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Moncrieff, J. & Kirsch, I. (2005) Efficacy of antidepressants in adults. BMJ, 331, 155157.
Moncrieff, J. & Cohen, D. (2005) Rethinking models of psychotropic drug action. Psychotherapy and Psychosomatics, 74, 145153.
Moncrieff, J. & Cohen, D. (2006) Do antidepressants cure or create abnormal brain states? PLoS Medicine, 3, e150.


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Authors' reply

  • J. Moncrieff (a1)
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Psychiatric disorders , treatment and validity- time to view things differently

sanil rege, career medical officer
25 September 2007

J moncrieff in her reply (Moncrieff, 2006) to Psychiatry and drugs ( Stern, 2006) made certain statements that I felt were nihilistic and portrayed psychiatry as being less evidence based than medicine. I attemptto provide a balanced view on her statements rather than a biased one sided view which I believe goes against the spirit of criticalthinking . Ialso attempt to rescue psychiatry from the accusation that current practice is based on poor evidence not by claiming that treatments are based on conclusive evidence but by showing that practice in general medicine has and still does to proceed on less than ideal evidence.

1. According to J.Moncrieff ‘ In general medicine drugs act on somelevel of the pathological process that generates the symptoms. In contrast there is no evidence that drugs used in psychiatric conditions act on specific neuropathological processes’.

Against this argument there is evidence that antidepressants have actions on neuronal growth and vulnerability trough BDNF and synaptic plasticity in the hippocampus and other brain structures (Reid & Stewart , 2001).Neuropathologically antidepressants affect responses via direct effects onsubcortical and frontal regions( Davidson et al, 2003) .Similar results are found with lithium in bipolar disorder ( Manji , 2003) . Atypical antipsychotics might ameliorate structural changes caused by the disease process underlying schizophrenia and effects of typical antipsychotics. ( Sherk , 2006) .

The comment also leads to the assumption that prescription in psychiatry is not evidence based whilst in general medicine treatments aregrounded in evidence. This is not true. The administration of many drugs such as antihypertensives and aspirin are not based on good evidence. The use of simple hypertensives for severe hypertension or aspirin in myocardial ionfarction is based on numbers needed to treat (NNT) of about 15- 40 (Bandolier, 1995) In contrast, NNT’s in psychiatry for use of medication for most disorders are in the range of 3-9 in most studies. (Pinson, 2003)

2. Secondly she states ‘No specific physical pathology has been established for any major psychiatric condition’.Against this statement, there are a number of studies that show specific neurophysiological, neuropathological and neurochemical changes in depression and schizophrenia ( Surguladze et al 2003 , Ross , 2006). There is some truth in the fact that the etiology of psychiatric disordershas not been clearly elucidated.This however should not stop the need to develop new drugs or use the currently available drugs. Medicationscan give us important clues about the etiology of psychiatric disorders eg; tryptophan depletion studies elucidated the role of tryptophan deficiency in depression prompting the role of serotonin and SSRI’s in depression. (Delgado, 1990). Medicine did not advance by abandoning their existing medications or their search for new medications but by focusing on etiology. Phthisis or tuberculosis as it was later called was treated symptomatically until the etiological agent was identified which prompted development of anti tuberculous drugs. Myxedema for example was also treated symptomatically until thyroid dysfunction wasfound to be the cause. Epilepsy still currently lacks the explanation of a clear biological correlates and treatment is not focused on etiology.

The difference between psychiatry and general medicine does not lie in the way treatments are adopted and administered but in the description of disorders. Many Medical disorders have been defined at a much more fundamental level whilst the majority of psychiatric disorders still continue to be defined by their clinical syndromes which often bring theirvalidity into question. Eg symptoms such as amotivation are seen in both depression and schizophrenia, features of psychosis are common to bipolar disorder and schizophrenia. What is necessary is an alternate conceptualization of psychiatric disorder. Eg limbic cortical dysfunction as a model for depression or bipolar disorder and schizophrenia collapsed into ‘psychotic spectrum disorders’ (Craddock & Owen , 2005)

Current research is based on the assumption that these syndromes arediscrete entities. One solution is to abandon a syndromal approach in research and focus on the neurobiological correlates of symptoms eg motivation which is mapped on to the anterior cingulate( abulic syndrome caused by ant cingulate dysfunction) modulated by the norepinephrine system. We need to focus on etiological mechanisms ofpsychiatric disorders and classificatory systems need to be based as such imparting greater validity to research.

