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

[Oliver3]

https://twitter.com/i/web/status/1035996271385792512

She does not.

Ok fair enough.
She does however concede that there is some correlation. Also this was from a year ago. I coulve sworn i read she'd said she has EDS but i could be wrong
But check out this doctors views that all these conditions are overlapping. I still don't think there is enough evidence to rule out CFS being a new form of EDS.
https://www.healthrising.org/blog/2...nic-fatigue-syndrome-center-complex-diseases/

 

[Oliver3]

I don't know about vascular EDS, but a quick check on Google reveals its prevalence is estimated to be between 1 in 50,000 and 1 in 200,000 people. So pretty rare, and due to this rarity alone, you can exclude the possibility of it playing any significant role in the general ME/CFS population.

I would even dispute that. Vascular EDS is thought to be rare, but it's a sliding scale. What i think we are seeing asVascular EDs is the very terrible end of the sliding scale. There are people in their 80's who have vascular EDS and yet it's supposed to kill everyone early. I just don't think the data has been properly assimilated. I don't want it to be EDS but i feelthat the prevalance is going to turn out to be much higher and fibro and cfs will have genetic underpinnings that share crossover with EDS, autism etc. The science behind EDS, as i understand it is not complete. There hasn't been enough research. And as i said before both Dr Ron Davies and his daughter have the disease. See the health rising article above which takls about the venn diagram nature of related diseases.

https://www.healthrising.org/blog/2...nic-fatigue-syndrome-center-complex-diseases/

 

[Oliver3]

scientific journals





ME/CFS is not a diagnosis of exclusion. If you look at the Canadian consensus criteria, they contain very specific symptoms that you must have in order to be given the diagnosis of ME/CFS.





Yes you do. Here are the diagnostic criteria for hEDS. In order to be diagnosed, as a adult you have to have at least a 4 on the Beighton scale of joint flexibility. If you do not have such joint flexibility, you cannot be diagnosed with hEDS.

No you don't You can have seized up as you age. The Beighton scale is just an incomplete very primitive test. As the article in health rising says:

The Beighton Test is a self-questionnaire that is often used to assess whether hypermobility is present. Dr. Chheda 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.

• Beighton Test

Hypermobility puts people at an increased risk of craniocervical instability and cerebral spinal fluid leaks. Dr. Chheda noted that if you go deep enough into a person’s history, you will sometimes find some very odd types of hypermobility as well as a history of physical trauma such as whiplash or other kind of head injury. For a person who is hypermobile, she said, it doesn’t take much trauma to cause craniocervical instability (CCI) or a spinal fluid leak.

She guessed that more than half of her patients have some kind of hypermobility: whether that consists of stretchy skin, the ability to pop their joints in and out or some other type of hyperflexibility.

For some people, hypermobility is the starting point of their disease. For others, the hypermobility comes on later – perhaps as a side-effect of mast cell activation.

 

[bread.]

ME/CFS is not a diagnosis of exclusion. If you look at the Canadian consensus criteria, they contain very specific symptoms that you must have in order to be given the diagnosis of ME/CFS.





Yes you do. Here are the diagnostic criteria for hEDS. In order to be diagnosed, as a adult you have to have at least a 4 on the Beighton scale of joint flexibility. If you do not have such joint flexibility, you cannot be diagnosed with hEDS.

Beighton Score every 4th person „can be positive“ for that test.

It might be and I definitely hope so that there is one underlying issue surrounding PEM (something like ido trap), but everything else looks like clusters of symptoms that can come from everywhere,

@JenB neurosurgeon considers her an EDS patient, she herself does not, I think personally she does so for many different reasons and probably for good reasons.

EDS is a collagen disorder with already 14 different types, talking to specialists in this disease it becomes clear it is more likely than not that there are probably another 10 types and that is without counting secondary induced collagene damage that is more likely in people with some polygenetic issues (which is also a genetic illness!).

 

[Oliver3]

Beighton Score every 4th person „can be positive“ for that test.


It might be and I definitely hope so that there is one underlying issue surrounding PEM (something like ido trap), but everything else looks like clusters of symptoms that can come from everywhere,

@JenB neurosurgeon considers her an EDS patient, she herself does not, I think personally she does so for many different reasons and probably for good reasons.


EDS is a collagen disorder with already 14 different types, talking to specialists in this disease it becomes clear it is more likely than not that there are probably another 10 types and that is without counting secondary induced collagene damage that is more likely in people with some polygenetic issues (which is also a genetic illness!).

What you said!

 

[Hip]

I am still interested in your authorative journals prevalence studies of me/cfs and especially heds, one big problem is that people just repeat stuff they have red somewhere and give bs authorative power where there should not be.

If you are interested in reading scientific papers from medical journals, then go to the PubMed medical database of papers, and enter the subject you are interested in into the search field.

Though it's often easier to search PubMed via Google, which is done by adding the command site:www.ncbi.nlm.nih.gov into your Google search. For example, if you want papers on ME/CFS prevalence, see this Google search on PubMed.

Note that disease incidence is not the same as disease prevalence; those are two different concepts.

Beighton Score is ridiculous, every 4th person „can be positive“ for that test.

Where do you get this information from?

Again, you are thinking in made up category boxes that have absolutely no value

Hold on, you started this thread introducing the idea that ME/CFS is a disease which arises in people with EDS or other connective tissue conditions. So you introduced these categories of ME/CFS and EDS, and you proposed a relationship between them.

Now you are claiming that these same categories you introduced have absolutely no value.

You cannot have it both ways: you cannot base your arguments on these categories, and then at the same time say the categories have no value. That's just contradicting yourself.

We alread know that me/cfs can be persistent hhv6 infection or cci, how many pieces of the „clear cut disease“ have to be cut out of the cake before you realise it is not one cake?

