Trial By Error: New Biopsychosocial Paper on Long-Covid and Somatic Symptom Disorder

By David Tuller, DrPH

Biopsychosocial Campaigners Target Long-Covid

New papers from the biopsychosocial campaigners often provide opportunities to highlight unwarranted assertions, misleading use of data, and, in particular–associations interpreted as if they were causal relationships and not, well, associations. An article co-authored by Trudie Chalder, a professor of cognitive behavioural therapy at King’s Collge London, and The article, positioned as an editorial, is called “Concern for Covid-19 cough, fever and impact on mental health. What about risk of Somatic Symptom Disorder?” It recycles years of biopsychosocial shibboleths promulgated by Professor Chalder and her fellow campaigners.

SSD is a construct outlined in the DSM-5 (the American Psychiatric Association’s guide to diagnoses). The term is often used interchangeably with related ones, including “medically unexplained symptoms” (MUS), “persistent physical symptoms” (PPS) and “bodily distress syndrome” (BDS), although they all differ somewhat in how they define their cohorts. As the editorial explains,  SSD “refers to persistent (6 months or more) and clinically significant somatic complaints accompanied by excessive and disproportionate health-related thoughts, feelings and behaviours regarding the symptoms.”

The SSD diagnosis contains a neat twist. Even patients with recognized illnesses like cancer can be diagnosed with SSD if they are viewed as having similarly “excessive and disproportionate” health-related fears and anxieties. That’s convenient for those interested in promoting psychological and psychiatric interventions. But rendering the diagnosis relies on determining what should be considered appropriate levels of health-related concern and what should be considered “excessive and disproportionate” for patients confronting serious disease. The potential for bias is self-evident.

Professor Chalder and other biopsychosocial campaigners are considered experts in this domain of illness, which in their own research they frequently refer to as MUS. Despite this expertise, she and others have demonstrated an unfortunate habit of mis-citing a seminal paper in the field in a way that more than triples the estimated costs of MUS to England’s branch of the National Health Service. On the back of such disinformation and a body of problematic research, they have engineered a major expansion of an NHS mental health program to include people with MUS.

The program, called Improving Access to Psychological Therapies (IAPT), was launched to provide cognitive behavior therapy (CBT) and related rehabilitative interventions for people with untreated anxiety and depression disorders. With the expansion to include MUS, the program has defined the category as including chronic fatigue syndrome (CFS), irritable bowel syndrome (IBS), and random somatic symptoms not identified as part of a syndrome. Not surprisingly, IAPT receives a shout-out in the new editorial. That raises the concerning prospect that long-Covid patients could find themselves being pushed toward IAPT, as if the interventions on offer were evidence-based treatment for their condition.

Purportedly definitive studies of the IAPT-type interventions have not turned out as planned. The PACE trial, which investigated a specialized form of CBT and graded exercise therapy (GET) for CFS, has been discredited in the eyes of much of the scientific community. An evidence review conducted for the development of a new ME/CFS guidance from the National Institute for Health and Care Excellence found most of the data for presumed benefits from these interventions to be of “very low” quality and the rest to be of “low” quality. The draft guidance from NICE, released in November, positions CBT as solely a supportive strategy and not as a treatment for the underlying condition, and it recommends against GET. That significantly undermines the argument for including ME/CFS in the IAPT program as an MUS.

More recently, major studies examining the use of specialized forms of CBT to treat irritable bowel syndrome and dissociative seizures (better known as “psychogenic non-epileptic seizures”) have hyped their findings while downplaying poor results, as I documented here and here. In fact, the online CBT program for IBS road-tested in the former study is now being marketed by a San Francisco company as an effective intervention for reducing symptoms, even though the study clearly documented that the benefits at one year were clinically insignificant.

Professor Chalder was a co-investigator not only of PACE but of the major IBS and dissociative seizure trials. Just saying.


