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Psychological Medicine
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ARTICLE CONTENTS
* Abstract
* Introduction
* Antidepressants
* Electroconvulsive therapy
* Alternative approaches
* References
DEPRESSION: WHY DRUGS AND ELECTRICITY ARE NOT THE ANSWER
Published online by Cambridge University Press: 01 February 2022
John Read [Opens in a new window] and
Joanna Moncrieff
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--------------------------------------------------------------------------------
John Read* Affiliation:
School of Psychology, University of East London, London E15 4LZ, UK
Joanna Moncrieff Affiliation:
Division of Psychiatry, University College, London, UK
*
Author for correspondence: John Read, E-mail: john@uel.ac.uk
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* Abstract
* Introduction
* Antidepressants
* Electroconvulsive therapy
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ABSTRACT
The dominant view within mental health services and research suggests that
feeling depressed is a kind of medical illness, partially caused by various
biological deficits which are somehow corrected by physical interventions. This
article critically appraises evidence for the effectiveness and value of
antidepressant drugs and electroconvulsive therapy (ECT), the two principle
physical treatments recommended for depression. It also describes the negative
effects of these interventions and raises concerns about how they impact the
brain. We propose an alternative understanding that recognises depression as an
emotional and meaningful response to unwanted life events and circumstances.
This perspective demands that we address the social conditions that make
depression likely and suggests that a combination of politics and common sense
needs to guide us in providing help for one another when we are suffering in
this way. This alternative view is increasingly endorsed around the world,
including by the United Nations, the World Health Organization and service users
who have suffered negative consequences of physical treatments that modify brain
functions in ways that are not well-understood.
--------------------------------------------------------------------------------
KEYWORDS
Depressionantidepressantselectroconvulsive therapyplaceboadverse effects
--------------------------------------------------------------------------------
Type Invited Review
Information
Psychological Medicine , First View , pp. 1 - 10
DOI: https://doi.org/10.1017/S0033291721005031[Opens in a new window]
Copyright Copyright © The Author(s), 2022. Published by Cambridge University
Press
INTRODUCTION
With the World Health Association and the United Nations calling for a paradigm
shift away from the medicalisation of human distress, new evidence about
millions of people struggling to get off antidepressants, and ongoing debate
about the value and safety of electroconvulsive therapy (ECT), it seems timely
to discuss these two longstanding treatments offered to us by biological
psychiatry's ‘medical model’ when we become sad or depressed.
Firstly, we acknowledge that treatments rest on, and are justified by,
assumptions about the nature, and causes, of what is being ‘treated’. Advocates
of so-called ‘antidepressant’ medications, and ECT, argue that the treatments
work by correcting underlying biological dysfunctions. These hypothesised
dysfunctions are proposed to be among the causes of the problematic cognitions,
emotions and behaviour that are referred to as ‘symptoms’ and that form the
criteria for diagnosing ‘mental disorders’ such as ‘Major Depressive Disorder’.
We, and others, have provided detailed reviews of evidence demonstrating that no
biological dysfunction that can be corrected by current treatments has been
found, and explained how alternative mechanisms can account for apparent
treatment effects including treatment-induced alterations to normal brain
functions as well as placebo effects (Breggin, Reference Breggin2008; Fosse &
Read, Reference Fosse and Read2013; Moncrieff, Reference Moncrieff2008;
Moncrieff & Cohen, Reference Moncrieff and Cohen2005; Rasmussen, Reference
Rasmussen2009; Read et al., Reference Read, Gibson, Cartwright, Shiels, Dowrick
and Gabbay2015; Read, Kirsch, & McGrath, Reference Read, Kirsch and McGrath2019;
Read & Sanders, Reference Read and Sanders2010; Speed et al., Reference Speed,
Moncrieff and Rapley2014; Valenstein, Reference Valenstein1988).
Although most clinicians subscribe to a biopsychosocial model of mental
disorder, the idea that treatments work by rectifying underlying biological
dysfunctions relegates the role of social and psychological factors to secondary
or indirect considerations, such as triggers of a supposed genetic
predisposition. Although holistic care is important in general medicine, the
primary focus is treating the physiological processes that give rise to symptoms
and health risks (Moncrieff, Reference Moncrieff2020). Therefore, equating
psychiatric conditions and treatments with medical ones implies the pre-eminence
of biological factors. This is reinforced with psychiatric language. Depression,
for example, is described as somehow causing abnormal feelings and behaviours,
as if it were a physical condition, even though those same feelings and
behaviours form the criteria for the diagnosis in the first place. For example,
the American Psychiatric Association (2021a) proclaims:
Depression (major depressive disorder) is a common and serious medical illness
that negatively affects how you feel, the way you think and how you act.
Until January 2021, the APA website advised:
Psychiatric medications can help correct imbalances in brain chemistry that are
thought to be involved in some mental disorders. (APA, 2021b)
The idea that biological factors ‘cause’ depression, even if in conjunction with
social circumstances, also presupposes that there is a mechanical and
predictable relationship between biology and human feelings and actions that
excludes the possibility of meaning and agency (Moncrieff, Reference
Moncrieff2020). Hence viewing depression as a medical disorder that somehow
originates in the brain and responds to brain-based interventions is
fundamentally inconsistent with understanding it as a ‘normal’ human emotion,
albeit sometimes extreme and disproportionate – that is as a meaningful reaction
to depressing events and circumstances (Moncrieff, Reference Moncrieff2020).
Although we will focus on the failure to establish that antidepressants and ECT
are effective or safe, we do so from the perspective that this approach,
focussed as it is on decontextualised, pathologised individuals or brains, is
flawed from the outset. For example, it cannot address the issues underlying
women being about twice as likely as men to receive either ‘treatment’. We are
not alone in calling instead for approaches that acknowledge the meaning of
depression, and address the common social origins of misery and sadness (e.g.
Brown & Harris, Reference Brown and Harris1978; Cromby, Harper, & Reavey,
Reference Cromby, Harper and Reavey2013; Johnstone et al., Reference Johnstone,
Boyle, Cromby, Dillon, Harper, Kinderman and Read2018; Puras, Reference
Puras2019).
