Contrary to a well known study by Demitrack, Straus et al. published in 1991, a recent study by Wood, Wessely et al. finds that salivary cortisols are higher in CFS patients than in healthy controls. The citation for the current paper is:

Wood B, Wessely S, Papadopoulos A, Poon L, Checkley S.
Salivary cortisol profiles in chronic fatigue syndrome.
Neuropsychobiology. 1998; 37(1): 1-4.

The abstract for this paper is as follows:

Salivary cortisol profiles (hourly sampling over a 16-hour period) of 10 patients with chronic fatigue syndrome (CFS) but without concurrent depressive disorder were compared with those of 10 healthy volunteers matched for age, sex and menstrual cycle. The mean saliva cortisol concentration over the 16-hour period was slightly but significantly greater in the patients than the controls (p < 0.05). These findings are at variance with earlier reports that CFS is a hypocortisolaemic state and suggest that in CFS the symptom of fatigue is not caused by hypocortisolaemia.

Dr. Mark Demitrack was recently asked by CFS-NEWS to comment on this paper. Demitrack et al. published a well known study in 1991 that indicated that cortisol levels were lower in CFS patients, the opposite of the current Wood et al. findings. Demitrack's remarks are as follows:

This report is a very interesting and well-done study which provides data contrasting with several reports (ours included) that have previously suggested a modest-centrally-mediated reduction in the tone of the hypothalamic-pituitary-adrenal axis. Heterogeneity in the biological phenotype of patients with CFS is not unexpected. We are now well aware that the population of individuals defined by the traditional criteria used to specify a case of CFS probably encompasses an etiologically heterogeneous group of people. Therefore, data with disparate results underscores the need for more careful description of the methods used to evaluate cases for study so that subsequent investigators can be sure that they are actually testing the same types of patients in their work (i.e., an apples to apples comparison, so to speak).

In the case of our report, the patients were ill for a longer duration of time, and in general had a broader mix of clinical phenomenology than appears in the sample reported by Wood, et al. Whether this is relevant to the differences in the results is not clear, and should be considered in future work. Given the complexity of the physiology of the HPA axis, and its close links to other biological systems (e.g., the immune system), not to mention its plasticity relative to other clinical events (e.g., the sleep-wake cycle), it is certainly reasonable to assume that different patterns of dysfunction may be evident depending upon the testing strategy employed and the particular patient population studied.

What these results do tell us is that the HPA axis of patients with CFS is different from what is seen in healthy individuals. Placing a statement like this in proper context and teasing apart cause from effect in this complex illness will have to await further study.