Themes from people’s experience of antidepressants

Many so-called treatment resistant depressed patients do not respond adequately to two antidepressant medications given one after another. The question of the efficacy of antidepressants is still an open issue in the scientific literature because of methodological problems with the clinical trials (see eg. previous post).

Crowe et al (2023) identified four themes from a meta-analysis of qualitative studies examining patients' experiences of antidepressant medication. These were:-

(1) The only option available. This was partly about the sense of ‘needing something’, often quite quickly. People were generally more accepting of taking antidepressants when in acute crisis but were more ambivalent about taking them outside this context. Some felt they had to take antidepressants because of what the doctor said and even felt bullied into taking them. Some said they got relief from their first prescription but over half in one study had a trial of more than one antidepressant before getting any relief. Not everyone took the medication as prescribed, with some deciding themselves when to take it and others choosing not to even take the prescription. Most participants described feeling that there was no other treatment option available and were desperate for relief.

(2) Stigma associated with ‘biochemical deficit’. Participants in 14 studies described how the medical construction of their experience as a biochemical abnormality was stigmatising. Participants may feel different or damaged and reliant on medical expertise. Having been positioned into a passive position with the doctor having control may have shamed some into taking medication. Just using medication itself was linked to the stigma by many. Most participants in this theme described being told they needed antidepressants for their ‘biochemical deficit’. For some the deficit was constructed as something that would require on-going treatment. The doctor may state as fact that the person was biologically flawed even though there was a lack of evidence for such a view. 

(3) Not myself. In weighing up the benefits and risks, participants in 6 studies, if they took medication, described it as helping their functioning, noticing improvement in mood and being given a sense of hope on starting. However, this was often offset by experiences in which they felt the medication was masking the real problem or altering their experiences of themselves and others. This was captured in one study where participants described unbearable side effects, undermining emotional authenticity, masking real problems and reducing the experience of control. Most people commonly experienced a flattening of emotional responses which included feelings of being ‘dulled’, ‘numbed’, ‘flattened’ or completely ‘blocked’, as well as descriptions of feeling ‘blank’ and ‘flat’, affecting their relationships with others and how they saw themselves. Some described how antidepressants made them feel worse than the original depression.

(4) A vicious cycle. Patients in 8 studies identified issues in relation to discontinuing antidepressants. They often described wanting to discontinue antidepressants but had a fear of relapse. Discontinuation was associated with withdrawal symptoms, ranging from mild to severe. Fear of relapse and the experience of withdrawal symptoms meant participants felt compelled to keep taking antidepressants when they no longer wanted to.

Disclosure of industry payments to the healthcare sector

I've mentioned Peter Gordon before (see previous post). He raised a petition for a Sunshine Act for Scotland in September 2013 to make it mandatory for healthcare workers (including academics and allied health professionals) to declare fully any payments from industry and commerce (see his blog post). 

The UK government has recently issued a consultation on disclosure of industry payments to the healthcare sector (see BMJ news report). This is based on a recommendation from the Cumberledge review that investigated the harm caused by the use of Primodos, sodium valproate and pelvic mesh (see BMJ news report). 

Peter argues that government proposals for disclosure need to go further (see his blog post). It will be interesting to see the Royal College of Psychiatrists' response to the consultation. Peter tells me that the College has given no response to the Cumberledge review. Still, two high profile media doctors have been persuaded to become conflict-free (see BMJ article). 

Updating psychiatry’s biology

I’ve mentioned John Dupré previously (see post). His book The metaphysics of biology: Elements in the philosophy of biology (2021) looks at four general philosophical perspectives on life: vitalism, materialism, mechanism and organicism. Vitalism is generally derided because it is seen as postulating a vital thing or substance that is unique to life. Materialism, in the sense of the non-existence of the immaterial, is obviously true but, in this sense, a narrow claim. It is often strongly associated with the thesis of mechanism that life can be explained as a machine. Organicism, like vitalism, asserts that different principles apply to living systems. As Dupre says, "The point of difference is that it is not that there are principles that don’t apply to matter, but that these principles apply only when matter is organised in a particular way.“

An organism exhibits a mode of organisation very different from a machine. It is more than the sum of its parts. Cells and bodies are not well-defined structures but actually stabilised processes (see eg. previous post). Vitalism attributes the wrong kind of specialness to life, but nonetheless, living beings have a purposiveness that cannot be derived from mere physical-chemical processes.

Psychiatry, therefore, needs to update its biology from mechanism to organicism. Mechanical explanations are insufficient for an account of the totality of human nature. Psychiatry's primary object is not the brain but the person living in relationships. This fundamental failure to appreciate this philosophical reality is damaging psychiatry.

Taking relational psychiatry forward

I completed two years in semi-retirement of a five year part-time PhD on ‘The foundations of critical psychiatry’ at the University Department of Psychology in Cambridge in 2017/9. My supervisor left after 4 terms and I couldn’t find a replacement! Still, I managed to write three articles in Royal College of Psychiatrists’ journals: (1) Twenty years of the Critical Psychiatry Network; (2) Critical psychiatry: An embarrassing hangover from the 1970s?; and (3) Toward a more relational psychiatry: A critical reflection. An interview with Awais Aftab expressing my views about critical/relational psychiatry is to be published in a forthcoming book. 

As I said in the interview, part of the reason I changed the name of my blog from critical psychiatry to relational psychiatry was to try to move on from debates about so-called anti-psychiatry and incorporate more recent perspectives from anti-cognitivist phenomenology and enactivism and the tradition from cultural psychiatry. Key contributions here would be: two books by Thomas Fuchs: Ecology of the brain: The phenomenology and biology of the embodied mind (2018) (see eg. previous post); and In defence of the human being: Foundational questions of an embodied anthropology (2021) (see eg. previous post); the book Enactive psychiatry by Sanneke de Haan (2020) (see eg. previous post); and the contributions over many years by Laurence Kirmayer (see eg. previous post) including the book Re-visioning psychiatry: Cultural phenomenology, critical neuroscience, and global mental health (2015), of which he was the first editor. 

