Monday, September 30, 2019

Foundations of the biopsychosocial model

Derek Bolton is giving a series of colloquia on Engel's biopsychosocial model, based on his book with Grant Gillett (ebook freely available, and references below taken from it). Gillett and he recognise the need for the biopsychosocial model in the light of "historical prejudices against psychosocial causation deriving from physical reductionism and dualism" (loc 132). Nonetheless, they seem to accept criticism of the model by authors, such as Nassir Ghaemi in The rise and fall of the biopsychosocial model, that its eclecticism makes it "vague, useless and even incoherent" (loc 132).

I have myself reviewed Ghaemi's book (see review and response from Ghaemi and my reply). It critiques psychiatric eclecticism and in my view wrongly blames this on Engel's biopsychosocial model. Ghaemi is correct to note the contribution of Roy Grinker, who appreciated the relevance of general systems theory to psychiatry (see my article). Engel suggested that systems theory provided a suitable conceptual basis for his biopsychosocial model. Bolton & Gillett think this is "fundamentally the right way to go" (loc 563). But they seem unaware that Engel's biopsychosocial model is not responsible for the eclecticism in psychiatry.

As I've said before (see eg. previous post), the real origin of the eclectic view in psychiatry is Anthony Clare's response to anti-psychiatry. As Bolton & Gillett say:
The way Ghaemi tells the story ... [is that] the biopsychosocial model arose in the context of competing general views about illness, favouring one or other of the social, the psychological/psychoanalytic and the biological. ... Ghaemi interprets the biopsychosocial model as an elegant ... solution to these ideological conflicts ... [as] if all participants won, [as] if they were not really in opposition at all, but were in fact all true general accounts of illness and healthcare in all aspects. (loc 237)
This was what Clare argued, not Engel. Clare wanted to avoid the ideological conflict created by anti-psychiatry and proposed eclecticism as a way forward.

Bolton & Gillett do realise that "this line of thought [ie. eclecticism] is not apparent in Engel's main papers" (loc 237). In some of Engel's other papers, he does make the general comment that biological, psychological and social must all be taken into account. Misuse of this statement by Ghaemi to mean that all three are more or less equally relevant in all cases and at all times, seems to convince Bolton & Gillett that Ghaemi has a valid point.

As I’ve said (see eg. my editorial and previous post), Engel’s original paper was in fact written to counter Ludwig (1975), who recommended a retreat to a rigid biomedical model in the face of the onslaught of anti-psychiatry. In the same year as Engel, Manschrek & Kleinman (1977) similarly argued for a critical rationality to replace the hubris (dogmatic biomedical) and semi-critical (eclectic) positions in psychiatry (see previous post).

I'm not convinced that Bolton & Gillett have fully appreciated this context. Engel was aware of the success of biomedicine in explaining physical diseases. As a psychosomatic physician, he was also mindful that many presentations to doctors do not necessarily have an underlying physical disease. He wasn't retreating to vagueness, but accepting of the uncertainties of medicine and psychiatry. I, too, have reviewed the book on Biopsychosocial medicine edited by Peter White (see my review), which Bolton & Gillett reference by quoting from The Lancet review of that book by McManus (2005). As McManus notes, "the broader view [of biopsychosocial medicine] is seen by biomedicine as irredeemably soft, with no clear methodology, measurement, or experimental manipulation". This isn't a reason for dismissing the psychosocial nature of some patient complaints; nor for having a negative assessment of Engel's biopsychosocial model.

Bolton & Gillett try to meet the challenges to the biopsychosocial model by suggesting that it needs to be made "specific to particular health conditions" (loc 456). From their point of view, Engel's biopsychosocial model is not really a general model, and this explains its vagueness. I'm not against looking at examples and specifics, but I don't think this is an adequate reason for undermining the generality of Engel's model. Bolton & Gillett do recognise the connection between patient-centred medicine (see previous post) and the biopsychosocial model and the centrality of this element for Engel (loc 2707). An integrated understanding of the whole person is required for all medical conditions.

Bolton & Gillett suggest that the foundational theoretical constructs of the biopsychosocial model need rethinking and reconceptualising. Again, I'm not convinced this is necessary as such, although I recognise there is a need to develop the biopsychosocial model as a philosophical and scientific theory of health, disease and healthcare. This is the strength of Bolton & Gillett's book. For example, they argue that information processing theory has moved biology on from understanding causes as merely physico-chemical. There is some truth to this view and Bolton & Gillett are correct that psychiatry should not be dualist or vitalist (see previous post). However, the mechanistic perspective remains pervasive in biology. Biology still needs to move onto a processual, organismic philosophy (see previous post), in the same way as indicated by Engel.

Bolton & Gillett argue against physicalism. Persons do need to be understood as biological processes. An integrated biopsychosocial model studies people within the framework of biology. A mechanistic conception of nature fails to provide a complete characterisation of living systems (see previous post). We need a new organismic biological perspective to enrich the integrated mind-brain understanding promoted by Engel for medical and psychiatric practice.

Monday, September 23, 2019

Scientists think antidepressants work but is the evidence biased?

Gemma Lewis and Glyn Lewis popularise their PANDA study (published in The Lancet Psychiatry) in The Conversation. The headline of their piece is 'Antidepressants work, but just not how scientists thought they worked'.

Even though the PANDA study did not find a significant difference in depression scores at 6 weeks between sertraline and placebo groups, the authors still claim antidepressants work. This is because they found evidence of a significant difference for anxiety symptoms and suggest the benefit of antidepressants is more for anxiety than depression. I'm not sure if they're saying that antidepressants should be renamed anxiolytics.

