What I wish Stephen Fry understood about mental health

The following letter, addressed to Stephen Fry, is written by Richard Bentall, professor of clinical psychology at the University of Liverpool.


Stephen Fry Screen-Shot-2016-03-01

Stephen Fry (Pic)


Dear Stephen,

You and I attended the same public school (Uppingham, in Rutland) at the same time, in the early 1970s, and our unhappy experiences there have undoubtedly helped to shape our different trajectories, which have led us to a shared interest in mental health.

In your case, your premature departure from Uppingham, and your adventures immediately afterwards, were documented in your wonderful book, Moab is my Washpot. Your subsequent openness about your own mental health difficulties, for which I salute you, has been an inspiration to other mental health sufferers.


In my case, despite a lacklustre academic performance which I attribute mainly to spending much of my adolescence feeling depressed and emotionally abused, I managed to make my way to university and eventually pursued a career in clinical psychology. (My brother, unfortunately, was much worse affected by his time at the school; his expulsion was the start of a long downward spiral that culminated in his suicide, an event that haunts me 20 years later, and which reinforces my determination to improve the public understanding of mental ill-health.)

I have now spent more than 30 years researching severe mental illness, focusing especially on patients with psychosis (who, in conventional psychiatry, are typically diagnosed with ‘bipolar disorder’ or ‘schizophrenia’). It is from this perspective that, reluctantly, I must now ask you to rethink the way that you portray these conditions to the general public. I know that you wish to demystify and destigmatise mental illness, which are surely laudable aims, but my worry is that some aspects of your approach may have the opposite effect from that which you intend.

Conventional psychiatry tends to decontextualise psychiatric disorders, seeing them as discrete brain conditions that are largely genetically determined and barely influenced by the slings and arrows of misfortune, and it was this perspective that was uniquely presented in your recent programme The Not So Secret Life of a Manic Depressive: Ten Years On. According to this ‘brain conditions’ view, psychiatric disorders occur largely out of the blue in individuals who are genetically vulnerable, and the only appropriate response is to find the right medication. Even then, it is usually assumed that severe mental illnesses are lifelong conditions that can only be managed by continuous treatment. However, research into severe mental illness conducted over the last 20 years (not only by me, although I have contributed) tells a more complex story.


To begin with, we now know to a level of certainty that diagnoses such as ‘bipolar disorder’ and ‘schizophrenia’ are not separate conditions [1]. Furthermore, there is no clear line between severe psychiatric disorders and healthy functioning [2], with the consequence that large numbers of people manage to live productive lives despite experiencing symptoms at some time or another, and without seeking help [3]. There is, for example, an international network for people who hear voices, many of whom manage perfectly well without psychiatric care [4]. (In my experience, psychiatrists are often troubled by this ‘fuzziness’ at the edges of mental ill health, which I find puzzling as doctors in physical health have no difficulties with handling arbitrary boundaries; there is no sharp dividing line between healthy and unhealthy blood pressure, for example.)


It also appears that the outcomes for severe mental illness are much more variable than was once thought. Longitudinal research suggests that a surprising number of people manage to make full or partial recoveries [5], even when not taking medication. A complication is that recovery means different things for different people; whereas psychiatrists typically think of recovery in terms of recovery from symptoms, patients more often emphasise the importance of self-esteem, hope for the future, and a valued role in society [6].


Of course genes play a role in making some people more vulnerable to psychiatric disorder than others, but the latest research in molecular genetics challenges simplistic assumptions about ‘schizophrenia’ and ‘bipolar disorder’ being primarily genetic conditions. The genetic risk appears to be shared across a wide range of diagnostic groupings — the same genes are involved when people are diagnosed with schizophrenia, bipolar disorder, ADHD and even, in some cases, autism [7]. More importantly, genetic risk is widely distributed in the population with hundreds, possibly thousands of genes involved, each conferring a tiny increase in risk [8]. Hence (to quote American genetic researcher Kenneth Kendler): ‘The genetic risk for schizophrenia is widely distributed in human populations so that we all carry some degree of risk’ [9].


Of course, some people (possibly yourself) have more of these genes than others, but the fact that so many are involved suggests that it is very unlikely that studying them will lead to therapeutic innovations any time soon. By contrast, consider Huntington’s disease, a terrible degenerative neurological condition that is caused by a single dominant gene with a known biological function. Many years after this gene was discovered there is still no sign of a medical therapy for this simplest of all the genetic conditions.