By claiming that drugs in psychiatry essentially do not work whilst those in general medicine perpetuates the dualism that already exists. This chemical dualism’ will be another addition to the organisational and conceptual dualism that pervades our practice currently. It also imparts one of the most serious forms of dualism , moral dualism implying thatpsychiatric patients are ill due to their poor coping mechanisms rendering culpability which medical patients are exempt from. I believe it is important to understand patients acceptance of these explanations proposed for illness and effects of drugs and work with the most suitable one. Moncrieff also claims that psychiatric medications actually create chemical imbalances. This might well be true but the hypothesis is not mutually exclusive and it is equally plausible and possible that psychiatric drugs correct the chemical imbalances .This maybe attributed to an active placebo effect, antidepressant effect and/or other non specific factors but in clinical experience many psychiatric drugs work and many patients benefit from them. This is because real life is very different from the artificial environment of a clinical trial. Medications are however not the complete answer by any means.

I agree with Moncrieff that the pharmaceutical industry has a greatinfluence on psychiatrists and our practice and in the current pluralisticworld this is difficult to avoid. They do offer simplistic neurotransmitter explanations that oversimplify complex conditions possibly for their own gains. I believe that it is here that skills of critical appraisal and Evidence based medicine ( EBM) are useful for the psychiatrist to interpret the evidence about medications for the patient and then use clinical experience, the social and biological circumstances of the patient and patient preference in decision making.

Finally, although I disagree with some of moncrieff's views I also feel that such opinions are valuable as they make the psychiatric profession exciting ,stimulate alternate conceptualizations of psychiatricillnesses, modify research and most importantly lead on to improvements intreatment.


1. Craddock , N and Owen, MJ . (2005)The beginning of the end for the Kraepelinian dichotomyBritish Journal of Psychiatry, 186, 364 - 366.

2. NNT and interpreting NNT – Bandolier Available from URL :

3. Davidson RJ, Irwin W, Anderle MJ, Kalin NH ( 2003). The neural substrates of affective processing in depressed patients treated with venlafaxine. American journal of psychiatry 160, 64-75.

4. Delgado, P.L. 1990. Serotonin function and the mechanisms of antidepressant action: Reversal of antidepressant induced remission by rapid depletion of plasma tryptophan. Archives of General Psychiatry, 47,411-418

5. Manji, H (2003). Depression,III American journal of Psychiatry 24, 160:1.

6. Moncrieff, J (2006). Author's replyBritish journal of Psychiatry; 189, 189. doi:10.1192/bjp.189.2.189

7. Pinson L. Gray GE.( 2003) Psychopharmacology: Number needed to treat : an underused measure of treatment effect. Psychiatric Services. 54,145-6.

8. Reid, I. C. & Stewart, C. A. (2001) How Antidepressants work. New perspectives on the pathophysiology of depressive disorder. British Journal of Psychiatry, 178, 299-303

9. Ross CA. Margolis RL. Reading SA. Pletnikov M. Coyle JT. (2006) Neurobiology of Schizophrenia .Neuron 52,139-53.10. Scherk H. Falkai P. (2006) Effects of antipsychotics on brain structure. Current Opinion in Psychiatry. 19,145-50.

11. Stern , R (2006) Promotion of psychiatric drugsBritish Journal of Psychiatry, 189, 188 - 189. doi:10.1192/bjp.189.2.188b

12. Surguladze , S, Keedwell , P , Phillips , M (2003)Neural systems underlying affective disorders. Advances in Psychiatric Treatment 9, 446 – 455..
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