ANTIDEPRESSANTS
ARE ANTIDEPRESSANTS ACTIVE PLACEBOS?
Certain drugs have been referred to as ‘antidepressants’ since the 1950s.
Despite this appellation, it is not clear that they have any specific
antidepressant effects. Hundreds of placebo-controlled trials suggest that
antidepressants are marginally better than placebo at reducing depressive
symptoms as measured by depression rating scales. Combining published and
unpublished studies suggests an effect size of around 0.3 across different
meta-analyses, which translates into a difference of around 2.0 points on the
commonly used Hamilton Depression rating scale (HAM-D) (Hamilton, Reference
Hamilton1960), which has a maximum score of 52 points. This has not been shown
to be a clinically relevant difference (Leucht et al., Reference Leucht,
Fennema, Engel, Kaspers-Janssen, Lepping and Szegedi2013; Moncrieff & Kirsch,
Reference Moncrieff and Kirsch2015). Matching HAM-D scores against Clinical
Global Impression scale scores (Guy, Reference Guy1976) suggests a difference of
8 points is required to indicate ‘mild clinical improvement’ and that a
difference of 3 points and below does not register as indicating any change.
Moreover, the small difference between antidepressant drugs and inert placebo
tablets does not confirm that the drugs have an antidepressant action. There are
other explanations for these small differences. At present, most drugs are
assumed to work according to a ‘disease-centred’ model of drug action, which
proposes that they act on the biological processes assumed to underpin symptoms,
in the same way as drugs do in most medical conditions, including non-curative,
symptomatic treatments (such as salbutamol for wheezing). However, an
alternative, ‘drug-centred’ model suggests that psychiatric drugs change mental
states and behaviour through the modification of normal brain functions (Table
1). This model highlights that psychiatric drugs are psychoactive substances
that alter normal thoughts, sensations, emotions and behaviours. These
alterations, along with physical alterations, may unblind people in
placebo-controlled trials. This may lead to amplified placebo effects among
those taking active drugs, especially since several antidepressant studies show
that people's beliefs about whether they are taking an active drug or a placebo
have substantial effects on the outcome (Chen et al., Reference Chen,
Papakostas, Youn, Baer, Clain, Fava and Mischoulon2011; Faria et al., Reference
Faria, Gingnell, Hoppe, Hjorth, Alaie, Frick and Furmark2017). Consistent with
this, it seems that almost any drug with psychoactive properties (one that
produces noticeable mental alterations) has equivalent effects to
antidepressants in depression, including benzodiazepines, stimulants, opiates,
buspirone and antipsychotics (Moncrieff, Reference Moncrieff2008).
Table 1. Alternative models of drug action (adapted from Moncrieff, Reference
Moncrieff2009; Moncrieff & Cohen, Reference Moncrieff and Cohen2005)
The mental and behavioural alterations produced by antidepressants (and other
psychiatric drugs and ECT) may also reduce or mask depressed feelings or other
‘symptoms’ of depression. Selective serotonin reuptake inhibitors (SSRIs) and
some other antidepressants have emotion-numbing effects, which may lead to a
reduction in the intensity of both depression and anxiety (Goldsmith &
Moncrieff, Reference Goldsmith and Moncrieff2011; Price, Cole, & Goodwin,
Reference Price, Cole and Goodwin2009; Read & Williams, Reference Read and
Williams2018). Antidepressants with sedative properties, for example, such as
the tricyclic antidepressants and some newer agents like mirtazapine, may help
with insomnia or reduce anxiety or agitation, all of which feature in depression
rating scales. The fact that differences from placebo are so small suggests
these effects are not particularly useful, however.
Other artefacts may also account for the differences between drugs and placebos
in randomised trials, such as selective publication (Turner, Matthews,
Linardatos, Tell, & Rosenthal, Reference Turner, Matthews, Linardatos, Tell and
Rosenthal2008), the conversion of continuous data into categorical outcomes
(Kirsch & Moncrieff, Reference Kirsch and Moncrieff2007), and the fact that many
participants in drug trials are already on medication, and are then withdrawn,
leading to withdrawal effects and increased likelihood of unblinding in the
placebo group (Hunter et al., Reference Hunter, Cook, Tartter, Sharma, Disse and
Leuchter2015).
ANTIDEPRESSANTS PERFORM POORLY IN CLINICAL PRACTICE
The majority of placebo-controlled trials have been conducted by the
pharmaceutical industry, which has an investment in inflating results, but
government-funded research also fails to confirm that antidepressants have
beneficial effects. The massive sequenced treatment alternatives to relieve
depression (STAR-D) study of gold-standard naturalistic antidepressant treatment
produced dismal results. Although the original publication suggested reasonable
remission rates of 37% at 12 weeks (Rush et al., Reference Rush, Trivedi,
Wisniewski, Nierenberg, Stewart, Warden and Fava2006), the study has been
criticised for the use of a secondary outcome measure, exclusion of early
dropouts and numerous other protocol deviations (Pigott, Reference Pigott2015;
Pigott, Leventhal, Alter, & Boren, Reference Pigott, Leventhal, Alter and
Boren2010). A subsequent analysis found that only 108 participants out of a
total of over 4000 recovered, remained well and completed the study, a figure
that is still based on the secondary outcome (Pigott et al., Reference Pigott,
Leventhal, Alter and Boren2010). For 14 years no data was published on the
primary outcome measure, the Hamilton rating scale. When independent researchers
eventually obtained the data it emerged that people given antidepressant
treatment along with high-quality care showed a reduction in their scores of 6.6
points after 12 weeks (Kirsch, Huedo-Medina, Pigott, & Johnson, Reference
Kirsch, Huedo-Medina, Pigott and Johnson2018). This is at the lower end of the
range of change seen in people on placebo in meta-analyses of randomised trials
(Gibbons, Hur, Brown, Davis, & Mann, Reference Gibbons, Hur, Brown, Davis and
Mann2012; Kirsch, Moore, Scoboria, & Nicholls, Reference Kirsch, Moore, Scoboria
and Nicholls2002; Sugarman, Loree, Baltes, Grekin, & Kirsch, Reference Sugarman,
Loree, Baltes, Grekin and Kirsch2014) and roughly half that in randomised trials
comparing different antidepressants (Rutherford, Sneed, & Roose, Reference
Rutherford, Sneed and Roose2009). This suggests that the conditions of being in
a randomised trial inflate drug effects and that, in real life, antidepressants
are no better than placebos.
