Metabolic abnormalities in chronic fatigue syndrome/myalgic encephalomyelitis: a mini-review

Abstract

Chronic fatigue syndrome (CFS), commonly known as myalgic encephalomyelitis (ME), is a debilitating disease of unknown etiology. CFS/ME is a heterogeneous disease associated with a myriad of symptoms but with severe, prolonged fatigue as the core symptom associated with the disease. There are currently no known biomarkers for the disease, largely due to the lack of knowledge surrounding the eitopathogenesis of CFS/ME. Numerous studies have been conducted in an attempt to identify potential biomarkers for the disease. This mini-review offers a brief summary of current research into the identification of metabolic abnormalities in CFS/ME which may represent potential biomarkers for the disease. The progress of research into key areas including immune dysregulation, mitochondrial dysfunction, 5'-adenosine monophosphate-activated protein kinase activation, skeletal muscle cell acidosis, and metabolomics are presented here. Studies outlined in this mini-review show many potential causes for the pathogenesis of CFS/ME and identify many potential metabolic biomarkers for the disease from the aforementioned research areas. The future of CFS/ME research should focus on building on the potential biomarkers for the disease using multi-disciplinary techniques at multiple research sites in order to produce robust data sets. Whether the metabolic changes identified in this mini-review occur as a cause or a consequence of the disease must also be established.

Influence of Regular Physical Activity on Mitochondrial Activity and Symptoms of Burnout—An Interventional Pilot Study

“…As described in more detail elsewhere [22,23], the sample consisted of twelve males (M= 45.8 years, SD = 6.8; range 36-65 years) suffering from burnout syndrome, based on Maslach's definition of occupational burnout. All participants continued working during their participation in the study.…”

“…Specifically, Picard et al [22] showed in their systematic review that compared to healthy controls, individuals with major depressive disorders had down-regulated mitochondrial activity. Likewise, Tomas and Newton [23] reported in their mini-review that compared to healthy controls, individuals with chronic fatigue syndrome had deteriorated mitochondrial dysfunction. Given this, it appeared plausible that also among individuals with burnout traits, mitochondrial activity should be dysfunctionally down-regulated.…”

“…First, the overlap between burnout traits and major depressive disorders [4,[17][18][19][20] and fatigue [21] are well documented. Second, there is sufficient evidence that in people with major depressive disorders [22] and fatigue [23] mitochondrial activity is decreased. Specifically, Picard et al [22] showed in their systematic review that compared to healthy controls, individuals with major depressive disorders had down-regulated mitochondrial activity.…”

“…The following three hypotheses and one research question were formulated. First, following others [22,23], we expected that at baseline and compared to healthy controls, mitochondrial activity would be lower in individuals with burnout traits. Second, following others [13][14][15][16], we anticipated that mitochondrial activity would increase following a 12 week program of physical activity.…”

Chronic fatigue syndrome: progress and possibilities

“…These data reinforce the low probability of finding any meaningful abnormality in the blood. A series of interesting but preliminary studies have used proteomics, metabolomics and microbiome analyses in cross‐sectional case–control studies of patients with CFS. As these approaches measure hundreds to thousands of variables, the studies have uniformly included tens of subjects only, and the technologies are relatively new and evolving, any preliminary findings require independent replication in larger cohorts.…”