HOW on earth is EDS or any other CTD not the soil in which ME flourishes?

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But if they are the same disease, how would this EDS develop overnight like ME/CFS does for many of us? I didn't develop sudden onset symptoms, but many people have been perfectly healthy and then one day woke up with what turned out to be ME/CFS after catching some infection. It doesn't make sense to me.
It's a good point but i made an analogy with autism. How can one person who has autism be so damaged and yet another be highly functioning, yet they both have autism?
Further to that Bob Naviaux has suggested that cfs has similar genetic possibilities to autism. The austic people are damaged in the womb, the cfs people are damaged by life.
No one person is going to express eds the same.
Out of interest, did it come on all of a sudden? Mine did...sort of. I felt a vulnerability there all my life but i got through life ok, then very stressful job and bam!
Think of EDS as a spectrum disorder like autism. Thats why the disease gets expressed more easily in some than others. The actual merchanics of that remain a mystery.
 

andyguitar

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But if they are the same disease, how would this EDS develop overnight like ME/CFS does for many of us? I didn't develop sudden onset symptoms, but many people have been perfectly healthy and then one day woke up with what turned out to be ME/CFS after catching some infection. It doesn't make sense to me.
No it does'nt make sense. Neither does the fact that me/cfs in children often gets better and does not come back. For EDS to be the same as me/cfs someone will have to come up with an explaination as to why children recover from it.
 

JenB

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My one additional comment is that I don’t think it is useful to say “hEDS is/is not the same as ME/CFS.” That was not how the question was framed and no one is saying that. It’s a straw man.

Moreover, not all people with hEDS have ME and not all people with ME have hEDS. However, there is a striking degree of colinearity, as striking IMHO as POTS or MCAS.

Re: children, from an EDS lens, many possible reasons. One, they stiffen and become more stable with age until they start falling apart as adults (see 2019 Bolognese talk). Two (in the case of boys, who are much more likely to recover) testosterone. Testosterone is associated with muscle mass, which help stabilize joints. Estrogen is associated with weaker ligaments/connective tissue.
 
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For a start, please just tell me a percentage of your symptoms that are not directly or indirectly connected to your connective tissue!
I' ve become convinced this is a key feature of: the decline our bodies . I am heteoZ for EDS supposedly. No fingerprints, likely have lower brain stem collapse. Sure feels likely.

These issues are somehow intimately related. and If connective tissue and collagen convey Qi, which I believe they potentially do, its further shows the connection between these forms of body processes and affiliated breakdown and impairment in proper body functioning.

They sure should be SURE more interested in Collagen Processes.
 
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For EDS to be the same as me/cfs someone will have to come up with an explaination as to why children recover from it.
I was a child, who recovered from :Eppstein Barr....four times at least. (at 10, 13, 15, and 22). When I was ten, I returned to school after being out for SEVERAL WEEKS at least, but was restricted from PLAYING at RECESS. Not restricted from: MATH.

At 66: nothing is recovered.

So I'm not convinced- if these children are recovering from viral infections...and have post viral fatigue..it simply might take more TIME, more subsequent STRESSORS, more toxin exposure (inevitable in current world)...and it probably takes a long time to: digest one's own muscle and collagen.
 
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My one additional comment is that I don’t think it is useful to say “hEDS is/is not the same as ME/CFS.” That was not how the question was framed and no one is saying that. It’s a straw man.

Moreover, not all people with hEDS have ME and not all people with ME have hEDS. However, there is a striking degree of colinearity, as striking IMHO as POTS or MCAS.

Re: children, from an EDS lens, many possible reasons. One, they stiffen and become more stable with age until they start falling apart as adults (see 2019 Bolognese talk). Two (in the case of boys, who are much more likely to recover) testosterone. Testosterone is associated with muscle mass, which help stabilize joints. Estrogen is associated with weaker ligaments/connective tissue.
Jennifer, is Dr Ron Davies vey aware of this?
 
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My one additional comment is that I don’t think it is useful to say “hEDS is/is not the same as ME/CFS.” That was not how the question was framed and no one is saying that. It’s a straw man.
I appreciate that you aren't saying this, but others are, so it's not a straw man per se.

And no, they are definitely not “the same disease.” They are each on their own probably a collection of many different conditions/subtypes.
I am glad you clarified your position, because from your newsletter I definitely got the impression that what you were saying was that there was no ME/CFS as a distinct condition at all, just a bunch of misdiagnosed conditions being diagnosed as ME/CFS. You didn't directly say this, but I understood it to be the logical implication of what you explained. My sister undersood it the same way.


