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Research into putative biological mechanisms of mental disorders has been of no value to clinical psychiatry

  • David Kingdon (a1) and Allan H. Young (a2)
Extract

In 1845 Griesinger declared that mental disorders were physical in origin (Kendell, 2001). The discovery of the bacterial cause of general paresis and the anatomical basis for Alzheimer's disease seemed to confirm this belief. However, is it still reasonable, a century later, to continue to devote increasing amounts of financial and expert human resource to pursuing further possible physical causes for mental disorders? The belief that there remain undiscovered and important biological causes for mental disorders continues to exert a major influence on the direction of research, practice and public education. But has it helped us to understand aetiology, improve management or destigmatise mental disorders?

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References
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Angermeyer, M. C. & Matschinger, H. (2005) Causal beliefs and attitudes to people with schizophrenia. Trend analysis based on data from two population surveys in Germany. British Journal of Psychiatry, 186 331334.
Baldessarini, R. Tondo, L. Davis, P. et al (2006) Decreased risk of suicides and attempts during lithium treatment: a meta-analytic review. Bipolar Disorders, 8 625639.
Bauer, M. Adli, M. Baethge, C. et al (2003) Lithium augmentation in refractory depression: clinical evidence and neurobiological mechanisms. Canadian Journal of Psychiatry, 48 440448.
Bentall, R. P. (2004) Madness Explained: Psychosis and Human Nature. Penguin Books.
Cade, J. F. (1975) Lithium – when why and how? Medical Journal of Australia, 1 (22) 684686.
Craddock, N. & Owen, M. J. (2005) The beginning of the end for the Kraepelinian dichotomy. British Journal of Psychiatry, 186 364366.
Cunningham Owens, D. G. Carroll, A. Fattah, S. et al (2001) A randomized controlled trial of a brief interventional package for schizophrenic out-patients. Acta Psychiatrica Scandinavica, 103 362369.
Gartside, S. E. Leitch, M. M. & Young, A. H. (2003) Altered glucocorticoid rhythm attenuates the ability of a chronic SSRI to elevate forebrain 5-HT: implications for the treatment of depression. Neuropsychopharmacology, 28 15721578.
Geddes, J. R. Burgess, S. Hawton, K. et al (2004) Long term lithium therapy for bipolar disorder: systematic review and meta-analysis of randomized controlled trials. American Journal of Psychiatry, 161 217222.
Guze, S. B. (1989) Biological psychiatry: is there any other kind? Psychological Medicine, 19 315323.
Hall, W. (2006) Is cannabis use psychotogenic? Lancet, 367 193195.
Kane, J. Honigfeld, G. Singer, J. et al (1988) Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine. Archives of General Psychiatry, 45 789796.
Kendell, R. E. (1975) The Role of Diagnosis in Psychiatry. Blackwell.
Kendell, R. E. (2001) The distinction between mental and physical illness. British Journal of Psychiatry, 178 490493.
Kendell, R. E. & Zeally, A. K. (1988) Companion to Psychiatric Studies. Churchill Livingstone.
Kingdon, D. (2006a) Health research funding: mental health research continues to be underfunded. BMJ, 332 1510.
Kingdon, D. (2006b) Psychological and social interventions for schizophrenia. BMJ, 333 212213.
Kingdon, D. G. & Turkington, D. (2005) Cognitive Therapy of Schizophrenia. Guilford.
Kingdon, D. Sharma, T. & Hart, D. (2004) What attitudes do psychiatrists hold towards people with mental illness? Psychiatric Bulletin, 28 401406.
Kingdon, D. Gibson, A. Turkington, D. et al (2007) Acceptable terminology and subgroups in schizophrenia: an exploratory study. Social Psychiatry and Psychiatric Epidemiology in press.
Kunugi, H. Ida, I. Owashi, T. et al (2006) Assessment of the dexamethasone/CRH test as a state-dependent marker for hypothalamic-pituitary-adrenal (HPA) axis abnormalities in major depressive episode: a multicenter study. Neuropsychopharmacology, 31 212220.
Lopez-Munoz, F. Alamo, C. Cuenca, E. et al (2005) History of the discovery and clinical introduction of chlorpromazine. Annals of Clinical Psychiatry, 17 113135.
Meaney, M. J. & Szyf, M. (2005) Maternal care as a model for experience-dependent chromatin plasticity? Trends in Neurosciences, 28 456463.
Myin-Germeys, I. Delespaul, P. & Van, O. J. (2005) Behavioral sensitization to daily life stress in psychosis. Psychological Medicine, 35 733741.
Nitrini, R. (2005) The cure of one of the most frequent types of dementia: a historical parallel. Alzheimer Disease and Associated Disorders, 19 156158.
Rathod, S. Kingdon, D. Smith, P. et al (2005) Insight into schizophrenia: the effects of cognitive behavioural therapy on the components of insight and association with sociodemographics – data on a previously published randomised controlled trial. Schizophrenia Research, 74 211219.
Read, J. Agar, K. Argyle, N. et al (2003) Sexual and physical abuse during childhood and adulthood as predictors of hallucinations delusions and thought disorder. Psychology and Psychotherapy, 76 122.
Teskey, P. (2006) What's in a name? A case for changing the ‘S’ word. Schizophrenia Digest, 4 3637.
Watson, S. Gallagher, P. Ritchie, J. C. et al (2004) Hypothalamic–pituitary–adrenal axis function in patients with bipolar disorder. British Journal of Psychiatry, 184 496502.
Watson, S. Gallagher, P. Smith, M. S. et al (2006) The dex/CRH test-is it better than the DST? Psychoneuroendocrinology. 31 889894.
Young, A. H. Gallagher, P. Watson, S. et al (2004) Improvements in neurocognitive function and mood following adjunctive treatment with mifepristone (RU-486) in bipolar disorder. Neuropsychopharmacology, 29 15381545.
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Research into putative biological mechanisms of mental disorders has been of no value to clinical psychiatry

