The key to demystifying long COVID-19 could come from studying another chronic condition : Article: Chicago Tribune: Leonard Jason

https://www.chicagotribune.com/opin...0220912-42gktniwobbcbblcbs56l6r7zu-story.html

 

Thank you to the authors for this.

But a point about hair loss.

The article says those with ME do not experience hair loss, but those with Long Covid do.

Early on with ME, I had hair loss.

This post has been copied and following discussion moved to Hair loss

 

"Those with COVID-19 have been exposed to the coronavirus, whereas those with ME/CFS have a variety of triggers, including the virus that causes mononucleosis."

This borders on fallacy. It implies a direct equivalence between a statistically significant population level correlation ( COVID 19 exposure followed by prolonged sequalae ) and a mass of statistically unentangleable patient reports which solely on the basis of implied correlation are described as "triggers".

The enthusiasm here to link A to B is understandable - equivalence of esteem between areas of research, appropriate funding, avoiding reinventing the wheel etc all apply. But ME/CFS research needs intellectual rigour and whatever the patient experience of x following y, correlation isn't necessarily causation and investigation is always needed to ascertain whether x and y are causally related.

We currently have no clear evidence that any given prior infection is a 'trigger' for anything in the disease process of ME/CFS and while prior infection is a reasonable basis for hypothesis formation regarding the development of disease in PwME, talking with certainty as though there is even such a thing as a trigger, let alone that there are known triggers is misleading, and worse accepting such certainty serves to curtail scientific rigour. We don't need yet another false orthodoxy to misdirect ME/CFS research.