As I've pointed out previously (eg. see post), despite antidepressant trials on average showing a statistically significant difference for active drug over placebo, the difference is small and there is a question about how clinically significant this difference is. Furthermore, methodological difficulties, such as unblinding, can bias the results, so it is possible that any statistically significant result is an artefact (see my Bias in controlled trials webpage). This is called the placebo amplification hypothesis of the apparent statistical advantage of antidepressants over placebo in clinical trials. It is difficult to prove and the debate about antidepressant efficacy is still open in the literature (see previous post), despite the Lewises apparently not being prepared to admit that their PANDA study may actually provide evidence that antidepressants are not effective.

Data is given on unblinding in the PANDA study, although the authors do not make very much of it. The authors knew of three incidents when participants opened the capsule to see if there was a tablet included, and these patients were withdrawn from the trial. The majority of participants did not think they were on active treatment, even though half of them were. More people on sertraline (46%) thought they were on active treatment than those on placebo (19%). People seem to have generally thought they were not on active treatment, and placebo patients were quite good at recognising this. Participants were able, therefore, for whatever reason, to distinguish sertraline from placebo, so it's misleading to say the PANDA trial was double-blind.

Despite what the authors seem to think, antidepressant trials are not adequately blinded (Even et al, 2000). The findings of the PANDA study may therefore merely reflect the authors bias (transmitted to the participants) that antidepressants are effective (although for some reason not detected at 6 weeks with depression scores). Antidepressants may merely be placebo panaceas for emotional problems.

Thursday, September 19, 2019

The validity of the distinction between functional and organic mental illness

A tweet by Mohammed Rashed has intrigued me. He says the distinction between functional and organic mental illness is not valid, and suggests it's a false distinction based on a misunderstanding of the concept of illness. The brevity of communication on twitter leaves me not understanding what he means.

I have argued that critical psychiatry seeks to restore the functional/organic distinction (eg. see previous post). It was abolished by DSM-IV (see eg. previous post) but this was a mistake.

Mental and brain activity need to be understood as a single biological response. The problem is that we tend to have a mechanical view of biology, which can make it difficult for psychiatry to integrate mind and brain (see eg. previous post). Mental dysfunction ie. functional mental illness, as much as brain disease ie. organic illness, is a medical condition resulting from pathological process.

We have always needed myths to understand illness, including madness (see eg. previous post). Relating symptoms to their underlying physical pathology was a major advance for medicine in the first half of the nineteenth century and still underlies our modern understanding of disease (see eg. previous post). Applying this anatomoclinical method in psychiatry was not as successful because it was not always very easy to relate mental conditions to underlying brain pathology. In fact, it led to an overenthusiastic search for anatomical localisation of mental illness in the second half of the nineteenth creating a brain mythology that was unrelated to empirical findings. Acceptance of the organic/functional distinction helped psychiatry to move on from such fanciful notions.

Of course acute brain disease can cause delirium and chronic brain disease can cause dementia. The symptom patterns of brain disease are different from functional illness, with a prominent disturbance of cognitive function, such as orientation. Clinicians are trained to assess and detect whether a psychiatric presentation may have an underlying organic basis by testing cognitive function in particular. To suggest that the distinction between functional and organic mental illness is invalid does not seem to make sense to me clinically, let alone conceptually.

Nor am I sure what understanding of illness Mohammed thinks we should have that will make it apparent that the functional/organic distinction is invalid. Technically a distinction has been made in the scientific literature between illness, which is the personal experience of symptoms and suffering, whereas disease is the underlying biological pathology (see eg. previous post). Disease is something an organ has; illness is something a person has. It's commonly assumed that the organic basis of mental illness will be found (see eg. previous post). Could this be what Mohammed means? If so, my claim is that the functional/organic distinction is more fundamental and critical psychiatry is a legitimate challenge to the disease model of mental illness (see eg. previous post).

I'm hoping this blog may help to clarify what Mohammed meant by his tweet. Once I've understood, maybe this issue does need to be taken forward in debate in a scientific article. There does need to be further discussion about the validity of the functional/organic distinction of mental illness.

Saturday, September 07, 2019

Reclaiming the term ‘biopsychosocial’

Joanna Moncrieff comments in a tweet on Niall McLaren’s Mad in America blog, saying that the biopsychosocial model is “just a phrase used to dress up biomedical reductionism”. I’ve commented before several times on the biopsychosocial model (eg. see previous post). I do understand what Jo means when she implies that psychiatrists who say they adopt a biopsychosocial model are really using a weaker version of biomedical reductionism (see eg. extract from my book chapter). And, as Niall indicates in his blog, despite Ronald Pies claim that psychiatry is biopsychosocial, Pies himself is quite biological in his approach to psychiatry (see previous post).

The definition of biopsychosocial has become quite confused and I have advocated using the term ‘sociopsychobiological’ (see previous post). But George Engel’s original biopsychosocial model was a deliberate challenge to biomedical reductionism and I think that critical psychiatry does take a biopsychosocial position (eg. see my article). What happened was that Anthony Clare (see previous post) deliberately avoided any ideological implications for psychiatry, encouraging an eclecticism as a way of dealing with the challenge of anti-psychiatry (see eg. my eletter [original layout has been lost on website upgrading]). We need to move on from this eclecticism (see eg. previous post). The original meaning of ‘biopsychosocial’ needs to be reclaimed by critical psychiatry.