Isn't the age of onset enough to differentiate though?

I understand that hEDS symptoms are present in childhood. Whereas ME/CFS is something that only appears at a particular point in your life, usually triggered by viral infection, before which you were healthy.


I think it is of great interest when two diseases manifest very similar symptoms, and worthy of full investigation, because if the symptoms are the similar, it's possible there may be shared pathophysiology.

However, I don't think there is any reason to assume that ME/CFS and hEDS are the same disease, just as there is no reason to assume that ME/CFS and celiac are the same, in spite of the fact that people with celiac are sometimes misdiagnosed with ME/CFS.
It’s definitely not as clear-cut as that. Some of it is the fuzziness around the hEDS diagnosis. There are plenty of people who have generalized joint hypermobility and no debilitating symptoms until they get a virus or other trauma and then start dislocating, and develop POTS, and then PEM. That’s a common story, as well as many presumed “de novo” cases of hEDS w/o family history. I’ve started engaging with PWhEDS about this and it’s clear there is no agreement about this among patients (which means clinicians also differ). Many people who don’t meet hEDS criteria say they have it b/c they have other features, etc. I don’t think anything is going to be clear until a gene or genes are found, and even then, it is unlikely to account for everyone in that diagnostic category.
Unfortunately, regarding age and onset patterns, Jen is correct. My doctor told me that EDS can suddenly worsen after a virus, car accident, or so forth.

On the other hand, I have both and they seem clearly different to me. They don't seem like the same disease at all. They have different stuff that makes them better or worse. The only part where it gets confusing is where there is some symptom overlap (such as dysautonomia and ill-defined GI issues/IBS).

However, there's enough that doesn't overlap that it doesn't seem confusing at all to me, that they seem to me to be two different, unrelated diseases that I have the misfortune to have both. I have a lot of family that has EDS-y stuff and hardly any of them are ME-type ill.

However because of reading posts here and elsewhere, I keep an open mind that I could be wrong and maybe they're more related than I think. I am just n=1. Or n=(some other small number) if we count my family.


There are a lot of discussions like these happening on social media/Twitter and most of my thoughts have already been laid out on Medium.
I appreciate that you feel overstretched, but I can't follow tons of different places and I suppose that others are like me. Maybe if you could post a specific link to a Medium post instead of citing an entire website or three?

However, as all the symptoms of ME can be caused by CCI and cervical stenosis, the former of which is associated with hEDS. That could be one explanation for the overlapping symptoms.
Moreover, not all people with hEDS have ME and not all people with ME have hEDS. However, there is a striking degree of colinearity, as striking IMHO as POTS or MCAS.
As interesting as it is, it doesn't matter how much the symptoms appear similar to some other disease. This is a phenomenon that exists throughout medicine. Lupus looks like every other disease known as well, just as an example. Lupus and Lyme disease are both called "the great imitator."

It's needful to look for what is unique and different, in order to diagnose stuff. That's one of the major problems with "fatigue:" it is not distinguishing. One needs to seek out the things that are distinguishing.


Naviaux (published) + Severely ill patient study (unpublished)
https://www.me-pedia.org/wiki/Hydroxyproline

There’s a third researcher who said his published metabolomics findings had implications for collagen. More to come on that.

If 50% of patients truly meet hEDS criteria, then of course these results would be confounded, unless they were found in both ME patients who do and do not meet hEDS criteria. No one has been designing their studies to ask that question, so no one knows.
You're talking about 50% of severly ill patients here, not 50% of all patients. I think it's important to be precise. We already suspect that more severely ill people have more comorbidities, for example
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1890280/
(we can probably safely assume that some of the fibromyalgia diagnoses should be instead diagnosed with some kind of EDS, possibly hEDS)


I
did two online polls and got about 60-80% of people saying “yes” they had post-onset changes.
You probably are aware of this, but after months of talking about Nightengales and CII and so on, a poll done by you is going to be highly skewed to people who think that these diseases have some kind of unique relevance to each other (morso than other comorbidities or other diseases that share symptoms).

I agree that it's good to have neglected diseases working together, but I think it's really premature to say that there's some logical grouping of some particular set of diseases.

Yes, I think it's great and needed to look into whether collagen disorders are related to ME, especially as there seem to be some findings that this could be important, or there could be a subset for whom this is relevant.