Other initiatives include the Relational Practice Movement, which has developed out of the therapeutic community movement (see eg. previous post). It has produced a Relational Practice Manifesto. Russell Razzaque has also produced a Relational Psychiatry vlog. He is now the Presidential lead for compassionate and relational care at the Royal College of Psychiatrists. It would be nice to think that the College could help to bring all these strands together to make psychiatry more relational. 

Still against the grain to be against biomedical psychiatry

I've managed to find a Psychiatric Times article by David Kaiser (1996) 'Against biologic psychiatry' which I thought had been lost in the ether. Unfortunately I can't find his associated articles that featured in the MHi 'Against the Grain' series. My critical psychiatry webguide, which originally was published on the Royal College of Psychiatrists' website in 2001 featured these articles. Some of the other links on the webguide are also now dead.

Kaiser's articles were also some of the first I posted on my list of articles critical of psychiatry, which I collected over many years on my Critical Psychiatry website. Again, many of the links in the list and on the Critical Psychiatry website in general are now dead.

As I indicated in the webguide, an advantage of the internet in the early days was that it provided a forum for critiquing biomedical psychiatry. In the modern days of social media, we have become used to everyone being able to express their views online about many things, besides psychiatry. Still, two of my first posted comments in the list of articles (see first and second), critiquing 1999 psychiatric journal articles about the biological basis of schizophrenia stand as much now as they did then. I didn’t bother submitting them to the journals as letters because they wouldn’t have been published! But I could self-publish on the internet. Kaiser's expression of his "dismay and outrage [at] the rise and triumph of the hegemony known as biologic psychiatry" doesn't seem to have had as much impact as it should have done from within psychiatry.

On psychiatric diagnosis

A diagnosis is a name for an illness or a disease. Technically, illness is the experience of symptoms and suffering and disease is the underlying biological pathology. People can be ill without have a disease and primary mental illness is an example where there is no underlying brain abnormality.

So, having a psychiatric diagnosis does not necessarily mean there is something wrong with your brain. And anyway, people are not their brains or bodies.

Psychiatry needs to abandon its biomedical framework

Campolonghi & Orrù (2023) argue that psychiatry needs to abandon its biomedical framework (see Mad in America research news). As they say, treating functional mental illness as brain disease "constitutes an illegitimate epistemological leap” which “leads to pseudoscientific (and unethical) practices”. 

As they go on, “biological processes and the brain are [of course] involved in enabling and mediating cognitive, emotional, and behavioral functions and responses”. However, "the consistent and systematic search for biological and neurological causes of distress and problematic behaviors conducted over more than a century" has not provided "any evidence or support for the existence of 'mental disorders' as natural kinds”.

The problem is that “psychiatry is not built upon physical sciences (as medicine is) and yet adheres to a (neo)positive-empiricist tradition”. Psychiatry will not find it easy to abandon its biomedical framework but it needs to do so in the interests of patients.

Improving compassion in mental health services

Elisa Liberati et al (2023) tackle the issue of the lack of compassion in acute mental health services, exposed, for example, by undercover reporting of abuse in psychiatric inpatient services (see eg. previous post). As they say, the preconditions for compassion in mental healthcare have been severely eroded.

The reasons for this are complex. There has always been a tendency for staff to dissociate themselves from the pain and distress experienced by services users. As Liberati et al say:-

Rising demand, resource shortages, and weak organisational support are causing staff burnout and disillusionment, compromising their ability to act compassionately. … These problems are especially acute in inpatient settings, where staff are often exposed to intense negative emotions and may experience vicarious trauma.

But this lack of compassion seems to have become worse over recent years with the rise of risk management. The challenge for staff is to maintain therapeutic relationships with patients in the context of an organisational bureaucracy which has become primarily concerned about its accountability and responsibility rather than concentrating on its main task of patient care. In this context, staff may practice defensively for fear of making mistakes and being blamed by the organisation. Such tension can lead to practice becoming too risk averse, prioritising service requirements over patient needs.

Risk management in mental health is not always applied sensibly (see eg. previous post). Emotional safety can actually be reduced by too much of a focus on physical safety and organisational risk. Rigorous adherence to procedures designed more to protect the organisation rather than patients may not really reduce risk but instead infantilise people, taking away their personal responsibility and thereby emotional safety. Relationships between staff and patients need to be prioritised in practice and developed to provide therapeutic services.

Biomedical understandings of mental illness can also objectify people by reducing their psychosocial problems to brain disease. Nonetheless, even biomedical services should act humanely. If staff cannot provide good quality care, their sense of professional integrity may feel violated. It may nonetheless be difficult to challenge ways of working which conflict with their values leading to the normalising of poor practice.

The lack of compassion in mental health services needs to be taken seriously and staff supported by service organisations in their supervision and training to provide good quality care. The rights of people with mental health problems must be promoted to improve the standards of modern mental health care (see eg. previous post).

Mystical views about overcoming depression

JAMA article (one of whose co-authors is the current NIMH Director - see previous post) on the potential and challenges of using psychedelics in the therapeutics of depression notes that “it is clear that psychedelics are not wonder drugs”. As it also notes, approving their use could promote a booming psychedelic drug industry, in the same way as approving medical cannabis did for cannabis, despite lack of scientific evidence for therapeutic efficacy. Approved psychedelics, like cannabis, are likely to be used outside any licensed indications.

Is the mystical-type experience induced by psychedelics of benefit in depression? Any effects of psychedelics in depression may merely be due to the placebo effect. Participants in trials can usually tell if they have been given psychedelic vs placebo, so trials are not double-blind, which makes them biased.

If one of the most biomedical of journals can see the disadvantages and risks of approving psychedelics for depression, then surely this needs to be taken seriously. Trouble is that I doubt it will, if only to meet the wish-fulling phantasies of psychiatry and people in general about overcoming depression with medication.