DO ANTIDEPRESSANTS CORRECT AN UNDERLYING BIOLOGICAL ABNORMALITY?
Despite claims by professional organisations and the pharmaceutical industry
that depression is due to a chemical imbalance that can be rectified by drugs
(e.g. APA, 2021b), there is no evidence that there are any neurochemical
abnormalities in people with depression, let alone abnormalities that might
cause depression. Where differences between people with and without depression
have been found, these are likely to be explained by prior use of
antidepressants and other medications; but in most areas, no consistent
differences have been found in any case (Moncrieff et al., Reference Moncrieff,
Stockmann, Amendola, Hengartner and Horowitz2021). Although the public,
internationally, continue to favour psycho-social explanations of depression
(Hagmayer & Engelmann, Reference Hagmayer and Engelmann2014; Read et al.,
Reference Read, Cartwright, Gibson, Shiels and Haslam2014; Read et al.,
Reference Read, Cartwright, Gibson, Shiels and Haslam2015), an increasing
proportion have been influenced to believe that depression is caused by a
chemical imbalance (Pilkington, Reavley, & Jorm, Reference Pilkington, Reavley
and Jorm2013), and across the world increasing numbers now take antidepressants
(OECD, 2020; Olfson, Wang, Wall, Marcus, & Blanco, Reference Olfson, Wang, Wall,
Marcus and Blanco2019). Seventeen per cent of the population of England were
prescribed an antidepressant in 2018 (Taylor et al., Reference Taylor, Annand,
Burkinshaw, Greaves, Kelleher, Knight and Marsden2019), and 14% of US adults by
2015 (Olfson et al., Reference Olfson, Wang, Wall, Marcus and Blanco2019). Yet
the number of people requiring services or going onto long-term disability due
to depression is increasing (Olfson et al., Reference Olfson, Wang, Wall, Marcus
and Blanco2019; Viola & Moncrieff, Reference Viola and Moncrieff2016).
ANTIDEPRESSANTS ALTER NORMAL MENTAL ACTIVITY AND BEHAVIOUR
Besides the fact that millions of people are taking drugs with little
demonstrable benefit, the dominance of the disease-centred model of drug action
has inhibited research into the nature of the various antidepressant drugs. We,
therefore, don't know the full implications and long-term consequences of taking
these drugs. Like other psychiatric drugs, they are psychoactive substances that
cross the blood-brain barrier and alter normal mental processes and behaviour by
changing the normal functioning of the brain. Evidence suggests that SSRIs
reduce the intensity of emotions, and produce apathy and demotivation, which are
associated with impairment of sexual function (Goldsmith & Moncrieff, Reference
Goldsmith and Moncrieff2011; Padala et al., Reference Padala, Padala, Majagi,
Garner, Dennis and Sullivan2020; Read & Williams, Reference Read and
Williams2018; Zahodne et al., Reference Zahodne, Bernal-Pacheco, Bowers, Ward,
Oyama, Limotai and Okun2012). A drug-centred model suggests that we need to
evaluate whether such changes might have worthwhile effects, when balanced
against their likely negative impact and other adverse effects.
ADVERSE EFFECTS OF ANTIDEPRESSANTS
Modern antidepressants are generally less toxic than their predecessors and
therefore less likely to be used for self-poisoning or suicide, as older
antidepressants frequently were (Henry & Antao, Reference Henry and Antao1992).
Many have fewer adverse effects, but they are not innocuous. SSRIs cause sexual
dysfunction in a large proportion of users, and more worryingly, some people
report that this persists after stopping the drug (Bala, Nguyen, & Hellstrom,
Reference Bala, Nguyen and Hellstrom2018). This is consistent with research with
young animals finding that sexual behaviour is negatively impacted by previous
use of SSRIs (Simonsen, Danborg, & Gotzsche, Reference Simonsen, Danborg and
Gotzsche2016). The prevalence of persistent effects is unknown, but even if it
is rare, it is a potential catastrophe given the huge numbers now using
antidepressants, and the increasing number of younger users. That long-term
antidepressant use may lead to persistent brain modifications is also evidenced
by the prolonged and severe withdrawal state they can induce (Framer, Reference
Framer2021; Hengartner, Schulthess, Sorensen, & Framer, Reference Hengartner,
Schulthess, Sorensen and Framer2020).
It has been recognised since the 1990s that current antidepressants are
associated with withdrawal effects (Haddad, Lejoyeux, & Young, Reference Haddad,
Lejoyeux and Young1998), but this has only recently started to receive serious
attention. A recent review suggests that around 56% of people experience
withdrawal effects after discontinuing antidepressants, and for 46% of those the
effects are severe (Davies & Read, Reference Davies and Read2019). In general,
the longer someone takes an antidepressant, the more likely they are to
experience a withdrawal reaction, and the more severe it will be (Horowitz &
Taylor, Reference Horowitz and Taylor2019). The adverse effects of withdrawal
can be so intolerable that some people trying to discontinue treatment have to
reduce by tiny amounts over many years, and accumulating evidence suggests that
the effects may even persist for months or years after the drugs are finally
stopped (Framer, Reference Framer2021; Hengartner et al., Reference Hengartner,
Schulthess, Sorensen and Framer2020).
The use of antidepressants also has potential negative psychological
consequences. Since antidepressants are associated with beliefs that depression
is caused by biochemical perturbations, their use may discourage people from
addressing the circumstances that caused their depression in the first place,
whether they be relationship problems, financial difficulties or something else.