  • David Kingdon (a1) and Allan H. Young (a2)
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eLetters

Author's response

David G Kingdon, Professor of Mental Health Care Delivery
28 November 2007

Pattanayak asserts that I am dismissive of biological advancements - not true, my hay fever benefits from them every summer - I’m simply tryingto identify their relevance to psychiatric practice. If such advancementsin understanding ‘putative biological mechanisms of mental disorder’ proved of concrete value to clinical psychiatry, I would be delighted but no single example has yet been given in these letters or the original debate which demonstrate this to be the case.

Hill says that genetic research helps in counselling patients but what he is describing is the relevance of discussing and providing evidence about the influence of family history. Any genetic component may relate to mental disorder but could it simply be the mediating effects of the genetics of vulnerability factors such as temperament? He adds some speculations about the interaction of biology and social circumstances andthe former’s possible role in conveying vulnerability to depression. HPA reactivity may be theoretically interesting but how does assessment of it contribute to clinical interactions? And how exactly, in the management ofchildhood maltreatment are ‘the presence (sic) of structural abnormalitiesin the brain ... highly relevant in clinical practice’?

If after decades of watching the ‘new dawn’, the sun still does not appear to have risen, could I suggest to Dr Al-Adwani and his colleagues that they turn round and look in a different direction? They may find that it has been rising behind them providing illumination of the way forward. Such a reorientation by psychiatry, to use psychosocial research as the foundation from which to address the major issues that exist, couldtransform our fundamentally flawed classification system (McHugh, 2005), appallingly stigmatising terminology (Kingdon, 2007b;Kingdon, 2007a) and manifestly confusing and ineffective explanations of mental conditions (Read et al, 2006).

Declaration of interest: none.

Reference List

1. Kingdon, D. (2007a) Down with schizophrenia. New Scientist, 196, 22.

2. Kingdon, D. (2007b) DSPD or 'Don't Stigmatise People in Distress': Invited commentary on ... Challenges in the treatment of dangerous and severe personality disorder. Advances in Psychiatric Treatment, 13, 333-335.

