Abstract
We propose an initial explanation for how myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) could originate and perpetuate by drawing on findings from critical illness research. Specifically, we combine emerging findings regarding (a) hypoperfusion and endotheliopathy, and (b) intestinal injury in these illnesses with our previously published hypothesis about the role of (c) pituitary suppression, and (d) low thyroid hormone function associated with redox imbalance in ME/CFS. Moreover, we describe interlinkages between these pathophysiological mechanisms as well as “vicious cycles” involving cytokines and inflammation that may contribute to explain the chronic nature of these illnesses. This paper summarizes and expands on our previous publications about the relevance of findings from critical illness for ME/CFS. New knowledge on diagnostics, prognostics and treatment strategies could be gained through active collaboration between critical illness and ME/CFS researchers, which could lead to improved outcomes for both conditions.
Highlights
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating illness that affects millions of people worldwide [1, 2]
We combine emerging findings regarding (a) hypoperfusion and endotheliopathy, and (b) intestinal injury in these illnesses with our previously published hypothesis about the role of (c) pituitary suppression, and (d) low thyroid hormone function associated with redox imbalance in myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS)
We propose that the sequence during critical illness—from splanchnic hypoperfusion to hypoxia, redox imbalance, altered gut microbiome, intestinal injury, gut-related endotoxemia, pro-inflammatory cytokines and systemic inflammatory— may contribute to explain the emergence of ME/CFS following a physiological insult
Summary
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating illness that affects millions of people worldwide (an estimated 800,000 to 2.5 million in the USA) [1, 2]. We propose that the sequence during critical illness—from splanchnic hypoperfusion to hypoxia, redox imbalance, altered gut microbiome, intestinal injury, gut-related endotoxemia, pro-inflammatory cytokines and systemic inflammatory— may contribute to explain the emergence of ME/CFS following a physiological insult. Some critical illness researchers have proposed a model that describes how NTIS is maintained by reciprocal relationships between inflammation (notably pro-inflammatory cytokines), O&NS and reduced thyroid hormone function, forming a “vicious cycle” [101, 173] This model can help to explain the perplexing failure to recover of some critically ill patients in ICUs that survive their initial severe illness or injury. The other elements for a “vicious cycle” which researchers have suggested perpetuate a hypometabolic and inflammatory state in critical illness are present in ME/CFS, including inflammation [140, 189], increased O&NS [190–192] and altered cytokine profiles [193, 194]
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