But of course it still could be something else. An autoimmune disease (more relvance to Lupus), a channelopathy (more relevance to myasthenia gravis). Or maybe it's most closely related to multiple sclerosis, or to mitochondrial or glycogen storage diseases.

At this point, most any option is valid. (Obviously not the hypochondriac/ deconditioning stuff, but just about anything else.)

And yes, ME/CFS can explain CT changes (more than skin) in anyone who has a) sudden onset changes and b) sudden onset MCAS. At least, I think that’s plausible. I’m sure you’ve already seen this, but: https://www.me-pedia.org/wiki/Collagen
What I don’t know about is muscle fatigability, as that’s not in the ICC.
If you haven't accounted for skin changes and muscle fatiguability, then you aren't able to say you can't differentiate EDS and ME.

sorry for the huge text; I didn't want this bit lost at the end of a long post.
 
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My one additional comment is that I don’t think it is useful to say “hEDS is/is not the same as ME/CFS.” That was not how the question was framed and no one is saying that. It’s a straw man.

Moreover, not all people with hEDS have ME and not all people with ME have hEDS. However, there is a striking degree of colinearity, as striking IMHO as POTS or MCAS.

Re: children, from an EDS lens, many possible reasons. One, they stiffen and become more stable with age until they start falling apart as adults (see 2019 Bolognese talk). Two (in the case of boys, who are much more likely to recover) testosterone. Testosterone is associated with muscle mass, which help stabilize joints. Estrogen is associated with weaker ligaments/connective tissue.
Yep, if i've overstated the case for emphasis, then i'm saying there is too much similarity for these 2 diseases, if it is two diseases not to be related. I can't believe its not been picked up by scientists until recently. It's so flamin obvious!
I wrote to the Open Medicine Foundation to look at the work of Liz Parrish. She's working with telemores and stemcells and has increased her own muscle mass and tissue strength by doing so. The people filtering info at OMF said stem cells weren't the way forward (i'm thinking they are deeply entrenched in the metabolic trap hypothesis) But surely stem cell therapy and regenberative medicine are going to be the way forward for victims of collagen loss and weak structures?
Prolotherapy can also be a way to stabilise neck ligaments..i hope the team know about these options
 
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But surely stem cell therapy and regenberative medicine are going to be the way forward for victims of collagen loss and weak structures?
It might depend on why the collagen loss is happening and how widespread it is.

In a genetic disease like EDS, this is baked into the genes and is in or near (supporting, or so on) virtually every tissue in the body.

Cells regularly die and get replaced. When they do, new cells are made with a copy of the original genetic information (or at least whatever the cells around previously had).

Stem cell therapy is more useful to regrow something like a tooth, that's localized to one place and where the original genetic information is intact (or good genetic information can be somehow supplied). Maybe someday it will be possible to do something as complex as a kidney.

When cells grow, they require signals to tell them what kind of cell to develop into. So you need either cells that already know what kind of tissue they are (differentiated) or you need undifferentiated tissue (pluripotent) but need to know how to tell it what kind of cell to be (or hope it works it out itself, but it usually doesn't do perfect at this presumably because the body is no longer developing). Scientists don't know how to make the signals (it's extremely complex, and the various signals are not all known).

Collagen makes up a lot of diverse tissue that's widely distributed, and would have to be from many cell types or recieve many different types of instruction sets.

Additionally, it would have to be redone every time there was cell turnover.
 
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It might depend on why the collagen loss is happening and how widespread it is.

In a genetic disease like EDS, this is baked into the genes and is in or near (supporting, or so on) virtually every tissue in the body.

Cells regularly die and get replaced. When they do, new cells are made with a copy of the original genetic information (or at least whatever the cells around previously had).

Stem cell therapy is more useful to regrow something like a tooth, that's localized to one place and where the original genetic information is intact (or good genetic information can be somehow supplied). Maybe someday it will be possible to do something as complex as a kidney.

When cells grow, they require signals to tell them what kind of cell to develop into. So you need either cells that already know what kind of tissue they are (differentiated) or you need undifferentiated tissue (pluripotent) but need to know how to tell it what kind of cell to be (or hope it works it out itself, but it usually doesn't do perfect at this presumably because the body is no longer developing). Scientists don't know how to make the signals (it's extremely complex, and the various signals are not all known).