If people attribute their improvement to taking antidepressants, rather than
recognising how they helped themselves, they will not develop confidence in
their own resilience and abilities which is likely to make them more vulnerable
to future episodes.
Research confirms that people may come to believe they need antidepressants to
stay well, and therefore become fearful of stopping them, leading to
ever-increasing numbers of long-term users (Eveleigh, Speckens, van Weel, Oude
Voshaar, & Lucassen, Reference Eveleigh, Speckens, van Weel, Oude Voshaar and
Lucassen2019; Maund et al., Reference Maund, Dewar-Haggart, Williams, Bowers,
Geraghty, Leydon and Kendrick2019). The longer antidepressants are used, the
greater their adverse effects, including the likelihood of severe and protracted
withdrawal syndromes.
ELECTROCONVULSIVE THERAPY
CORRECTING A BIOLOGICAL DEFICIT?
As is the case for antidepressants, the various biological deficits that are
supposedly corrected by ECT have never been demonstrated. The earliest two
claims about how ECT works, and what it was supposedly correcting, are
interesting.
The first was a supposed ‘biological antagonism’ between ‘schizophrenia’ and
epilepsy (Fink & Sackeim, Reference Fink and Sackeim1996). If you had one you
couldn't have the other. While some doctors treated epilepsy by injecting the
blood of ‘schizophrenics’ (Kalinowsky, Reference Kalinowsky1986), others were
using various techniques, including insulin and eventually electricity, to
induce seizures in ‘schizophrenics’.
The second claim was that ECT works because it causes brain damage, thereby
erasing painful memories and/or simplifying thought processes. In Reference
Freeman1941, Walter Freeman, who imported ECT to the United States, wrote, in a
paper entitled ‘Brain Damaging Therapeutics’:
The greater the damage, the more likely the remission of psychotic symptoms….
Maybe it will be shown that a mentally ill patient can think more clearly and
more constructively with less brain in actual operation (p. 83).
Another psychiatrist explained:
There have to be organic changes or organic disturbances in the physiology of
the brain for the cure to take place. I think the disturbance in memory is
probably an integral part of the recovery process. I think that it may be true
that these people have for the time being at any rate more intelligence than
they can handle and that the reduction in intelligence is an important factor in
the curative process…. Some of the very best cures that one gets are in those
individuals whom one reduces almost to amentia. (Myerson, Reference Myerson1942,
p. 39)
These quotations concerned the use of ECT for ‘schizophrenia’, but the idea that
the procedure worked in this way was also applied to depression, at least until
the 1960s. The principle UK psychiatry textbook of the period attributed the
effects of ECT to the ‘disruption by the fit and the subsequent period of
amnesia of recently acquired morbid patterns of behaviour and reaction’
(Henderson & Gillespie, Reference Henderson and Gillespie1962, p. 335).
A neutral observer would assume that the effects on the brain of repeatedly
passing sufficient electricity through it to cause seizures are likely to be
negative. ECT advocates, however, tend to interpret abnormal brain changes
caused by multiple electrocutions as beneficial, sometimes even linking them to
reduced depression. They don't consider that the changes might be negative or
might be characterised as brain damage. To do so would revert to the original
1940s theory that ECT works because it causes brain damage.
A similar line of argument was resurrected, 70 years later, by researchers who
reported that ECT reduces the ‘functional connectivity’ of the brain (Perrin et
al., Reference Perrin, Merz, Bennett, Currie, Steele, Reid and
Schwarzbauer2012). Our neutral observer might assume the researchers would be
concerned by this rather worrying side effect. Instead, they celebrated having
discovered how ECT works. They posited a supposed ‘hyperconnectivity’ that
somehow causes depression, and which is somehow corrected by ECT. Other ECT
advocates, meanwhile claim to have found the opposite; that ECT works because it
increases functional connectivity (Wei et al., Reference Wei, Bai, Chen, Ji, Hu,
Xie and Tian2018).
Still other ECT proponents, meanwhile, acknowledge that we simply don't know
what brain changes lead to the temporary lift in mood that some people
experience, or what biological deficits are being corrected. Max Fink, a very
famous ECT advocate, admitted, 83 years after the first ECT: ‘Studies to decode
the mechanism by which such interventions improve serious illnesses are sorely
needed’ (Fink, Reference Fink2021, p. 151).
A recent audit of 36 ECT patient information leaflets in England found that 22%
acknowledged that it is not known how ECT works. Nevertheless, 78% claimed it
corrects some deficit in the brain (Harrop, Read, Geekie, & Renton, Reference
Harrop, Read, Geekie and Renton2021).
Freeman's old idea of ‘brain-damaging therapeutics’ does receive some support
from contemporary evidence. A 2013 review concluded:
The temporarily improved scores on depression instruments following ECT reflect
the combination of frontal and temporal lobe functional impairments and
activation of the hypothalamic pituitary adrenal (HPA) axis and the
mesocorticolimbic dopamine system. These effects as well as other detailed
changes observed in structures such as the hippocampus appear consistent with
those typically seen after severe stress-exposure and/or brain trauma. (Fosse &
Read, Reference Fosse and Read2013, p. 6)
Furthermore, bilateral ECT causes more memory loss/brain damage than unilateral
(Sackeim et al., Reference Sackeim, Prudic, Fuller, Keilp, Lavori and
Olfson2007), and is more effective in the short-term (Read & Arnold, Reference
Read and Arnold2017), suggesting that cognitive impairment and temporary
‘improvement’ result from the same brain process.
So, as is the case for ‘antidepressants,’ the story of ECT appears to be one of
a biological intervention being claimed to correct biological deficits, but in
reality having negative effects on healthy brains, some of which are
misconstrued as signs of improvement.
MEDICAL INTERVENTION OR EXPECTANCY EFFECT?
