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EDS and ME - is there a connection?

Discussion in 'Fibromyalgia and Connective Tissue Disorders' started by Jonathan Edwards, Jan 20, 2018.

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  1. Sly Saint

    Sly Saint Senior Member (Voting Rights)

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    Article by someone with both EDS and ME:
    Mast Cells & Collagen Behaving Badly
    My journey with Ehlers-Danlos Syndrome, M.E. & Mast Cell Disease

    "Following on from my blog post on Types of Fatigue I was asked by one of my followers to do a post on the various types of pain I experience. When I was healthy I, like most people, had only ever experienced short-term acute pain for which an end was in sight and had no idea how difficult living with a chronic pain condition could be. Pain, like fatigue, is often talked about as a single entity but there are lots of different types of pain sensations which are often difficult to describe, but I’ve given it a bash below."

    https://mastcellblog.wordpress.com/tag/hypermobility/
     
    Stuart, Justy, Binkie4 and 1 other person like this.
  2. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    An interesting history @Michelle. The detail you give allows me to get a pretty good idea of the biomechanics over 20+ years. And with that detail the 'diagnosis' of EDS does not actually add anything. (I will come back to that.) An unlucky bimalleolar fracture can produce lifelong disability, especially if there are knock on biomechanics effects on other joints. No need for a paediatrician to talk of growing pains.

    I think it is very plausible that muscle disuse can contribute to joint instability after a period with ME. But that would be biomechanically distinct from joint laxity based on ligaments, which is the basis of mobility in EDS, although the consequences may overlap.

    I am tempted to think that maybe a number of PWME develop joint instability from reduced muscle use. That would not be EDS, it would be the effect of ME.

    I think we can exclude that. Loss of blood supply to a joint does not lead to laxity or instability. If it leads to anything it would be death of cartilage with arthritic change that is very obvious. These things are not difficult to work out from examining patients. The problem is that most rheumatologists know almost nothing about joint physiology. I tried to get questions on this included in proposed final rheumatology exams but my colleagues said it was too technical and science based!!

    That seems to me a pity - you were let down. I see no reason why a specialist properly trained in joint biology could not have given you a detailed explanation of what was going on and what to expect. And there would be no real need to use the term 'EDS' as we probably agree. BUT, without that luxury it makes sense that a name provides some sort of handle that at least appears to provide a justification for problems in the social context.

    I guess what worries me is that using EDS as a justification for problems that are actually part of ME itself runs the danger of perpetuating the underrating of the importance of ME itself as a source of disability. Nancy Klimas is supposed to have said that ME is worse than AIDS. I am not sure about that but I am pretty sure it is much more disabling than hEDS. I have a feeling that doctors providing the EDS label are really doing the ME cause no favours. ME is the big problem.
     
  3. Skycloud

    Skycloud Senior Member (Voting Rights)

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    Interesting thought. So this is one of the things I'm wondering now about my sister; it might make an alternative sense of her problems. I could do with asking her more questions.

    I'm a bit shocked!
    However, it took a third rheumatologist to look at my sisters x-rays to see she has hip dysplasia, both hips. I suppose they weren't expecting to see it in someone in their 40's and/or they didn't know well enough what normal looked like.
     
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  4. MsUnderstood

    MsUnderstood Senior Member (Voting Rights)

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    @Andy , @Amw66 , @Barry , @Binkie4 , @Invisible Woman , @Inara , @MErmaid , @MeSci , @Mij , @ScottTriGuy , @Trish

    I'm responding here (rather than on my original thread -- hence, the "tags" above) because this is where the bulk of the EDS discussion has taken place. I'm just back from an interesting appointment at the genetic clinic.

    Once again, I was impressed with the young doctor (late 30's, perhaps) involved in my evaluation. He seemed to respect my medical knowledge, and expressed confidence in the ability of informed patients to self-diagnose using Doctor Google. Although aware of ME, he admitted not knowing much about it. He gave no indication that he perceives ME as other than a genuine physiological illness.

    First, he confirmed my internist's suspected diagnosis based on medical history and a physical assessment (eg. hypermobile joints; body components that collapse in ways they shouldn't; and soft, stretchy skin). However, he doesn't call conditions like mine Ehlers-Danlos. He prefers to think of what has traditionally been called Ehlers-Danlos Syndrome Hypermobility (hEDS) as falling somewhere along the "hypermobility spectrum".

    Whereas other (true?) types of EDS each have a genetic test that identifies a single gene that is responsible for the connective tissue defect, no single gene has been found for hEDS (terminology used here for simplicity). He said that during the past several years, numerous advanced labs around the world using sophisticated gene sequencing equipment have looked, but have not found a single gene. This does not mean that the cause isn't genetic. Rather, the current belief is that hEDS is caused by a number (perhaps hundreds) of genes. He assured me that researchers are still working on the problem.

    This doctor said there is enough evidence involving familial symptom clusters to definitively say something is happening in these patients. He confirmed what patients already know -- that hypermobility often occurs in those with mast cell issues and autonomic problems (POTS, NMH, BP, HR, temperature control, etc.) The link is apparent regardless of where (from which medical issue) the investigation starts.

    For me, it was deemed unnecessary to actually do genetic testing since it is unlikely a single-gene cause would be found. The doctor apologized that he could offer nothing beyond what I am already doing to manage a very complex collection of medical issues. Regardless, I considered the appointment worthwhile, and left glad to have had the opportunity to consult with such a kind and compassionate man.
     