Understanding why serotonin does not cause depression

Allan Young, one of the co-authors of the recent article that indicated that serotonin is implicated in depression (see last post), is quoted in Herald Scotland (see analysis article) as saying that “Any criticism of the chemical imbalance theory truly misunderstands why it was developed and used by researchers and clinicians”. I’m not quite sure what he means by this. As I understand it, the motivation to continue the serotonin hypothesis is to encourage people to take their antidepressant medication. How people have understood the serotonin hypothesis (chemical imbalance theory) is that depression is caused by low serotonin. Young says this theory is too simplistic. But I’m not sure what he believes instead.

He suggests the theory was developed to explain how “brain changes occur in depression in a more accessible way”. Again, it’s not clear what he means by this. But this seems to be the crux of the problem. Are the brain changes in depression any different from ‘normal’? Depression is a personal condition. Of course it’s mediated by the brain. That’s commonsense and not rocket science. People don’t need a chemical imbalance theory to understand that.

Young's convinced that “brain changes do occur in the brain of depressed people”. He seems to be saying that these changes cause depression. He’s got muddled that people are their brains (eg. see previous post). Of course I have a brain. If I was depressed I would still have a brain. But that brain is not me, whether I’m depressed or not. It doesn’t cause my depression.

The conclusion of the umbrella review by Moncrieff et al was that there is no convincing evidence to support the theory that depression is caused by low serotonin. Young says this conclusion is wrong. It isn’t! Psychiatrists like Young need to move on from an outdated, misguided physical disease model of mental illness. Otherwise he won’t understand why the serotonin theory of depression needs debunking, even the less simplistic version he wants to promote, whatever that is.

What does it mean to say that serotonin is implicated in depression?

As I explained in a recent post, psychiatrists find it difficult to give up the serotonin theory of depression. A paper in Molecular Psychiatry, written by multiple authors, many of whose academic psychiatric careers have been dependent on believing a version of the theory, argues that the evidence clearly indicates the serotonin system is implicated in depression. I want to look at what this statement means.

The paper concludes that "acute tryptophan depletion and decreased plasma tryptophan in depression indicate a role for 5-HT [serotonin] in those vulnerable to or suffering  depression, and that molecular imaging suggests the system is perturbed". Note that the paper does not say that depression is caused by low serotonin. The serotonin hypothesis has not been proven, which is what people have often been led to believe. The argument seems to be that further research is justified, I guess particularly in the two areas highlighted of tryptophan depletion and serotonergic molecular imaging.

Any statements in the paper in favour of the serotonin theory of depression are not couched in terms of causation. For example, as in the title of the paper, the serotonin system is said to be implicated in depression, not necessarily a causal factor in depression. The brain contains large numbers of neurones that transmit signals by releasing neurotransmitters, such as serotonin. Of course depression is mediated by the brain. Is any more than this tautologous statement being made by suggesting that the serotonin system is implicated in depression? I guess the serotonin system must be implicated in some way, which is unclear at present, as it is part of total brain processes. But that is very different from suggesting that depression is due to an abnormality of serotonin in the brain.

Moncrieff at al (2023) make this point in their response to this paper, including commenting on other letters written in reply to their original umbrella review. As they say, 

We would agree that many brain processes, including the serotonin system likely play a complex, though poorly understood, role in emotion and behaviour, including depression. Yet such ideas are different from the specific claim that depression is caused by low serotonin levels or serotonin activity (often communicated to patients) that our review specifically examines.

Psychiatrists will continue to find it difficult to give up the serotonin theory of depression because they believe antidepressants are effective. As nearly all antidepressants have an effect on serotonin, as far as they are concerned, this mechanism must be how they work. Questioning whether antidepressants are any better than placebo creates grave concern for the professional viability of psychiatrists, as does debunking the serotonin theory of depression. Psychiatrists need to give up such a vulnerable basis for their practice.

Labelling differences between people as neurodevelopmental

I want to take further what I was saying about ADHD in a recent post. Over recent years, ADHD has been classified as a neurodevelopmental disorder with identification of comorbidity between ADHD and autistic spectrum disorder (ASD). Claims that ADHD is a genetic condition (see previous post) are consistent with the hypothesis of a genetic neurodevelopmental continuum of intellectual disability, ASD, ADHD and other childhood conditions including tic disorders. The concept of neurodiversity (see article in The Atlantic), meaning intrinsic diversity of brain function, implies that neurodevelopment disorders are not necessarily pathological but may merely represent brain differences. 

People are different. The clamour to find a psychiatric diagnosis to explain our difficulties, eccentricities and odd behaviour may not necessarily increase our understanding of the reasons for these problems and differences. Admittedly these may be difficult to understand, at least initially, but that doesn't mean that we shouldn't try. These issues are complex and differences between people are not just due to their brains or genes. I agree with advocates of neurodiversity about human rights and the need for society to adapt to individual differences. That doesn’t necessarily mean, however, that increasing the diagnosis of ADHD and other neurodevelopmental diagnoses is the answer to understanding and managing our differences from others.

Barriers to debunking the serotonin theory of depression.

I concluded my article on 'Towards a more relational psychiatry: A critical reflection' with the sentence:-

Rather than psychiatric practice being based on the notion that primary mental illness will be found to have a physical cause, psychiatry needs to move on to a more relational practice.

I just want to elaborate what I mean by this in relation to the umbrella review that confirmed there is no convincing evidence to support the theory that depression is caused by low serotonin (see previous post). Even though antidepressants may be serotonin re-uptake inhibitors, they do not seem to correct an imbalance or deficiency of serotonin in the brain (see another previous post). 

This may well be surprising to patients and the general public who have been led to believe in the serotonin theory of depression. Simplistic notions of the serotonin theory have actually been untenable for some time (see eg. previous post). Psychopharmacologists gave up the theory ages ago but it persists in clinical practice as a way of persuading patients to take their medication. I'm sure the fundamental faith of psychiatry that primary mental illness will be found to be due to brain disease will continue. Doctors find it difficult to accept that depression hasn't something to do with serotonin because antidepressants can be serotonin re-uptake inhibitors. They are convinced antidepressants work, so this must be due to their effect on serotonin. 

