How do we understand depression?
The discussion as to whether the source of mental disorders is in the brain or in society has a long history. In
The myth of mental illness, Thomas Szasz pointed out that a disease or disorder is due to defects or functional impairment (16). As soon as impairments or defects are detected, the diseases are by definition no longer mental disorders, but neurological, metabolic or genetic diseases, as the case may be. The assertion that mental disorders are a myth is therefore a tautology, according to Szasz.
Illustration: The Journal of the Norwegian Medical Association
This does not prevent many researchers from firmly maintaining the belief that depression is to be understood as a brain disorder, but at the same time attaching weight to genetic and environmental factors. It is still argued that depression is due to serotonin deficiency, injury and inflammation, neurodegeneration and mitochondrial dysfunction
Depression is studied at different analytical levels in biological, psychological and social theories. The fact that the brain is the source of all the mind's activity does not mean that research on the brain is always the most fruitful analytical level for understanding thoughts and experiences. In a one-sided biological approach, there is a risk of confusing cause and effect and individualising and biologising social problems. When unemployment and loneliness increase the prevalence of depression, it is not self-evident that these are matters for neurobiological studies.
No matter how much or how little biology there is in a depression, the context must be important. Depression seldom strikes in a vacuum. For example, Dalgard et al. demonstrated a dose-response relationship between stress and the occurrence of depression
(18). If one is going to biologise mental problems, one must avoid an overgeneralisation that does not take account of what we all know: that our feelings are bound up with the life we live.
Topical book: Johann Hari. Lost connections. Uncovering the real causes of depression – and the unexpected solutions. London: Bloomsbury, 2018
Mental problems are classified without account being taken of
why the person has the problems in question. The clinical treatment must start where the classification system leaves off, i.e. with an understanding of why this particular person has these problems. The critics are right in maintaining that neither diagnostics nor treatment can be context-free.
Between 2006 and 2013, the number of girls in Norway aged between 14 and 17 taking antidepressants increased by 70 %
(19). This is difficult to reconcile with a purely biological interpretation of the problem. There must be something else driving developments.
A study by Einar Kringlen et al. showed that the prevalence of depression and other mental disorders is far lower in the county of Sogn og Fjordane than in Oslo
(20). The authors believe that the difference in prevalence is due to social stability and closer ties among people in the former county. If they are right, measures that increase a sense of belonging, fellowship and trust among people must reduce the prevalence of depression.
Many people perceive depressive problems as a reaction to the conditions they live under. Many feel that they struggle with individual problems, and they prefer to understand their specific problems rather than to be told which abstract category they belong to.
Instead of diagnostics and psychotropic drugs, the critics of the biomedical paradigm want normalising approaches, socially oriented solutions, inclusion of those who are less fortunate and social activism. Above all, many want a less paternalistic psychiatry, and more equality between expert and patient. It would do Norwegian psychiatry no harm to listen to these ideas.
Home from the office, standard routine. Coffee and newspapers, back to the keyboard. Search on PubMed: "Depression + serotonin + hypothesis + review". The review articles firmly maintain the theory. The latest edition of
JAMA Psychiatry drops into the Inbox: editorial from Oslo on the NMDA receptor-antagonist esketamine for treatment-refractory depression (21). The authors write that the disease mechanism may be related to the NMDA receptor. The same reasoning as those who launched the serotonin hypothesis. Are we going round in circles? I log out and finally read something on paper – Ivan Illich's classic from 1974. Of everything I have read today, he is undoubtedly the most correct – there is a nemesis pervading medicine (22), p. 919): "By transforming pain, illness and death from a personal challenge into a technical problem, medical practice expropriates the potential of people to deal with their human condition in an autonomous way and becomes the source of a new kind of un-health."