital (and some might say obvious) question: ‘what might have happened to make the groups different?’ I would not for a moment dispute that such researchers are well-intentioned folk. They may have a deep knowledge of neurology and access to some very fancy technology. However, they often don’t seem to grasp the simple fact that a primary function of the brain is to respond to the environment.

One of the findings underpinning our model is that there are some striking similarities between the brains of traumatised young children and those of people diagnosed with schizophrenia. Perhaps the most important is in the way that the nervous systems (the ‘HPA axis’, to be precise) of the two groups respond to stress. We’ve been told for decades that the reason that people who experience ‘psychosis’ are sensitive to stress is genetic. It now seems that for many people the cause of such heightened sensitivity may lie elsewhere: in early trauma.

This goes to the heart of whether the much touted ‘bio-psycho-social model’ and its alter ego the ‘stress-vulnerability model’ really do what it says on the tin, and offer a genuine integration of nature and nurture.  I argue in my book Models of Madness that these terms can sometimes disguise what is still fundamentally a biological explanation of our experiences. We’re told that stress can play a role, but only in people who already have a supposed genetic predisposition. Life events, even serious and  traumatic ones,  are relegated to the role of ‘triggers’ of an underlying genetic time bomb. Bio-genetics enthusiasts claim that the ‘vulnerability’ part of the equation must be genetic. This conveniently ignores the fact that the inventors of the model, Joseph Zubin and Bonnie Spring, stated in their seminal 1977 paper that the vulnerability can be acquired from early life events. As Michael Caine used to say, ‘Not a lot of people know that’.

This all reminds me that a few years back Robin Murray, Professor of Research at London’s Institute of Psychiatry, announced from a Canadian conference stage that ‘The schizophrenia wars ended in the 1970s’. I couldn’t help raising my hand and pointing out that the occupying force in a colonial war is usually quick to announce the end of hostilities, and that the war would not be over until the occupying forces withdrew to the appropriate boundary.

It is remarkable then that the relationship between trauma and psychosis – heresy just 15 years ago – is now one of the strongest and most consistent findings in our field. How times have changed – and how quickly. I now hear people saying ‘What’s all the fuss about? We always knew that – nothing controversial there’. Some of the most scathing critics of our first few papers are now happily putting their names on papers confirming the relationship. I was moaning about the ‘hypocrisy’ of all this to my colleague Richard Bentall recently and he replied ‘John, John, – you’ve won and you’re still bitching!’

The ‘victory’ had never felt so real as when I heard some wonderful news from New Zealand towards the end of last year. An abuse survivor had twice been denied financial aid in relation to subsequent mental health problems because two ‘experts’ – employed by the agency responsible for making such payments – had stated that there is no evidence that child abuse can cause psychosis. However, in the final appeal a psychiatrist summarised the substantial literature which attests otherwise. The judge upheld the appeal and I’ll admit I took some naughty pleasure in the NZ’s national Sunday newspaper quoting me as saying that the first two psychiatrists, ‘either knew nothing about the many studies documenting the relationship between child abuse and psychosis or were trying to mislead the judge’.

Another area where research is challenging the simplistic medical model type thinking in mental health is that of interventions. More and more studies are giving the lie to the pharmaceutical company propaganda which would have us believe that their products are targeted, specific ‘treatments’ for identified brain problems. My second recent paper reported an online survey of 1,829 people taking antidepressants. It revealed some astonishing levels of psychological and interpersonal adverse effects. For example, 60% of people reported feeling emotionally numb, 42% said that the drugs reduced positive as well as negative emotions, and 39% felt that they cared less about others whilst on the drug. Other effects are already well documented but we were surprised at their sheer frequency: 62% reported sexual difficulties (rising to 72% for men), and 39% reported feeling suicidal, rising to 55% in 18-25 year olds. Withdrawal effects, often dismissed as rare or imagined – were reported by 55%. Those who had been more depressed when the drugs were first prescribed were no more likely than others to experience these effects, suggesting that they were drug-related rather than symptoms of the depression itself.

Although biologically-rooted explanations of distress and pharmaceutical treatments are still prevalent, it seems that both professionals and the public are increasingly exploring alternatives. All over the world – with the sole exception of the USA – surveys reveal that the public, including service users and carers, tends to take the common-sense view that mental health problems are related much more closely to the events and circumstances of our lives than to biological factors such as genetics or brain chemicals. When it comes to help the public also strongly prefer psychological and social approaches over drugs, electroshock therapy or hospitals. Only a minority of professionals seem intent on continuing to ignore experience and push the idea that mental health problems are essentially problems with our brains. And those people are getting older by the minute. Things have changed unbelievably in 20 years. Hopefully, if we all keep pushing, in whatever way our circumstances allow, our mental health services will finally become evidence-based, effective and humane.

About the author

John Read is Professor of Clinical Psychology and Director of the Clinical Psychology Programme at Liverpool University. You can follow him on Twitter @ReadReadj