Chronic fatigue syndrome: A response to the Lancet review by Prins et al

Authors

Abbot NC, Spence V

Institution

Vascular Diseases Research Unit, The Institute of Cardiovascular Research, Ninewells Hospital and Medical School, Dundee, UK

Publication

Abbot NC, Spence V. Chronic fatigue syndrome: A response to the Lancet review by Prins et al. Lancet 2006; 367: 1574.

Full text

The Seminar by Judith Prins and colleagues (1) purports to review chronic fatigue syndrome with emphasis on “scientific aspects”, yet it falls far short of this aim. Research on biomedical aspects of the syndrome is covered only perfunctorily (318 words in a 4900 word review), yet much work has already been done by others (2), and the role of definitional issues in understanding clinical trial results is barely addressed. The overwhelming focus of the Seminar is on one model of chronic fatigue syndrome — the biopsychosocial model, a construct which contrasts with the biomedical model which implies that a primary disease entity exists and that biopsychosocial aspects are secondary (the two models discussed in the report to the UK Chief Medical Officer in 2002 (3)). The biopsychosocial model is supported only by researchers with a professional interest in psychosocial aspects of illness who have acquired the funding to test their hypotheses. In fact, the evidence base for the usefulness of this model in chronic fatigue syndrome consists of a small number of clinical trials (eight discrete trials have used cognitive behavioural therapy (CBT): five positive and three negative for the intervention) which, even by their own standards, have relatively unspectacular results. For example, Prins’ own clinical trial (4) described in the review as having “cure of chronic fatigue syndrome as its explicit goal of therapy”, reported no improvement on the fatigue severity endpoint in 56 of 83 patients after 8 months and in 38 of 58 after 14 months. The result was significantly better than in the control groups, but was modest nevertheless, in line with the findings of another positive trial for CBT (5) which concluded that, although providing some benefits, CBT was “not a cure”. Surveys of patients’ groups, limited as evidence yet surely not meaningless or valueless, emphasise the same point: a survey of some 2000 patients (3) reported that only 7% of respondents found cognitive behavioural therapy ‘helpful’, compared with 26% who believed it made them ‘worse’, the remaining 67% reporting ‘no change’. Indeed, a large body of professional and lay opinion considers that this essentially adjunctive technique has little more to offer than good medical care alone, and questions what specific additional therapeutic value it brings to, say, the 79% of patients in the survey quoted above who answered that they had severe pain sometimes, much of the time, or all of the time. The central point, which was not addressed by Prins and colleagues, is that, for patients with chronic fatigue syndrome (and there are some 20,000 members of support groups in the UK alone), the biopsychosocial model offers relatively little, yet it dominates the canvas in terms of research funding and exposure in professional journals instead of being a small part of the overall clinical and scientific picture.

References

1. Prins JB, van der Meer JW, Bleijenberg G. Chronic fatigue syndrome. Lancet 2006; 367: 346–355.
2. Carruthers BM, Jain AK, De Meirleir KL et al. Myalgic encephalomyelitis/chronic fatigue syndrome: clinical working case definition, diagnostic and treatment protocols. J Chronic Fatigue Syndrome 2003; 11: 7–115.
3. Working group on CFS/ME (Chronic Fatigue Syndrome/Myalgic Encephalomyelitis). Report to the Chief Medical Officer of an independent working group. Accessed from www.doh.gov.uk on Feb 10, 2006.
4. Prins JB, Bleijenberg G, Bazelmans E et al. Cognitive behaviour therapy for chronic fatigue syndrome: a multicentre randomised controlled trial. Lancet 2001; 357: 841–7.
5. Deale A, Husain K, Chalder T, Wessely S. Long-term outcome of cognitive behaviour therapy versus relaxation therapy for chronic fatigue syndrome: a 5-year follow-up study. Am J Psychiatry 2001; 158: 2038–42.

Comment by ME Research UK

Letters to scientific journals like the Lancet are constrained by the number of words they can contain, and the number of references that can be given at the end (in this case five). For that reason, we could report only what we considered to be the essential flaw of the Prins et alreview, namely that it proclaims the biopsychosocial model of ME/CFS at the expense of the biomedical model which — in the words of the report to the Chief Medical Officer of 2002 — assumes that a primary disease entity exists and sees ME/CFS as “…a condition where illness results from a specific pathological defect in physiological functioning, mediated at organ, tissue, cellular and/or molecular level”.