3. McHugh, P. R. (2005) Striving for coherence: psychiatry's effortsover classification. JAMA, 293, 2526-2528.

4. Read, J., Haslam, N., Sayce, L., et al (2006) Prejudice and schizophrenia: A review of the 'mental illness is an illness like any other' approach. Acta Psychiatrica Scandinavica, 114, 303-318.
... More

Conflict of interest: None Declared

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Putative biological mechanisms in psychiatry

Premal J Shah, Consultant psychiatrist
28 November 2007

It is interesting that the debate (1) has been framed in terms of thevalue of apparent ‘biological mechanisms’. This could imply that there are other putative mechanisms or approaches which do have value. Whilst asking this specific question is useful for debate, the mirror question, that of the clinical value of putative psychological mechanisms ought to be debated as well, and could prove even more controversial.

It is perhaps a marker of the state of current psychiatry where the ‘biological/ psychological’ dichotomy in psychiatry still evokes extreme views, and keeps resuscitating a mindless (and brainless) Descartian dualism, where psychosocial interventions and models are somehow seen as holistic and superior working with the mind, the ‘biological’ being the lesser ‘brain science’. Of all people, psychiatrists need to overcome these dualistic tendancies and simply try and refine what treatments work for our patients, without assuming that treatments give insight into the aetiology of disorders.

Particularly worrisome is Professor Kingdon’s assertion that a model of mental disorder is true on the basis that patients and the general public understand it, that it fits with their model of mental disorder, and supports psychosocial interventions. This is because it argues againstscientific rigour, overlooks the fact that science often challenges conventional and accepted wisdom, and assumes psychosocial interventions are, somehow, not medical. On the strength of that argument, we would haveneeded to accept conventional wisdom at Gallileo’s time that the Earth wasflat, because that was what the general public accepted. Indeed, such an argument seems to favour democratically electing scientific fact, invokingmodern day ‘truthiness’ and practicing postmodernism. Following such an approach would not allow us to practice medicine for the patient’s benefit, but rather for the benefit of the patient’s ideology. Perhaps we need rid of the shackles of dualism, and instead concentrate our efforts on defining what is best for our patient, regardless of treatment modality.

REFERENCES

1.Kingdon D, Young AH. Research into putative biological mechanisms of mental disorders has been of no value to clinical psychiatry.Br J Psychiatry.2007;191:285-90

Dr. Premal J Shah, Honorary Senior Lecturer, Consultant in General Psychiatry, Royal Edinburgh Hospital, Morningside Terrace, Edinburgh EH10 5HF. Tel No. 0131 537 6000

Declaration of interest- none.
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Conflict of interest: None Declared

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Skepticism is welcome, dismissal is not

Raman D Pattanayak, M.D;Senior resident
31 October 2007

Kingdon (1) has provided his perspective suggesting the dismissal of biological advancements and alternatively, promotion of psychosocial research. This is our humble attempt to challenge some of the points raised by him.

To discard the biological advances for being unable to pin-point the ‘exact etiology’ or ‘cure’ is unjust. It has remained elusive in entire medicine as a speciality (90% of hypertension is idiopathic sans any ‘cure’; so is epilepsy).We never forget to take our anti-hypertensive pills, why make an exception for psychiatric illnesses.

As for the statement made by Kingdon (1) "…research into psychosocialmechanisms, which has been much more productive." We refer to a recent meta analyses by Luborsky (2) which revealed that the effect size attributed to specific therapy techniques is only 0.2 and common factors such as therapist-client alliance found to be more important (3). This casts doubts over the clinical relevance of 400 different types of psychotherapies. Absence of large scale well controlled trials on efficacyof psychotherapy versus pharmacotherapy in major mental illnesses further leaves us wondering.Further, the abandonment of once prevalent theories about ‘latent homosexuality’ , ‘refrigerator mothers’ and ‘schizophrenogenic families’ only begs us to be doubly cautious before accepting empirical evidence as absolute.

