Saturday, October 31, 2020
Saturday, October 17, 2020
Friday, October 16, 2020
Monday, October 12, 2020
To investigate further why so many people were unwilling to even try stopping their antidepressant medication despite it not being indicated, Eveleigh at al (2019) interviewed some of the participants in the trial. They found that fear (of recurrence, relapse, or to disturb the equilibrium) was the most prominent barrier, and prior attempts fuelled these anticipations (see eg. previous post). Another important barrier was the notion that antidepressants are necessary to correct deficient serotonin levels (see previous post). As Verbeek-Heida & Mathot (2006) found, the fear and uncertainty about stopping were stronger than the fear and uncertainty about continuing. Users of antidepressants tend to think they are better off 'safe than sorry' by continuing medication (see another previous post). Patients are uncertain and fearful about what they will be like without medication (Leydon et al, 2007).
The evidence for what it is worth is that continuing antidepressant treatment reduces the risk of relapse. Relapse rates in discontinuation trials can be substantial. Although fear of relapse may be biasing the results of such studies through unblinding, doctors have to be realistic that discontinuing antidepressants may not be easy. Patients tend to think doctors should take responsibility for initiating contact about discontinuation (Bosman et al, 2016), but in practice this tends not to happen. A good proportion of the increase in antidepressant prescribing over recent years is because of long-term repeat prescribing (see previous post).
Taking antidepressants can be identity altering (see previous post). Patient's preferences and concerns affect their decisions about medication (Malpass et al, 2009). These sort of factors should have been obvious to doctors (see my book chapter). As I keep emphasising, psychological factors cannot be denied in causing antidepressant discontinuation problems (see eg. previous post). The question is whether they are a sufficient explanation or whether underlying clinically significant brain changes also contribute (see last post).
(With thanks to a MIA blog post by Peter Simons)
Thursday, October 08, 2020
She also mentions the harms caused by psychiatric drugs. For example, antipsychotic medication can cause brain shrinkage, although I think the clinical significance of this finding is unclear (see eg. previous post). Antidepressant discontinuation problems may have become better recognised since a formal complaint made to the Royal College of Psychiatrists two years ago (see eg. previous post). I actually think that believing the disease-centred model of antidepressant action is likely to increase the risk of discontinuation problems (see another previous post).
Joanna defends what she calls a drug-centred rather than disease-centred model of drug action (see eg. another blog post from her). As she also notes, psychiatrists may have an outcome-based understanding of drug action, without necessarily any apparent particular commitment to an explanation of the drug's action. I certainly don't believe in the disease-based model, but still prescribed psychotropic medication when I was working because the evidence, for what it is worth, is generally said to be that such medication is effective within NICE guidelines. It was difficult for me to refuse a request for medication within these parameters. This is despite my scepticism about the evidence (see eg. previous post) and recognition that any effect may be due to placebo (see eg. another previous post). I don't want to undermine people's belief in their medication, but not everyone is helped in the clinical trials and the difference between placebo and active medication in these trials is generally much smaller than most people realise. Because of psychological factors, I was very aware of the risk of discontinuation problems and often it seemed easier for patients maintained on medication to continue with it rather than stop (see eg. another previous post).
An advantage of the drug-centred model is that it makes us realise, as Jo says, "how little we really know about these drugs". Modern psychopharmacology started with the introduction of chlorpromazine in the 1950s. When testing drugs for treatment of protozoal infections and parasitic worms, chlorpromazine was noted to have strong anti-histamine properties. It was therefore investigated with allergic patients and reported to cause drowsiness. This 'drowsiness' effect was explored by Henri Laborit, a French surgeon, using chlorpromazine to potentiate anaesthesia with other agents by preventing surgical shock. He reported it induced 'detachment' in his patients, suggesting it produced an 'artificial hibernation' because of its hypothermic and hypnotic qualities. Jean Delay and Pierre Deniker, therefore, investigated the potential for the drug on its own at higher doses in calming manic patients. Their papers talked about chlorpromazine causing a 'chemical lobotomy' different from other sedatives. They coined the term 'neuroleptic syndrome' referring to a slowing down of motor activity, affective indifference and emotional neutrality. Trials of chlorpromazine undertaken by Heinz Lehmann in Montreal facilitated the new drug's introduction to North America. Extrapyramidal effects, such as parkinsonism, were difficult to differentiate from any anti-psychotic properties.
Imipramine, the first antidepressant, has a similar chemical structure to the phenothiazines, like chlorpromazine, but different psychoactive effects. Initial trials in schizophrenia failed but it was said to be spectacularly effective in vital depression (see previous post). As Jo says, the SSRI antidepressants seemed to be "relatively innocuous" compared to the tricyclic antidepressants, like imipramine. She speculates about how they might be "changing the brain in significant ways that we do not understand".
The trouble is that these are only speculations and psychological dependence could be a sufficient explanation of antidepressant discontinuation problems (see eg. previous post). I agree with Jo that we should concentrate on psychiatric harm (see eg. another previous post) and the way to do that is to be much clearer about the pharmacological effects of psychotropic medication. I was much cleare about the effects of neuroleptics and tricyclics when I first started in psychiatry than SSRIs which are relatively inert.
