Is ME due to Ehlers-Danlos Syndrome "stretchy veins"

Thansk to Janet for this 2013 article abstract which made me think - skin is so important in temperature regulation
Perhaps some skin defect also affects us cauing our cold intorlearnce an contributing to heat intolerance - just guess ing here.

2013 May 15. doi: 10.1111/jcmm.12060. [Epub ahead of print]

Mechanobiological dysregulation of the epidermis and dermis in skin disorders and in degeneration.
Ogawa R, Hsu CK.

Source
Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, Japan.

Abstract
During growth and development, the skin expands to cover the growing skeleton and soft tissues by constantly responding to the intrinsic forces of underlying skeletal growth as well as to the extrinsic mechanical forces from body movements and external supports.

Mechanical forces can be perceived by two types of skin receptors: (1) cellular mechanoreceptors/mechanosensors, such as the cytoskeleton, cell adhesion molecules and mechanosensitive (MS) ion channels, and (2) sensory nerve fibres that produce the somatic sensation of mechanical force.

Skin disorders in which there is an abnormality of collagen [e.g. Ehlers-Danlos syndrome (EDS)] or elastic (e.g. cutis laxa) fibres or a malfunction of cutaneous nerve fibres (e.g. neurofibroma, leprosy and diabetes mellitus) are also characterized to some extent by deficiencies in mechanobiological processes.

Recent studies have shown that mechanotransduction is crucial for skin development, especially hemidesmosome maturation, which implies that the pathogenesis of skin disorders such as bullous pemphigoid is related to skin mechanobiology.

Similarly, autoimmune diseases, including scleroderma and mixed connective tissue disease, and pathological scarring in the form of keloids and hypertrophic scars would seem to be clearly associated with the mechanobiological dysfunction of the skin.

Finally, skin ageing can also be considered as a degenerative process associated with mechanobiological dysfunction.

Clinically, a therapeutic strategy involving mechanoreceptors or MS nociceptor inhibition or acceleration together with a reduction or augmentation in the relevant mechanical forces is likely to be successful. The development of novel approaches such as these will allow the treatment of a broad range of cutaneous diseases.

Published by Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

 

You know those pics of EDS people where they lock their knees and their calf bends out backwards in a sort of arc? Well, both my husband and oldest son have that. In fact my oldest son raised a few eyebrows as he began walking and his legs bent back like that. (He's the one with failure to thrive until he was 4 and now has type 1 diabetes)
It makes me wonder if both my husband and I carry a gene and if so what that means for the kids...

I note that failure to thrive (my oldest son and my 5th child both had this - my dd nearly died) and EDS are linked.
FtT is also linked with type 1 diabetes. and autoimmune is sometimes linked with EDS too. What a tangled web. But what an interesting one.

I will have to see what happens.

 

I lock my knees too, I can't even stand normal because my legs are too weak, they start to buckle if I don't lock them.

 

Allyson, I was wondering about a few medical issues and illnesses if they are EDS related. Are anueurysms in arteries related? My uncle had one, but he's morbidly obese so it could just be from obesity. He also had very poor blood circulation in his legs, could be POTS but in his case more likely due to obesity.
My mother got disease of Ledderhose, Raynaulds phenomenon, poli neuropathy, had surgery for bursitis, prurigo, artrosis, osteoporosis (I read somewhere it is linked to EDS, I got it as well and my father and his sister too), glaucomia, cornia dystrophia, cataract and scorliose (I used to have it before I broke my back, but it got straightened out by breaking my back it seems). She got a few other things but don't think it's related (no article mentioned the other things)
We had a lot of people die of heart failure, but all at an old age and one was a heavy smoker and another was a heavy smoker and obese. We had one ancestor die young of a stroke. And one ancestor who was very ill and had a 'weak constitution' as they called it back then but we don't know what she had.

 

Hey VM

Yes most of those are CLASSIC symptoms
scoliosis
aneurysms
Reynauds
eye problems

also soft skin
bursitis yes i have read - and i have wrist gangions too
have not read about osteoporosis but cannot see why not as bone is mostly? all/ connective tissue
as is lymph - hence perhaps immune involvement.
they are encouraging EVERY one now with ANY type of EDS to get a cardiac utrasound as a matter of urgency to detect potential cardiac issues - esp i think problems in aortic arch - and with your family histroy i would get one pronto.
Yes often wonder about all those people you read about with "sickly disposition" in the past. poor things.
We are so lucky to have the internet to connect with others

Once we may have been burned as witches..... is that over yet?


