In respect of triggers for the condition (as opposed to predisposing factors), a number were noted in paragraph 3.3.2 of the report. Of particular importance to this case are the following two:
"Infections: Good-quality evidence indicates that certain infections are more common triggers for [CFS] than others. Glandular fever, viral meningitis and viral hepatitis are followed by [CFS] in about 10% of cases of the primary infection. [CFS] can follow infections with herpes viruses. Influenza and 'flu-like infections can trigger [CFS], but common upper respiratory tract infections do not seem to.
Life events: The evidence that life events can trigger [CFS] is weak. Severe life events are much more likely to provoke a mood disorder, which can be misdiagnosed as [CFS]. However, clinical and patient experience suggests that increased 'stress' may be common around the onset of symptoms or a triggering event, such as infection. It is unclear whether this is as a triggering, a predisposing or a maintaining factor. Stress is also recognised as a trigger for setbacks."
In short, the report concluded that there was good evidence indicating that certain infections (including chickenpox, a herpes virus) may trigger CFS. Evidence that life events may do so was considered weak; but there appeared to be at least a temporal association between the onset of CFS and increased stress. Otherwise, the relationship between stress and the condition was regarded as unclear.
In addition to that authoritative paper, I was referred by Dr Weir to four academic papers, in which the authors seek to add to the knowledge of the relationship between life events and CFS. The paper most heavily considered was S Hatcher and A House, "Life events, difficulties and dilemmas in the onset of chronic fatigue syndrome: a case control study", Psychological Medicine, 2003, 33, 1185-92. It considered 64 CFS patients. In relation to marked difficulties with life events (as opposed to a severe event, such as the loss of a loved one) in the three months before onset, there was a statistical difference between the patient group (more) and the controls (less). However, (i) a number of the controls refused to take part, and the controls were questioned by way of a questionnaire rather than interview, introducing an obvious source of bias; (ii) particularly in relation to marked difficulties patients identified in the three months before onset, there was considerable risk of association bias; (iii) in relation to marked difficulties in the year before onset, there was no statistically significant difference between patients and controls; and (iv) the numbers involved were so small that this study has no great statistical potency. The results do not appear to have been replicated.
Of the other two papers, one (I E Salit, "Precipitating Factors for the Chronic Fatigue Syndrome", J Psychiatr Res, 1997, 31(1), 59-65)) concerned 134 CFS patients. In 72% of them, CFS started with an apparently infectious disease. In 85%, stressful events appeared common in the year before onset, compared with only 6% of the controls. However, it predates the Working Party Report, and was presumably taken into account in it; and it is in any event statistically weak. The conclusion is no stronger than it is likely that CFS is multifactorial in origin; acute events (including infections) may trigger CFS; and patients in which it does may be "quite vulnerable, based on the occurrence of many stressful events". Webster Marketon et al, "Stress hormones and immune function", Cellular Immunology, 252 (2008) 16-26, reviewed data relating to the effects of stress on the immune system, in particular in relation to delayed wound healing, impaired responses to vaccination and the development and progression of cancer. That paper appears to be of little assistance in respect of the issues before me. The final paper (E Sundbom et al, "Possible influence of defences and negative life events on patients with chronic fatigue syndrome: a pilot study", Psychological Reports, 2002, 91, 963-978) was not referred to at the trial, and readily concedes its own statistical limitations.
Dr Weir accepted the conclusions of the Working Party report, and accepted that there are insufficient data to confirm a hypothesis that stress and CFS have a causal relationship; he said he believed there was such a link because of his clinical experience. Prof Cleare (who was a member of the Key Group of the Working Party) said that, in his view, none of these studies and indeed none of the collected academic and clinical experience and wisdom since 2002 undermines or significantly changes the views and conclusions of the Working Party report with regard to trigger. I agree: there is no evidence before me which significantly changes the position with regard to trigger as set out in that report.
