Myalgic Encephalomyelitis is clear to see in the blood

[andyguitar]

Am I missing something?

The research was more about looking for what the difference is between me/cfs and the general population than trying to find a single biomarker.

 

[pamojja]

I am NOT trying to be a Negative Nelly, but this was my takeaway from the original linked reference:

"No diagnositc biomarker"

Am I missing something? (Please be gentle in your response, thank you.)

Well, one can perceive it from a different perspective.

My main ME/CFS symptom in the very mild category of PEMs only became dominant with additional chronic PAD and COPD. It took me years to realize it as such, already present before those following chronic conditions. And mistook it as a secondary consequence. No more, since the symptoms of PAD and COPD both went into remission first.

Since I couldn't find a helpful experienced practitioner, I monitored progress and regress with as many as possible lab-markers. Discerning the usual normal lab reverence ranges, from optimal ranges. And employed comprehensive life-style changes and supplementation.

Throwing as many possible nutrients and herbs at those lab markers for nudging them to improve, not only ceased the symptoms of COPD, and the walking-disability from PAD 3 years later, into remission. But another 3 years later, even PEMs. I still have a small energy envelope of 3-4 hours work only, needing 10 hours of sleep. But now the consequence isn't PEMs for many days (exhaustion, pains and brain-fog), but tolerable back pain, gone the next day already.

So lab-markers can be made a useful tool in multiorgan damage. Insulin resistance, NAFLD and Inflammation I all fought with comprehensive lifestyles and supplementation. Some lab-markers resisted going to the optimal range, but overall they all improved together with remissions.

However, with mild ME/CFS only. So individual results will definitely vary.

 

[Viala]

Thats going to depend on the the individual @Viala The research shows traits and should not be seen as a diagnosis of all who have me/cfs. Having a trait really just raises the possibility that a disease might be present. The individual will need their own diagnoses using whatever tests are currently used used by the medical profession.

I wish that studies like this one would point in the right direction, a hypothesis that would include each ME/CFS case and explain differences between us, including having remissions. There must be a common denominator somewhere there and it should be seen in a large study. Unless some traits went under the radar.

 

[andyguitar]

There must be a common denominator somewhere there and it should be seen in a large study. Unless some traits went under the radar.

There is something coming up in the near future that may well help. The DEcode ME study. A genetic analysis of about 20,000 me/cfs patients which is looking to find what makes a person susceptible to me/cfs. Should be published in a couple of months. So maybe putting research like this together with that will lead to treatments.

 

[Wishful]

Am I missing something?

One thing I noticed: they talk about not finding any single difference, but they don't claim that their combination of factors can be used as a diagnostic test either. That's what makes me think the findings might just be an artifact of the methodology. We live such different lives from "healthy controls" that there are likely many differences not directly related to the ME mechanism.

It's too bad that they didn't expand the study to include samples post-exertion (PEM state) as well as pre-exertion. I'm thinking of that study that showed a difference in muscle recovery between PWME and controls. I think ME is more likely to show dynamic differences (rate of change of some factor) than static ones (blood sampled once only).

There's another possible reason for the differences found: blood from PWME were taken under different circumstances than from controls. PWME might have been more stressed about the tests (worried about PEM from the experience), or it might take more physical and cognitive effort to travel to give the sample.

If PWME are supposed to have chronic inflammation and liver disease and insulin resistance, shouldn't there be more postings here about having those diseases and getting better by treating them? If the blood markers for those things are so minor that the typical tests don't reveal them, it's more likely that they're just an artifact of the study, rather than an insight into ME's mechanism.

 

[Oliver3]

I know an alcoholic with diabetes, liver damage, brain damage who has a shed load of energy.
He still smokes , drinks and generally shouldn't be as able to move around has he does.
Baffling that I'm trying every modality to stay afloat and he's doing everything that should sink him but doesn't.
Resilience is the great mystery

 

[Treeman]

If PWME are supposed to have chronic inflammation and liver disease and insulin resistance, shouldn't there be more postings here about having those diseases and getting better by treating them?

I have constant swollen tender lymph nodes and experience frequent urination and dehydration. Test show no inflammation and no diabetes? Somethings going on but current tests show no problems and have for decades?

 

[Violeta]

I have constant swollen tender lymph nodes and experience frequent urination and dehydration. Test show no inflammation and no diabetes? Somethings going on but current tests show no problems and have for decades?

I have frequent urination, dehedration, always thirsty. This is diabetes insipidus. Something wrong with the hypothalamus.

I'm glad you brought that up, I was spending too much time on the hippocampus tonight.

 

[Treeman]

I have frequent urination, dehedration, always thirsty. This is diabetes insipidus. Something wrong with the hypothalamus.

All my hormone tests are normal too?

 

[Violeta]

All my hormone tests are normal too?