Like antidepressants, the story of ECT is also the story of the power of placebo
effects (Lambourn & Gill, Reference Lambourn and Gill1978; Johnstone et al.,
Reference Johnstone, Deakin, Lawler, Frith, Stevens, McPherson and Crow1980;
Rasmussen, Reference Rasmussen2009; Read & Bentall, Reference Read and
Bentall2010; Ross, Reference Ross2006). Positive expectations affect prescribers
as well as patients. They influence perceptions of recovery as well as recovery
itself. Neurologist John Friedberg (Reference Friedberg1976, p. 31) pointed out
that the rapid spread of ECT across Europe and the USA in the 1940s took place
despite there being no studies comparing recipients and non-recipients, and that
‘the influence of ECT was on the minds of the psychiatrists, producing optimism
and earlier discharges.’
The standard placebo in ECT studies, known as ‘sham ECT’ (SECT), is the
administration of the general anaesthetic but not the electricity or subsequent
convulsion. A review of the literature on placebo responses to ECT concluded:
‘Rigorously defined endogenously depressed patients did exceptionally well with
sham ECT, just as well as with real ECT’ (Rasmussen, Reference Rasmussen2009, p.
59).
In the 84 years since the first ECT there have only been 11 randomised
placebo-controlled studies (RCTs) for its target diagnosis, depression, all
before 1986 (Read & Bentall, Reference Read and Bentall2010). A recent review,
involving Dr Irving Kirsch, Associate Director of Placebo Studies at Harvard
Medical School, highlighted the poor quality of the 11 studies (Read et al.,
Reference Read, Kirsch and McGrath2019, p. 64):
Only four studies describe their processes of randomisation and testing the
blinding. None convincingly demonstrate that they are double-blind. Five
selectively report their findings. Only four report any ratings by patients.
None assess Quality of Life. The studies are small, involving an average of 37
people.
Furthermore:
Four of the 11 found ECT significantly superior to SECT at the end of treatment,
five found no significant difference and two found mixed results (including one
where the psychiatrists reported a difference but patients did not).’
No studies showed that ECT outperforms placebo beyond the end of the treatment
period (Read et al., Reference Read, Kirsch and McGrath2019). Two of the least
flawed studies reported follow up data. One produced a near-zero effect size
(0.065) in favour of ECT (Johnstone et al., Reference Johnstone, Deakin, Lawler,
Frith, Stevens, McPherson and Crow1980), the other a small effect size (0.299)
in favour of SECT (Lambourn & Gill, Reference Lambourn and Gill1978).
Nevertheless, all five meta-analyses of these flawed studies somehow conclude
that ECT is effective. They pay little or no attention to the shortcomings of
the studies, fail to comment on the high response to sham ECT, and don't
identify any evidence on long-term effects (Read et al., Reference Read, Kirsch
and McGrath2019). The Food and Drug Administration (2020) in the US mandates
that ECT machines have signs next to them stating: ‘The long-term safety and
effectiveness of ECT treatment has not been demonstrated.’
The meta-analyses fail to identify any evidence that ECT prevents suicide, as
often claimed. Numerous studies have found ECT recipients are more likely than
other patients to kill themselves (Munk-Olsen, Laursen, Videbech, Mortensen, &
Rosenberg, Reference Munk-Olsen, Laursen, Videbech, Mortensen and Rosenberg2007;
Read, Bentall, Johnstone, Fosse, & Bracken, Reference Read, Bentall, Johnstone,
Fosse, Bracken, Read and Dillon2013a). In a recent study 14 810 ECT patients
were 16 times more likely to try to kill themselves than a matched control group
of 58 369 (Peltzman, Shiner, & Watts, Reference Peltzman, Shiner and Watts2020).
Even after controlling for ‘demographic, clinical, and service use
characteristics,’ including psychiatric diagnoses and inpatient admissions, the
ECT patients were 1.3 times more likely to have killed themselves (a
non-significant difference). A study using the Danish National Patient Registry
also found an increased risk of suicide in patients who received ECT compared to
equally depressed non-ECT patients (Jorgensen, Rozing, Kellner, & Osler,
Reference Jorgensen, Rozing, Kellner and Osler2020),
Another recent study, using the Swedish national registry, claimed its findings
‘support the continued use of ECT to reduce suicide risk in hospitalised
patients who are severely depressed’ (Ronnqvist, Nilsson, & Nordenskjold,
Reference Ronnqvist, Nilsson and Nordenskjold2021). The overall difference in
suicides over 12 months between the ECT group (1.1%) and the non-ECT group
(1.6%) was small. The difference was significant, but only for patients who were
psychotic, not for those who were depressed but not psychotic. Nor did the
difference hold for people under 45. Furthermore, at 3 months (at which point
any difference might more reasonably be attributed to ECT than at 12 months)
there had been no significant overall difference. More importantly, ‘Suicide was
defined as death caused by intentional self-harm (ICD-10 codes X60-X80) or by an
event of undetermined intent (ICD-10 codes Y10-Y35).’ Emails to the authors
failed to determine how many of the events they counted as suicide had, instead,
been ‘events of undetermined intent’.
The most recent study found that 1524 homeless US veterans who received ECT had
made significantly more suicide attempts, at 30 days follow up, than 3025
matched homeless veterans who hadn't had ECT. The difference remained
significant at 90 days and 1 year (Tsai, Peltzman, Watts, & Shiner, Reference
Tsai, Peltzman, Watts and Shiner2021).
In the only recent meta-analysis, from the Institute of Psychiatry in London
(Mutz et al., Reference Mutz, Vipulananthan, Carter, Hurlemann, Fu and
Young2019), just one sham ECT study (Brandon et al., Reference Brandon, Cowley,
McDonald, Neville, Palmer and Wellstood-Eason1984) contributed to their ‘network
meta-analysis’ (involving comparisons of different types of treatments). Thus,
after more than 80 years, only one placebo study was considered robust by the
Institute. Strangely, another relatively high-quality study, the well-known
Northwick Park study (Johnstone et al., Reference Johnstone, Deakin, Lawler,
Frith, Stevens, McPherson and Crow1980), which found much smaller effects of
ECT, was excluded because, according to the authors, it ‘cannot be obtained’. It
had been published in the Lancet. Furthermore, the one study they did include
(Brandon et al., Reference Brandon, Cowley, McDonald, Neville, Palmer and
Wellstood-Eason1984) was classified, by the reviewers themselves, as having a
‘high risk’ of bias. Nevertheless, they announced that two of the four types of
ECT they claimed to have assessed are more effective than placebo (and two are
not), even though the only sham-ECT study they included assessed only one of
those four types (bilateral ECT) (Read et al., Reference Read, Kirsch and
McGrath2019, pp. 88, 89).
