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Stressful life events have long been supposed to act as a precipitating factor for rheumatoid arthritis (RA).1 In 1860 Fuller expressed the opinion that “...when the rheumatic poison is present in the system, any disturbing circumstance, even of temporary duration, such as overfatigue, anxiety, grief or anger, by rendering the system more susceptible of its influence, may prove the accidental or exciting cause of the disease...”.2 In modern terms, the rheumatic poison may reflect the underlying immunological process preceding RA.3 James has highlighted the stressful life events to support his contention that low androgen values are a contributory cause of RA.4
We have studied serum testosterone values in healthy subjects who later developed RA. The preliminary results were not in line with the hypothesis that low values of testosterone play an aetiological part in RA.5 We would like to propose another pathway by which stressful life events could precipitate RA. As recently reviewed, there is evidence for cigarette smoking as a risk factor for RA.6 It has been observed that depressed mood significantly predicts lung cancer but not any other form of cancer.7 A possible explanation is that depressive persons tend to smoke more often and to inhale the smoke more intensively than others and, thus, to have an increased risk of lung cancer.7 This model can probably be generalised from depression to other psychological disorders and from lung cancer to other smoking related diseases.
Thus, the experience of stress may exert its influence on RA through smoking.
Dr Aho does not respond to the point I was trying to make in my letter.1-1 I was drawing attention to what may be a rare phenomenon but which nevertheless exists—that is, a stressful life event causing a remission (not an exacerbation) in rheumatoid arthritis (RA). The word “stressful” needs careful qualification. Of the two cases I cited, one was an 86 year old lady (my aunt) who was at the scene of, if not subject to, a strike of lightning. This was a terrifying experience for her. The other case was of a lady whose husband and son died in close succession. Such experiences are unusual in their severity and suddenness, and contrast with the more routine misfortunes that comprise the adverse circumstances more frequently recorded in psychological life events questionnaires. The point is important because one may suspect that the immediate physiological response to such acute shocks is quite different to the physiological response to more minor adverse events. The latter are associated with depression; and depression is associated with low steroid hormone values in both sexes, and, ex hypothesi, to exacerbation of RA.
However, acute shocks of the sort described may be expected to have different effects on the androgen levels of men and women. In men, pituitary regulation lowers gonadal testosterone secretion: whereas in women, adrenal androgens would be expected to be raised in response to acute shocks.1-2
Thus, if I am correct, adverse life events will cause amelioration of RA if, and only if (a) the events are sudden and severe, and (b) the patient is female.
If either of these is not fulfilled, then I would expect adverse life events to be associated with exacerbation of RA. The point is testable and should be tested.
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