I have not forgotten the walking tips you requested above - brain fog today but will ge to it

I think you said you are booked in for a genetics appraisal?

Keep us posted on how it goes if so. Good idea.

Cheers
Ally

 

re obesity - my own personal theory is that it may result from the inactivity EDS causes


makes a lot of sense - and leads to type 2 diabeties too

both my mother and granmother had both

and famliy history is very important in diagnosis of EDS - like all genetic diseases.


my doc thought with EDS we are just seeing the tip of the iceberg - it is widely uneeridagnosed so lots of people could have it and not know and type 2 diabeties is endemic ATM'

anyway in about 2 years they wil have gentic test for this so good to be on the books already when that happens

And the more people they see with it the more seeriously they will take it and the more research will be done.

A

 

my sister has scoliosos. She has a bar cemented down her spine to straighten it.
Both my parents were very overweight and these days dad would be labeled obese. The massive rise in obesity and type 2 diabetes is one of those areas where politics are at play. Sad how powerful groups in both pharma and farming can block progress.
There are apparently only 3 EDS specialst centres on the UK.

I hope they'll get a clear, straight forward and cheap test for this soon.

 

Shell i read th atscoliosis occurs because th ligaments and tendons around the spinea re too strethy so spine does not for m straight - sounds feasible

yes i suspect that as this ilness is widely underdiagnosed there may be a strong link to obesity that is not realised due to the inability to exercise among other things....leading in turn to type 2 diabeities.


Professor Rodney Grahame is at University College Londonn and is supposed to be excellent for EDS.

 

"Causes of dysautonomias are not fully understood, but they are thought to include hereditary connective tissue diseases, especially Ehlers-Danlos Syndrome. In a study on orthostatic intolerance and EDS, it is suggested that the co-occurrence of these syndromes can be attributed to the abnormal connective tissue in dependent blood vessels of those with EDS, which permits veins to distend excessively in response to ordinary hydrostatic pressures. This in turn leads to increased venous pooling and its hemodynamic and symptomatic consequences."

Journal Pediatr. 1999 Oct;135(4):494-9.
Orthostatic intolerance and chronic fatigue syndrome associated with Ehlers-Danlos syndrome.
Rowe PC, Barron DF, Calkins H, Maumenee IH, Tong PY, Geraghty MT.

 

and no, you do not always "know " you have EDS as
Kirsty Burmeister says: [emphasis mine]

quote

I didn’t realize I had Ehlers-Danlos Syndrome for the first 30 years of my life. I just knew I was weird.

Having a connective tissue disorder (with all the strange, seemingly unrelated medical problems that go along with it) and not even knowing it has led to several awkward moments. Like…

The time I passed out and half the dorm floor tried to give me CPR.
I was eighteen and had just moved into a new dorm. A couple of the other girls walked into the bathroom while I was cutting my hair. One of them asked if she could wield the scissors and I happily handed them over (hey, free haircut!) A few more girls wandered through the bathroom, but stopped to chat.

My new pal was snipping a few stray strands at the back of my neck and… I woke up being hauled into the dorm hall. I had just started to open my eyes when I heard a shout of, "Does anyone know CPR?!" I regained my senses enough to "thanks, but no thanks" them on that one and explain that randomly passing out was just something I did from time to time. None of those girls were very interested in hanging out with me after that.

.......

The time a cute guy complimented my appearance… my apparently undead appearance.
I was sixteen and on a trip with a bunch of other teenagers from all over the country. We’d stopped to grab a burger and one of the most attractive guys in our group sat down at my table. During a lull in the conversation he says, "You have a really cool look."

Mentally batting my eyelashes, I replied, "Oh, yeah?"

"Yeah, your eyes are kinda blue where they should be white…and you have really dark circles. You look like a vampire. It’s really cool."
Sixteen years later, I’ve yet to come up with a response to that.

 

Here is an abstract onthe muculocontractural ype of EDS

2013 May 23. [Epub ahead of print]

Loss of dermatan sulfate epimerase (DSE) function results in musculocontractural Ehlers-Danlos syndrome.


Müller T, Mizumoto S, Suresh I, Komatsu Y, Vodopiutz J, Dundar M, Straub V, Lingenhel A, Melmer A, Lechner S, Zschocke J, Sugahara K, Janecke AR.

Source
Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria.