Saturday, October 03, 2020
As I've also mentioned before, there actually was some value in the work of anti-psychiatry (see previous post). It shouldn't be seen merely as a negative contribution to psychiatry. As I wrote in my editorial, "it is difficult to accept that there was no value in the approach and what may be more beneficial is to look for the continuities, rather than discontinuities, with orthodox psychiatry" (see also my essay review). Personally I've always tended to emphasise the links of critical psychiatry (which I differentiate from anti-psychiatry) with mainstream psychiatry (see another previous post).
The term 'anti-psychiatry' was coined by David Cooper (see eg. previous post). It came to incorporate earlier writings by R.D. Laing, Michel Foucault, Erving Goffman and Thomas Szasz. It was most associated with the views of Laing and Szasz, who actually had very different perspectives (see eg. another previous post). Szasz, for example, equally rejected both mainstream psychiatry and Laing’s views. The emphasis on therapeutic communities in the Laingian version of anti-psychiatry led to positive developments such as the Philadelphia Association (see previous post) and the Arbours Association. The anti-institutional concerns of anti-psychiatry contributed to the rundown of the traditional asylum, with political impact such as that of Franco Basaglia in Italy (see previous post). The application of social labelling theory to mental illness, for example by Thomas Scheff (see my book review), had particular implications in the study 'On being sane in insane places' by David Rosenhan, which caused a crisis of confidence for psychiatric diagnosis at least for American psychiatry (see previous post). This was countered by the development of DSM-III. There were also international perspectives to anti-psychiatry, such as: French anti-psychiatry, particularly identified with Gilles Deleuze and Felix Guattari; Frantz Fanon in Algeria; and Jan Foudraine in the Netherlands (see my book chapter).
Maybe the term 'antipsychiatry' (without the hyphen) should now be reserved for the argument for the abolition of psychiatry (see previous post). But, I'm afraid it's still being used in the same way (eg. in the Psychology Today blog post mentioned above) as it was originally by mainstream psychiatry to denigrate any criticism, including valid criticism, of the biomedical model in psychiatry. I think this usage goes back to articles such as that by Martin Roth (1973).
In the article, Roth frames the debate about anti-psychiatry as an attack on the deterministic scientific nature of psychiatry. He recognises that this issue raises difficult philosophical questions and creates a need to reconcile deterministic concepts of causation with the inner experience of free will. He sees psychiatry as making progress towards this end by, for example, being able to describe the medical and social profile of those who commit suicide. He believes the Enlightenment represented the replacement of moralistic and transcendental attitudes with rational and deterministic explanations.
Roth is correct that the conflict between determinism and free will is ultimately unresolvable. However, critical psychiatry does not take the same positivistic view of biological and biomedical sciences. In fact, the postpsychiatry version of critical psychiatry explicitly sees such a modernist agenda as untenable (see eg. previous post).
A mechanistic worldview, which Roth calls science, confers an apparent advantage by providing a predictive and systematic way of understanding and manipulating nature. However, this leaves the phenomenon of life in an equivocal position because it cannot be totally stripped of its intrinsic purposiveness (see previous post). Rene Descartes (1596-1650) regarded both animate and inanimate matter by the same mechanistic principles. Animals are therefore machines; and human physiology is also 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.
Although Georg Ernst Stahl (1659-1734) claimed erroneously that living things possess a vital entity, his dualistic notion was different from Descartes, in that he differentiated organic life from the inorganic, not the soul from the body. Unlike Descartes, the soul and body were not separate but integrated in the organism. Stahl originated an organismic perspective in the life and human sciences. This perspective formed the basis for Stahl having an emphasis on psychosomatic medicine, and a focus on clinical medicine rather than the physical sciences.
Despite what Roth implies about the modernism of enlightenment thinking in the second half of the eighteenth century, the critical philosophy of Immanuel Kant (1724-1804) was clear that it is absurd and futile to expect to be able to understand and explain life in terms of merely mechanical principles of nature (see previous post). A mechanistic conception of nature fails to provide a complete characterisation of living systems. Organisms, unlike machines, are self-organising and self-reproducing systems. Different modes of explanation are therefore required for teleological and mechanical points of views.
What's needed is a pragmatic approach which focuses on nature and experience and the centrality of the organism-environment interaction. Life’s dynamic, systemic and purposive character needs to be promoted as a way of moving on from physico-chemical reductionism, which tends to eliminate the meaning of human action. Life is continuously and dynamically preserving its internal environment and is therefore a perpetual stream of matter and energy, better understood as a process than a static unchanging entity (see previous post).
Roth rightly recognises that it is the mechanistic approach to mental illness that is being criticised and notes the difficulties in identifying the social cause of mental illness. But his reason for rejecting a social perspective is not valid. This is because he expects social explanations to be determinist, which they are not. Moreover, he resorts to genetic factors to avoid environmental explanations. I agree with Roth’s conclusion that constructive endeavour is required to resolve the manifold problems of contemporary psychiatry. However, his labelling of any criticism of the biomedical model of psychiatry as ‘anti-psychiatry’ has hidden the extent to which the critique of reductionism and positivism in psychiatry is valid. Modern apologists for psychiatry by labelling their critics as ‘anti-psychiatry’ are doing the same. Instead they should examine how much psychiatry reduces people to objects and uses an inappropriate mechanistic psychology and biology.