CFS as Hibernation

Spent 3 days in a bad mood. Apparently cleaning the bathroom the day after walking 2 mi and then walking 2 mi again the day after was too much. The cumulative effect of exertion is still alive and well; it is only less pronounced because my tolerance to exertion went up.  I'll have to go back to cleaning the bathroom in lieu of, not in addition to, the (bi-daily) walk.

Now, today's topic. The UCSD researchers announced this week that they discovered anomaly in the metabolomics of CFS patients. Out of 600 or so metabolites they tested, 80% were severely reduced compared to matched controls. From this, they speculated that CFS patients are in a hibernation state like Dauer worms. For some reason, the body is mistakenly putting the patients in a hypometabolic state that only allowed survival and no more, at a great expense to the quality of life.

One issue with this theory is that humans don't hibernate. Dauer worms and bears can slow down their metabolism, lower body temperature and burrow into a hole or cave. For humans, hibernation means death unless fed and taken care of by other humans. That not a viable evolutionary strategy generation after generation. So it can't possibly be an evolutionary adaptation. Perhaps it is an ancient cellular level response (they call it CDR, or cellular danger response) mistakenly activated. But that still does not explain slew of neurological CFS symptoms. Worse yet, you can't explain with the hibernation theory the ability to exert normally only to get sick the next day.  (If you are in a dauer state, you should not be able to exert at the first place). So, for now,  the metabolic anomaly is more likely than not yet another symptom of CFS rather than the cause of it.

The problem with CFS research that I see is that researchers focus on their specialties and then speculate whatever the anomaly they find as the cause of CFS. Thus, virus people blame EBV, psychiatrists blame depression, endocrinologists blame HPA axis, and geneticists blame genetic expressions. Now we can add to that growing list gut microbiome and metabolomics.  It's the proverbial blind men and the elephant. What we need is a creative thinking, as recently done in schizophrenia and alzheimer's, that can put together all these clues and zero in on the real cause, so that we can come up with a real solution. The problem is, with only $5 million dollars out of NIH's gazillion dollar budget allocated to CFS research, it's not going to attract a lot of researchers. Quantity usually leads to quality in research, and we need that quantity to solve this problem.

As far as I am concerned, CFS is still a neuromuscular disorder, mediated by the immune system.
I think the term Myalgic Encephalomyelitis will ultimately proven right, except that it is the inflammation sensitivity, not the inflammation itself. And the paper's finding that the metabolic response was the opposite to the response to infection or inflammation only proves that there is no infection or actual inflammation in CFS.