Cognitive behavioural therapy normalises HPA axis dysfunction in chronic fatigue syndrome [P.6.077]

Cleare, A. J., Roberts, A., Papadopoulos, A. , Chalder, T. and Wessely, S. (2004) Cognitive behavioural therapy normalises HPA axis dysfunction in chronic fatigue syndrome [P.6.077]. European Neuropsychopharmacology, 14 (Supp 3). S389. ISSN 0924-977X

Full content URL:

CBT normalises HPA axis dysfunction in CFS

Request a copy
[img] PDF
Cognitive Behavioural therapy normalises HPA Axis Dysfunction.pdf - Whole Document
Restricted to Registered users only

Item Type:Article
Item Status:Live Archive


There is increasing evidence that there is dysfunction of the hypothalamo-pituitary-adrenal (HPA) axis in patients with chronic fatigue syndrome (CFS). Studies have found hypocortisolism, impaired HPA axis responses to stimulation with a variety of challenges, and enhanced glucocorticoid receptor sensitivity. However, it remains unclear the extent to which these changes may reflect an underlying pathophyalology, or instead occur secondary to a number of consequences of the illness itself, including sleep disturbance, physical inactivity and deconditioning, chronic stress and medication use. In this study, we recruited 70 patients with CFS who were not taking psychotropic or other medication known to affect the KPA axis. Baseline HPA axis assessment was undertaken using: 24 hour urinary free cortisol (n=70); sequential diurnal salivary cortisol measurement (0800-2200) (n=59); and cortisol response to CRH challenge (n=41). Patients were then treated with a standard package of 12-15 sessions of Ct)T over 6 months, and the tests were repeated. On completion of CBT, patients reported clinically significant improvement in terms of
fatigue, psychiatric symptorm and disability. Accompanying this, there was an increase in salivary free cortisol, both in terms of the total ouput measured as the AUC (pre-treatment mean (SD): 68.2 (19.6) nmol/1.h, post treatment: 79A (21.8) nmol/1.h, P<0.05 by paired t-test) and the mean value (6.00 (1.70) nmol/1 pro-treatment, 6.82 (1.71) nmol/1 post-treatment, P<0.05). There was a non-significant rise in the 24-h UFC after CBT (76,7 (50,0) nmol/2dh to 85,7 (49,7) nmol/2dh), Accompanying the increased cortisol levels, there was an increase in the adrenal cortex cortisol response to CRH, which went from 226 (170) nmol/hh before treatment to 291 (167) nmol/hh after treatment (P<0.05). The degree of baseline HPA axis dysfunction was also predictive of the response to CBT. Overall, 43% of patients were rated as very much better or much better using the Clinical Global Impression. Compared to treatment-responders, treatment non-responders showed lower UFC values at baseline (responders 100.34-68.2 nmol/d, non-reaponders 68.84-41.6 nmol/d, P<0.05) and had less diurnal change in their salivary cortisol levels indicating a flattened circadian profile. We conclude that the t-IPA axis dysfunction in CFS is at least partly reversible by CBT Since CBT acts to reverse hypothesised maintaining factors in CFS such as sleep disruption, physical deconditioning, fluctuation in patterns of rest and activity and levels of stress, amongst others, it seems likely that these factors are also partly responsible for the HPA axis dysfunction. There is further support for this contention from studies that have failed to find HPA axis changes in those
prospectively followed in the early stages of fatiguing illnesses such as after glandular fever. Furthermore, greater impairment of the HPA axis is related to a poorer outcome after CBT, adding further weight to the suggestion that low cortisol levels are one of the maintaining factors in CFS.

Keywords:Chronic fatigue syndrome, HPA Axis, cognitive behaviour therapy, hypocortisolism
Subjects:A Medicine and Dentistry > A300 Clinical Medicine
C Biological Sciences > C841 Health Psychology
Divisions:College of Social Science > School of Psychology
ID Code:15845
Deposited On:31 Oct 2014 11:21

Repository Staff Only: item control page