[Update from Sept. 2018 here!] 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.
In both cases, the answers don’t apply solely to Eriksen’s hypothesis regarding clumps of EBV-infected immune cells. Indeed, his description of the gut has implications for any explanation that involves a disruption of the central and/or autonomic nervous system (probably that’s all of them).
Gut problems
Eriksen writes: There are two gut-related aspects of ME/CFS that a comprehensive hypothesis like mine should be able to explain: A) Many people with ME/CFS have symptoms that seem to stem from the intestinal system, such as abdominal pain, bloating, diarrhea, and food sensitivity. B) Some studies suggest that the intestinal bacterial flora of ME/CFS patients is different from that of healthy controls.
These aspects can be explained by my hypothesis. Understanding the anatomy and the role of the nervous system is the key. The intestinal wall and the connective tissue around the gut are, literally speaking, full of nerves, nerve endings, and bundles of nerve cells. These nervous structures control the peristaltic movements of the gut, they control the composition and magnitude of the secretions into the gut, and they convey sensations of pain. There are also nervous sensors that surveil the microenvironment in the gut. The majority of these nervous structures are linked to the autonomic nervous system and the central nervous system. So, a widespread glial activation may influence many aspects of how the gut functions. And fluctuations in the glial activation (e.g. after physical activity) may induce fluctuations in how the gut functions. Glial activation can, therefore, explain the ME/CFS-symptoms that stem from the intestinal system.
The intestinal bacteria are dependent on the “foodstuff” they get inside the gut. This “foodstuff” that the bacteria get inside the gut is determined not only by our diet but also by the quality and magnitude of the food components that reach different parts of the intestine. And the composition of these food components depends on the secretions from the intestinal wall, secretions from the liver via the biliary duct system, and the secretions from the pancreas. For example, when we eat fat, biliary secretions from the liver are poured into the small intestine, decomposing the fat, and making it easily absorbed from the gut. Without biliary secretions at the correct time after the meal, a lot of fat will reach the colon instead of being absorbed. Bacteria in the colon that like fat will then proliferate. And so on. Thus, it seems obvious to me that the intestinal bacterial flora will be influenced by disturbances in the nervous system that control the intestinal functions. Those who are in doubt could take a look at this paper: Rolig et al., Plos Biol February 16, 2017.
Timing (and a metaphor!)
Eriksen writes: Glial cell activation is often a complex process with several elements and different types of cell reactions. Some of the reactions (e.g., cell proliferation) may build up over weeks and months, and may take a long time to cool off. Other reactions (e.g., waves of calcium-flux disturbances) can perhaps best be likened to a hurricane that comes in from the Caribbean Sea, sweeps across Cuba and Florida, and subsides after a few days.
Tracy Duvall 