Our modern understanding of illness and disease as bodily pathology has been remarkably successful in elucidating biological processes of disease. Doctors should take a person-centred approach to attain an understanding of the patient as well as the disease. For psychiatry in particular, the danger is that medicine may treat patients more as objects than people by reducing their problems to brain disease.

After decades of intense neuroimaging research, there is still no neurobiological account of any functional psychiatric condition (see eg. previous post). Psychiatry must stop identifying the brain with the person. People’s experience and relationships with others are at the core of depression and cannot be identified with neuronal or biochemical processes, such as serotonin imbalance or deficiency. We may find it attractive to try and simplify the relationship between mind and brain, but it may well be an enigma we cannot solve. We have to accept the integration of mind and brain in the person. Of course brain disease can cause mental disorder, but it may well not make sense to see depression as being in the brain. Depression is mediated by the brain but there may be no brain abnormality as such. This is what psychiatry will continue to find difficult to accept.

Creating panaceas for emotional and other mental health problems

I want to look at some of the wider implications of the BBC Panorama programme exposure of private ADHD clinics. I'm not convinced the NHS is necessarily coping any better than private services with the burgeoning demand for psychiatric diagnosis of emotional and other mental health problems, of which ADHD is just one of the diagnoses for which remedies are being sought. A uncritical biomedical approach to ADHD can be an excuse for licensed fraudulence (see previous post). 

Panorama is not the first media programme to highlight the exploitation of ADHD diagnosis (eg. see previous post). Adult ADHD is a relatively new diagnosis, as ADHD was originally a diagnosis made in children with symptoms of hyperactivity, impulsivity and inattention. Such behaviours may be displayed when children feel frustrated, anxious, bored, abandoned, or in some other way stressed. The increasing diagnosis of ADHD in children, over many years now, has been compounded by diagnosis in adults without a previous childhood diagnosis, considered to have been a major unrecognised condition (see eg. my article). Many psychiatrists see this as an example of the overmedicalisation of mental health problems (see another previous post), which at least partly explains why adult ADHD services have generally been hived off into a special service, mostly with massive waiting lists.

Not all negative emotions and experiences should be labelled as mental disorder. A moral panic about mental health may encourage the packaging of our everyday problems as conditions that can be diagnosed and treated. The reality is not always so simple (see eg. previous post). As this is mental health awareness week, it is perhaps worth highlighting how destigmatisation campaigns seem to have encouraged this oversimplification (see another previous post). Services themselves also ironically have encouraged the expansion of demand, apparently with the misguided notion that a perseverative call for more funding will provide the answer. The cultural process of seeking to create panaceas for emotional and other mental health problems doesn’t always work and may create more problems than it is worth. 

Changing how mental disorders are studied and managed

As Caio Maximino (2023) says in History of Psychiatry, the "over-reductionist neo-Kraepelinian approach" has been criticised for decades. Like me, he also argues that these criticisms tend to disregard and not make as much as they should of advances in enactivism and phenomenological psychiatry (see eg. previous post). Biomedical psychiatry essentially ignored George Engel’s call for a more integrative approach by continuing with its ontological position that mental phenomena are brain phenomena, even if this is now understood in an eclectic biopsychosocial way (not originally what Engel meant - see eg. previous post). But what's needed is a new epistemology that recognises "the complexity of the relation of biology with interpersonal, social and cultural factors (see another previous post). I have tried to summarise all this in my paper 'Towards a more relational psychiatry: A critical reflection' (see yet another previous post).

Value for psychiatry of the explanation/understanding distinction

Joseph Gough (see Gough (2021) and Gough (2023)) seems to me to wrongly undermine the value for psychiatry of the explanation/understanding distinction from Dilthey. True, Jaspers notion of un-understandability as a basis for defining organic disorders does not hold up. And the apparent incomprehensibility of psychosis can be understood (see Wendler & Fuchs (2023)). 

But there is a very real sense in which we may not be able to say what causes functional mental health problems in physical terms. Relationship with antecedents is not linear but more circular (see previous post). This does not mean that it's not important to try and understand the reasons for mental health problems, even that they may provide a kind of explanation (see another previous post). Naturalistic explanations are inadequate because of the need to take a holistic personalistic view of mental health problems. Mind and body are integrated in the organism but this does not really dissolve the mind-body problem, merely acknowledge it can’t be solved.

Psychiatrists, antidepressants and suicide

David Healy (who I have mentioned before, see eg. previous post and a review of one of his books) has published a blog post on his website, which he provocatively entitles a 'Royal College of Psychiatrists' suicide note'. His post was in response to a letter written by the President of the Royal College about newspaper articles citing a study by John Read (2023) that David reviewed for the Ethical Human Psychology and Psychiatry journal, which also published an accompanying paper from David. 

John's study examined a data set summarizing 7,829 media reports of Coroners’ inquests in England and Wales between 2003 and 2020 that mentioned antidepressants (ADs). This information was collected on the AntiDepAware website. Overdose of antidepressants was not always the cause of death. John concludes:-

The data set we have summarized here confirms the findings of drug trials showing that ADs are ineffective for many people. The reports document the deaths of several thousand people who killed themselves despite being on ADs, and more than a thousand who actually used the drugs that were supposed to alleviate their depression to kill themselves.

As John also says, the paper has "few firm conclusions". Not many people will be surprised to learn that antidepressants do not necessarily prevent suicide; nor that some people take overdoses of their prescribed medication. I'm not sure that this information really reinforces questioning about whether antidepressants are effective, although I agree this is a major issue (see eg. previous post).

Not that whether antidepressants cause suicide is not also a major issue (see previous post). It's just that I don't think John's study adds too much to this debate either, despite the hype. Nor do I think David's accompanying paper really takes the issue forward. David describes two clinical scenarios, one of for which he was an expert witness at the inquest. As he says, "Coroners have actively steered" him to blame mental illness rather than medication for the cause of death. He is convinced these two cases were antidepressant-induced deaths. 

