Myalgic encephalomyelitis, commonly known as chronic fatigue syndrome or ME/CFS, is a disease of many mysteries. Even the most fundamental questions remain unanswered: how does ME/CFS develop, and how can patients recover?
Researchers across the globe are addressing different aspects of this enigma. They seek to uncover a fundamental disruption that underlies the array of symptoms – or at least to identify an exclusive test result, or biomarker, that a general practitioner could use in making a diagnosis. Some labs focus on immune function, others on the gut microbiome, aerobic energy, or brain inflammation, among others.
Promising results are common, but two recent studies of cell metabolism have garnered special attention for their potential in both aiding diagnoses and explaining what goes wrong.
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I took a physiology course so you don’t have to! I’ve combined some surprising basics with key terms and research on myalgic encephalomyelitis (aka chronic fatigue syndrome) into less than six minutes. And I’ve tried to keep it fairly simple.
Here’s the script: Continue reading
My wife and I recently saw Jennifer Brea‘s film Unrest at the AFI DOCS festival. We both found it moving. Here’s my review – and my reaction as a person with ME/CFS:
After reading my original posts on his hypothesis (summary, interview, and comments) explaining ME/CFS (myalgic encephalomyelitis, or chronic fatigue syndrome), Dr. Willy Eriksen sent me additional information regarding a couple of remaining questions. These are: 1) how his model accounts for problems in the gut and 2) how glial cell activation could require weeks to die down after rituximab treatment but only days for post-exertional malaise (PEM). I’ll provide his answers here, although I’ve inserted them in the original posts as well. Continue reading
This interview with Dr. Willy Eriksen, a research professor at the Norwegian Institute of Public Health, is the second of three blog posts on his hypothesis regarding the cause of and potential cure for myalgic encephalomyelitis, aka chronic fatigue syndrome (ME/CFS). Here I ask Eriksen to elaborate on his published hypothesis. So please see the first post for a summary of his hypothesis in relatively plain language—or, if you have access, read his journal article, “The spread of EBV to ectopic lymphoid aggregates may be the final common pathway in the pathogenesis of ME/CFS.”
In the third post, I consider Eriksen’s model in comparison to other recent research and my own experience. Continue reading