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

[Sly Saint]

Before the COVID-19 pandemic, 1.5 million people in the U.S. were estimated to have myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS, with an annual economic impact of $36 billion to $51 billion. Due to COVID-19, the total ME/CFS prevalence could rise to between 5 million and 9 million people. This would cause the annual U.S. economic impact to rise to $149 billion to $362 billion in medical expenses and lost income.

Certainly, we need to study ME/CFS to find ways of reducing this medical and economic harm. Yet, few funds have been devoted to ME/CFS. In contrast, more than $1 billion dollars has been allocated to the study of COVID-19 in the U.S. Reluctance to fund ME/CFS research might be due to there being multiple potential causes of the syndrome and that it is more scientifically justified to focus research on an illness such as COVID-19 that has clear viral cause.

However, what might be considered a limiting factor in studying ME/CFS could actually provide scientists a window into understanding long COVID-19. There is growing evidence of multiple similarities between patients with long COVID-19 and patients with ME/CFS (who have tested negative for COVID-19).

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

 

[DokaGirl]

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

 

[CRG]

"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.