How to determine causality in such cases is not easy. What worries me about David's position is that he tends to take a physicalist approach to medication and not necessarily consider how people react to the taking of medication (see previous post). How people react to the act of prescribing in itself when they are feeling desperate does need to be taken into account. Antidepressant prescribing may well be a factor in suicide, but it is not necessarily due to the effect of the medication on the brain.

Cultural-ecosocial approach to psychiatry

Gómez-Carrillo et al (2023) argue for the value of a cultural–ecosocial approach to integrating neuroscience in psychiatric theory and practice. I’ve mentioned before (eg. see previous post) that relational psychiatry brings together a cultural-ecosocial psychiatry with developments from anti-cognitivist phenomenological and enactive accounts of psychopathology. Gómez-Carrillo et al also make this link in their article by explicitly recognising the importance of 4E cognition, which examines how cognition is embodied, embedded, enacted, and extended. As they say, "training in systems thinking and social science needs to be a key feature of psychiatric education”.

Mediated by the brain not necessarily the same as caused by the brain

Further to my last post, it may be worth thinking a bit more about why psychiatry, and neuroscience in general, have taken us down the route of the mereological fallacy. It’s become very common to view ourselves in terms of our brains (see eg. previous post). This, of course, has particular implications for psychiatry.

The reason this happens is because people no longer want to make a distinction between the psychological and the biological. It is said to be a false separation (see eg. another previous post). The fear is that the mind/body split of Cartesianism is being perpetuated by seeing mental disorder as psychological, said to be implying it is not biological (see eg. yet another previous post). Better to do away with any distinction at all, is the thought.

As I've said before (see eg. previous post), René Descartes (1596–1650) was the first to apply a natural-scientific mechanistic approach to life  Animate and inanimate matter were understood by the same mechanistic principles. Animals were, therefore, regarded as machines; and human physiology was also seen as mechanistic. Descartes stopped short, though, of including the human mind in this mechanistic framework. The soul was denied any influence in physiology. Descartes thereby avoided the materialistic implication that man himself is a machine. The split he created between mind and brain is what is referred to as Cartesianism. 

One of the first to challenge this perspective was Georg Ernst Stahl (1660–1734). He claimed that living things possess an immaterial soul, although he did not necessarily mean a transcendent soul, that provided the key element of movement to matter within the living body. His ‘dualistic’ notion was different from that of Descartes, in that he differentiated organic life from the inorganic, not the soul from the body. Unlike Descartes, he proposed that the soul and body are not separate but integrated in the organism. Despite his vitalism, Stahl originated a holistic perspective in the life and human sciences. This perspective formed the basis for his emphasis on psychosomatic medicine, and a focus on clinical medicine rather than the physical sciences. But his vitalism is as much derided, now, as Cartesianism. Although it makes sense to distinguish life from inanimate matter, a more modern way of expressing this is through enactivism, rather than vitalism (see eg. previous post). 

The mereological fallacy helpfully highlights that even though mental disorder is mediated by the brain, this does not imply that it is necessarily represented in the brain. Of course, cerebral disease or abnormality can cause mental disorder. But the vast majority of mental disorder is functional, not structural. It is not represented in the brain as such. It doesn’t make sense to see it as being in the brain. Even delirium and dementia caused by cerebral disease should not be seen as being in the brain as such. It’s people that become delirious or demented, not their brains. But the cause of organic mental disorder, such as delirium and dementia, is abnormality in the brain, whereas for functional disorder, it is not. It is more to do with the whole person, not just the brain, and cannot be understood mechanically. The mental is as much biological as the physical. Because the assumption is that mediation by the brain means that all mental disorders must be in the brain, people fail to recognise that mental disorders are not always in the brain. Being more careful and avoiding language to say that the brain is the person would be a start towards that realisation.

People are not their brains

I have been thinking about the implications of the mereological fallacy (see previous post) for psychiatry. Psychiatry must stop identifying the brain with the person (see eg. another previous post). 

People need to be understood as wholes, as their brains are only part of them. The brain mediates cognition, emotions and behaviour but it is not the brain that perceives, thinks, feels and acts. It is people as a whole that do that (see eg. yet another previous post).

Brain disease or abnormality can cause mental disorder. Such organic mental disorders can be due to a primary brain disorder or secondary to a systemic illness, or result from an exogenous toxic agent, or be due to physical withdrawal of an addictive substance. But not all mental disorder is due to brain disease or abnormality. Mental disorder shows through the brain but not necessarily in it.

Brain disease can be detected when assessing for mental disorder by disturbances of sensorium and cognitive functioning (see eg. previous post). In particular, level of consciousness, orientation, attention and memory are affected. Jaspers in his General Psychopathology referred to the "state of consciousness" as the "momentary whole" of the "psychic state". Brain disease may be detected by its effects on consciousness and that sense of wholeness.

Depression and schizophrenia, as examples of functional mental disorders, need to be understood in meaningful context. But the meaning of dementia, as an example of an organic mental disorder, could be said to be more to do with brain abnormality. It's people that become demented rather than their brains, as such, but the brain abnormality of dementia, whether Alzheimer’s or whatever, affects the wholeness of people's experience of themselves.

Publication bias in antidepressant trials

Erick Turner was a former US Food and Drug Administration (FDA) reviewer. At the FDA he was aware of publication bias due to negative results of trials tending not to be published. As he says in an interview with Ayurdhi Dhar from Mad in America (see edited transcript and podcast), there was a “disconnect between what clinicians were seeing and what the FDA reviewers were seeing, and what was known to the FDA and the pharmaceutical industry”. 

I’ve always argued that the apparent small difference between antidepressant and placebo in clinical trials could be due to placebo amplification because of unblinding (see eg. previous post). Although maybe unlikely, I suppose it’s possible that publication bias could completely explain this artefact. Certainly the pharmaceutical industry has taken advantage of the clinical reluctance to consider this issue, although publication bias also plagues psychotherapy trials. As Erick says, the decision as to whether a clinical trial is “good science shouldn’t depend upon whether the results were statistically significant”.