Abstract

The sulfated polysaccharide dermatan sulfate (DS) forms proteoglycans with a number of distinct core proteins. Iduronic acid-containing domains in DS have a key role in mediating the functions of DS proteoglycans. Two tissue-specific DS-epimerases, encoded by DSE and DSEL, and a GalNAc-4-O-sulfotransferase encoded by CHST14 are necessary for the formation of these domains. CHST14 mutations were previously identified for patients with the musculocontractural type of Ehlers-Danlos syndrome (MCEDS). We now identified a homozygous DSE missense mutation (c.803C>T, p.S268 L) by the positional candidate approach in a male child with MCEDS, who was born to consanguineous parents. Heterologous expression of mutant full-length and soluble recombinant DSE proteins showed a loss of activity towards partially desulfated DS. Patient-derived fibroblasts also showed a significant reduction in epimerase activity. The amount of DS disaccharides was markedly decreased in the conditioned medium and the cell fraction from cultured fibroblasts of the patient as compared to a healthy control subject whereas no apparent difference was observed in the chondroitin sulfate (CS) chains from the conditioned media. However, the total amount of CS disaccharides in the cell fraction from the patient was increased ∼1.5-fold, indicating an increased synthesis or a reduced conversion of CS chains in the cell fraction. Stable transfection of patient fibroblasts with a DSE expression vector increased the amount of secreted DS disaccharides. DSE deficiency represents a specific defect of DS biosynthesis. We demonstrate locus heterogeneity in MCEDS and provide evidence for the importance of DS in human development and extracellular matrix maintenance.

 

and this on in from Answers for Erin

My heart is pounding out of my chest! I just called Cleveland Clinic and told the genetic counselor that I was extremely upset with them for being so dismissive when we brought Erin to them. I told her exactly how we were made to feel and that it "would behoove Dr M to learn some bedside manners because regardless of the letters after his name I can assure you that he is not God and does not know everything." I can't remember a time in the past six months that I have had to stand up to someone out of such intense pain. I then told her that through no help whatsoever from them we have learned that our daughter has the MTHFR abnormalities and that through our own research we have found that she more than likely has EDS-HM. I asked for the name and number for the ombudsmen and told her that I will be sending a letter to share with the hospital board how we were made to feel. Don't ever stop fighting. If your gut is telling you that there is something wrong and the doctors are not listening keep knocking on doors and researching and demanding answers. You never know when someone is going to decide to listen and you never know which simple test is going to reveal a key.

 

Just in from Physiscian Heidi A Collins - thanks so much Heidi

I posted this on another group and was subsequently urged to share here:

A few links on sinus and AV node ablation and POTS / dysautonomia (SHARE FREELY, ESPECIALLY WITH YOUR DOCTORS!!!)

As background, a few years ago, experts agreed that joint hypermobility syndrome and EDS are one and the same.

In a VERY IMPORTANT article by authors including Dr Rodney Grahame, a British Rheumatologist world-famous for his knowledge regarding joint hypermobility and EDS (I believe he has been knighted or something, as he is “Sir Rodney Grahame”), the authors document that dysautonomia is very, very common in hypermobile patients http://www.ncbi.nlm.nih.gov/pubmed/12867232: “Orthostatic hypotension, postural orthostatic tachycardia syndrome, and uncategorized orthostatic intolerance were found in 78% (21/27) of patients compared with in 10% (2/21) of controls.” This fact is widely acknowledged among experts taking care of EDS patients. The point is, if you have EDS, you are more likely than not to have some form of dysautonomia!

From Dr Grubb – widely recognized as THE WORLD’s EXPERT on POTS and dysautonomia in people with EDS (From 2006, before JHS and EDS were considered to be the same disorder) http://www.ncbi.nlm.nih.gov/pubmed/16426415 and http://www.iranep.org/Articles/POTS%20%20JCE%202006.pdf:

“Recent studies have suggested that up to 70% of patients with hypermobility syndrome may suffer from some form of orthostatic intolerance. Adolescents with the developmental form of POTS frequently have been noted to have features of JHS. Studies are currently under way to better elucidate this potential relationship.”

“The differentiation between POTS and IST is important as radiofrequency catheter ablation of the sinus node can make PD POTS patients markedly worse, and rarely seems to benefit patients with hyperadrenergic POTS.”

More from Dr Grubb (in 2008) http://circ.ahajournals.org/content/117/21/2814.full.pdf: “…catheter ablation of the sinus node rarely leads to improvement in patients with hyperadrenergic POTS and often makes those with the PD form worse.”

