Discriminating Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and comorbid conditions using metabolomics in UK Biobank, 2024, Huang et al

Perhaps the OI/hypertension discussion might benefit from my experience. I am not alone, but I have BOTH hypertension and NMH, neurally mediated hypotension. My hypertension is constant, my OI is usually suppressed except when very tired, such as my two and a half days without sleep earlier this week. During my Tilt Table Test maybe twenty odd years ago, my blood pressure crashed to zero and my cardiologist was about to call the crash cart when his treatment restored my bp enough to regain consciousness.

Given that maybe most of us have a new type of OI (eighty percent if I recall correctly), if it can be called that, with hypoperfusion of the brain, that does not show up on conventional TTT, we still do not know nearly enough to answer these questions. This is the kind of complicated that makes it no surprise that researchers still have not figured it out.

To me, metabolomics data is critical in our path forward. Of course I am biased, my background is in biochemistry.

For the record I consider I have ME, if pacing well I have minimal fatigue (but it takes only tiny amounts over my limit to have it crash back), I have been diagnosed with CFS four times (ME was not being used much back then), and may have been sick 56 years now after measles encephalitis as a child, though it really kicked up several notches after a stomach flu in 1985, several years before I was diagnosed as having antibodies to a coxsackie virus (1989).

 

I developed OI after reactivation of both HHV6 and EBV 11 years after PVFS/ME onset. I'm referring it OI because it's the only term we have at this time. We don't have a proper term for what we're experiencing for that either. It certainly exacerbates the pathophysiology of delayed PEM and we don't understand that yet either.

 

I understand what you're saying and wasn't trying to diminish anyone's experiences. The severity of the patient is very important. What I was trying to convey was that focusing more on the distinctive set of symptoms that we all share in common such as delayed PEM.

I think we'll find that there are different types of ME, like there are with MS, in which there are 4.

 

I have seen lipid homeostasis issues in cells from multiple tissues from pwME (some of these are experiments with Chris) and I do want to specifically look at membranes in a future project

 

Hypertension is in reference to ongoing elevated blood pressure at rest.

Orthostatic hypotension is the dramatic drop and sustained drop of blood pressure upon standing outside of a normal range. POTS is the dramatic rise and sustained rise of heart rate upon standing outside of a normal range.

Hypertension had no significance to ME/CFS, this isn't related to orthostatic issues.

 

Depends on the study, certainly severity matters if you were to develop an objective marker for clinical trials. It remains an important need for this disease.

In terms of studying the pathology of the disease or developing a diagnostic. It may not matter but it also may matter, the cause of severity is unknown.

One might simply think a severe patient has a more severe pathology of ME/CFS, but that may not be the case. A severe patient may have an accumulation of undefined co-morbidities that exacerbate their physical condition and remain unaccounted for.

 

The delay in PEM is very likely related to RNA, there are many processes in the body that take 24-48 hours to alter path.

The exacerbation that occurs in response to this new path is of course interesting.. what is biologically happening.

 

From what I hear, delay in PEM changes to nearly immediate when people are very severe. If this is actually the same phenomenon, then a process that only occurs consistently after over 24 hours wouldn't make sense.