The power of psychiatry to shape our sense of self

The belief that mental illness will be shown to be caused by the brain dominates psychiatric thinking. Of course brain abnormalities can cause organic mental illness, such as dementia and delirium. But most mental illness has not been shown to be caused by brain abnormalities. Research has failed to identify such definite biomarkers of functional mental illness. Biomedical psychiatry is more like a faith that people are expected to believe than a proven scientific practice.

Having such a basis for practice does not seem to matter, as biomedical approaches dominate mental health services. Although psychosocial interventions are used, medication plays a key role in treatment. People are encouraged to believe that medication is correcting a brain abnormality that has caused their mental health problems.

The biomedical hypothesis has obvious attractions, even if it seems to oversimplify. Understanding the reasons for mental health problems are generally complex and in a sense unprovable. Being able to latch onto a physical, more mechanical, explanation may seem to offer more certainty. But such mechanistic thinking fails to provide a complete characterisation of human beings and life in general. Organisms are self-organising and self-reproducing systems unlike inanimate objects. The brain is only part of a person, who needs to be understood as a whole.

Believing in the hope that mental illness can be fixed in the brain may, therefore, alter our understanding of ourselves. If we are no more than the operation of our brains, then our subjective sense of meaning is reduced. People deserve more from psychiatry than to be treated as objects.

Sealing over emotional problems with medication

I’ve never been convinced that any apparent response to antidepressants is more than placebo. Although short-term clinical trials may show a small advantage for active treatment over placebo, it is possible that this difference could be a artefact because of methodological problems with the trials and bias in the literature (see eg. previous post).

Placebos have effects because of patients’ belief in their treatment. These positive hopes about the effectiveness of antidepressants may be reinforced by the serotonin myth or other hypothesised brain mechanisms of antidepressant action. Patients are encouraged to take their medication by doctors telling them that their depression is due to a brain problem that is corrected by medication. However, by believing the myth that depression is caused by brain abnormalities, the real reasons for emotional problems may not be recognised and corrected. In other words, although emotional difficulties may be sealed over by taking medication because of the placebo effect, patients haven’t necessarily improved their understanding of the reasons for their problems. They do not necessarily incorporate their experience in a properly integrative way.

Beliefs about medication can therefore be powerful and the disadvantages of relying on medication need to be recognised. Believing treatment has been effective because of its antidepressant action, when the apparent benefit has really been due to placebo, can leave people feeling that their emotional problems have not really been solved. This may well be true because the social situation that caused the depression has not changed. Patients do not necessarily feel they have made a proper recovery or returned to their true self. Masking the real problem can create a sense of inauthenticity with the experience of flattening and numbing of emotional responses.

Avoidance of stress by taking medication is not necessarily an irrational coping strategy. Many people when they are depressed are in a desperate situation. It may well be understandable that they latch on to whatever is offered to them to make a recovery. Taking medication may seem like the only possible option available. But if there is an improvement, leading patients to have faith in the medication, it can mean that they continue on the medication becoming psychologically dependent on it over time. They become fearful about upsetting the mental equilibrium acquired through taking medication. No wonder they may have discontinuation problems.

Sealing over emotional problems with antidepressant medication can therefore cause withdrawal problems and emotional numbing as nocebo effects (see eg. previous post). Using medication as a coping strategy may not necessarily produce the better outcome obtained through incorporating emotional problems into patients’ life narratives. However difficult it may be, recovery from a depressive episode can be transformative.

The origins of the concept of autism

The concept of childhood autism originated independently in the work of Leo Kanner and Hans Asperger. The original paper by Kanner (1943) ‘Autistic disturbances of affective content’ has been re-examined by Sausalito & Kocha (2025) in History of Psychiatry. Kanner described 11 cases in children with what he called "extreme autistic aloneness". Eugene Bleuler (1911) had identified the symptom of an active turning away from external reality to a preponderance of inner life as ‘autism’ and saw it as fundamental to ‘schizophrenia’, a term which he originated (see eg. previous post). Kanner emphasised that his cases were unlike schizophrenia because such aloneness had always been present rather than being a withdrawal from participation in the outside world. As Sausalito & Kocha point out, this relationship between Kanner’s autism and childhood schizophrenia tends to be overlooked today. 

Michael Rutter (1978) clarified the definition of autism based on Kanner's paper by identifying the key symptoms of general failure to develop social relationships; language retardation with impaired comprehension, echolalia and pronominal reversal; and ritualistic or compulsive phenomena. He also emphasised that autism and learning disability frequently coexist, although differentiating autism from learning disability on the basis of particular cognitive deficits that involve language and central coding processes. When I trained Rutter's perspective tended to influence the diagnosis of autism, which was rare, certainly in adults without a childhood diagnosis, and, if made, tended to be related to learning disability.

Another paper in History of Psychiatry focused on the history of Asperger's autism (see previous post). Lorna Wing (1981) resurrected Asperger’s original 1944 German paper and popularised the term Asperger’s syndrome, introducing the autistic triad of difficulties in social interaction, communication and imagination. She saw autistic spectrum disorder (ASD) as a group of disorders of development with life-long effects, having this triad of impairments in common. The spectrum included but was wider than the original syndromes of Kanner and Asperger. Rise in the incidence and prevalence of autistic diagnoses followed the change of criteria and the introduction of the spectrum. ASD over recent years is seen as part of neurodiversity, reframing various conditions such as ADHD, dyslexia and autism as differences rather than deficits (see eg. previous post). These historical perspectives on autism help to make sense of the epidemic increase in neurodevelopmental diagnoses and highlight the subjective aspect of psychiatric diagnosis. 

Psychiatric diagnosis is merely a hypothetical construct. We too easily assume such concepts are entities of some kind. They are justified by their clinical utility, but the ever expansion of the notion of neurodiversity questions its value. Diagnoses are relative rather than absolute concepts with inevitable fuzzy boundaries between syndromes. More fundamentally, speculative notions about the causal biological basis of psychiatric diagnoses, like autism, mean than people tend to be reduced to their brains when they are given a psychiatric diagnosis. People are more than their brains and the reasons for their mental health difficulties, such as autism, may not be explained by brain abnormalities at all (see eg. last post). The kind of person they are, for example, may be more to do with their family origins and personal development than their brain. 

When I trained, schizoid personality disorder (SCD) was a diagnosis that overlapped with what is now seen as autism. It was originally a non-psychotic diagnosis of people that shared the feature of social aversiveness in schizophrenia. The key symptoms of SCD are social isolation and emotional detachment. It tends to be a diagnosis made in adults whereas autism was a diagnosis originally made in children. SCD in adults has now been replaced, at least to some extent, by higher functioning autistic spectrum in people without an original diagnosis in childhood, although signs of autistic traits in childhood are recognised retrospectively. Correspondingly, ASD diagnosis in children has also increased. 

The subjective aspects of psychiatric diagnoses are to be expected because diagnoses are merely idealised descriptions. There will be inevitable unreliability in their application. Of more concern is whether the diagnostic construct is valid. What worries me is when concepts like autism are seen as natural kinds, in the sense of being seen as reflecting the objective structure of the world. People are inevitably different and how well they relate to others and express themselves will of course vary. Blaming the brain for such difficulties may be more to do with wishful thinking than reality (see eg. previous post). Autism, like ADHD (see eg. previous post), is not a neurological condition as such. Of course it is mediated by the brain, but it’s not necessarily caused by it.