HOW on earth is EDS or any other CTD not the soil in which ME flourishes?
- Thread starter bread.
- Start date
When I said trolling, I was referring to @bread.'s comments where he initially said (incorrectly) that "there is absolutely zero prevalences of any of these diseases that you cant trust- how would you".
And then later, when I provided ready-made Google search which listed these studies, he refused to look at it, and continued to ask me for info about prevalences.
And then later, when I provided ready-made Google search which listed these studies, he refused to look at it, and continued to ask me for info about prevalences.
I'm only messing..things were getting a little heated. I believe you bread, i've thought this was EDS for a long time and Hip, all's good. I'm looking forward to the 7th of September. If Ron still thinks he can cure this and itis EDS, he'll be a damn miracle worker. here's to hoping.
OK, so you are saying that all prevalence rate studies are wrong because you believe that there is no clearly defined way to diagnose ME/CFS.
Well that is not really true: ME/CFS does not have a biomarker, but it is a reasonably defined illness, if you properly follow diagnostic criteria such as the CCC.
Because there is no biomarker, ME/CFS is defined by criteria which are based on symptoms. These criteria will also involve exclusions. For example, in the CCC, it says:
Thus if you are positive for the CCC symptom criteria, and you do not have any of these excluded illnesses, then by definition you have ME/CFS.
Now, it is often mentioned that ME/CFS may involve different subsets; some people for example talk about viral versus autoimmune subsets (though there's little evidence to support such a distinction). And most people would agree that ME/CFS likely involves several subtypes.
But that does not mean that the prevalence studies are incorrect.
Anyway, I thought you were trolling, but I now understand the point you were trying to make. So I apologize for suggesting you might be trolling. (Though I do not agree with your point).
Well that is not really true: ME/CFS does not have a biomarker, but it is a reasonably defined illness, if you properly follow diagnostic criteria such as the CCC.
Because there is no biomarker, ME/CFS is defined by criteria which are based on symptoms. These criteria will also involve exclusions. For example, in the CCC, it says:
Thus if you are positive for the CCC symptom criteria, and you do not have any of these excluded illnesses, then by definition you have ME/CFS.
Now, it is often mentioned that ME/CFS may involve different subsets; some people for example talk about viral versus autoimmune subsets (though there's little evidence to support such a distinction). And most people would agree that ME/CFS likely involves several subtypes.
But that does not mean that the prevalence studies are incorrect.
Anyway, I thought you were trolling, but I now understand the point you were trying to make. So I apologize for suggesting you might be trolling. (Though I do not agree with your point).
Last edited:
Hip i think we are going to have to agree to disagree. Time is going to tell. You obviously don't think EDS is a major player whereas me and perhaps i can speak for Bread, feel that the diagnostic criteria for both diseases are not robust enough to actually mean too much when EDS, Fibro, Lups, CFS etc all lhave overlapping symptoms. The criteria you mention are not biomarkers therefore by definition are not rigorous. All the above mentioned diseases are connective tissue diseases...so whats the correlation??? It seems increasingly obviously both known and unknown EDS types play a role in CFS. We will have to wait and see won't we?
@Oliver3 I am not discounting the possibility that hEDS may predispose to ME/CFS.
But I am calling into question the views expressed in this thread that it is impossible to distinguish ME/CFS from EDS, and the views that we can know nothing about the prevalence of ME/CFS or hEDS in the general population.
But I am calling into question the views expressed in this thread that it is impossible to distinguish ME/CFS from EDS, and the views that we can know nothing about the prevalence of ME/CFS or hEDS in the general population.
The geneticist that diagnosed me was very clear that my hEDS diagnosis voided my Fibro dx (at least in his eyes).
@Hip I do not agree that everyone here has EDS or even that you can have it without hypermobility (that remains to be seen), but I really do think that many of us have been misdiagnosed (in my case purposely by a rheumatologist) at some point. I think docs get frustrated that they do not have answers for patients like us and try to get us out the door with a label. It seems unfair, and only the most persistent will ever really know the truth.
