Increased HDAC in association with decreased plasma cortisol in older adults with chronic fatigue syndrome

Hypocortisolism is a frequent finding in individuals with chronic fatigue syndrome (CFS) with other research findings implying potential dysregulation of glucocorticoid signaling.Glucocorticoid signaling is under the influence of several pathways, several of which are of interest in the study of CFS. Oxidative stress and decreased antioxidant capacity are known to disrupt the hypothalamic–pituitary–adrenal (HPA) axis (Epel et al., 2004) and the presence of histone deacetylases (HDAC) could also impact glucocorticoid signaling. The intent of this pilot study was to investigate the relationship among oxidative stress elements, select HDAC’s (2/3) and glucocorticoid receptor signaling in an elderly sample with CFS. Findings suggest increased histone deacetylase activity, lower total antioxidant power, in the context of decreased plasma cortisol and increased plasma dehydroepiandrosterone concomitant with decreased expression of the encoding gene for the glucocorticoid receptor. These findings support the presence of HPA axis dysregulation in elderly individuals with CFS.

► Individuals with CFS display increased expression of HDAC 2 and 3, concomitant with decreased plasma cortisol.
► Those with CFS demonstrate lower total antioxidant power concomitant with down-regulation of the encoding gene NR3C1.
► Signaling dysregulation may exist in CFS, with increased HDAC expression along with reduced NR3C1 and cortisol expression.