Are Circulating FGF21 and NT-proBNP promising novel biomarkers in ME/CFS, 2020, Joan Charles Domingo et al

Full title:
Are Circulating FGF21 and NT-proBNP promising novel biomarkers in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome?

https://www.liebertpub.com/doi/abs/10.1089/ars.2020.8230

 

FGF21

Source is Wikipedia

 

Animal studies are a waste of time, money and lives. I have spent years studying this.

 

Do you have any links to articles or suggested reading on this? Would be interesting to have an overview article of how often results in animal studies do or do not translate to trials in humans.

 

Small holes and gaps???

 

Sci hub link, https://sci-hub.se/10.1089/ars.2020.8230

Fukuda selection criteria.

 

Dead end. I know it’s just my case but I had NT-proBNP measured as part of a battery of cardiovascular procedures and tests to look at my heart and the NT-proBNP results were almost zero.

Unfortunately, I was only able to get these tests in my third year or so of illness and wished I was able to examine this when I was having the heart arrhythmia issues triggered by the viral infection in the first year. They couldn’t find anything wrong with my heart after the arrhythmia mostly went away.

 

Here is a link to a PR blogpost on the subject: Cancer researcher slams requirement for animal models | Phoenix Rising ME/CFS Forums

There are several others. I can't write them now.

Animal studies almost always fail in humans.

 

In the second post, by @Michiel Tack.

 

To be fair animal studies of normal organ function (like immune cells) have been essential to the development of a wide range of life saving treatments. What has been a huge waste of time is animal models of disease causation.

 

As the virologists and immunogists on TWIV microbe TV point out:

"Mice lie and monkeys exaggerate" in experiments destined for human beings. That said, how else is one to start?

For new therapeutic molecules, basic safety and probable dosage is always tested on animals first. Lab science knows a lot about mice.

 

My serum FGF-21 was tested some three years ago by a London, UK immunology lab as part of a study on mitochondrial dysfunction. My serum FGF-21 levels were found to be "very low". I was told that Oxford had also seen very low levels in adult patients with MECFS. The researchers had no explanation.

 

Very interesting.

 

@J.G do you have poor fasting tolerance?

 

They are indeed. FGF-21 - I was told in writing - is under ongoing investigation as a potential biomarker for certain mitochondrial disorders where it is found in elevated levels. FGF-21 is also found elevated in some patients with *defined* respiratory chain defects.

Which, taken together, begs the question whether the patients in this Spanish MECFS study cohort suffer from actual core / true MECFS, or from a mitochondrial defect manifesting in a similar way. Alternatively, there could be separate ME cohorts, one with low FGF-21 of unknown etiology, one with sharply elevated FGF-21. Or perhaps PEM accounts for the difference, somehow.