In your programme, you did not attempt to link your own mental health difficulties to circumstances despite the fact that your story suggested that episodes had been triggered by specific events on at least two occasions (after bravely confronting an extreme homophobe in Uganda, and after extensive jet travel). More importantly, perhaps for understandable reasons, you seemed reluctant to explore any possible connections between your difficulties now and your experiences earlier in life. In fact, recent epidemiological studies have pointed to a wide range of social and environmental factors that increase the risk of mental ill health [10], some of which I am guessing you may be familiar with from personal experience.


These include poverty in childhood [11] and early exposure to urban environments [12]; migration [13] and belonging to an ethnic minority[14] (probably not problems encountered by most public school boys in the early 1970s) but also early separation from parents; childhood sexual, physical and emotional abuse; and bullying in schools [15]. In each of these cases, the evidence of link with future psychiatric disorder is very strong indeed — at least as strong as the genetic evidence. Moreover, there is now good evidence that these kinds of experiences can affect brain structure, explaining the abnormal neuroimaging findings that have been reported for psychiatric patients [16], and that they lead to stress sensitivity and extreme mood fluctuations in adulthood [17]. And of course, there are a myriad of adult adversities that also contribute to mental ill health (debt [18], unhappy marriages[19], excessively demanding work environments [20] and the threat of unemployment [21], to name but a few). Arguably, the biggest cause of human misery is miserable relationships with other people, conducted in miserable circumstances.


Why is all this important? Well, for one thing, many psychiatric patients in Britain feel that services too often ignore their life stories, treating them more like surgical or neurological patients than people whose difficulties have arisen in response to challenging circumstances. In the words of Eleanor Longden, a well-known voice hearer and mental health activist: ‘They almost always ask what is wrong with you and hardly ever ask what happened to you’ [22].


Patients are routinely offered powerful drugs as shown in your programme (I am not saying they don’t have a place) but very rarely the kinds of psychological therapies that may help them to come to terms with these kinds of experiences, or even practical advice (debt counselling probably has a place in the treatment of depression, for example).

Patients’ dissatisfaction with an exclusively medical approach is well founded, because research has shown that this approach has been extraordinarily unsuccessful, despite what clinicians often assert. Whereas survival and recovery rates for severe physical conditions such as cancer and heart disease have improved dramatically since the end of the Second World War [23], recovery rates for severe mental illness have not shifted at all [24]. Even more surprising, you might think, those countries which spend the least on psychiatric services have the best outcomes for severe mental illness [25] whereas those that spend the most have the highest suicide rates [26]. No doubt, if we understood the psychological mechanisms that lead from childhood misfortune to mental illness, we could do more to help people. However, research funding in mental health is being almost exclusively channelled into genetic and neurobiological studies, which have little realistic prospect of yielding practical interventions.


To make matters worse, research shows that exclusively biological theories of mental illness contribute to the stigma experienced by mental health patients, which I know you want to reduce [27]. The more that ordinary people think of mental illness as a genetically determined brain condition, and the less they recognise it to be a reaction to misfortune, the more they shun mental health patients. The biomedical model of mental illness, which your programme showcased, makes it all too easy to believe that humans belong to two sub-species: the mentally well and the mentally ill.

Finally, the biomedical approach entirely neglects the public health dimension of mental illness. Given the evidence from epidemiological studies, we can almost certainly dramatically reduce the prevalence of mental illness in the population by, for example, addressing childhood poverty and inequality, figuring out which aspects of the urban environment are toxic (you might or might not be surprised to know that living close to a park appears to provide some protection against mental illness [28]) and by ensuring that all of our children experience more benign childhoods than the ones we experienced. We cannot do any of these things if we spend all of our time peering into test tubes.


Let my finish by saying, Stephen, that I have the highest respect for you, and I thank you for your efforts to reach out to people who are suffering from mental illness. Please continue with this important work. But please, from now on, do so in a more balanced way.


Richard Bentall



[1] The literature on this is complex, but includes studies of patients with symptoms along the schizoaffective dimension (e.g. Tamminga, C.A., Pearlson, G., Keshavan, M., Sweeney, J., Clementz, B., & Thaker, G. (2014). Bipolar and Schizophrenia Network for Intermediate Phenotypes: Outcomes across the psychosis continuum. Schizophrenia Bulletin, 40 suppl 2, S131-S137. doi:10.1093/schbul/sbt179); statistical studies of symptom variation (e.g. Reininghaus, U., Priebe, S., & Bentall, R.P. (2013). Testing the psychopathology of psychosis: Evidence for a general psychosis dimension. Schizophrenia Bulletin, 39, 884-895) and studies showing shared genetic contributions to apparently different psychiatric disorders (e.g. Lichtenstein, P., Yip, B.H., Bjork, C., Pawitan, Y., Cannon, T.D., Sullivan, P.F., & Hultman, C.M. (2009). Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a population-based study. Lancet, 373, 234-239).