The folks on dinet.org nicely summarize Drs Shen’s and Grubb’s longstanding experience. From http://www.dinet.org/what_to_avoid.htm:

“Ablation of the sinus node may be detrimental to POTS patients. A Mayo Clinic study reported short-term success in five of seven ablated patients with inappropriate sinus tachycardia and postural orthostatic tachycardia features (Shen, Low, Jahangir, Munger, Friedman, Osborn, Stanton, Packer, Rea & Hammill, 2001). However, long-term outcomes were disappointing in these patients. None of the patients experienced complete eradication of symptoms. A follow-up evaluation showed no vast improvement in symptoms, despite better heart rate control. A later publication states ‘in our laboratory, sinus node modification, total sinus node ablation, or atrioventricular nodal ablation is not recommended for patients with inappropriate sinus tachycardia who have autonomic evidence of postural orthostatic tachycardia’ (Shen, 2002).”

“Ablations have reportedly been detrimental to some POTS patients who were misdiagnosed as having inappropriate sinus tachycardia. After the apparently successful elimination of their ‘sinus tachycardia’, they were left with profound orthostatic hypotension (Grubb & Karas, 1999).”

More on the research by Shen et al in 2001 http://www.ncbi.nlm.nih.gov/pubmed/11270703: “Sinus rate can be effectively slowed by sinus node modification. Clinical symptoms are not significantly improved after sinus node modification in patients with inappropriate sinus tachycardia and postural orthostatic tachycardia. A primary subtle autonomic disregulation is frequently present in this population. Sinus node modification is not recommended in this patient population.”

Again, from Shen http://www.ncbi.nlm.nih.gov/pubmed/12438812: “In conclusion, the precise role of sinus node modification in patients with inappropriate sinus tachycardia remains to be determined. Sinus node modification could be considered in patients with inappropriate sinus tachycardia with persistently increased heart rate in the absence of any autonomic abnormalities. Autonomic laboratory testing should be performed to exclude any evidence of autonomic dysregulation. Clinical research on the pathophysiology of inappropriate sinus tachycardia should be pursued vigorously.”

Many think the “no ablation” policy applies only if POTS has been officially diagnosed. However, look closely at Shen’s advice as an experienced clinician: “Sinus node modification could be considered in patients with inappropriate sinus tachycardia with persistently increased heart rate in the absence of any autonomic abnormalities.” In case you didn’t catch it, that’s “IN THE ABSENCE OF ANY AUTONOMIC ABNORMALITIES” and “EXCLUDE ANY EVIDENCE OF AUTONOMIC DYSREGULATION”!!!

This next one is particularly scary, but fortunately with a (supposedly) happy ending. A positive spin is put on the fact that someone decided to ablate the sinus node. When it was “unsuccessful”, they had to ablate the AV node AND put in a dual chamber pacemaker. From http://www.ncbi.nlm.nih.gov/pubmed/21539639 “After unsuccessful sinus node ablation, atrioventricular node ablation and dual chamber pacemaker implantation was performed, which dramatically improved her symptoms and eliminated syncope. Atrioventricular node ablation could modify the cardiac autonomic balance and thereby suppressed the excessive orthostatic sympathetic activity.”

If it were me, I would damn sure want to be certain that all possible non-invasive management was exhausted, and (as Drs Grubb and Shen would advise) a thorough workup is undertaken to determine the underlying pathophysiology of the inappropriate tachycardia and find out with certainty whether any autonomic dysregulation is at play (whether it is POTS or ANY OTHER primary or secondary dysautonomia), before undergoing two risky procedures to “remove” my heart’s built-in pacemakers and another risky procedure to put in an artificial dual chamber pacemaker, which requires further procedures when batteries need replacement and leads need adjusting. Just sayin.

 

My uncle isn't just obese because of inactivity, he over eats, he eats whole cakes in once. He wouldn't have to be obese if he ate a healthy diet. But he doesn't care about his health. He's literary eating himself to death it's a miracle he's still alive now, he's 80. Guess he's lucky. His brother (my father) and sister eat healthy and don't overeat, they are slim.

