Western psychiatry is living on borrowed time. There is now compelling evidence to support the assertion that the discipline with overarching responsibility for reducing human distress is fundamentally flawed, routinely delivering interventions that are of limited effectiveness, discriminatory and that often do more harm than good to the recipients (Sidley, 2015 TFTM). The clamour for radical change is growing louder and louder, while the sources of dissent broaden.
Under these circumstances one would expect a responsible medical discipline to initiate a period of intense reflection on their practices, to acknowledge their mistakes, and express regret for the widespread harm caused by their stubborn insistence that human suffering is a manifestation of some form of brain abnormality. But no, not psychiatry; there’s too much at stake. Fearful of losing its place at the top table of medical specialities, and not wishing to upset its pharmaceutical paymasters, the psychiatric establishment digs in and defends the indefensible.
In the arena of research and academia, biological psychiatrists have evolved a range of stock responses to deny culpability. So when specific criticisms, along with the empirical evidence to support them, are published in the scientific journals biological psychiatrists resort again and again to the same mantras intended to protect their profession. Here are three of psychiatry’s most common head-in-the-sand retorts to valid, evidence-based concerns about their core practice; a further three will follow in the second part of this blogpost.
1. The critic lacks expertise or objectivity
Rather than addressing the specific criticism, a standard psychiatry ploy is to undermine the credibility of the person raising the concern. When challenged, psychiatry’s first-line response is to try to discredit the attacker. The person highlighting the flaws is accused of engaging in a ‘turf war’, self-promotion or of representing some extreme political movement intent on anarchy. Alongside this knee-jerk tactic, psychiatry strives to defuse alternative approaches, neutralising them with dubious claims that ‘we are already doing that’.
This tactic, commonplace on social media, can also be seen in the academic literature. An early example of this manoeuvre occurred in 1968 with the reaction to George Crane’s conservative assertion that as many as a quarter of all hospitalised psychiatric patients suffered with tardive dyskinesia (an enduring disorder characterised by uncontrollable movements of tongue, face, lips and limbs) and that the psychotropic drugs were the most likely cause of this often permanent affliction. (Crane, 1968). Crane’s valid concerns provoked personal attacks from his fellow psychiatrists who accused him of poor scientific practice and lack of objectivity (Kline, 1968; Moncrieff, 2013, p78).
Contemporary examples of these character assassinations can be seen in the reactions to the work of Robert Whitaker, an American author and award-winning science journalist. Although a vocal and high-profile critic of biological psychiatry, Whitaker’s written appraisals are always comprehensive, meticulous and thoroughly researched. Despite this, his work frequently evokes personal attacks from prominent members of the psychiatric establishment. For example, on a popular Canadian radio programme in 2015, psychiatrist Jeffrey Lieberman (a former head of the American Psychiatric Association) described Whitaker as ‘a menace to society’ who has ‘an ideological grudge against psychiatry’. In the same interview, Lieberman also undermines Whitaker’s journalistic credentials with the slur, ‘God help the publication that employed him’.
2. The harm is a result of the underlying illness, not our treatments
For several decades, when confronted with evidence that their ‘treatments’ are damaging their patients, psychiatry has routinely strove to attribute the alleged negative consequences to some underlying disease process associated with the ‘mental illness’. Two prominent examples of this head-in-the-sand approach to criticism are the brain abnormalities associated with long-term ingestion of antipsychotics and the memory impairments following electro-convulsive therapy (ECT).
Advanced imaging techniques and post-mortem examinations have provided substantial evidence that the degree of brain-cell degeneration corresponds to the amount of antipsychotics ingested – in other words, the greater the drug intake, the greater the brain shrinkage (Sidley, 2015, p158). The primary responsibility of any medical profession is to do no harm, so one might reasonably expect that reports suggesting one of the mainstays of their treatment armoury is linked to neural decay would trigger caution, concern, even urgency within psychiatry.
On the contrary.
Biological psychiatrists have attempted to explain away these brain abnormalities as the consequence of some assumed, underlying schizophrenic disease process (Andreasen et al., 2011 ) or ‘continuous pathophysiological process … that warrants further study’ (Hulshoff Pol & Kahn, 2008, p354). Even when a potential deleterious role for antipsychotics is acknowledged, it is relegated to a supplementary contributor alongside some assumed ‘disease process’ (Cahn et al, 2002, p1002). A recent, high-profile study (Goff et al., 2017) regurgitated a similar conclusion: ‘it is not possible to conclude from available clinical imaging studies whether the brain volume loss observed during the course of illness is attributable to antipsychotics or to the underlying illness’. The aforementioned Jeffrey Lieberman took the self-serving defensiveness to a ludicrous degree – perhaps best described as head, torso and limbs in the sand – with his definitive conclusion, expressed in the Columbia University Psychiatry Department press release, that ‘antipsychotic medications do not have negative long-term effects … on the brain’.
