Abstract
Cortisol is a key regulator of the immune system, energy metabolism, and stress, yet its relevance to fatigue experienced by people with relapsing-remitting multiple sclerosis (RRMS) remains uncertain. We examined cortisol secretory activity in RRMS and its association with fatigue severity between-individuals and within-individuals (day-to-day) using a case-control ecological momentary assessment design. While undergoing usual daily routines, 38 people with RRMS and 38 healthy control participants provided saliva samples at strategic time-points over 4 consecutive weekdays to measure the cortisol awakening response (CAR; 0, 30, and 45 min after awakening) and the diurnal cortisol slope (DCS; 6 quasi-random samples provided between 1000 h and 2000 h). Recalled fatigue was measured at baseline, and daily fatigue was measured as the mean average of momentary fatigue ratings provided alongside each DCS sample. Multilevel modeling found CAR output was greater in RRMS than controls, and recalled fatigue in RRMS was associated with both lower waking cortisol level and larger awakening response. Day-to-day, the CAR was not associated with same-day fatigue levels in RRMS. Cortisol appears to have a role in fatigue experienced in RRMS, but whether it is a causal factor remains unclear.
Highlights
Multiple sclerosis (MS) is a disease characterized by autoimmune-mediated inflammatory demyelination and neurodegeneration (Compston and Coles, 2008)
There are several mechanisms by which cortisol, the adrenal product of the hypothalamic— pituitary—adrenal (HPA) axis, may be relevant to MS fatigue: (1) cortisol is generally considered the primary endogenous regulator of immune inflammation (Chrousos, 1995); (2) cortisol is an important regulator of energy metabolism via glycogenesis promotion (Sapolsky et al, 2000); and (3) while several reviews highlight a positive association between stressful experience and risk of MS symptom exacerbation (Mohr et al, 2004; Artemiadis et al, 2011), cortisol is fundamental within the stress response (Dickerson and Kemeny, 2004)
The cortisol awakening response (CAR) area under the curve ground (AUCg) and area under the curve increase (AUCi) analyses were based on 258 assessment days (84.8%) nested within 75 participants (37 relapsing-remitting multiple sclerosis (RRMS); 38 Control); one participant provided no valid CAR
Summary
Multiple sclerosis (MS) is a disease characterized by autoimmune-mediated inflammatory demyelination and neurodegeneration (Compston and Coles, 2008). Current understanding of the etiology of MS fatigue is uncertain, with many disease-mediated mechanisms and secondary factors such as depression and sleep dysfunction potentially implicated (Induruwa et al, 2012). There are several mechanisms by which cortisol, the adrenal product of the hypothalamic— pituitary—adrenal (HPA) axis, may be relevant to MS fatigue: (1) cortisol is generally considered the primary endogenous regulator of immune inflammation (Chrousos, 1995); (2) cortisol is an important regulator of energy metabolism via glycogenesis promotion (Sapolsky et al, 2000); and (3) while several reviews highlight a positive association between stressful experience and risk of MS symptom exacerbation (Mohr et al, 2004; Artemiadis et al, 2011), cortisol is fundamental within the stress response (Dickerson and Kemeny, 2004). Our understanding of unstimulated cortisol secretory activity in MS and its relevance to MS fatigue is limited, in daily life
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