The 2019 review concluded:
Given the high risk of permanent memory loss and the small mortality risk, this
longstanding failure to determine whether or not ECT works means that its use
should be immediately suspended until a series of well designed, randomised,
placebo-controlled studies have investigated whether there really are any
significant benefits against which the proven significant risks can be weighed.
(Read et al., Reference Read, Kirsch and McGrath2019, p. 64)
Esteemed British Clinical Psychologist, Professor Bentall (Reference
Bentall2020) commented:
I believe that Read and his colleagues have done an important service in
pointing out the parlous state of ECT research … ECT is a classic failure of
evidence-based medicine.
A subsequent discussion regarding the ethics of ECT concluded:
Although most of the medical literature states that ECT is an effective and safe
technique, there is no conclusive evidence of long-term effectiveness
(González-Pando et al., Reference González-Pando, González-Menéndez,
Aparicio-Basauri, Sanz de la Garza, Torracchi-Carrasco and Pérez-Álvarez2021).
THE SIX DEFENCES AGAINST HAVING NO ROBUST EVIDENCE
There are six standard responses used to try to counteract the absence of any
robust evidence that ECT is better than placebo (Read, Reference Read2022) (see
Table 2).
Table 2. The six defences against the continuing absence of any evidence of
efficacy from adequate randomised, placebo-controlled studies (RCTs) of ECT
The first is that it has been used for so long that it must be effective.
Unfortunately, the history of psychiatry is littered with treatments considered,
by intelligent, well-intentioned doctors, to be safe and effective, which turned
out to be neither, such as lobotomies.
The second is that it is unfair to apply today's standards of evidence-based
medicine to studies conducted 40 or 50 years ago. Perhaps so, but this
acknowledges that there is no robust evidence It also begs the question: why
have none been conducted since 1985?
The third defence, an attempt to answer the above question, is that it is
unethical to conduct studies that withhold a treatment which we believe works
from severely depressed, suicidal patients. Arguing that we can't find out
whether X actually does work because withholding X is unethical because we
believe it works, renders ECT proponents beyond the realms of normal science and
evidence-based medicine. (It also implies that 39 colleagues, the authors of the
11 RCTs, who did engage in the scientific process, were unethical).
The fourth is to argue that RCTs aren't essential because other types of studies
can be relied upon, such as comparisons with antidepressants or between
different types of ECT, along with clinical impressions. The sham-ECT trials
clearly demonstrate a powerful placebo effect, however, that will confound other
types of evidence. Furthermore, a review of these non-placebo studies found that
‘89% produced no meaningful follow-up data beyond the end of treatment, and none
investigated whether ECT prevents suicide.’ (Read & Arnold, Reference Read and
Arnold2017).
The fifth is to acknowledge the absence of evidence of any benefits beyond the
end of the treatment period but argue that this doesn't matter because you can
maintain the short-term effects with antidepressants. The claim requires
forgetting that ECT is primarily recommended for ‘treatment-resistant
depression’, i.e. for people for whom the drugs have proved ineffective.
The sixth defence is to shoot the messenger. Researchers and ECT recipients who
question the efficacy and highlight the adverse effects of ECT, are often
publicly denigrated, by ECT advocates, as ‘anti-psychiatry ideologues’,
‘extremists’ ‘Scientologists’ and ‘non-medical zealots’, whose work is ‘biased
polemics written masquerading as science’, ‘garbage’, ‘dangerous misinformation’
or part of a ‘guild war’ between professions. See, for example, comments from
psychiatrists in response to Medscape's coverage of the Read et al. (Reference
Read, Kirsch and McGrath2019) review (Vlessides, Reference Vlessides2020). The
President and Chair of the International Society for ECT and Neurostimulation
recently accused authors (including two ECT recipients) who had published some
inconvenient findings (Read, Hancock, & Cunliffe, Reference Read, Hancock and
Cunliffe2021a) of being ‘ideologically driven’, of ‘spreading misinformation’
and of having ‘questionable motives’ (Coffey & Kellner, Reference Coffey and
Kellner2021).
THE ACTUAL EFFECTS OF ECT
The fact that the temporary lift in mood experienced by some ECT recipients is
primarily a placebo effect, would not matter if it weren't for the fact that
repeatedly passing sufficient electricity through the human brain to cause a
seizure does have effects on the brain. As already discussed, these effects are
sometimes acknowledged but presented not as damage but as a beneficial
correction of an imagined pathology (Perrin et al., Reference Perrin, Merz,
Bennett, Currie, Steele, Reid and Schwarzbauer2012). Many of the changes,
however, are the same as those documented after brain trauma (Fosse & Read,
Reference Fosse and Read2013, p. 6).
