From The Independent Tuesday May 14 2013 – We need to change the way we talk about schizophrenia If we only ever talk about schizophrenia in the context of a violent murder, is it any surprise that the public think people with mental illness are dangerous?
From The Observer Sunday 19 May 2013 – Mental illness: the claim that abuse is behind psychosis is irresponsible Oliver James’s assertions are unhelpful and risk demonising people
Eye Movement Desensitization Reprocessing Therapy. It’s on page 11 via this link – No 67 Spring 2013 http://www.yourvoicesheffield.org/media/YV67final.pdf
At first Denise looks for quick and painless solutions; then, in rehab, she courageously begins to work her way through the problems of Borderline Personality Disorder, depression and substance abuse.
- Stress and how to avoid becoming overwhelmed.
- Why your emotions matter to you and to others.
- What you can do to harness the energy of your emotions and make them work for you.
- How you can become calm, energized, focused and more aware of yourself and others.
Changing Diets, Changing Minds – The Importance of Nutrition For Behaviour, Learning and Mood: Putting Research Into Practice
Start Date: June 06 2013
End Date: June 06 2013
Duration: 9.30am to 4.30pm
Location: Inverness IV2 3BL
Venue: Lecture Theatre, The Green House, Beechwood Business Park
It gives us great pleasure to announce an opportunity to hear from Professor Michael A Crawford of Imperial College, London – an internationally acclaimed expert on the role of nutrition in brain development and function. At this special one-day event, he will be joined by Dr Alex Richardson and Dr Bernard Gesch, senior researchers at the University of Oxford and leading experts in the links between diet and behaviour, and Mr David Rex, specialist child health dietitian at Highland Council.
The programme for the day has been designed for a multi-disciplinary audience of professionals, policy makers, researchers from academia and industry, and other interested groups and individuals. It will give all participants the chance to hear about and discuss the links between nutrition and mood, behaviour and learning in children and adults – both in the general population, and in special groups such as those with developmental or mental health conditions.
Find out how our food choices, and those of the people we care or provide for, could be affecting our wellbeing and performance – at home, at school or in the workplace.
- How does what we eat affect the way we feel, think and behave?
- What’s the truth about sugar and fat? Could some of our favourite foods really be toxic and addictive?
- Does nutrition really make a difference to children’s behaviour and learning? If so, what are the implications for conditions like ADHD, dyslexia or autism?
- What’s the evidence that dietary interventions could reduce antisocial behaviour?
- Can diet help in the prevention and management of mental health conditions like depression, psychosis and dementia?
- Improving food choices – what can be done, and who should be doing it?
Find out from our panel of experts what the real truth is about the food we consume, and what it’s doing to our brains as well as our bodies. Join in the discussion about the impact of modern day diets, their implications for the public health crisis, and what can be done to improve outcomes for both current and future generations.
This event will provide you with opportunities not only to learn about the latest research findings, but also to ask your own questions and get answers that may influence some of the decisions you have to make every day.
This event will also be available by interactive webinar.
‘Dietary fats and human brain development: implications for the nutrition of mothers and infants’
Prof Michael Crawford (Imperial College, London; Institute of Brain Chemistry and Human Nutrition)
‘The Importance of Diet for Children’s Behaviour and Learning’ and ‘The Role of Nutrition in Mental Health and Wellbeing’
Dr Alex Richardson (Founder Director, FAB Research; Senior Research Fellow, University of Oxford; Author of ‘They Are What You Feed Them’)
‘Nutrition and Antisocial Behaviour – Is there a Causal Link?’
Dr Bernard Gesch (Research Scientist, University of Oxford)
‘Practical dietary approaches to ADHD, autistic spectrum disorders and related conditions: What works in practice?’ and ‘Improving children’s food choices: theory and best practice’
David Rex (Dietitian, Health & Social Care – Children’s Services, Highland Council; lead public health role, food & health in schools, nurseries and children’s residential units; and provides specialist Dietetic advice for children with Autistic Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD).
An essential event for:
Local Government Policy Makers | Education and Health Professionals | Researchers from Academia and Industry | Professionals working in Social Services and the Justice System | Caterers and Food Producers | School Meal Stakeholder Groups | Charities, Support Groups and Voluntary Organisations | Parents, Carers and other Interested Individuals
Standard (Public Sector, Health, Education, Local Authority) – £79
Concessionary (Students, Support Groups, Charities) – £49
FAB Research Associate Members – £29
Interactive Webinar – £49* (free to FAB Associate Members)**
*Includes access to the webinar on the day and for one month post-event via the FAB Audio/Video Library. For continuing access, consider a subscription to FAB Research – see below.
**Subscribe to FAB Research as an Associate Member today and enjoy free access not only to this webinar, but also to our library of eventcasts and other resources, including footage of our recent event with US Pediatric Obesity specialist, Professor Robert Lustig MD in London, March 2013. Join up here FAB Research Associate Membership.