Association Is Not Causation

It was predictable back in March that the biopsychosocial campaigners would seek to colonize the predicted cohort of post-Covid-19 patients suffering from profound fatigue and other non-specific symptoms. So this editorial holds no surprises.

Let’s stipulate that, yes, anxiety and depression and related states likely play a role in how symptoms are experienced. And anxiety and depression can express themselves in any number of ways–panic attacks, for example. But that stipulation is a far cry from presuming all unexplained symptoms should be attributed to anxiety and depression and related states. One corollary of that presumption is the apparent rejection of the possibility that undiscovered or as-yet poorly understood biomedical processes could be implicated in phenomena that at the moment remain “unexplained.” The history of medicine is littered with such errors.

Before addressing long-Covid, the editorial mentions an apparent association of feelings about and reactions to Covid-19 with somatic complaints, citing a study from last year that assessed this kind of association. “In the United Kingdom general population, covid-19 related anxiety has been found to predict general somatic symptoms, particularly fatigue, followed by gastrointestinal symptoms,” notes the editorial.  

The cited article was a cross-sectional study, in other words, participants responded to a set of questions at a single point in time. The investigators used a novel scale to measure “Covid-19 anxiety” and also assessed symptoms. Those more anxious about Covid-19 reported greater somatic symptomology. The biopsychosocial assumption is that the Covid-19 anxiety is itself generating these somatic symptoms.

A major limitation of cross-sectional studies, like the one cited by the editorial, is the impossibility of distinguishing cause from effect. Studies with this one-point-in-time design can measure associations between indicators. The chronology of events, and therefore the possibility that one thing caused another–cannot be determined. And that is the case here.

The word “predict”–which was also used in the title of the cited study–could be easily interpreted as suggesting or implying causality. In this instance, however, it is being used in a statistical sense. The findings of the cited study could easily have been flipped around and rephrased to indicate that “general somatic symptoms, particularly fatigue, followed by gastrointestinal symptoms, have been found to predict covid-19 related anxiety.” When data are cross-sectional, both statements would be true.

During a pandemic, some people will be anxious and depressed and could become hyper-conscious of bodily sensations. But the reverse is also true–people currently experiencing bodily sensations would have legitimate reason for heightened anxiety about whether or not they might have covid-19. The cited paper acknowledged this issue in the limitations section, noting that “the temporal ordering of the variables cannot be established, and so the potential problem of reverse causation cannot be ignored.” But that doesn’t stop the biopsychosocial campaigners from treating this “potential problem” of interpretation as an afterthought relegated to the “fine print” of limitations sections, not a serious hole in their argument.

When it comes to long-Covid itself, the editorial continues in this vein, suggesting that the profound fatigue and other prolonged, non-specific symptoms as a likely result of biopsychosocial processes at work rather than pathophysiological ones. Highlighting irritable bowel syndrome as a parallel example, the editorial notes that “the developmental course of post-infectious IBS is also understood to be initially triggered by infection but maintained by social, psychological and behavioural factors.” These maintaining factors, per the editorial, include “negative illness beliefs, all or nothing behaviour, anxiety and depression.”

Let’s be clear: This is how the biopsychosocial campaigners hypothesize the developmental course of post-infectious IBS. Not surprisingly, they also have an intervention to offer for IBS–namely CBT, as outlined in the IAPT program. But the evidence for the effectiveness of CBT for treating the debilitating symptoms of IBS is no more reliable than the body of CFS research that has now been deemed in the NICE review as of poor quality.

In summing up, the editorial asserts that biopsychosocial models “provide a parsimonious route to the recognition that persistent multi-system symptoms can be produced by the interaction of physiological, cognitive, behavioural, emotional and social factors.” In fact, the most parsimonious and obvious explanation of the noted associations between symptoms and mood states such as “Covid-19 anxiety” is this: In a great many cases people are experiencing organic dysfunctions that have not yet been diagnosed or identified, which then cause them anxiety and distress–not least because the symptoms are often dismissed as arising solely from anxiety and distress.

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