As well as the short-term memory loss, which is widely acknowledged, between 12%
(Sackeim et al., Reference Sackeim, Prudic, Fuller, Keilp, Lavori and
Olfson2007) and 55% (Rose et al., Reference Rose, Wykes, Leese, Bindmann and
Fleischmann2003) of ECT recipients suffer persistent or permanent memory loss
(typically defined as 6 months or longer) (Read & Bentall, Reference Read and
Bentall2010; Read et al., Reference Read, Kirsch and McGrath2019). Even the
American Psychiatric Association (2001) acknowledges that ‘ECT can result in
persistent or permanent memory loss.’ One of the USA's two manufacturers of ECT
machines recently filed for bankrupticy following ‘five lawsuits related to the
company’s SpECTrum device, leading to the debtors being unable to obtain
products liability insurance to cover the device’ (Mecta, 2021). Meanwhile
British law firm, Freeths, is preparing multiople lawsuits on behalf of ECT
patients (Freeths, 2021). The other USA manufacurer, Somatics, owned by
psychiatrist Richard Abrams, recently added ‘permanent brain damage and
permanent memory loss’ to its list of risks (Somatics, 2018). For example:
My long-term memory was destroyed. Memories of childhood friends, memories of
major events I attended, memories of my training as a psychiatric registrar. I
started struggling with simple spelling and calculations. …. I never told
colleagues about this, as I felt ashamed. But I started talking to other people
who had ECT and realised I am not alone. (Brink, Reference Brink2020)
Furthermore, ECT causes adverse psychological and emotional effects (Johnstone,
Reference Johnstone1999; Wells et al., Reference Wells, Hancock and Honey2021).
It also carries a small risk of mortality (Read et al., Reference Read, Bentall,
Johnstone, Fosse, Bracken, Read and Dillon2013a, Reference Read, Kirsch and
McGrath2019). A review of 82 studies found that one in 39 ECT patients (25.8 per
1000) experience ‘major adverse cardiac events’ (Duma et al., Reference Duma,
Maleczek, Panjikaran, Herkner, Karrison and Nagele2019), the leading cause of
ECT-related deaths.
The recent audit of information sheets in England found that people were not
well informed about the risks of ECT. 28% failed to acknowledge the risk of
long-term/persistent/permanent memory loss (Harrop et al., Reference Harrop,
Read, Geekie and Renton2021) and none informed women and older people, the two
demographic groups most likely to receive ECT, that they are at particularly
high risk (Sackeim et al., Reference Sackeim, Prudic, Fuller, Keilp, Lavori and
Olfson2007). Few leaflets presented clear information on mortality and cardiac
risks (Harrop et al., Reference Harrop, Read, Geekie and Renton2021).
Two audits of how ECT is administered in England (Read, Harrop, Geekie, &
Renton, Reference Read, Harrop, Geekie and Renton2018; Read et al., Reference
Read, Hancock and Cunliffe2021a; Read, Harrop, Geekie, Renton, & Cunliffe,
Reference Read, Harrop, Geekie, Renton and Cunliffe2021b) found inconsistent but
generally poor practice, including little evidence of adequate assessment of
cognitive damage. The more recent of the two concluded:
Given the apparent failure of current monitoring and accrediting of ECT clinics
in England, by the Royal College of Psychiatrists' ECT Accreditation Service
(ECTAS), an independent government-sponsored review is urgently needed.
A campaign for such a review (Johnstone & Cunliffe, Reference Johnstone and
Cunliffe2020; Read, Reference Read2020) has broad support, including Mind
(England's largest mental health charity), the Royal College of Nursing, the
Association of Clinical Psychologists, Headway (the brain injury association),
and cross-party MPs including Dr Rosena Allin-Khan, the Shadow Mental Health
Minister.
ALTERNATIVE APPROACHES
We are suggesting that antidepressants and ECT can change an individual's mental
state by modifying normal brain activity. In someone with depression, these
mental changes are superimposed onto pre-existing depressed feelings, which may
temporarily obscure them. Although this situation is routinely understood as an
improvement of the depression itself, this is because the brain and
mind-altering properties of these procedures are ignored. Temporarily dampening
down depressed feelings with brain manipulations may sound helpful for some
serious situations, but the long-term consequences of these interventions have
not been adequately researched. Procedures that change normal brain functions
should be expected to have adverse effects, some of which may be long-lasting,
and this seems to be the experience of numerous people who undergo ECT or take
antidepressants long-term. We need much more information on long-term
consequences before we deem it safe to continue prescribing these techniques
Furthermore, believing you have a brain disease requiring medical intervention
can be profoundly disempowering. It encourages people to view themselves as the
victims of their biology, to adopt pessimistic views about recovery, increases
self-stigma and discourages people from taking active steps to improve their
situation (Deacon & Baird, Reference Deacon and Baird2009; Kemp, Lickel, &
Deacon, Reference Kemp, Lickel and Deacon2014; Read, Haslam, & Magliano,
Reference Read, Haslam, Magliano, Read and Dillon2013b). Amongst the general
population and mental health professionals biological causal beliefs (genetic,
biochemical imbalance etc.) about ‘mental health problems’ have been
consistently linked to negative attitudes (Kvaale, Haslam, & Gottdiener,
Reference Kvaale, Haslam and Gottdiener2013; Lebowitz & Ahn, Reference Lebowitz
and Ahn2014; Loughman & Haslam, Reference Loughman and Haslam2018; Read et al.,
Reference Read, Haslam, Magliano, Read and Dillon2013b).
So, if antidepressants and ECT are not helpful and are potentially unsafe, how
should we help one another when we feel depressed or distressed? Understanding
depression and anxiety as emotional reactions to life circumstances, rather than
the manifestations of supposed brain pathology, demands a combination of
political action and common sense. There is longstanding evidence on how
deprivation and social adversity make people vulnerable to depression
(Bjorkenstam, Pebley, Burstrom, & Kosidou, Reference Bjorkenstam, Pebley,
Burstrom and Kosidou2017; Brown & Harris, Reference Brown and Harris1978;
Cacioppo, Hughes, Waite, Hawkley, & Thisted, Reference Cacioppo, Hughes, Waite,
Hawkley and Thisted2006; Hoebel, Maske, Zeeb, & Lampert, Reference Hoebel,
Maske, Zeeb and Lampert2017; Postmes, Wichmann, van Valkengoed, & van der Hoef,
Reference Postmes, Wichmann, van Valkengoed and van der Hoef2018). Social
prescribing is now a recognised intervention for depression, currently being
tested in trials (Lewellyn, Reference Lewellyn2019). Psychotherapy (Cuijpers et
al., Reference Cuijpers, Quero, Noma, Ciharova, Miguel, Karyotaki and
Furukawa2021), cognitive therapy (Cuipers et al., Reference Cuipers, Berking,
Andersson, Quigley, Kleiboer and Dobson2013; Wampold et al., Reference Wampold,
Minami, Baskin and Callen Tierney2002), exercise (Schuch et al., Reference
Schuch, Vancampfort, Richards, Rosenbaum, Ward and Stubbs2016) and mindfulness
(Reangsing, Rittiwong, & Schneider, Reference Reangsing, Rittiwong and
Schneider2021) have all been shown to be beneficial. However, helping someone in
distress is not primarily a scientific activity - it is an essentially human
one. Common sense suggests that the conditions needed to lead an emotionally
balanced and fulfilling life, relatively free of major ongoing worry and
distress, include a dependable income, housing, secure and rewarding employment,
engaging social activities, and opportunities to form close relationships. Some
people may need relationship counselling or family therapy, others support with
employment or finances. People who feel severely depressed for a long time may
simply need to be cared for, reassured with kindness and hope, reminded of times
when they have felt good, and kept safe until they feel better, which they often
do with time.