Did you get vasopressin level tested?

 

[Treeman]

Did you get vasopressin level tested?

Not sure, I’ll look into it, have you had the test?

 

[Viala]

There is something coming up in the near future that may well help. The DEcode ME study. A genetic analysis of about 20,000 me/cfs patients which is looking to find what makes a person susceptible to me/cfs. Should be published in a couple of months. So maybe putting research like this together with that will lead to treatments.

That's good news, I am looking forward to it. Methylation issues should be seen in such study, that would be something we could work with.

One thing I noticed: they talk about not finding any single difference, but they don't claim that their combination of factors can be used as a diagnostic test either. That's what makes me think the findings might just be an artifact of the methodology. We live such different lives from "healthy controls" that there are likely many differences not directly related to the ME mechanism.

I've been thinking about methodology as well. Everything depends on it and the final effect can be the same as with creative accounting. Doesn't have to be done on purpose, just some computing error that changes the outcome and that's all it takes.

Also set normal ranges may skew the conclusions. I wonder how many of these findings are brushed off as 'normal', they may be normal for controls, but if we have a whole bunch of seminormal factors counted in hundreds, that can create a whole cascade and result in this disease. Normal ranges may not be normal for us. Maybe that's why they can't find any specific biomarker, ME/CFS can be a multitide of biomarkers that are slightly off the normal ranges.

For example one study found that there are changes in our aminoacids compared to controls, and the conclusion was that we do not need supplementation because they're still within ranges. But if our bodies burn muscles to provide needed aminoacids, then it changes everything, especially when supplementation of some of these aminoacids brings relief.

 

[Violeta]

Not sure, I’ll look into it, have you had the test?

No, doctors just kept testing me for bacterial infections. Not one ever mentioned diabetes insipidus. I had to figure it out for myself. I don't feel as though the test is necessary. I wouldn't take the drug for it.

Just looking up more about it now. Do you tend to have low blood pressure?

Have you had neurotransmitters tested?

 

[Treeman]

Just looking up more about it now. Do you tend to have low blood pressure?

Have you had neurotransmitters tested?

No and no. I also came to the end point of diabetes insipidus. I do have a lot of the symptoms and it’s something I will follow up on.

 

[cfs since 1998]

https://www.medrxiv.org/content/10.1101/2025.05.28.25328245v1
This paper might be a better one for seeing ME/CFS in the blood, however it hss not been peer reviewed yet.

"Focused secretome analysis supported intensified regulatory interactions related to immune activity, inflammation, vasculature, and metabolism. Validation of measurements using antibody-based methods confirmed findings for a selection of proteins. The uncovered serum proteome patterns in ME/CFS patients help clarify a multifaceted pathophysiology and offer a foundation for future therapy and biomarker discovery efforts."

 

[Wishful]

ME/CFS can be a multitide of biomarkers that are slightly off the normal ranges

It can also be abnormalities in places other than the blood. If the abnormalities are highly localized in the brain, the only signs in the bloodstream would be far downstream and depend on the individual, so there wouldn't be a pattern common to the majority.

 

[Viala]

It can also be abnormalities in places other than the blood. If the abnormalities are highly localized in the brain, the only signs in the bloodstream would be far downstream and depend on the individual, so there wouldn't be a pattern common to the majority.

So there would be patterns, only difficult to diagnose. Hence the issues with methodology, diagnostics and conclusions. You do it the wrong way and you'll have only noise, no real results. Although in this disease there should be something visible in our blood, but like I said, if it flies under the radar of normal ranges, we won't find anything this way.

 

[Oliver3]

The research was more about looking for what the difference is between me/cfs and the general population than trying to find a single biomarker.

I'm wondering how many of them have eds gene or the rccx genes.
It's so ckear to me it's a huge player with everything else downstream

 

[andyguitar]

if we have a whole bunch of seminormal factors counted in hundreds, that can create a whole cascade and result in this disease.

There may be many semi normal and some abnormal factors coming from 1 trait. So for instance if liver dysfunction is present there could be many things that are abnormal but not causing symptoms but a couple that do. I think looking for traits is a good strategy and could explain why different patients have different symptoms. As I said these things need to be looked at on an individual basis. Some may have 1 trait others 3. That would explain why some are very badly affected, others less so.

 

[pamojja]

Some may have 1 trait others 3. That would explain why some are very badly affected, others less so.

Not necessarily. Beside NAFLD with non-circulated nodules, rather high inflammation from various infections, and T2D. I also had tubercles from tuberculosis, small airway disease from COPD, and CKD stage1. To name a few. But was in the mild ME/CFS category only.

So even with many more conditions than just marker of slightly raised inflammation, liver enzymes and insulin resistance, one can suffer those rather strong and a zillion other conditions, but mild ME/CFS only.