Cellular bioenergetics is impaired in patients with CFS (2017) Tomas, Strassheim, Newton et al

[Saturnation]

With CPET data for ME or strictly defined CFS the problems are not found in sedentary controls.

But in my opinion using CPET is really a bad idea, given what it will do to someone with ME. So it's good that they didn't do CPET in the study and at the same time it's bad?

If they were to make an earnest attempt to find low functioning mitochondrial in control groups and failed then this would be a big step towards finding an objective test for ME and cohorts and that would be huge? Which was kind of the point I was initially trying to make in the first place...

 

[alex3619]

But in my opinion using CPET is really a bad idea, given what it will do to someone with ME.

There is risk in CPET technology. It is totally unsuitable for severe patients. Its why we need a validated blood test or other investigatory marker.

However a great many patients have used CPET. Nearly all recover in a week or two from what I have read. This level of risk is also found in procedures like lumbar punctures. Its also for research that I think its justified. Patients have to decide if the risk is worth the benefit to the science. Many do CPET themselves for the data they get which helps them manage their PEM.

I first got involved in metabolic testing in 1993. I was a test subject. Most of us have low metabolic rate. That was measurable even back then. This research was not published, I think, though I could be wrong as only one paper by this investigator is on PubMed and there were at least seven papers I think. Or was it four? It was too long ago for my memory to be reliable.

For the record my metabolic rate was consistently low. That was as a mild patient.

 

[Valentijn]

I guess it's just the current nature of medical research that the title of the paper infers findings that the research doesn't actually totally support?

Not really ... there is impairment, regardless of cause.

I'm wondering if that paper doesn't just show that low mitochondrial function is only a symptom of fatigue and not that fatigue is a symptom of low mitochondrial function?

Fatigue is a symptom. Symptoms are caused by a disease or other states. Symptoms are not caused by symptoms, though multiple symptoms may have the same source. So I don' think it makes any sense for a state to be a symptom of a symptom.

I'm also not sure why you believe fatigue is relevant. Fatigue isn't what results in sedentary behavior in ME patients - it's PEM which does that, and more immediate forms of exercise intolerance, muscle weakness, OI,etc.

 

[Andy]

Cara Thomas gives the MEA a summary explanation of this research - http://www.meassociation.org.uk/201...getic-deficiencies-in-mecfs-13-november-2017/

 

[alex3619]

Fatigue is a symptom. Symptoms are caused by a disease or other states.

This is one of my major concerns. One of the reasons, in my view, that diseases like depression, fibro, and ME have no cures, aside from complexity, is this confusion between a symptom and a disease. Its a category mistake. Depression, for example, is not a disease, its a symptom of disease. Treating depression with antidepressants is like giving aspirin for chronic headaches, without trying to find the cause and fixing it.

 

[Little Bluestem]

Muscle and perhaps other tissue also needs to be tested.

What he said!

 

[Mithriel]

I'm wondering if that paper doesn't just show that low mitochondrial function is only a symptom of fatigue and not that fatigue is a symptom of low mitochondrial function? If you take a normal healthy human and run them into the ground over a week, then test them I suspect that you might find low mitochondrial function in them as well.

There was an article in the New Scientist a few weeks ago about deconditioning. They said that birds "train" for long migrations by putting on fat and sitting about a lot. In humans, we seem to keep our bodies at a low level of "fitness" but when we need more efficiency we get it because the watse products of anaerobic respiration make the mitochondrial numbers increase and improves aerobic fitness.

It seems to me that this means experiencing fatigue should make a normal person increase their mitochondrial function.

Doctors use the CPET testing for lots of diseases and accept one day testing as an accurate result to on which to base treatment, so , in a sense, it has already been tested on lots of diseases. Remember that the physiologists found the results unbelievable and had to be persuaded the machines were not faulty.

A high blood sugar is accepted as proof of diabetes without every disease in the world being tested. A single instance of VO2 max dropping in a person with ME is a sign of something profoundly wrong whether it is unique to ME or not.

 

[alex3619]

A single instance of VO2 max dropping in a person with ME is a sign of something profoundly wrong whether it is unique to ME or not.

This relates to another common medical mistake. ME cannot be proven. The physiological problems in ME patients do have tests though. So what is wrong to a great extent can be demonstrated by tests. No disease diagnostic test does not mean no physiological tests.

The issue with ME diagnostic tests is no longer test sensitivity, or the capacity to find it. Its about specificity, or being sure its not due to something else. Yet that is not considered a problem with depression especially when diagnosed with written instruments, and for which there is either no known specificity or the data implicates very very weak specificity at best. Medicine loves pseudoscience, poor standards, and even quackery, and defends them. That has to change.