  5. Binkie4

    Binkie4 Senior Member (Voting Rights)

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    @MsUnderstood
    I think most of us can tolerate disappointment or lack of progress when treated with kindness and compassion. And I'm glad he treated ME as nothing but a physiological illness.
     
  6. Inara

    Inara Senior Member (Voting Rights)

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    @MsUnderstood, that sounds very interesting and informative, thank you!
     
  7. chrisb

    chrisb Senior Member (Voting Rights)

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    Shouldn't the title be "EDS and ME-is there a loose connection?"
     
  8. Barry

    Barry Senior Member (Voting Rights)

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    Now there's a bit of dark'ish humour for you!
     
  9. Karen S

    Karen S Established Member

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    I became ill after a virus in 1990 and was diagnosed with M.E in 2003. However, some of my symptoms were not linked to M.E as life progressed nor some symptoms prior to 1990. It is now obvious I have EDS (prob type 3 now known as HEDS) and I have an appt in April to confirm which type. They are not the same thing. I suspect people with EDS get overlooked as I did with all symptoms being linked to M.E. It is possible to have both. HEDS and Joint Hypermobility Spectrum Disorder are not the same thing either. There is a good book published by Redcliff that explains the differences between HEDS and JHSD. Unless someone with M.E has easy bruising, skin that tears and is stretchy and has multiple ligament/tendon/muscle tears as well as hypermobility, they are unlikely to have EDS.
     
  10. Sly Saint

    Sly Saint Senior Member (Voting Rights)

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    I'm not posting this because I am a disciple or follower of Dr Hyde but because not having any knowledge on the subject, I would like some idea of how much of the info is true or feasible.

    He writes:

    "
    The possible role of genetic susceptability in M.E.-like patients
    Ehlers Danlos Syndrome (EDS)
    One of the more severe forms of acute onset vascular M.E. is Ehlers
    Danlos Syndrome. There is not one Ehlers Danlos Syndromes but at
    least 8 varieties. Some cause such severe anatomical and physiological
    changes that the child does not survive infancy. Probably each of the
    EDS variants are all genetic based illnesses although I have never seen
    a genetic study published on each of the subtypes. One of these EDS
    subtypes is important in any discussion on the subject of M.E., which I
    will now briefly outline.
    I have only seen Ehlers Danlos in women. Their illness tends to be
    severe and often misdiagnosed. Whether this is a variant of M.E. only
    time will tell but if it is not it should be placed in this group for the
    moment. The patient usually falls ill sometime after the age of 16-18.

    Up until this moment there is no indication of any M.E. or CFS like
    abnormality. It is possible they may have previously been diagnosed
    with hyper-reflexia or as a child they may have amused their friends
    by their double joint manifestations. Probably all EDS have abnormal
    connective tissue in their blood vessels. These patients all seem to have
    fallen ill immediately after an untyped infectious episode or following
    an immunization. I believe these women have a genetic disease and it
    is either turned on by a specific virus or alternatively by some aging
    trigger.
    These hyper-reflexive EDS patients tend to be light sensitive, and
    suffer from severe Dysautonomia with one or more of the following:
    POTS (orthostatic tachycardia syndrome), IST (inappropriate sinus
    tachycardia, and NMH (neurally mediated hypotension).

    Marfan Syndrome
    Marfan syndrome in its extreme form is quite easy to recognize and is
    due to an inherited genetic trait of the connective tissue. The classical
    Marfan patient is a tall thin, thin-headed individual with long limbs
    hands and fingers and long narrow feet. In the extreme form the
    patient develops severe aortic and valvular pathology that today can be
    replaced where previously many of these patients died before reaching
    20-30 years. These patients are easily recognized by their parents and
    their physicians. Wikipedia has an excellent review of the pathological
    findings in these extreme patients.
    Our problem is not the classical easily diagnosed Marfan individual but
    in the wide variety of expression of this genetic illness. These milder
    disease forms of patients often are missed and not diagnosed as Marfan
    syndrome but present with a history of gradual onset fatigue syndromes
    and as with its close cousin, Ehlers Danlos Syndrome they should be
    considered in the differential diagnosis
    In my patient physical examination check-list, I have a triad of
    progressive illnesses. Hyper-extensive syndrome, Ehlers Danlos and
    Marfan disease. All three are associated with fatigue syndromes and
    dysautanomia. The three are not related but they do form a progressive
    cause of the dysautanomia family of pathologies. My check-list of
    Marfan features is as follows:"

    taken from http://www.hfme.org/Other/DefinitionBooklet_Sept_2011.pdf

    if it is a load of twaddle I will gladly delete it.:)
     
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  11. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    I would not delete it because it is of interest. However, it is twaddle, or pseudoscience. It is completely unsubstantiated by any reliable observations and in places is actually incoherent, or at least plain wrong.

    I am unclear where all this guff originates from but it has clearly been around for at last fifteen years, probably more like twenty five. There was none of it in 1979.

    What intrigues me is that the literature on EDS and putative associations with POTS and 'MCAS' in general says nothing at all about ME or CFS. There is talk of pain but not specific ME symptoms. Even the cover of the Redcliffe book does not mention fatigue and it mentions just about everything else.
     

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