Affiliations: School of Nursing, DePaul University, Chicago, IL, USA | Center for Community Research, DePaul University, Chicago, IL, USA
Note: [] Correspondence to: Matthew R. Sorenson, School of Nursing, DePaul University, 990 W. Fullerton Ave, Suite 3000, Chicago, IL 60614, USA. Tel.: +1 773 325 1887; Fax: +1 773 325 7282; E-mail: [email protected]
Abstract: A wide array of physiologic mechanisms has been proposed to explain the symptomatology and pathogenesis of chronic fatigue syndrome. One consistent finding points to potential disruptions of hypothalamic-pituitary-adrenal (HPA) axis functioning concomitant with hypocortisolism. While there are divergent theories, evidence has been found for a possible lack of responsiveness on the part of the HPA axis to challenge, a pattern of glucocorticoid resistance, and disruption or dysregulation of the expected diurnal cortisol pattern among patients with CFS. Some authors offer that CFS is the result of a maladaptive stress response, one that is under the influence of genetic variance or epigenetic influences. Recent research demonstrates a lack of messenger RNA encoding for the glucocorticoid receptor, with evidence pointing toward histone deacetylases. The intent of this review is to highlight these findings supporting dysregulation of the HPA axis in CFS.