This year I was told at an ME clinic that hEDS is no big deal, there is no way it is the root of my problems and I was making entirely too big a deal about the whole thing. The big deal that I made was to question if there was a basis for hEDS causing any of the issues. That ended the trust in that relationship.
@Hip I do not agree that everyone here has EDS or even that you can have it without hypermobility (that remains to be seen), but I really do think that many of us have been misdiagnosed (in my case purposely by a rheumatologist) at some point. I think docs get frustrated that they do not have answers for patients like us and try to get us out the door with a label. It seems unfair, and only the most persistent will ever really know the truth.
This year I was told at an ME clinic that hEDS is no big deal, there is no way it is the root of my problems and I was making entirely too big a deal about the whole thing. The big deal that I made was to question if there was a basis for hEDS causing any of the issues. That ended the trust in that relationship.
Last edited:
Yes, again, there are no clear diagnostics but it could well be couldn't it. It's gonna be intersting when we have the ability to double down and analyse variabilities in a much more precise way.
Just looked on jennifer Brea's twitter feed and she's talking a lot about heads. interestingly she just posted a video which in part gave the interesting fact that the entire US gymnastic team is hypermobile and yet unaffected. She's wondering what the trigger can be or if it's just waiting there in the wings to appear.
Just looked on jennifer Brea's twitter feed and she's talking a lot about heads. interestingly she just posted a video which in part gave the interesting fact that the entire US gymnastic team is hypermobile and yet unaffected. She's wondering what the trigger can be or if it's just waiting there in the wings to appear.
I understand that you and @bread. have a personal theory that ME/CFS is really EDS. However, you have not provided any significant evidence or theoretical justification for your theory. So it's hard to discuss you opinions anyway, because there is very little substance to them that can be discussed.
You also have personal views on the inadequacy of diagnostic criteria of ME/CFS and EDS, and you believe that because of this claimed inadequacy, it is not possible to distinguish these two diseases. But again you have not provided any evidence to support your statement (in terms of references to studies or other medical literature).
Now, if you presented some interesting ideas or evidence that can link ME/CFS and EDS, then I am all ears. But so far, all I have heard is opinions without supporting evidence.
You also have personal views on the inadequacy of diagnostic criteria of ME/CFS and EDS, and you believe that because of this claimed inadequacy, it is not possible to distinguish these two diseases. But again you have not provided any evidence to support your statement (in terms of references to studies or other medical literature).
Now, if you presented some interesting ideas or evidence that can link ME/CFS and EDS, then I am all ears. But so far, all I have heard is opinions without supporting evidence.
There is one flaw in your argument. There's virtually no research done on EDS and even less so on the comparisons with the two diseases. Tell me how me and my friend differ. He has heds, i have CFS.
He has pots. thats a tick for me. He has Pem. Tick for me. He has dysautomnia. Tick for me. He has thinnish skin. Tick for me. He scored quite a few of points on the Beighton scale. I have hypermobile toes, thats it. Then again, i have a herniaand other weak connective tissues. He has orthastic intolerance. Thats a tick fo rme. He has problems with cold extremes. Tick fo rme. He has sympathetic activation and mastcell problems. Ticks for me So basically he scored a few points more than me on a questionable score, all the rest of his symptoms are identical.
To further confuse things you can score on the beighton scale and be hypermobile and be healthy. This area is so underresearched, that as i understand it, it's pretty new to most scientists and gets very little funding. Just seeing whether somones fingers bend back is no, to my mind comprehensive. How does it take into accopunt mitral valve prolapse, ibscolon spasticityvaricose veins etc etc etc All of the symptoms i mentioned are common to both conditions and fibromyalgia and lupus...so what is the correlation.?
My feeling is that its a collagenbased problem from the start and cfs is under that umbrella.
I did provide you the work of Dr Chedda. an ex HIV and infectious disease specialsit with lots of clinical experience in CFS here is the quote from the article
'The Beighton Test is a self-questionnaire that is often used to assess whether hypermobility is present. Dr. Chedda noted, though, that people who don’t score positive on the Beighton Test or who don’t fit the criteria for Ehlers Danlos Syndrome (EDS) may still be hypermobile. She recently had a patient who scored low on the Beighton Test and seemed perfectly normal except she was able to pop her shoulder and hip in and out – which she promptly demonstrated.'