Reducing overprescribing in the NHS

The Department of Health and Social Care (DHSC) produced a report in September 2021 to reduce overprescribing of medication. According to the Sunday Express (see article), NHS England is due to unveil a scheme in the spring aimed at weaning the health service off a culture of ‘a pill for every ill’. 

As the DHSC report says, what’s needed to reduce overprescribing is already known: shared decision-making with patients; better guidance and support for clinicians; more alternatives to medicines, such as physical and social activities and talking therapies; and more Structured Medication Reviews (SMR) for long-term health conditions. The problem is that “Many patients do not feel that they experience a compassionate, coordinated service that pays enough attention to their individual needs, assets, values, preferences and priorities”. The College of Medicine (see webpage) launched its Beyond Pills Campaign in 2022. A cultural change to reduce the reliance on medication and to support shared decision-making would be very welcome, not least for mental health services.

Does psychotropic medication work?

Horatio Clare and Femi Oyebode have made a valiant effort to provide a balanced perspective in the radio series ‘Is psychiatry working?’. In the fourth episode, they ventured into the controversial area of medication, and I just wanted to make a few comments. I hope the final two episodes may help to explain why psychiatric services have become too dysfunctional and fragmented, although that might be for another series.

Almost as a kind of disclaimer, the programme had to say that there is no doubt that psychotropic medication helps millions of people round the world. But what is meant by such a statement? Individual experience may be that psychotropic medication helps. For others it may not be of benefit. Clinical trials tend to show an advantage over placebo for eg. antidepressants, but maybe not as great as is commonly assumed and a good proportion of people do not respond to antidepressants, even in the clinical trials. The efficacy of antidepressants is in fact still an open issue in the scientific literature because of methodological problems with the clinical trials (see eg. previous post).

The dynamic of the doctor-patient relationship is important even when medication is used. It is difficult for people to accept that so-called antidepressant efficacy may merely be due to the placebo effect (see eg. another previous post). Even cognitive neuropsychological theories, as for example described by Catherine Harmer in the programme, tend to assume that medication works through brain effects. Of course a placebo effect, which is not a brain effect, in itself can make people think more positively and seem to help their depression.

Although Joanna Moncrieff said that antidepressants make people physiologically dependent, the programme did not really deal with this issue (see eg. previous post). The extent to which taking medication can be an identity-altering experience tends to be underestimated (see eg. another previous post). Of course psychotropic medication can have physiological effects. But the whole edifice of modern psychiatry has been built on psychotropic medication being more than placebo and the fear is that it will come crumbling down if this were not true. Not a very firm basis for practice in my view. Psychiatry, of course, existed before the modern psychopharmacological era and isn’t just about medication.

Truth about psychiatric diagnosis

The study by Rosenhan (1973) published in Science has probably always been difficult to believe. I’ve said before, though, that psychiatry doesn’t need to be so defensive about it (see eg. previous post). DSM-III was motivated to improve the reliability of psychiatric diagnosis by introducing operational criteria, at least partly due to the challenge of the Rosenhan study, because Robert Spitzer thought unreliable diagnoses must be invalid. 

The Rosenhan study was actually more designed to challenge the validity rather than reliability of psychiatric diagnosis. Andrew Scull (who I’ve mentioned before eg. see previous post) has recently published an article in History of Psychiatry summarising the evidence that the study was fraudulent. Six of the seeming nine original participants are said to have never been traced. Data from one of the participants was not included in the Science report and this psychology student at the time of the study, who became an academic psychologist, published his own more positive account of his experience (see article). 

At the very least, Rosenhan (1973) is biased, inaccurate, dishonest and exaggerated its findings. As Andrew says, there is a "possibility that they [ie. the six missing participants] may still surface" but he thinks it is more likely they "never existed at all". 

I know of two reports of modified repeats of the Rosenhan study. Because they are later, both were done in the context of the rundown of the traditional psychiatric hospital. Although all Rosenhan's pseudopatients were said to have been admitted to hospital, both these reports suggest that feigning an auditory hallucination does not now generally lead to admission, maybe because of the pressure on beds. Scribner (2001) used 7 volunteers with long well documented histories of chronic schizophrenia, six of whom were actually denied treatment and turned away. The baseline histories were therefore very different from Rosenhan (1973), whose pseudopatients were said not to have had a history of mental disorder. 

The other report was from the book Opening Skinner's Box (2004) by Lauren Slater. Interestingly, she too has been accused of never conducting her study (see article). As she says in the book in her chapter on Rosenhan:

Psychiatry as a field is, of course, predicated on the belief that its own professionals know how to reliably diagnose aberrant mental conditions and to make judgments based on those diagnoses about a person’s social suitability

Interestingly again, she seems to suggest that Martin Seligman, an eminent psychologist, was one of Rosenhan's pseudopatients, which is not mentioned by Scull (2023). As far as I know, Seligman is still alive, so it may be possible to check this.

Slater herself has a "formidable psychiatric history" and was admitted to a psychiatric hospital aged 14. She does not deny the reality of mental illness. Slater says she used someone else's name, so that she wasn't recognised, and denied any psychiatric involvement in the past. She relates that she presented herself nine times saying she was hearing a voice, and that, although she was treated kindly and was not admitted, she was prescribed a total of 25 antipsychotics and 60 antidepressants. Almost every time she says she was given a diagnosis of psychotic depression.

I suppose Rosenhan could be said to have had more impact on psychiatry as a social scientist than Andrew (except maybe Andrew’s influential dismissal of Foucault in the literature - see eg. previous post)! Not excusing Rosenhan's behaviour, but I think the scientific literature is plagued by such dishonesty as Rosenhan's. There is evidence, though, that at least aspects of his Science paper are correct. Certainly it was possible for a person who is not mentally ill to obtain admission to psychiatric hospital and mislead psychiatrists into diagnosing schizophrenia. Maybe this has always been the main message that people have taken from the study. Rosenhan does seem to have elaborated the details to reinforce his conclusion that psychiatric diagnosis is subjective and does not reflect inherent patient characteristics.