It is universally accepted that electro-convulsive therapy (ECT) – a psychiatric treatment where sufficient electricity to trigger a grand-mal seizure is passed through the brain – causes some degree of memory loss. Furthermore, there is substantial evidence that for a significant proportion of recipients this amnesia may endure, or even be permanent (for a review, see Read et al., 2013).
Once again, the psychiatric establishment attempts to explain away this troublesome finding by denying that the erosion of autobiographical memories is a direct consequence of ECT. For example, McGuffin and Farmer (2008) claim that this deficit was due to the ‘unimproved depressive illness’. Similarly, the UK’s Royal College of Psychiatry information website, after mentioning that some people ‘complain’ of permanent memory loss, goes on to state that, ‘It is not clear how much of this is due to the ECT, and how much is due to the depressive illness or other factors’.
The self-serving notion that the documented damage to patients is a result of underlying illness rather than the psychiatric interventions might be more plausible if empirical research had indicated that ‘schizophrenia’ and ‘depression’ were the products of an inherent, progressive brain disease; no such evidence exists. Consequently, these head-in-the-sand explanations in some ways parallel a bygone age where a powerful group of people inflict prolonged beatings on others to drive out evil spirits and then attribute the subsequent physical injuries to the internal demons.
3. We are on the cusp of a major scientific breakthrough
For more than half a century, psychiatry has claimed to be on the cusp of a scientific discovery that will transform our understanding of ‘mental illness’. The focus of their research endeavours – lavishly funded by the pharmaceutical industry – has often concerned the identification of specific genes for ‘schizophrenia’ or ‘depression’. Biological psychiatrists excitedly tell us that their work teeters on the brink of a game-shifting discovery, one that will prove that severe mental health problems are bona fide brain diseases.
Despite their frenetic efforts, such a breakthrough remains elusive. We’ve heard many grand claims linking fundamental brain abnormalities (biochemical and structural) to an array of mental health problems but none of them have been substantiated as representing primary causes of human suffering. Indeed, upon further consideration, any reliable brain differences between those tagged with a psychiatric diagnosis and those not seem more likely to be a consequence of the ‘treatments’ rather than constituting a biological basis for the distress.
This head-in-the-sand response continues. When challenged about the ineffectiveness of its core practises, psychiatry implores us to be patient and await the great reveal of a revolutionary breakthrough. In 2011, Ronald Pies (a high-profile American psychiatrist) announced that progress in neuroscience indicated that ‘psychiatry may be on the brink of a unified model of so-called mental illness’. A similar tone was adopted by Goff et al. (2017) in their reaction to the robust finding that many people with psychotic experiences fare better without antipsychotic drugs. This self-proclaimed group of expert psychiatrists concluded that this ‘subgroup of patients require further study, including the development of biomarkers that will enable a precision medicine approach to individualized treatment’.
The overarching message is there is no need to worry about the ineffectiveness of core psychiatric interventions, nor the damage being inflicted on millions of people, because biomarkers, precision medicine and a unifying model of mental illness are just around the corner.
A further three head-in-the-sand responses will be discussed in the second part of this blog.
Andreasen, N.C., Nopoulos, P., Magnotta, V., Pierson, R., Ziebell, S. & Ho, B.C. (2011). Progressive brain change in schizophrenia: a prospective longitudinal study of first-episode schizophrenia. Biological Psychiatry, 70, 672 – 79.
Cahn, W., Hulshoff Pol, H.E., Lems, E.B., van Haren, N.E., Schnack, H.G., van der Linden, J.A. et al. (2002). Brain volume changes in first-episode schizophrenia: a 1-year follow-up study. Archives of General Psychiatry, 59, 1002 – 10.
Crane, G.E. (1968). Dyskinesia and neuroleptics. Archives of General Psychiatry, 19, 700 – 703.
Hulshoff Pol, H.E & Kahn, R.S. (2008). What happens after the first episode? A review of progressive brain changes in chronically ill patients with schizophrenia. Schizophrenia Bulletin, 34(2), 354 – 366.
Kline, N.S. (1968). On the rarity of ‘irreversible’ oral dyskinesias following phenothiazines. American Journal of Psychiatry, 124, 48 – 51.
McGuffin, P. & Farmer, A. (2008). Biological treatments of depression and anxiety.
In R. Murray et al (Eds). Essential Psychiatry, Cambridge: Cambridge University
Moncrieff, J. (2013). The Bitterest Pills: The troubling story of antipsychotic drugs. Palgrave, Macmillan.
Read, J., Bentall, R., Johnstone, L., Fosse, R. & Bracken, P. (2013). Electro-convulsive therapy. In J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis.Routledge.
Sidley, G. (2015). Tales from the Madhouse: An insider critique of psychiatric services. PCCS Books: Monmouth.
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