There is no scientific evidence for some of these suggestions. We learn how to
support our fellow humans through our life experience, through being cared for
ourselves, and sometimes through art and literature. Classifying anxiety,
depression and other emotional reactions as mental diseases or disorders
obscures the relation between our moods and our circumstances. It leads society
to believe that social structures are unchangeable. Instead, we need to listen
carefully to the message that people's emotional reactions convey, and endeavour
to create a society in which all people can flourish. This approach to
understanding and helping people with ‘mental health problems’ is increasingly
endorsed by professionals and political bodies, as well as service user
organisations. The United Nations Special Rapporteur, Dr Dainius Pūras, a
Lithuanian psychiatrist, recently wrote:
Current mental health policies have been affected to a large extent by the
asymmetry of power and biases because of the dominance of the biomedical model
and biomedical interventions. This model has led … to the medicalisation of
normal reactions to life's many pressures, including moderate forms of social
anxiety, sadness, shyness, truancy and antisocial behaviour. (Puras, Reference
Puras2019)
The World Health Organization (2021) echoed these sentiments in its ‘Guidance on
Community Mental Health Services’ which argues that social determinants of
mental health are being neglected, resulting in ‘an over-diagnosis of human
distress and over-reliance on psychotropic drugs to the detriment of
psychosocial interventions’. The document offers 22 examples of alternatives to
drugs and electricity (Read, Reference Read2021).
Similarly, the British Psychological Society has published reports on depression
(Bowden, Shankar, Cooke, & Kinderman, Reference Bowden, Shankar, Cooke and
Kinderman2020) and mental health more generally (Cooke, Reference Cooke2017;
Johnstone et al., Reference Johnstone, Boyle, Cromby, Dillon, Harper, Kinderman
and Read2018) that suggest that brain-based understandings and treatments rest
on false assumptions, and call for alternatives to uninformative and potentially
stigmatising diagnoses, and for treatments that address the role of trauma,
power structures and social adversity (Johnstone et al., Reference Johnstone,
Boyle, Cromby, Dillon, Harper, Kinderman and Read2018; Read & Harper, Reference
Read and Harper2020).
A plethora of international organisations representing people who have been
harmed by psychiatric treatments, including ECT and antidepressants, also call
for a different approach to understanding and treating depression. James Moore,
founder of Mad in the UK (http://www.madintheuk.com) and the Let's Talk
Withdrawal podcast (http://www.letstalkwithdrawal.com), came to realise that he
had not been adequately informed about the risks and benefits of
antidepressants, and was ‘coerced and led on a merry dance, ultimately to the
detriment of my health, my confidence, my family and my social life’. He
concludes:
Psychiatric drugs can't address isolation, poverty, inequality, racism,
intolerance, hatred, bigotry, sexism, etc., but they can mask those things.
Perhaps that is why they are so successful. The blame is placed on us, the
patient, for being broken because it obviates the need for powers that be to
take any action to address those underlying causes of distress and suffering
(Moore, Reference Moore2018).
FINANCIAL SUPPORT
This paper received no specific grant from any funding agency, commercial or
not-for-profit sectors.
CONFLICTS OF INTEREST
JR has received royalties for: Read J, Dillon J (eds) (2013) ‘Models of Madness:
Psychological, Social and Biological Approaches to Psychosis’, Routledge, which
includes a chapter on ECT which he co-authored. He currently holds the unpaid
positions of Chair of the International Institute for Psychiatric Drug
Withdrawal [https://iipdw.org], and Member of the Board of Trustees of the
Hearing Voices Network, England [http://www.hearing-voices.org]. In 2021 he
received a fee from a law firm as an expert witness on an ECT case.
JM has received royalties for: Moncrieff, J. (2020) ‘A Straight Talking
Introduction to Psychiatric Drugs' (2nd ed.) PCCS Books; Moncrieff, J. (2013)
‘The Bitterest Pills: The Troubling Story of Antipsychotic Drugs', Palgrave
Macmillan; Moncrieff, J. (2009) ‘The Myth of the Chemical Cure: A Critique of
Psychiatric Drug Treatment', Palgrave Macmillan; and Rapley, M., Moncrieff, J.,
& Dillon J. (eds.) 'Demedicalising Misery', Palgrave Macmillan. She is a
co-applicant on the NIHR-funded REDUCE study of antidepressant discontinuation,
and CI on the RADAR study of antipsychotic reduction She currently holds the
unpaid positions of co-Chair of the Critical Psychiatry Network
(www.criticalpsychiatry.co.uk) and Board Member of the Council for Evidence
Based Psychiatry (http://cepuk.org).
--------------------------------------------------------------------------------
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View in content
Table 1. Alternative models of drug action (adapted from Moncrieff, 2009;
Moncrieff & Cohen, 2005)
--------------------------------------------------------------------------------
View in content
Table 2. The six defences against the continuing absence of any evidence of
efficacy from adequate randomised, placebo-controlled studies (RCTs) of ECT
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