Health rising blog post, by Cort Johnson, 18 April 2017: The Stanford Paradox: Elevated Energy Production Found in Chronic Fatigue Syndrome (ME/CFS)
Producing energy is a big problem in Chronic Fatigue Syndrome (ME/CFS). In fact it’s probably the problem in ME/CFS, which is why the findings of mitochondrial dysfunction and lowered ATP production have made sense. When the metabolomics studies suggested that chronic fatigue syndrome (ME/CFS) was a hypometabolic state, the field seemed set: energy production (ATP) was low and the mitochondrial activity probably was too. Fatiguing disease and low ATP production: it seemed to make so much sense.
Then came the study with the eye-catching title: “Elevated Energy Production in Chronic Fatigue Syndrome Patients.” It suggested that far from being low, cellular energy production was actually abnormally high in ME/CFS patients. Even for a field that’s had more than its share of inconsistent findings, that was a real lu-lu.
The results, though, could not be ignored. They didn’t come from a small research group but from the Xinnan Wang Lab at Stanford. Last year the lab – which is devoted entirely to studying the mitochondria – made headlines with its potentially seminal finding in Parkinson’s disease. It uncovered a defect that prevented Parkinson’s patients from removing their mitochondria as their mitochondria start to wear out. That defect left those mitochondria pumping toxins into the brain. Because the defect was present in different types of Parkinson’s patients, it suggested that a “mitochondriopathy” might lie at the core of the disease.
Plus the patient samples in the Wang ME/CFS study came from some of our best ME/CFS experts. Plus it was funded by an ME/CFS group – the Chronic Fatigue Initiative – that hires only the best researchers. There was no looking past this result.