Contact Information: Fiona O’Fee firstname.lastname@example.org 01463 667318
From Richard Bentall:
Last week, Dr Frank Hirth of King’s College London was on Radio 4 saying that his research into the neural circuitry of the fruit fly might help us understand neurodevelopmental disorders such as schizophrenia. To cut a long story short, I got copied into some correspondence about this between Dr Hirth and a colleague and was moved to join in as follows:
My friend and colleague Dave Pilgrim forwarded me your email to him, which I feel moved to reply to. I am copying in various colleagues who are as concerned as I am about the naive biological reductionism that seems to be dominating media discussions of mental health these days. Briefly, the problems with this view when applied to ‘schizophrenia’ are:
(i) Schizophrenia is a meaningless construct
There is no syndrome of schizophrenia and nobody can agree on who is schizophrenic. To my knowledge, no statistical study has ever identified a cluster of symptoms that correspond to the Kraepelinian concept or its subsequent revisions. Most recent studies have converged on a multidimensional model that incorporates all psychosis diagnoses (schizophrenia, schizoaffective disorder, bipolar disorder, delusional disorder, depression with psychotic features etc) within five dimensions of positive symptoms, negative symptoms, cognitive dysfunction, depression and mania/excitability, or even more complex structural models (see Demjaha, A., et al. (2009). Combining dimensional and categorical representation of psychosis: the way forward for DSM-V and ICD-11? Psychological Medicine, 39, 1943-1955 and, one of my own papers, Reininghaus, U., Priebe, S., & Bentall, R. P. (in press). Testing the psychopathology of psychosis: Evidence for a general psychosis dimension. Schizophrenia Bulletin, available online). In recent field trials, the proposed DSM-V criteria for schizophrenia generated a derisory kappa of 0.46, showing that clinicians working with a precise definition of the disorder and following a diagnostic interview often could not agree on who was schizophrenic and who was not (Regier, D. A., et al. (2013). DSM-5 field trials in the United States and Canada, Part II: Test-retest reliability of selected categorical diagnoses. American Journal of Psychiatry, 170, 59-70)!
(ii) Heritability coefficients are misleading
It is often forgotten that heritability coefficients are, actually, just fancy correlation coefficients. We all know, or should know, that correlation does not necessarily prove causality. Heritability coefficients are statements about populations and not individuals so that it is wildly misleading to suggest that high heritability = mostly genetically caused (for a detailed discussion of this, see Bentall, R. P. (2009). Doctoring the mind: Why psychiatric treatments fail. London: Penguin.).
In fact, precisely because heritability coefficients are correlations which attempt to parse up the variance in a trait to genetic and environmental causes, low variance in the environment leads to inflation of the apparent effects of genes. This is why, for example, IQ is highly heritable in middle class families (where environmental variation is low) but very low in working class families (where environmental variation is high) (Turkheimer, E., et al. (2003). Socioeconomic status modifies heritability of IQ in young children. Psychological Science, 14, 623-628). Also, heritability coefficients assume an additive model of genes and environment, which is wildly implausible given what we know know about how genes work. Again, assuming an additive model when there are G x E interactions leads to massive inflation of heritability and an underestimate of environmental effects (Dickins, W. T., & Flynn, J. R. (2001). Heritability estimates versus large environmental effects: The IQ paradox resolved. Psychological Review, 108, 346-369). This is probably why, as you know, molecular estimates of heritability are generally much lower than those based on the methods of classical genetics. The ‘missing’ heritability in these studies is probably phantom heritability.
Incidentally, you will also know from the genetic studies that you cite, that the consensus amongst geneticists is now that many common alleles (perhaps many hundreds) probably each confer a tiny risk of all kinds of severe mental illness. Although some CNVs have much higher association with psychosis, they account for only a small proportion of patients and are also associated with intellectual disabilities and autism (Owen, M. J. (2012). Implications of genetic findings for understanding schizophrenia. Schizophrenia Bulletin, 38, 904-907. doi: 10.1093/schbul/sbs103). This is further evidence, if ever it was needed, that schizophrenia is a meaningless construct and confirms the impossibility of devising a genetic test for the disorder.
(iii) There is massive evidence that environmental factors are causal in severe mental illness
The implications of ii above are that you can’t estimate environmental influences from heritability estimates – you have to look for them and measure them in their own right. Recent studies have pointed to a wide range of environmental factors associated with psychosis. These include social disadvantage, migration, living in cities and various forms of victimisation. I attach a recent meta-analysis I conducted on the evidence linking childhood adversity to psychosis (Varese, F., et al. (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.) The bare odds ratio between childhood trauma was stable across methodologies (retrospective/prospective) and came in at about 3, much higher than any association with common alleles. More importantly, there is evidence of a dose response effect, with ORs climbing to around 50 for children who have been multiply traumatised. Reaction in the psychiatric community has sometimes been bizarre, with convoluted attempts to explain away the data (see a recent editorial I wrote about this, also attached).