It is not a rigorous test. be prepared to reevaluate where this is headed as i thinkthese diseases are too related not to be related!!
He has pots. thats a tick for me. He has Pem. Tick for me. He has dysautomnia. Tick for me. He has thinnish skin. Tick for me. He scored quite a few of points on the Beighton scale. I have hypermobile toes, thats it. Then again, i have a herniaand other weak connective tissues. He has orthastic intolerance. Thats a tick fo rme. He has problems with cold extremes. Tick fo rme. He has sympathetic activation and mastcell problems. Ticks for me So basically he scored a few points more than me on a questionable score, all the rest of his symptoms are identical.
To further confuse things you can score on the beighton scale and be hypermobile and be healthy. This area is so underresearched, that as i understand it, it's pretty new to most scientists and gets very little funding. Just seeing whether somones fingers bend back is no, to my mind comprehensive. How does it take into accopunt mitral valve prolapse, ibscolon spasticityvaricose veins etc etc etc All of the symptoms i mentioned are common to both conditions and fibromyalgia and lupus...so what is the correlation.?
My feeling is that its a collagenbased problem from the start and cfs is under that umbrella.
I did provide you the work of Dr Chedda. an ex HIV and infectious disease specialsit with lots of clinical experience in CFS here is the quote from the article
'The Beighton Test is a self-questionnaire that is often used to assess whether hypermobility is present. Dr. Chedda noted, though, that people who don’t score positive on the Beighton Test or who don’t fit the criteria for Ehlers Danlos Syndrome (EDS) may still be hypermobile. She recently had a patient who scored low on the Beighton Test and seemed perfectly normal except she was able to pop her shoulder and hip in and out – which she promptly demonstrated.'
It is not a rigorous test. be prepared to reevaluate where this is headed as i thinkthese diseases are too related not to be related!!
Last edited by a moderator:
This is from the Ehlers danlos society:
There is not enough information about fatigue in hEDS, it is also unclear how many patients diagnosed with CFS actually really have EDS. Clinical trials are needed to improve healthcare and to assess the effect of treatment. The influence of mental health on treatment is also not clear.
As you see, we cannot quote research when there isn't any. Similarly we can't really call CFS CFS unless we get a biomarker. Your criteria are so vague, it could be heds, eds fibro.
If we continue to use this basic ideas about EDs and CFS then we are gonna stay stuck. It's bloody obvious there is so muchg cross over. Youre a pedant, which can be good, but i'm a global thinker and i'm going on clues from Dr Ron davies, Jennifer Brea, my own experiences and the laughable criteria you champion as being able to tell these two diseases apart.
There is not enough information about fatigue in hEDS, it is also unclear how many patients diagnosed with CFS actually really have EDS. Clinical trials are needed to improve healthcare and to assess the effect of treatment. The influence of mental health on treatment is also not clear.
As you see, we cannot quote research when there isn't any. Similarly we can't really call CFS CFS unless we get a biomarker. Your criteria are so vague, it could be heds, eds fibro.
If we continue to use this basic ideas about EDs and CFS then we are gonna stay stuck. It's bloody obvious there is so muchg cross over. Youre a pedant, which can be good, but i'm a global thinker and i'm going on clues from Dr Ron davies, Jennifer Brea, my own experiences and the laughable criteria you champion as being able to tell these two diseases apart.
This is wrong. If 50% of PWME have hEDS (I have heard this), then the general ignorance most ME/CFS clinicians have about hEDS is no longer defensible. They should be attending EDS conferences or doing EDS CMEs.
And what about people, like me, in that other 50%, who do not have hEDS by any definition but have all of its cousins?