Those who don’t learn from mistakes in past are condemned to repeat it….We quote this in context of past 100 years of dementia research. Alzheimer’s initial findings were dismissed as non-specific and most tributes on his death in 1915 did not even mention this, now significant, discovery. Psychological theories of dementia (‘elderly neglect / loneliness’) were in vogue till 1960s. Ironically, we often dismiss the biological theories despite the preliminary evidence and go on to ‘believe’ the psychological theories without challenging the very basis ofthat belief.

Finally in response to the issue of enhanced stigma associated with illness model, the study showing enhanced suicidlity (4) cannot be overgeneralised and it would be erroneous to undermine the well recognised benefits and enhanced compliance after psycho-education.Patients have a ‘right to know’ about the mental illness. We can draw a parallel with HIV or cancer.Have we ever considered shifting away from their biological causation because of stigma or enhanced suicidal risk respectively. How to educate and update the general public with the available information in the most appropriate way is the researchquestion ,concealing the evidence is unfortunately not an answer.

Current clinical practice rests on a consensus about BPAD,Schizophrenia,OCD and ADHD as primary biological diseases with stronggenetic component and psychosocial factors contributing to the disease process in contrast to 1950s, thanks to contribution from biological research. We agree with Young(1) when he brings up the biopsychosocial model. Understanding all the complexities of biology is a ‘process’ and cannot be over in this short period of biological research.

We can be optimistic at best and skeptical at worst about the clinical relevance of biological contribtions but cynicism and dismissal would be a big mistake.

REFERENCES:

(1)Kingdon D, Young AH.Research into putative biological mechanisms of mental disorders has been of no value to clinical psychiatry.Br J Psychiatry.2007;191:285-90

(2)Luborsky, Rosenthal, SIguer, Andrusyna, Berman, Levitt, Seligman,Krause. "The Dodo bird verdict is alive and well - mostly". Clinical Psychology: Science and Practice.2002;9:2-12

(3)Messer SB, Wampold BE.Let's Face Facts: Common Factors Are More Potent Than Specific Therapy Ingredients. Clinical Psychology: Science andPractice.2002;9 :21-5

(4)Cunningham Owens DG, Carroll A, Fattah S, Clyde Z, Coffey I, Johnstone EC.A randomized, controlled trial of a brief interventional package for schizophrenic out-patients. Acta Psychiatr Scand.2001;103:362-9
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Conflict of interest: None Declared

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Biology is psychiatrys new dawn

Andrew Al-Adwani, Consultant psychiatrist
12 October 2007

With Kingdon's view, which seems to say because we haven't found it why bother looking, all scientific endeavour would come to a halt. To propose that genetic research has not contributed to our ability to offer counselling is to ignore the extremely high heritabilty of bipolar disorder and the schizophrenias and the advice we are able to offer in light of our knowledge. We have not even begun to skim the surface as faras research into the biological mechanisms underlying the major mental disorders is concerned, and more recent findings, such as the doubled or greater risk of developing a schizophrenic illness as a consequence of cannabis use, open yet more doors for researchers to explore the contents beyond. The fact that our tools are crude and our knowledge shallow does not justify giving up our search as with this attitude no heavenly body, beyond those visible to the naked eye, would have been discovered. The biological basis of all the major mental illnesses, and their often successful chemical treatment, could only be dismissed by those blinded bydogma. The fact that our drug treatments have, for the most part, been discovered serendipitously does not render them any the less valuable and to dismiss these discoveries would also lead to the dismissal of the discovery of antibiotics or radiology for example. We have refined our treatments on the basis of many chance discoveries and long may the tradition of research for researches sake continue and thereby provide us with new therapeutic opportunities. The claims for cognitive therapy as the answer to all our problems are thankfully receding and allowing for a more enlightened mindset to regain centre stage. ... More

Conflict of interest: None Declared

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