(iv) Brain studies do not provide clear evidence of neurodevelopmental disorder in psychosis
The evidence linking the basal ganglia to psychosis is far from clear cut. The best evidence is from response to antipsychotics, but recent studies suggest that only about 20% of patients show a genuine clinical response (Marques, T. R., et al. (2011). The different trajectories of antipsychotic response: antipsychotics versus placebo. Psychological Medicine, 41, 1481-1488). In any case, abnormal basal ganglia activity could just as likely be attributed to environmental factors – animal studies show that chronic victimisation leads to sensitisation of dopamine pathways in this part of the brain (Selten, J.-P., & Cantor-Graae, E. (2005). Social defeat: Risk factor for psychosis? British Journal of Psychiatry, 187, 101-102).
Current structural and functional neuroimaging studies of psychosis are probably not to be trusted for a variety of complex methodological reasons (Ioannidis, J. P. A. (2011). Excess significance bias in the literature on brain volume abnormalities. Archives of General Psychiatry, 68, 773-780; Button et al. (2013), Power failure: Why small sample size undermines the reliability of neuroscience, Nature Reviews Neuroscience, published online 10 April 2013; doi:10.1038/nrn3475 – this study estimated that the median statistical power of 461 individual fMRI studies contributing to 41 separate meta-analyses was 8%!), not least the emerging evidence that drugs affect brain structure (Ho, B.-C.,et al. (2011). Long-term antipsychotic treatment and brain volumes. Archives of General Psychiatry, 68, 128-137).
In any case, the observed abnormalities could well be the consequence of social and environmental factors (Hoy, K., et al. (2011). Childhood trauma and hippocampal and amygdalar volumes in first–episode psychosis. Schizophrenia Bulletin. doi: 10.1093/schbul/sbr085).
(v) A narrow neurodevelopmental approach is damaging to patients
There is little evidence that the biological approach to psychiatry is benefiting patients. Outcomes for patients suffering from ‘schizophrenia’ have not improved since the Victorian age and an increasing number of people are disabled by psychiatric conditions. This is precisely the opposite to what has happened in physical medicine, where genuine advances have led to improved outcomes and reduced disability (see my Doctoring the Mind, and also Whitaker, R. (2005). Anatomy of an epidemic: Psychiatric drugs and the astonishing rise of mental illness in America. Ethical Human Psychology and Psychiatry, 7, 23-35). Just as importantly, although it is often assumed by doctors that promoting a biological understanding of psychosis will reduce stigma, empirical research provides strong evidence that the opposite is the case, and that biological models actually promote stigma (Read, J., et al.(2006) Acta Psychiatrica Scandinavica, 114, 303-318; Angermeyer, M. C., et al. (2011). Biogenetic explanations and public acceptance of mental illness: systematic review of population studies. British Journal of Psychiatry, 199, 367-372.)
The claim that biological research (on flies or whatever) will one day lead to a cure for schizophrenia is a common rhetorical trick designed to gain publicity and guarantee grant funding. I have no problem with research on the CNS of flies, which seems valuable in its own right. But linking flies to schizophrenia (whatever that is) is really about self-promotion and is damaging to the interests of patients.
Members of International Health Humanities network may be interested in an upcoming event. As part of a series of workshops for the Leverhulme-funded project “Fashionable Diseases: Medicine, Literature and Culture” at the Universities of Northumbria and Newcastle, we are pleased to welcome Professor Ian Hacking (Philosophy, University of Toronto) on 15th May 2013, 10:30am at the MEA House Auditorium, Northumbria University.
Professor Hacking will give a lecture entitled ”‘Making Up People’ Reconsidered” exploring the ways in which new scientific classifications of diseases such as multiple personality disorder and autism may affect experiences of them and thus give rise to a new type of person and way of being. You may wish to read the following article in preparation for the event: Ian Hacking, “Kinds of People: Moving Targets.” Proceedings of the British Academy 151 (2007): 285-318.
All are warmly invited to attend. See the poster below for details.
Dr. Anita O’Connell
Department of Humanities
· The problem with diagnosis
· Take a critical and thoughtful perspective on traditional ways of understanding voice hearing and visions.
· Understand the potential pitfalls of the claims made from other therapies.
· Take a respectful and ethical approach to the experience of voice hearing and visions.
· Understand the potential connection between trauma and voice hearing and visions.
· Develop new ways of talking to and working with people who experience voices and visions.
My article on EMDR therapy is on page 11
Guest Post by Dawn Willis : Bedding In, Bedding Out with Liz Crow – A tweet call and virtual participation information.