Byron Hyde would probably say it’s the ground in which it flourishes: https://www.me-pedia.org/wiki/Comorbidities_of_Myalgic_Encephalomyelitis#Clinical_perspectives
And Peter Rowe has been banging this drum for years: https://www.me-pedia.org/wiki/Neural_strain, which may be an important intersection between hEDS and ME.
And what about people, like me, in that other 50%, who do not have hEDS by any definition but have all of its cousins?
Byron Hyde would probably say it’s the ground in which it flourishes: https://www.me-pedia.org/wiki/Comorbidities_of_Myalgic_Encephalomyelitis#Clinical_perspectives
And Peter Rowe has been banging this drum for years: https://www.me-pedia.org/wiki/Neural_strain, which may be an important intersection between hEDS and ME.
You need 248 cases to test 1 SNP that you already suspect. To identify an unknown SNP, you must test more locations, so more cases are needed.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3480678/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3480678/
That would require access to some competent physician. Sorry. No testing is available to me unless i can work out how to travel many states away while being homebound and needing to keep my legs elevated and lie down a lot. Sleeper cars in trains are super expensive, especially the ones with the included bathroom.
Over the years, I've heard a number of speculations on this forum similar to yours, that ME/CFS is really just a manifestation of some other known disease.
For example, I heard the opinion that ME/CFS is just an undiscovered form of MCAS. Or that ME/CFS is just an unusual form of hypothyroidism. Or that ME/CFS is just another form of fibromyalgia.
We also know that ME/CFS has similar symptoms, and sometimes some shared pathophysiology, to anemia, hepatitis B, hepatitis C, celiac disease and others.
In all cases, there is some overlap of symptoms and sometimes pathophysiology, but that's not enough to say that ME/CFS is really just a manifestation of some other disease X.
The argument you are presenting as evidence that ME/CFS is the same as hEDS could also be applied to all the other examples I just mentioned. So you can see the problems with this argument.
I agree it is certainly interesting when diseases manifest very similar symptoms, and personally I am always trying to find commonalities between diseases similar to ME/CFS, in case those diseases might throw some light onto the nature of ME/CFS. But that does not mean conflating the diseases.
It is a precise box, which tries to maintain distinctions. Whereas the argument I hear from you and @bread. sounds more like a desire to blur the distinction between diseases.
If you blur distinctions in this way, you may end up concluding that ME/CFS is a form of eEDS, which is a form of MCAS, which is a form hypothyroidism, which is a form of fibromyalgia, which are all the same as anemia. I don't think that really helps anyone.
Generally speaking, medical diseases are often similar to other diseases. That's why there is a thing called differential diagnosis, which enables you in most cases to distinguish similar diseases.
You are clearly surprised and interested by the symptomatic similarities between ME/CFS and HEDS. And I agree it is interesting. But it is common in medicine to have different diseases with similar symptoms; and it would be rather foolish to lump all diseases with similar symptoms under the same name.
Heart valve disease is linked to enterovirus infections of the valves. Enterovirus infection of course is often found in ME/CFS, so the higher prevalence of mitral valve prolapse in ME/CFS conceivably might be explained by this.
Note that viral infection can trigger the immune system to secrete connective tissue-degrading enzymes such as matrix metalloproteinases (MMP) and neutrophil elastase. So this may be how chronic viral infections in the tissues can remodel connective tissues. Bacteria also make their own connective tissue-degrading enzymes, which they utilize to "burn" holes through tissue so that they can spread and infect more areas of the body.
When I first caught my ME/CFS triggering Coxsackie B4 virus, it very quickly started to cause a number of connective tissue changes in my body: sudden onset receding gums, sudden onset skin wrinkling, and sudden onset pelvic girdle laxity. I detail my sudden soft tissue changes in this post.
In fact, one of the first areas of medical research I started reading about when my virus hit was connective tissue-degrading enzymes like MMPs.
So if there is a connection between hEDS and ME/CFS in terms of shared connective tissue symptoms, it may be these matrix metalloproteinase and neutrophil elastase enzymes which explain it.
But the difference between hEDS and ME/CFS is that the former is hereditary, whereas the latter is acquired usually after an episode of viral infection.
Last edited: