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

bread.

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Prolotherapy made my CCI worse and ME/CFS which had gone into partial remission resurface with a vengeance. Be careful with cervical Prolo.

Do you have an explanation for yourself why this could have worsened your condition? do you have eds or hypermobility?
 
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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.
This write up makes every kind of sense to me. It also (sort of?) renders something evident but not sure if I can insist. Looking back, I could identify a kind of slow-onset phase for my illness and later that same year, a rapid-onset event which rendered everything a lot worse. I remember the time around which I developed some energy difficulty and changes, and then I remember the acute event (very vividly) which then rendered my condition cognitively debilitating.

However, what if the event which brought on slow-onset symptoms was not ground zero for my ME/CFS but something in fact predisposed me to the onset? An accident, a fall, a condition which only manifested a decade later or more... Genotyping/phenotyping is complex and there are a lot of borderline conditions, all mutations and variations interact. What to make of the concept of "acquired" if it isn't "hereditary" but a notion that is borderline and tentative, a mix of nature and nurture, as several conditions already are?

This is just my way of thinking out loud. I'm also pretty sure I've read a few times (and recently on Dr Hyde's new write up) that ME patients will have had a history of "allergic precondition."

His description of "allergic precondition" is expressly interesting to me. I have a very long and evident history (going as far as childhood) of allergic reaction, hay fever, acne, flaking scalp (later), and seborrheic dermatitis.

In my opinion @Hip I think that even the "acquired" descriptor of ME/CFS requires that we maintain an analytical view of our past, beyond "slow-onset" or "rapid-onset" terms, that we truly appreciate the purpose of a potential "precondition" in Hyde's terminology.
 

Hip

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Looking back, I could identify a kind of slow-onset phase for my illness and later that same year, a rapid-onset event which rendered everything a lot worse.
There could be a number of reasons for that dual-phase onset. In my own case, I first developed pretty severe IBS around 9 years before being hit with virally triggered ME/CFS. That I believe was the first phase in my descent into ME/CFS.

My IBS I suspect was also pathogen-triggered, as I was perfectly fine one minute, and then I had constant severe diarrhea non-stop, along with a lot of fatigue, sudden-onset anxiety, increased allergies, and other symptoms which became permanent symptoms.

Then a few years later, I had a very unfortunate serious chronic exposure to pesticides, due to a major spillage of a bottle of pesticide in my home, which I was not aware of (otherwise I would have got the hell out of there). This brought some major symptoms of its own.

This was not yet ME/CFS though; that only hit many years later after a viral brain infection. But I think the IBS and pesticide exposure set the stage for the virus to trigger ME/CFS.

IBS is one of the most common comorbid conditions to ME/CFS, and I suspect it helps set the scene for ME/CFS to later appear. One study found 92% of ME/CFS patients had IBS in their lifetime (compared to 18% for healthy controls). And major exposure to pesticides has been shown in a Scottish study to increase the risk of later developing ME/CFS by a factor of 4.


In your case, the "slow-onset phase" you experienced could, for example, have been exposure to toxins such as mold or pesticides, which are both found to increase the risk of later developing ME/CFS. Or it could have been due to acquiring some new pathogen (virus or bacterium) — a pathogen which did not trigger full ME/CFS, but caused some minor fatigue etc symptoms to appear.

I caught the virus which triggered my ME/CFS from kissing on a date. And there is also a good chance I caught my presumed IBS pathogen from kissing as well, since I just started dating a new girl at the time the IBS first appeared. So it's pretty easy to pick up new pathogens.
 
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There could be a number of reasons for that dual-phase onset. In my own case, I first developed pretty severe IBS around 9 years before being hit with virally triggered ME/CFS. That I believe was the first phase in my descent into ME/CFS.

My IBS I suspect was also pathogen-triggered, as I was perfectly fine one minute, and then I had constant severe diarrhea non-stop, along with a lot of fatigue, sudden-onset anxiety, increased allergies, and other symptoms which became permanent symptoms.
The list of symptoms mirror my onset phase very closely, which comprised of returning from a trip abroad to find I was dealing with unpredictable IBS, increasing fatigue, need to hold my neck with hands while seated, reddish nodules between tops/soles of feet. Could a pathogen/enterovirus have been sexually transmitted regardless of the circumstances of my trip? Yes.

A stressful and new environment including harsh weather towards the Fall of the same year was my own breeding ground for contracting ME/CFS. I got ill while heading back to my dorm, started coughing harshly, and within seconds, developed a high-grade fever. I passed out on my bed and was eventually rushed out by an ambulance. Mono could not be detected by a viral test that was run that same day. I remember the doctor's exact phrasing. I remember him saying it was an unspecific viral reaction or something like that.

Maybe ME/CFS is not an illness which contends with latent or abortive infections at its core. Enterovirus can trigger a EBV reactivation. My IgG anti-EBNA titers tested differently over one year (first time they back negative, meaning it seemed as if I did not have antibodies for EBV; whereas in June these antibodies were detected). My EBV titers remained at 152-154 u/mL over the space of a year.

From my perspective (and since enterovirus is still not at the exact stage of being necessarily treatable though I have heard of the Rega compounds), testing for enterovirus could be useful, though it could also be very interesting to test for MMP9 levels, seek deeper neurological testing (since in the write up of Dr Hyde, this is essentially a disease which inflicts brain damage), and/or also look at other factors (my CRP fluctuated between <1 last year and slightly >5 this year).
 

Hip

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though it could also be very interesting to test for MMP9 levels
Yes, it would be interesting. Though none of the CCI positive patients have tested for MMP-9 to my knowledge, so it's not known if there is any relation between this connective-tissue degrading enzyme and CCI. I could not find any studies showing a connection either.

Furthermore, MMP-9 is not the only enzyme which can degrade connective tissue: there is a list of about two dozen different MMPs which do this (and another list here). So it may not be MMP-9 which is weakening the ligaments, but some other MMPs.

I read just now that the main collagen in ligaments is collagen type I (this paper says 95% of the ligament collagen is type I). So as a wild guess, possibly any MMP which can degrade collagen type I might be a suspect for causing CCI. MMP-1, MMP-2, MMP-8, MMP-13 and MMP-14 all degrade collagen type I.

According to those lists, MMP-9 only acts on the substrates: gelatin, elastin, collagen type IV, and collagen type V.

Then there is autoimmune attack on the ligaments, where the ligament can become thicker and weaker due to the inflammation (this is called pannus), which is a known mechanism of CCI. Pannus is found in the autoimmune disease rheumatoid arthritis. Because pannus swells as well as weakens ligaments, the enlarged ligament can press on the brainstem and cause brainstem compression.



At this stage, it's just pure guessing about how an infection might lead to CCI. Dr Henderson lists infection as one of the causes of CCI, but I could not find any info on the mechanism. So my guess is that MMPs are involved, but this is only pure speculation.

However it's interesting that in my CCI survey, around half the ME/CFS patients positive for CCI had a rapid onset to their ME/CFS (full-blown ME/CFS within days) after an acute infection. So infection often seems to be involved in CCI ME/CFS.
 
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However it's interesting that in my CCI survey, around half the ME/CFS patients positive for CCI had a rapid onset to their ME/CFS (full-blown ME/CFS within days) after an acute infection. So infection often seems to be involved in CCI ME/CFS.
Infection seems to play a role (additionally, reactivated or chronic). If I were to guess at this time, I would be inclined to say that for me, it was brought on over a sufficiently long stretch of time by, at earliest, a combination of trauma (physiological) and precondition (toxins).

I won't hide that I've done all the harmful stuff. I've gotten into accidents / falls and taken one or two knocks to the back of the head and then another at the front; there's a small forehead scar. I've ingested pesticides off of fruit and got badly poisoned (summer of 2006), and I've most likely caught one or two nasty pathogens over the years.

Thank you for the MMP resources. I can honestly only hope that whatever we're doing, some if it can reverse or undo the damage caused by whatever it is that is farther upstream: neuro-immune exhaustion, brain damage, virus. If I test for anything of note I will let you know. Not sure what's available to test here re: MMPs.
 
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What you find on Google of course is not automatically correct. You have to rely on authoritative sources, such as studies or systematic reviews published in high quality scientific journals. The prevalence figures I refer to come from such journals.





I am not assured by your opinion that there are no correct prevalence data for ME/CFS. Where are the facts and authoritative sources to support your view that the ME/CFS prevalence figures are not correct?





There are clearcut distinctions, and a good doctor who gives you all the right tests can distinguish between ME/CFS and other diseases with similar symptoms.

Hypermobile EDS you cannot mistake for ME/CFS, because the former involves measurable joint hypermobility, whereas ME/CFS does not involve hypermobility.
Well, in terms of ME or CFS not involving measurable joint hypermobility, lots of us do have hypermobile joints. Not enough to qualify for EDS, I don't think. But I am no expert in EDS. So maybe I am misunderstanding what you are saying. I do know some EDS patients and they are clearly not like me. One can't maintain enough stability to walk at all without injury.
I used to think I was limber, but before I got the standard post-viral diagnosis of M.E., I was told my joints were hypermobile. And the doc who treats me for POTS says lots of his patients pass the "palm to the floor" test. I assume that vascular issues play into all this. Like migraine, etc.

Please excuse me if I am not understanding your reasoning here.
 

Hip

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Well, in terms of ME or CFS not involving measurable joint hypermobility, lots of us do have hypermobile joints. Not enough to qualify for EDS, I don't think.
In order to qualify for a diagnosis of hypermobile EDS, your joints need to be mobile enough to get a score of at least 4 on the Beighton scale of joint flexibility. Plus you ave to satifiy other criteria. Here are the diagnostic criteria for hEDS.

Remember also that hEDS is something you are born with, whereas ME/CFS is something you acquire usually after a viral infection.

And hEDS is not a disease, it's a genetic feature. Many people with hEDS are perfectly healthy. Dr Bolognese in one of his videos points out that all the people in the Olympic gymnastics teams from any country are EDS people.
 

bread.

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In order to qualify for a diagnosis of hypermobile EDS, your joints need to be mobile enough to get a score of at least 4 on the Beighton scale of joint flexibility. Plus you ave to satifiy other criteria. Here are the diagnostic criteria for hEDS.

Remember also that hEDS is something you are born with, whereas ME/CFS is something you acquire usually after a viral infection.

And hEDS is not a disease, it's a genetic feature. Many people with hEDS are perfectly healthy. Dr Bolognese in one of his videos points out that all the people in the Olympic gymnastics teams from any country are EDS people.

Could you please point me to the paper or study that says hEDS is a genetic feature that you have to be born with?

I would be more than interested, as are many other hEDS patients.

(There is an ongoing study that looks for a genetic root cause for what you call a genetic feature, the chances they will find something are rather slim.)

Could you please point me to the paper or study that says that all gymnasts going to the Olympics have EDS or is that only what one neurosurgeon says?

How do you know that gymnasts with hEDS are perfectly healthy? Also, do you know the average age of the Olympics gymnasts' team?

According to your own standards, you should not say what you are saying here.

I will say it again the Beighton Score is an insufficient method to diagnose you with a systemic disease (what you call genetic feature) and is only used because of a lack of a biomarker, every specialist of hEDS and EDS will tell you so.
 

Hip

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Could you please point me to the paper or study that says
I've learn from previous discussions with you that you don't give any credence to scientific papers; you have your own opinions, and you won't let any pieces of scientific fact get in the way of them; so can you tell me, what benefit would arise from providing those papers?



But for the benefit of those here who do generally have credence in medical science, the NHS website describes EDS as "a group of rare inherited conditions that affect connective tissue."
 
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I've learn from previous discussions with you that you don't give any credence to scientific papers; you have your own opinions, and you won't let any pieces of scientific fact get in the way of them; so can you tell me, what benefit would arise from providing those papers?
There are no such papers that would secure your claims at this point in time, as you (probably) know.

It would be very easy to post the papers here, so why you do not? I would be glad to be proven wrong indeed.

There is absolutely no evidence that I do not give credence to any well planned scientific papers which makes your post questionable at best.

I want to say that I do not feel offended by your post.

EDIT:

You edited your second paragraph into your post. That is alright, does not prove you correct though:

hEDS is at this point not connected to any specific genetic variants, there are some ideas and small studies (that claim to have found variants), but no real proof yet, due to small sample size.

If you think otherwise, again, I would be happy to be convinced I am wrong by a study that has found specific gene variants. Personally, I think hEDS is a genetic disease, but there is no proof yet.
 
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Hip

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There are no such papers that would secure your claims at this point in time, as you (probably) know.
I have not looked at individual papers, so I don't know.

But when a science-based organization such as the NHS makes a statement on its website, that statement is a deeply considered one, based on surveying all the available scientific evidence. So a statement like the one on the NHS website that carries more weight and is better than any single research paper, and better even than a systematic review.



I don't know if you are aware that there are different levels or weights of scientific evidence:

A single study on a subject is called a primary source or primary study, and it the lowest level of evidence. As you know, when you get several primary studies examining the same subject, you may get contradictory results from one study to the next. This is why a single primary study is not considered very reliable.

Next up, in terms of weight of scientific evidence, is a systematic review, which is known as a secondary source, and is a study which examines the results of multiple primary studies, and sort of averages out the results of all the primary studies, and from the overall trend of all these primary sources, comes to a conclusion.

Finally you have tertiary sources, which include things like academic medical textbooks, encyclopedias, the NHS, NIH or CDC websites, that take all the available evidence, including multiple systematic review studies, and then state a considered conclusion about our current understanding of a subject.

So when the NHS or the NIH says EDS is an inherited (genetic) disease, that's the highest level of scientific evidence.



Incidentally, if you look at what the NHS says about ME/CFS, you see that they correctly state that:
It's not known what causes CFS/ME, but there are a number of theories – for example, it may be triggered by an infection, or certain factors could make you more likely to develop the illness.


If you want a recent systematic review study on EDS, then this paper says:
Ehlers-Danlos syndromes (EDS) are a clinically and genetically heterogeneous group of heritable connective tissue disorders characterized by joint hypermobility, skin hyperextensibility, and tissue fragility.

EDS were first described by Hippocrates in 400 BC as a condition with joint laxity and multiple scars.
 

Hip

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Sorry, my mistake: the above EDS paper I quoted is not in fact a systematic review (a systematic review is one which examines multiple primary studies and weighs up the evidence); but it is a review of the topic of EDS.