Collagen makes up a lot of diverse tissue that's widely distributed, and would have to be from many cell types or recieve many different types of instruction sets.

Additionally, it would have to be redone every time there was cell turnover.
Thanks for the info
So gene therapy could be a possibility, Crispr or relengthening telomeres to reverse where are bodies were at in the ageing process might be a possibility.


Liz Parrish in the above link has experimented on herself with increasing muscle mass and biological and metabolic signs of ageing. I trust the womans motives as she came to this to try and cure her son's type 1 diabetes
 

JenB

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The best I can do @Foxglove is point you here https://link.medium.com/5pVq7N93wZ and say take a look at the theory section.

There are some intensive, ongoing discussions on Twitter with people with hEDS and co-morbid hEDS & ME. Also in the ME/CFS CCI FB Group, where many pwme are now getting hEDS diagnoses. However the latter is not for debate or discussion but geared more toward people actively pursuing structural diagnoses.

We all have to pick which platforms we are active on and wish I had more time to write here. I will check in here when I can.
 
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I appreciate that you aren't saying this, but others are, so it's not a straw man per se.


I am glad you clarified your position, because from your newsletter I definitely got the impression that what you were saying was that there was no ME/CFS as a distinct condition at all, just a bunch of misdiagnosed conditions being diagnosed as ME/CFS. You didn't directly say this, but I understood it to be the logical implication of what you explained. My sister undersood it the same way.






Unfortunately, regarding age and onset patterns, Jen is correct. My doctor told me that EDS can suddenly worsen after a virus, car accident, or so forth.

On the other hand, I have both and they seem clearly different to me. They don't seem like the same disease at all. They have different stuff that makes them better or worse. The only part where it gets confusing is where there is some symptom overlap (such as dysautonomia and ill-defined GI issues/IBS).

However, there's enough that doesn't overlap that it doesn't seem confusing at all to me, that they seem to me to be two different, unrelated diseases that I have the misfortune to have both. I have a lot of family that has EDS-y stuff and hardly any of them are ME-type ill.

However because of reading posts here and elsewhere, I keep an open mind that I could be wrong and maybe they're more related than I think. I am just n=1. Or n=(some other small number) if we count my family.



I appreciate that you feel overstretched, but I can't follow tons of different places and I suppose that others are like me. Maybe if you could post a specific link to a Medium post instead of citing an entire website or three?



As interesting as it is, it doesn't matter how much the symptoms appear similar to some other disease. This is a phenomenon that exists throughout medicine. Lupus looks like every other disease known as well, just as an example. Lupus and Lyme disease are both called "the great imitator."

It's needful to look for what is unique and different, in order to diagnose stuff. That's one of the major problems with "fatigue:" it is not distinguishing. One needs to seek out the things that are distinguishing.



You're talking about 50% of severly ill patients here, not 50% of all patients. I think it's important to be precise. We already suspect that more severely ill people have more comorbidities, for example
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1890280/
(we can probably safely assume that some of the fibromyalgia diagnoses should be instead diagnosed with some kind of EDS, possibly hEDS)


I
You probably are aware of this, but after months of talking about Nightengales and CII and so on, a poll done by you is going to be highly skewed to people who think that these diseases have some kind of unique relevance to each other (morso than other comorbidities or other diseases that share symptoms).

I agree that it's good to have neglected diseases working together, but I think it's really premature to say that there's some logical grouping of some particular set of diseases.

Yes, I think it's great and needed to look into whether collagen disorders are related to ME, especially as there seem to be some findings that this could be important, or there could be a subset for whom this is relevant.

But of course it still could be something else. An autoimmune disease (more relvance to Lupus), a channelopathy (more relevance to myasthenia gravis). Or maybe it's most closely related to multiple sclerosis, or to mitochondrial or glycogen storage diseases.

At this point, most any option is valid. (Obviously not the hypochondriac/ deconditioning stuff, but just about anything else.)




If you haven't accounted for skin changes and muscle fatiguability, then you aren't able to say you can't differentiate EDS and ME.

sorry for the huge text; I didn't want this bit lost at the end of a long post.
Jennifer wrote a great piece here which basically encapsulates my feelings on what i understand is going on as a layman
https://medium.com/@jenbrea/are-a-subset-of-us-members-of-a-lost-tribe-ee8942f35577
 

JenB

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And I agree muscle fatigability is really important but it’s not included in the ICC, nor is it required in the CCC, even though Ramsay thought it should be a required symptom. My polls aimed for better or worse to make use of the diagnostic instruments we have. They are not science but they can be useful for prototyping ideas.