What worries me is that Andrew’s complete dismissal of Rosenhan’s study as fraudulent may reinforce the case that psychiatric diagnosis is objective, which it isn’t in any absolute sense. The limitations of psychiatric diagnosis do need to be acknowledged (see eg. previous post). If psychiatric diagnosis is meaningful, there will be inevitable inconsistencies.

Conversation about critical/relational psychiatry

I've posted a summary (see link) of my views about critical/relational psychiatry, which is to be published in a forthcoming Oxford University Press book adaptation (late 2023) of  'Conversations in Critical Psychiatry' edited by Awais Aftab. The essential message of critical/relational psychiatry is that primary mental illness cannot be reduced to brain disease. Such a view tends to be dismissed or marginalised as it may be difficult to believe and accept. Of course mental illness has something to do with the brain, people say. Is critical/relational psychiatry really suggesting otherwise?

Of course it isn’t! The brain mediates our thoughts, emotions and actions, including mental illness. This statement is of course true. But biomedical psychiatry’s claim is that mental illness will be shown to be due to an abnormality in the brain, even that there is considerable evidence already to come to this conclusion. This hypothesis may seem to stand to reason, but it doesn’t. Let me explain.

Abnormalities of the brain can of cause cause mental symptoms. Such is the case for example with a brain tumour. Definite neurological signs may also be present in cerebral disease. Fortunately such organic conditions tend to cause symptoms affecting cognitive functioning that usually allow them to be distinguished from non-organic mental illnesses, like schizophrenia or depressive illness. Primary mental illness, not caused by brain disease, is functional and not structural. It shows through the brain but not in it.

Acknowledging this situation has advantages for psychiatric practice. It should mean that people are not reduced to their brains. They must not be treated as objects. Clinical work needs to be focussed on understanding patients’ histories and mental states and formulating their problems in those terms. Treatment needs to be about supporting them to deal with their problems.

This basic message needs reinforcing in the current mental health system which has become too dysfunctional and fragmented. Psychiatry needs to move on from an outdated belief in mental illness as brain disease.

The Joint Committee on the draft Mental Health bill has produced an impressive report (see eg. last post and twitter thread of what the Committee sees as the highlights. Also, see the walkthrough of conclusions and recommendations by Alex Ruck Keene.). I particularly welcome the Committee’s not necessarily expected recommendation to abolish Community Treatment Orders (CTOs) for civil patients. Although it is keen for the Mental Health Bill to be passed into legislation as soon as possible, it also promotes the need for ongoing reform. The Committee helpfully recommends the creation of the post of Mental Health Commissioner and the introduction of pilots for patients to be able to appeal to a slimmed down Mental Health Tribunal about treatment plans. It makes helpful recommendations about incorporating reference to the principles of racial equality, choice and autonomy, least restriction, therapeutic benefit and person as an individual on the face of the Act.

Although it expresses concern that the introduction of conditional discharge for restricted patients may be overused, the Committee only recommends close monitoring of implementation with a statutory review after 3 years. My main concern about the report is that it does not seem to have considered the need to improve the right to an independent second opinion from a person of the patient’s choice, rather than just from a Second Opinion Approved Doctor (SOAD) appointed by the Care Quality Commission (CQC). As I said in a previous post, the strengthening of the role of SOAD is welcome, but this should be taken further by making the second opinion process even more independent. I think this is particularly the case in the context of developing the role of the Tribunal to consider treatment decisions and I would argue that eventually SOADs could be abolished.

The Committee emphasises the need for adequate resourcing of the MHA changes and sees it as essential that a detailed plan for resourcing and implementation is produced on introduction of the Bill. I look forward to seeing the government's response.

Legislating for Mental Health Act (MHA) reform

My understanding is that the Joint Committee on the draft Mental Health bill should be producing its report this week (see its tweet). I just want to pick up on aspects of the additional written evidence submitted to the Committee since the original batch (see previous post). 

Supplementary written evidence by the Chair and Vice-Chairs of the Independent Review of the Mental Health Act helpfully highlights the need to improve the quality of advocacy services (see twitter thread; also guidance from NICE on how to commission and deliver effective advocacy services) and to enable the Mental Health Tribunal to challenge treatment decisions (see another twitter thread). NHS England expresses concern about the power of supervised discharge (see twitter thread). A letter from from the Joint Committee on Human Rights recommends improvements in MHA complaint handling (see another twitter thread). 

I look forward to seeing how the Committee deals with these and other issues in its report to take forward the Mental Health Bill.

Reimagining psychiatry

Diana and Nik Rose have a Psychological Medicine article entitled ‘Is ‘another’ psychiatry possible?’. They discuss postpsychiatry (see eg. previous post), Open Dialogue,  the Power, Threat and Meaning Framework (PTMF) (see eg. another previous post) and service user involvement in research in this context. As they say, the leaders of the psychiatric establishment are unlikely to accept “reduction in their claims that they are the exponents of highly effective, neurobiological based, targeted treatment of brain disorders”. 

I’ve always said it’s unrealistic to expect a paradigmatic shift in psychiatric practice because the hope of finding a biological basis for mental illness will never go away completely. But the extent to which it’s understood that this belief is wishful thinking may change. Psychiatry does need to become more open minded, more self-critical and less dogmatic in its beliefs and claims. 

Psychiatric practice is too based on speculation

Although psychiatrists generally admit that brain science has not advanced to the point where discernible biological lesions or genetic abnormalities have been found that are reliable markers of functional mental disorder, they tend to assume in practice that such markers will be found. Their clinical work is backed up by a vast research effort motivated to uncover the biological basis of mental illness. Treatments, such as medication, are presumed to correct abnormalities in the brains of mentally disordered people.

There are of course brain impairments that cause mental symptoms. These can primarily be divided into acute and chronic presentations. Acute conditions present with a toxic confusional state or delirium, for example related to the general effects of disease in the body. Chronic irreversible conditions are dementia, such as Alzheimer's disease. Such organic presentations can be differentiated on clinical examination of the mental state, as they have cognitive symptoms and signs affecting intellectual functioning, such as orientation (time, place, person), concentration, attention, memory and level of consciousness. These cognitive abnormalities tend not to be present with functional disorders.