[2] Again, the literature on this is complex, but includes psychological studies of people with psychosis-prone personality traits (Raine, A. (2006). Schizotypal personality: Neurodevelopmental and psychological trajectories. Annual Review of Clinical Psychology, 2, 291-326), including sub-clinical bipolar traits (e.g. Bentall, R.P, Myin-Germeys, I., Smith, A., Knowles, R., Jones, S.H., Smith, T., & Tai, S. (2011). Hypomanic personality, stability of self-esteem and response styles to negative mood. Clinical Psychology and Psychotherapy, 18, 397-410) and also ‘psychometric’ studies which use complex statistical methods (‘taxometrics’) to discover whether there are any natural breaks in the continuum between healthy functioning and psychiatric disorder (e.g. Haslam, N., Holland, E., & Kuppens, P. (2012). Categories versus dimensions in personality and psychopathology: A quantitative review of taxometric research. Psychological Medicine, 42, 903-920).


[3] There are many epidemiological studies which show a surprisingly high prevalence of psychotic-like experiences in the general population. See, for example, Johns, L.C., & van Os, J. (2001). The continuity of psychotic experiences in the general populations. Clinical Psychology Review, 21, 1125-1141. This phenomenon has been demonstrated in respect to bipolar symptoms; see for example, Merikangas, K.R., Akiskal, H.S., Angst, J., Greenberg, P.E., Hirschfield, R.M.A., Petukhova, M. and Kessler, R.C. (2007) Lifetime and 12-Month prevalence of bipolar spectrum disorder in the National Comorbidity Survey Replication. Archives of General Psychiatry, 64, 543-552


[4] http://www.intervoiceonline.org/


[5] See, for example, Harding, C.M., Brooks, G.W., Ashikage, T., & Strauss, J.S. (1987). The Vermont longitudinal study of persons with severe mental illness: II. Long-term outcome of subjects who retrospectively met DSM-III criteria for schizophrenia. American Journal of Psychiatry, 144, 727-735, and Harrow, M., & Jobe, T.H. (2007). Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications: A 15-year multifollow-up study. Journal of Nervous and Mental Disease, 195, 406-414.


[6] Morrison, A. P., Shryane, N., Beck, R., Heffernan, S., Law, H., McCusker, R., & Bentall, R.P. (2013). Psychosocial and neuropsychiatric predictors of subjective recovery from psychosis.Psychiatry Research, 208, 203–209.


[7] Psychiatric Genomics Consortium. (2013). Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs.Nature Genetics, 984-994. Note that this finding, from analyzing DNA, is completely consistent with the results of population genetic studies such as Lichtenstein et al. (2009) ibid.


[8] The International Schizophrenia Consortium. (2009). Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature, 460, 748-752.


[9] Kendler, K.S. (2014). A joint history of the nature of genetic variation and the nature of schizophrenia. Molecular Psychiatry. doi:10.1038/mp.2014.94

[10] For a recent review, see Bentall, R.P., de Sousa, P., Varese, F., Wickham, S., Sitko, K., Haarmans, M., & Read, J. (2015). From adversity to psychosis: Pathways and mechanisms from specific adversities to specific symptoms. Social Psychiatry and Psychiatric Epidemiology, 49, 1011-1022.


[11] See, for example, Wicks, S., Hjern, A., & Daman, C. (2010). Social risk or genetic liability for psychosis? A study of children born in Sweden and reared by adoptive parents. American Journal of Psychiatry, 167, 1240-1246.


[12] Vassos, E., Pedersen, C.B., Murray, R.M., Collier, D.A., & Lewis, C.M. (2012). Meta-analysis of the association of urbanicity with schizophrenia. Schizophrenia Bulletin, 38, 1118-1123.


[13] Cantor-Graee, E., & Selten, J.P. (2005). Schizophrenia and migration: A meta-analysis and review. American Journal of Psychiatry, 163, 478-487.


