Eriksen’s ME/CFS hypothesis: my comments

[Update from Sept. 2018 here!] In two other posts, I summarize Dr. Willy Eriksen’s hypothesis for the cause of and cure for myalgic encephalomyelitis, aka chronic fatigue syndrome (ME/CFS), and I interview Eriksen. Here I—a well-educated sufferer but no biologist or physician—consider this model in the light of other research and my own experience. In other words, I’m thinking about it in print. While I have questions and reservations, I think Eriksen might be right about some important aspects of ME/CFS.

Comparison to research

One of my frustrations with the recent metabolomic and gut-focused studies of ME/CFS is that they don’t provide a sufficient account of what originally went wrong and why the symptoms change over time. Symptoms change for days because of post-exertional malaise (PEM), but they also change for much longer periods because of diverse traumas, including over-exertion, infection, and courses of medicine. Personally, I’d like to know how Robert Naviaux, for example, explains PEM or these longer plateaus in symptoms. Eriksen at least attempts to account for both.

Where his hypothesis stops, however, is where these other studies pick up. I find Eriksen’s claim of compatibility with the metabolomic studies and Ron Davis’ work to be promising: glial cell activation might directly or indirectly lead to the release of whatever molecule in the bloodstream is causing cells to go into the cell danger response.

(Further, it’s intriguing that glial cells emit and receive ATP as a purinergic signal, which would fit with Davis’ and Naviaux’ models and allow for a more complex chain of signaling. See this and this for more.)

In any case, his model is consistent with a lot of diverse research, which he cites.

Comparison to experience

Here’s my specialty—I’ve been working on this for more than six years! In short, I find that Eriksen’s hypothesis could account for some mysteries in my experience with ME/CFS, but, to my mind, others remain, including the process of PEM.

Questions answered plausibly

Eriksen’s hypothesis:

  • Accounts for the evidence of ongoing infection with the Epstein-Barr virus (EBV), even when EBV can’t be found in the bloodstream and it isn’t the noticeable infection that immediately precedes the onset of symptoms.
  • Explains changes in my symptoms over time.
    •  For example, getting a back infection near my spine was like getting ME/CFS all over again, and it changed the severity of my condition and the relative intensity of various symptoms.
  • Accounts for how I can trigger PEM more easily and quickly on a bad day than on a good one.
  • Accounts for how I can trigger PEM by a lot of low-intensity activity or a little high-intensity activity.
  • Explains how different people have different symptoms.

 Questions remaining

  • PEM?
    • For me PEM isn’t simply a deepening of symptoms that already exist, as Eriksen’s writing appears to assume. PEM engenders new symptoms, too. Most especially, during PEM I always suffer from an intense, exhausting ache that radiates from the center of my torso. This symptom turns on and off discretely like a switch (although it does take several minutes to hit fully). Others, I think, get ‘brain fog’ in a similar fashion.
    • Also, I’ve had an experience when I grossly overextended myself through physical activity – yet, as far as I could tell, I completely avoided PEM. Probably I entered ketosis. I can envision complex ways in which this is compatible with Eriksen’s model, but is it? In short, I think the answer might be more complex than a straightforward increase in glial cell activation.
  • Cure?
    • My biggest question is whether this is a realistic cure, as opposed to a potential treatment. As I understand it, our bodies should already have T-cells that can attack EBV. Maybe, as in multiple sclerosis, the T-cells in ME/CFS are defective against EBV. Would a mass infusion of defective T-cells really reach all pockets of infection and wipe them out?
  • Not just plausible but true?
    • Of course, the biggest question is whether there are EBV-infected ectopic lymphoid aggregates that trigger glial activation and, ultimately, ME/CFS as we know it. I hope someone seeks and obtains the funding to put Eriksen’s hypothesis to a test.

3 responses to “Eriksen’s ME/CFS hypothesis: my comments

  1. Pingback: ME/CFS: Eriksen on gut issues and timing | Tracy Duvall

  2. Pingback: Eriksen’s ME/CFS hypothesis: interview | Tracy Duvall

  3. Pingback: Eriksen’s ME/CFS Hypothesis: An Update | Tracy Duvall

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