I myself would be obese if I didn't watch what I eat. I have been overweight for 10 years in the past (with short periods of being slim in between) till I had enough of it (its hard to dance when there is a big belly in the way) and was afraid of my health. It took me 3 years to loose it! But I have been a healthy weight for more than a year now and it feels so much better

Btw you mentioned eye problems, I have a deformed cornea and it's very thin, I need a transplant but I don't know if people with EDS accept transplanted body parts well. Do you know? It will need to be done some time in future as I can barely see with that eye and my other eye is deteriorating slowly as well. Being able to see with one eye only already caused me to slip on something I didn't see and fall and break my back, I'm scared next time I'm not so lucky and break my neck and will be worse off.

 

I'm sorry that someone said that, that's not nice being 16 and getting a comment like that

 

i think he meant it in a good - goth - kind of way - not realising they were symptoms of EDS

here is more info from Dr Heidi Collins - thanks Heidi!

Adapted from a lengthy comment I originally made on the national EDNF FB page related to EDS and multiple “overlapping” disorders, including magnesium imbalance and gut problems. I posted the following text on the Michiana EDNF and Michigander Zebras group pages a few days back, and thought I would re-post here. As always, SHARE THIS INFO FREELY, ESPECIALLY WITH YOUR HEALTHCARE PROVIDERS.

EDS is a primary condition affecting connective tissue. If the primary condition could go away, any condition secondary to it should theoretically disappear. Since nobody has figured out how to make EDS go away, we are stuck with practically innumerable secondary conditions, as connective tissue is in every tissue of the body.

All EDS patients should educate themselves regarding the basics of the autonomic nervous system, including the enteric nervous system, which governs gut function.

Many people understand that the autonomic nervous system controls the “fight or flight” response. Specifically, the sympathetic portion of the autonomic nervous system drives the “fight or flight” response.

Far fewer realize that the autonomic nervous system controls the “rest and digest” response that offsets and balances the “fight or flight” response. Specifically, the parasympathetic portion of the autonomic nervous system drives the “rest and digest” response.

Enter the enteric nervous system.

Directly from Wikipedia: “The enteric nervous system (ENS) or Intrinsic nervous system is one of the main divisions of the autonomic nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system. …the enteric nervous system is sometimes called a ‘second brain’” http://en.wikipedia.org/wiki/Enteric_nervous_system

The enteric nervous system resides in the gut. Although it is subject to control from the brain and spinal cord, if connections are severed between brain, spinal cord, and enteric nervous system, the enteric nervous system will function independently (as if it has a mind of its own.)

I find the following documents from http://foodintolerancemanagementplan.com/ very nicely describe the enteric nervous system in easily readable terms. See: Understanding the Human Gut and the Enteric Nervous System (ENS) http://foodintolerancemanagementplan.com/documents/Understanding%20the%20Human%20Gut%20and%20the%20Enteric%20Nervous%20System.pdf

The same site lists numerous detailed references regarding enteric nervous system health, including dietary management of enteric disorders. See: Helpful Resources and Links and Research Papers, Studies and Donations http://foodintolerancemanagementplan.com/documents/helpful%20resources%20&%20links.pdf

For example: Evidence-based dietary management of functional gastrointestinal disorders. The FODMAP approach. http://www.ncbi.nlm.nih.gov/pubmed?term=20136989)

I will quote directly from “The enteric nervous system: New developments and emerging concepts” http://www.um.edu.mt/umms/mmj/PDF/329.pdf :

“The ENS controls gut motility and secretion via local reflexes that are triggered by local distension of the intestinal wall, distortion of the mucosa, and chemical contents in the lumen. This neuronal regulation of GI functions is due to the liberation of specific neuromediators synthesized by functionally defined enteric neurons. In addition, ENS is involved in the control of immune and inflammatory processes throughout the gut. Thus, it is not surprising that any damage to ENS circuitries and in the neurotransmitters systems results in a wide array of gut disorders, including motor impairments, which are characterized by high morbidity. … with a markedly compromised patient’s quality of life and occasional fatal outcomes. …Besides a few exceptions, the mechanisms through which neural diseases cause gastrointestinal dysfunction, including motor abnormalities, remain poorly understood.”

Also: “ENS express all neurotransmitters so far known in CNS (more than 30 neurotransmitters). These include classical neurotransmitters such as acetylcholine (Ach), noradrenaline, serotonin, GABA and glutamate, but a great number of other neurotransmitter and hormones also participate in the regulation of functions in the GI tract: vasoactive intestinal polypeptide (VIP), nitric oxide, galanin, motilin, adenosine triphosphate, tachykinins, etc.”

