Wednesday, September 23, 2015

Discovered: the underlying metabolic problem in ME

@ sciforschenonline:

The Aerobic Energy Production and the Lactic Acid Excretion are both Impeded in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Mark Vink, Family Physician/GPwSI, Soerabaja Research Center, The Netherlands

Background: In this study the muscle bioenergetic function in response to exercise in severe ME was explored to see if the underlying metabolic problem in ME, responsible for the severe difficulties with trivial exercise, and the severe loss of muscle power, could be discovered.

Methods: Inorganic phosphate, creatine kinase and lactate were measured in a former Dutch National Field Hockey Champion, who is now a patient bedridden with severe ME, before and 5 minutes after very trivial “exercise”, from which his muscles needed 12 hours to recover.

Results: Inorganic phosphate and creatine kinase were both normal, however, lactate after this trivial exercise was very high, and further testing showed that a second batch of lactic acid was excreted after the same exercise with a 6-fold delay, showing that the lactic acid excretion was impaired and split into two. And this was delayed up to 11- fold by eating closer to the exercise.

Conclusion: This study found that in severe ME, both the oxidative phosphorylation and the lactic acid excretion are impaired, and the combination of these two is responsible for the main characteristic of ME, the abnormally delayed muscle recovery after doing trivial things. The muscle recovery is further delayed by immune changes, including intracellular immune dysfunctions, and by lengthened and accentuated oxidative stress, but also by exercise metabolites, which work on the sensitive receptors in the dorsal root ganglions, which in severe ME are chronically inflamed, and are therefore much more sensitive to these metabolites, which are produced in high quantities in response to trivial exercise, which for ME patients, due to the underlining metabolic problem, is strenuous exercise. And a similar problem is most likely responsible for the abnormally delayed brain recovery after doing trivial things.

This study also shows that the two metabolic problems are the result of an impaired oxygen uptake into the muscle cells or their mitochondria and in combination with the Norwegian Rituximab studies, which suggest that ME is an autoimmune disease, it is suggestive that antibodies are directly or indirectly blocking the oxygen uptake into the muscle cells or their mitochondria.


Johnnyd said...

Thanks Dr. Speedy. If we were to assume the best about the research and funding world ( a pretty big assumption, I know ) -- personally I think tying together the autoimmune components some researchers have found, such as Fluge and Mella, with the metabolic components would be a huge step forward.

Hope said...

Thanks, Dr. S.
Would be very interesting if this study can be replicated with a larger N and information about the diagnostic criteria used for inclusion in the study as a patient with severe ME.

Hope said...

Thanks for the journal article link. Just read first bit of it, available online free, not just the abstract, and Dr Vink clearly distinguishes between ME, Ramsey, and CFS.
Unfortunately my severe ME stops me reading any more now. Hope to come back to it another day. Fortunately some of the time I can read critically.

Dr Speedy said...

Important article and if we could replicate in a larger trial and tie things together that would be fantastic. But this study clearly shows that there's a major metabolic problem in severe ME


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