I am also not saying it’s impossible to distinguish between ME and hEDS: these are very different diagnostic criteria and it’s very clear that I meet (or rather, used to meet) one in spades and the other, not by 1000 miles. Rather that for two people who meet the ICC, it’s impossible to say that one person’s ICC symptoms constitute “true ME” while another’s is caused by hEDS and is somehow “not ME.” Of course there are many many PWhEDS who do not meet ICC or have PEM (but a much greater than expected number who do).

The “do you meet the ICC?” question was geared toward PWhEDS.

The skin change question was asked separate and geared toward PWME only.


I have very deep training in statistics and am very aware of the biases of social media polls.

The Navaiux study used a different sample than the Severely ill patients study and included mild and moderate patients (is my understanding).

EDIT: and I believe the “50% of PWME have hEDS” is Ron Davis paraphrasing Dr. Kaufman’s estimate of his own practice. I would need to check in with Dr. Kaufman to confirm. There is obviously nothing published. And what I was trying to say is that the elevated hydroxyproline findings could be universal, or they could be an artifact of so many PWME having hEDS, and have nothing to do with ME at all (at least not directly). No studies subset between PWME w/ hEDS and PWME w/o.
 
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Gingergrrl

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And I agree muscle fatigability is really important but it’s not included in the ICC
I apologize for butting into this thread on page 5 (and my question is not geared toward JenB even though I am quoting her). I am confused to read that the ICC Criteria does not include muscle fatiguability?! Is this correct?

I recently started another thread after I learned that the ICC includes "ion transport issues" (because that really surprised me). But I assumed for sure that the ICC included muscle fatiguability... Isn't that at the core of ME/CFS? If it's not, then it definitely reinforces that I was not (initially) properly diagnosed b/c progressive muscle fatigue and muscle weakness were absolutely core symptoms for me prior to treatment.

Interesting thread.
 

JenB

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I apologize for butting into this thread on page 5 (and my question is not geared toward JenB even though I am quoting her). I am confused to read that the ICC Criteria does not include muscle fatiguability?! Is this correct?

I recently started another thread after I learned that the ICC includes "ion transport issues" (because that really surprised me). But I assumed for sure that the ICC included muscle fatiguability... Isn't that at the core of ME/CFS? If it's not, then it definitely reinforces that I was not (initially) properly diagnosed b/c progressive muscle fatigue and muscle weakness were absolutely core symptoms for me prior to treatment.

Interesting thread.
I think it may be more accurate to say that it includes but does not require
 

Gingergrrl

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So not required in CCC, not described ICC at all (I think)
All of these different criteria are so confusing to me so I can only imagine how it must seem to the outside world to sort it all apart. I don't want to take this thread off-track and maybe I will copy your post above to my thread re: ion transport issues being part of the ICC Criteria. That shocked me but I think muscle fatiguability not being part of the ICC Criteria shocks me even more!
 

percyval577

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I think we must be logical pretty precise. The difficult to grasp CFS symptoms may be neurological, esp. delayed PEM and the possibility of pacing, whereas CCI and EDS are tissue diseases. It might be like so:

--------------> CFS symptoms -------------->
comorbidities...............................................................................................comorbidities
<----(maybe other parts/units of the body ) <----

EDS or CCI are - at least so far - a comorbidity, and obviously there can be relationships, and they can even be so strong - as it seems ATM - that an influence on them may heal CFS.

But this does neither say, that CFS would have been caused by say CCI - it could be the other way around, and due to the circle a surgery is a good influence - nor does it deny that there might be other influence in other PwCFS (or perhaps even in the same).

If we say that CFS must be - in an underlying manner - caused by EDS or CCI (b/c of the encouraging successes of CCi surgery), it might be also discouraging or misleading for other ppl.

There have been reports that ppl have been substantially improved from CBT (though the most detoriated). WHY? How is it possible? Maybe these ones who have major psychological problems and got sick from viruses can evade the effects of the triggering event by inducing some changes in XY(and these ones who havn´t major psychological problems, can´t -). A member recently told that she (former he) would have recovered from changing the biological sex, thereby probably inducing changes in XY.

This must be taken into account. Maybe they had CCI? Maybe you can heal your EDS supported CFS but not your EDS?
 
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