In my opinion, the two most critical concepts touched upon in the quoted text are:

1) The ENS controls gut motility and secretion via local reflexes that are triggered by local distension of the intestinal wall, distortion of the mucosa, and chemical contents in the lumen. Connective tissue is what allows the intestinal wall to distort and distend when needed. This is where the connection lies between EDS and gut disorders!!!

2) Adrenaline and noradrenaline (epinephrine and norepinephrine) are catecholamines. When catecholamines have gone haywire (for example, in dysautomic conditions such as POTS), of course the enteric nervous system (and thus, the gut) is very specifically affected!!!

POTS is just one of the dysautonomic conditions which can occur in persons with or without EDS. For those familiar with POTS, it isn’t just about tachycardia. It’s a SYNDROME which includes gut disorders. POTS involves either an intrinsically “broken” autonomic nervous system (a primary dysautonomia) or an autonomic nervous system without intrinsic pathology that subsequently “misbehaves” due to specific controlling circumstances (a secondary dysautonomia). In the case of POTS comorbid with EDS, POTS is believed almost certainly to occur as a condition secondary to EDS. (The jury is still out as to exactly WHY EDS causes POTS, but there is little dispute regarding the high incidence of EDS sufferers who struggle with POTS.) In the broadest sense, both patients and practitioners need to understand that persons with dysautonomia can experience symptoms in ANY system affected by the autonomic nervous system. In fact, ALL systems are modulated by the autonomic nervous system; this means that dysautonomia can wreak havoc with just about anything! Perhaps the most commonly acknowledged symptoms are cardiovascular (tachycardia, orthostatic intolerance, fatigue, etc.), gastrointestinal (malabsorption, dysmotility, IBS, constipation, etc.), and amplification of pain in general. (Of course, the fact that the list of dysautonomia-associated symptoms are seemingly infinite – and the fact that dysautonomia is not “easy” to treat – is why dysautonomia generally makes practitioners want to hide under a rock when their patients mention it.)

Bottom line: for many of those with EDS, gut difficulties likely relate heavily to the enteric nervous system and are often associated with autonomic dysfunction such as POTS.


A few more links that are worth looking at:

Direct Effect of Catecholamines on Bacterial Growth: A New Mechanism by Which Stress can Influence Digestive Health and Disease http://www.brainimmune.com/index.php?option=com_content&view=article&id=1594%3Adirect-effect-of-catecholamines-on-bacterial-growth-and-intestinal-mucosabacteria-interactions-a-new-mechanism-by-which-stress-can-influence-digestive-health-and-disease&catid=56%3Areviews-and-viewpoints&Itemid=413

Stress at the intestinal surface: catecholamines and mucosa-bacteria interactions. http://www.ncbi.nlm.nih.gov/pubmed?term=20941511


Understanding and controlling the enteric nervous system. http://www.ncbi.nlm.nih.gov/pubmed?term=12473304


Catecholamines and Vasopressin During Critical Illness http://medicina.iztacala.unam.mx/medicina/Catecholamines%20and%20Vasopressin%20During.pdf

Enteric nervous system - Wikipedia, the free encyclopedia
en.wikipedia.org
The enteric nervous system (ENS) or intrinsic nervous system is one of the main divisions of the autonomic nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system.[1]

 

I am no ecpert on eyes sorry VM - but i know they feature prominently in EDS issues - there are a couple of related articles not oo far above in this thread. And you would want someone who knowsa bout EDS to do the surgery and anything related to eyes whould be given top priority. If i see anythin specific i will post it for you.


And there is a good fb page on EDS articles. I will find the link and post it here for you soon. you mightalso post that question on MI Zebras fb page as there seem to be some knowledgeable peeps there.



A

 

some more info on CT

http://www.britannica.com/EBchecked/topic/132995/connective-tissue

 

Hi Justy sorry i missed this i think - nothe wiki page is not great

the main thing is that they say sommething that peopl overlook - that the lines between the different categories are very blurred and there is considerable overlap between the types .
My point is you say you do not need to be lying flat - but lying flat may tax you less than sitting even though you are not aware of it - I am not sure and i know that does not work fo eveyone - some people cannot lie flat and I have read why somewhere but lost the article.

I as ctually hoping this thread would stimulate people to look at their body's reactions to different things and see if there are patterns that make sense based on this theory. SO far lot of people with ME have now been diagnosed with EDS or CTDs so it is going somewhere for some of use at least.

Cheers

Ally

 

nanong i notice that the mast cells are all embedded in connective tissue and wonder if there could be a link there to mast cell theory - some overlap?.