Mental disorders are of course mediated through the brain, but it is a conceptual mistake to regard non-organic disorders as being in the brain. People become mentally ill, not their brains. Functional mental disorder needs to be understood in the context of life, social, family and personal development and current situation. It may not be possible to 'prove' what causes mental illness, and it may be very difficult to make sense of some presentations, such as psychosis, but nonetheless any treatment needs to focus on providing the support and understanding to help people recover from their difficulties as much as they are able and wish to do so.

Mental health treatment online can exploit people

Article in The Wall Street Journal exposes how advertising and other strategies to promote expansion of treatment by digital mental health companies are motivated more by profit and not really improving patient care. For example, heavy advertising of ADHD self-diagnosis online (see eg. MediaMatters article) has encouraged people to seek prescription for stimulant medication. Exploitation of this situation by Cerebral Inc. has been described in four podcasts: Uncontrolled Substances. It isn’t just medication but also other physical treatments and psychological therapy that are being oversold on the internet (see eg. previous post). 

Medicine has always exploited patients but the move to online treatment because of the pandemic may have made this situation more obvious. In the end, it’s also the doctors and other health professionals that need to take responsibility alongside corrupt business practices (see eg. another previous post). 

Causal concepts of disease

I’ve emphasised before (eg. see previous post) how medicine changed in the nineteenth century. K. Codell Carter in his book The rise of causal concepts of disease (2003) mentions how James L. Bardsley, a prominent British physician, in 1845 thought that diabetes ‘has been traced by some patients to sleeping out the whole of the night in a state of intoxication’. This shows how much our ideas of disease before our modern anatomoclinical understanding were influenced by patients’ opinions themselves.

Codell Carter describes the development of what Robert Koch called the aetiological standpoint which understood disease as having natural, universal and necessary causes. He also suggests in the last chapter of the book that how we characterise disease may change in the future. 

The domination of medical thought by the aetiological standpoint has prevented the proper understanding of functional mental illness. Psychiatry’s credibility is wrongly dependent on a biological aetiology of mental illnes, despite brain abnormality not being a sufficient explanation of functional mental illness. Psychiatry’s still stuck in the nineteenth century in its search for natural, universal and necessary causes of mental illness.

Relational psychiatry not merely an embarrassing hangover from 1970s

I have been re-reading my editorial in BJPsych Bulletin entitled ‘Critical psychiatry: An embarrassing hangover from the 1970s?’. I conclude that “Critical[/relational psychiatry] can be understood as a non-eclectic, biopsychosocial, neo-Meyerian approach to psychiatry based on Kant’s critical philosophy”. 

I just thought it may be worth explaining a bit more what I mean by this. I’m arguing that critical/relational psychiatry is not new. Although it’s often seen as a continuation of the anti-psychiatry of the 1960/70s, associated with R.D. Laing and Thomas Szasz, in fact it has a longer pedigree and was actually present in the origins of modern psychiatry in the Enlightenment. 

As described by Foucault in History of madness (see previous post), critical engagement of reason with itself in the Enlightenment brought psychiatry into existence as a distinct discipline. Early psychiatrists identified mental alienation and delusional thinking. The asylums became a specific form of institutional care, built to accommodate people needing treatment for mental illness, rather than such people being, for example, kept in the workhouse. The mentally ill were seen as deserving of poor relief on the basis of their mental state. The twentieth century saw the development of community care making the asylum increasingly irrelevant. Even in modern welfare, though, the mentally ill receive sickness and disability benefits, rather than unemployment benefit.

Anthropological understanding in the Enlightenment, viewing human beings as psychophysical entities, created the idea of the possibility of a natural scientific approach to psychology. However, Immanual Kant developed an alternative pragmatic approach to anthropology. He was clear that life could not be explained in mechanical terms and that psychology is descriptive and cannot be reduced to biology (see eg. previous post). This perspective was eclipsed by positivism later in the 19th century with the progress in understanding of physical illness in biological terms. The expectation was that mental illness would also be understood as a dysfunctional biological process (see previous post). However, it would have been better if psychiatry had stuck with Ernst von Feuchtersleben’s understanding of psychiatry (see eg. previous post) based on Kant’s critical philosophy. To reduce mental illness to brain disease is not possible in principle (see yet another previous post). 

Since then, there have been attempts to recreate an anti-reductionist perspective in psychiatry. For example, although he was not as explicit as he should have been, Adolf Meyer developed a psychobiological approach to psychiatry as an alternative to positivistic psychiatry (see eg. previous post). He was clear that psychopathology needs to be studied functionally in experiences and social interactions rather than at the level of neurobiology. This is not to deny the importance of organic conditions, such as delirium and dementia. Meyer's system never really took hold as a systematic theory, at least partly because he was prepared to compromise with biomedical perspectives, even if he disagreed with them. His views were also eclipsed by a reassertion of biomedical ideas over recent years in so-called neo-Kraepelinianism, developed as a response to anti-psychiatry (see eg. another previous post). 

Another example would be George Engel’s paper in Science in which he suggested there was a need for a new medical model, which he called the biopsychosocial model (see previous post), to replace the biomedical model. The trouble is that ‘biopsychosocial’ over recent years has become an ill-defined basis for psychiatric practice meaning that biological, psychological and social are all more or less equally relevant in all cases and at all times in psychiatric assessment. This eclecticism has been critiqued by Nassir Ghaemi and does seem to have outlived its usefulness (see eg. previous post). 

So, in summary, critical/relational psychiatry is a truly biopsychosocial model. It is not eclectic. It adopts the psychobiological model of Adolf Meyer but not his tendency to compromise with biomedical perspectives. It seeks a return to the Kantian origins of psychiatry, as, for example, expressed by Ernst von Feuchtersleben, to provide a more integrated critical perspective on modern psychiatry (see previous post).