[14] Veling, W., Susser, E., van Os, J., Mackenbach, J.P., Selten, J.P., & Hoek, H.W. (2008). Ethnic density of neighborhoods and incidence of psychotic disorders among immigrants. American Journal of Psychiatry, 165, 66-73.


[15] For a meta-analytic summary of the effects of childhood adversity (separation from parents, bullying, childhood abuse) see Varese, F., Smeets, F., Drukker, M., Lieverse, R., Lataster, T., Viechtbauer, W, Read, J, van Os, J. and Bentall, R.P. (2012). Childhood adversities increase the risk of psychosis: A meta-analysis of patient-control, prospective and cross-sectional cohort studies. Schizophrenia Bulletin, 38, 661-671. doi:10.1093/schbul/sbs050


[16] Sheffield, J.M., Williams, L.F., Woodward, N.D., & Heckers, S. (2013). Reduced gray matter volume in psychotic disorder patients with a history of childhood sexual abuse. Schizophrenia Research, 143, 185-191.


[17] Glaser, J.P., Van Os, J, Portegijs, P.J., & Myin-Germey, I. (2006). Childhood trauma and emotional reactivity to daily life stress in adult frequent attenders of general practitioners. Journal of Psychosomatic Research, 61, 229-236.


[18] Meltzer, H., Bebbington, P., Brugha, T., Farrell, M., & Jenkins, R. (2013). The relationship between personal debt and specific common mental disorders. European Journal of Public Health, 23, 108-113.


[19] Wade, T.J., & Pevalin, D.J. (2006). Marital transitions and mental health. Journal of Health and Social Behavior, 45, 155-170.


[20] Stansfeld, S. & Candy, B. (2006). Psychosocial work environment and mental health: A meta-analytic review. Scandinavian Journal of Work, Environment & Health, 32, 443-462.


[21] Barr, B., Taylor-Robinson, D., Scott-Samuel, A., & McKee, M. Suicides associated with the 2008-10 economic recession in England: Time trend analysis. British Medical Journal, 345, e5142. doi:10.1136/bmj.e5142




[23] See Chapter 1 of my book Doctoring the mind: Why psychiatric treatments fail (Penguin, 2009) for evidence on historical recovery rates for cancer and heart disease.


[24] This was first pointed out by Richard Warner (1985) in his bookRecovery from schizophrenia: Psychiatry and political economy. New York: Routledge & Kegan Paul. For a recent meta-analysis of the historical data, see Jääskeläinen, E., Juola, P., Hirvonen, N., McGrath, J.J., Saha, S., Isohanni, M., & Miettunen, J. (2013). A systematic review and meta-analysis of recovery in schizophrenia. Schizophrenia Bulletin, 39, 1296-1306. doi:10.1093/schbul/sbs130


[25] Sartorius, N., Jablensky, A., Ernberg, G., Leff, J., Korten, A., & Gulibant, W. (1987). Course of schizophrenia in different countries: Some results of a WHO comparative 5-year follow-up study. In H. Hafner, W.G. Gattaz, & W. Janzarik (Eds.), Search for the causes of schizophrenia (Vol. 16, pp. 909-928). Berlin: Springer. See, for more recent data, Saha, S., Chant, D., Welham, J., & McGrath, J.A. (2007). A systematic review of the prevalence of schizophrenia. PLoS Medicine, 2. e141.


[26] See, for example, Shah, A., Bhandarkar, R., & Bhatia, G. (2010). The relationship between general population suicide rates and mental health funding, service provision and national policy: A cross-national study. International Journal of Social Psychiatry, 56, 448-453; and also Rajkumar, A.P., Brinda, E.M., Duba, A.S., Thangadurai, P., & Jacob, K.S. (2013). National suicide rates and mental health system indicators: An eological study of 191 countries. International Journal of Law and Psychiatry, 36, 339-342.


[27] See Read, J., Haslam, N., Sayce, L., & Davies, E. (2006). Prejudice and schizophrenia: A review of the ‘mental illness is an illness like any other’ approach. Acta Psychiatrica Scandinavica, 114, 303-318, and Angermeyer, M.C., Holzinger, A., Carta, M.G., & Schomerus, G. (2011). Biogenetic explanations and public acceptance of mental illness: systematic review of population studies. British Journal of Psychiatry, 199, 367-372.


[28] van den Berg, A.E., Maas, J., Verheij, R.A., & Groenewegen, P.P. (2010). Green space as a buffer between stressful life events and health.Social Science and Medicine, 70, 1203-1210…..


Credit: The Spectator

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