We know neither of these things. There is no definitive evidence that ME/CFS can be caused by viral infection. There's evidence linking ME/CFS to infection, but as I would hope you appreciate, association does not imply causation.

And at this stage it is far, far too early to say that CCI causes ME/CFS. We are seeing the beginnings of a very interesting association, but nothing further than that can be said at this stage.

Science is a careful process based on meticulous and painstaking work which eventually produces solid evidence.

Dr. Chheda 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.

It's interesting what Dr Chheda is observing, or thinks she is observing, but we really need to see a published study on this.

Vascular EDS is thought to be rare, but it's a sliding scale. What i think we are seeing asVascular EDs is the very terrible end of the sliding scale.

I am not really seeing your point. Perhaps you can elaborate. Most medical parameters are on a continuous scale; you need to decide when a parameter becomes pathological, and then draw a line between pathological and normal.

You can have seized up as you age.

Maybe, but no medical test is 100% accurate, this is something all doctors know. Every medical test, no matter how sophisticated, will produce incorrect results on a certain percentage of occasions. What is important is how often the test is correct, and how often it gives false results.

 

[bread.]

what you call me/cfs could be partly eds, what some call eds could be partly me/cfs, how would you know, there is no biomarker for neither of this diseases (in regards to heds and not other forms of eds) and therefor extremely prone to error and subjectivism.

The overall arch is that me/cfs is more likely in people with collagene disorders, it does not matter if you call it EDS or something else, but so far we have to go with heds.

Just try the Beighton score, I have asked around 40 people that I know to do so, nearly 30% were positive or borderline. That is interesting isn‘t it?

 

[Hip]

you also can not show me your prevalence studies which you claim to have an authorative quality to it and I ask myself why?

I provided a link above which searches PubMed for prevalence studies. All you have to do is click the link. This not only provides the prevalence studies you asked for, but also demonstrates how to conduct a PubMed search, which you may find useful in future when looking for medical info.

Just try the Beighton score, I have asked around 40 people that I know to do so, nearly 30% were positive or borderline. That is interesting isn‘t it?

Better still, I have made use of the PubMed database I introduced you to, and found this study (full paper here) on the Beighton score in the general population in Australia.

As you can see from table 2 of the study, in adults of 20 to 39 years old, 7% had a Beighton score of 4 or higher. And for adults of 40 to 59, 1.5% had a Beighton score of 4 or higher.

So I don't know where you got your 30% figure from.

 

[percyval577]

Generel speaking:

maybe EDS or hEDS can be an underlying cause,

but they will not explain the most characterizing "symptoms" of ME/CFS anyway, which is:

1. potentially delayd PEM
2. the possibility of Pacing (the same amount of exertion!)
3. the wide range of concrete symptoms in generel (as reported on the forum), and influences

In case of CCI it is also thinkable that it has developed as a result of a rather likely existing but unknown core (or a trigger of both),
and due to the nature of pathways to interact in a web-like structure, it can allow for a (hopefully lasting) major influence.
Considering especially 1. and 2. I would call this good luck.

 

[Oliver3]

These diagnoses/critera for illness definition are built on shifting sands. I came to EDS as a possible cause for myself after starting to notice connective tissues. the more i looked the more vfs and EDS seemed very very similar.
The work done on EDS itself is scant. After decades looking at say breast cancer, it was only then realised its many different forms and not one illness, hence the meds only working for some. If thats true for a well studied disease like breast cancer, then we are in the wilds with EDS
The symptoms are almost identical. It's certainly worth looking into. I remember the chair speaker at the OMF conference saying that regenerative med and stem cell therapy in particular may be the therapy one day. It was an off the cuff remark but it made me think .
I hope they start to look at the stem cell pioneer Liz Parrish. She's working in Panama to be able to work on stem cell therapies. I'm sure by now she's had CFS patients through her door. Would love to know whats happened there.

 

[Oliver3]

My point about say vascular eds is that it's supposed to kill everyone bylate 40's tops and yet there are people living with it into their 80's. So what are the mitigating factors that allowed them to survive? Is it like autism, where yu can have virtual complete shutdown of a person and in another case someone who is high functioning, Yet they both have autism. We don't have the scientific dexterity to say ok, this severe type is actually this expression on the phenotype and this mild version is this expression on the phenotype , so we call them both autism. One is severe, one isn't. But why? hence i'd question the prevalence data. If someone on the mild epxression of say vascular eds lives to 90 then dies of a brain bleed, it's just 'age' . So what we think we are seeing as age could be just the mild version of vascular eds that is totally survivable and what is a killer is the most potent expression on the phenotype. You could say it's conjecture, but all science is conjecture, all scientific 'rules' subject to change..We just don't know yet, but i have a feeling there will be lotsof cross over with these 2 at the moment, seperate diseases.
I hope to god it is not EDS. I want a quick metabolic trap fix but even if it is EDS, i'm sure there will be therapies, particularly nutritional ones that will help us.

 

[bread.]

I did not say that 30% have a Beighton score that is positive in my own little study with my GP, I said 30% are positive or borderline

THIS shows just how completely random and useless this test is, it has little relevance for you to understand if you suffer from a connective tissue disorder, yes even a hypermobility disorder, it only tells you whether or not the joints you are testing are hypermobile or not There is no magic algorithm behind this score that will tell you if your gut is disdended and unfunctional, same for your heart and bloodvessels.

You can be negative for Beighton and have a complete hypermobile spine and gut issue hanging and sagging down in your pelvis, you are negative for Beighton and you are still positive for heds for every eds practitioner you will ever see.


Lets say you are borderline negative for Beighton, then you do 2 months of yoga and many sun salutations, it is likely you will be positive after that, this will be decisive of whether or not you have EDS.

 

[valentinelynx]

This is plain ridiculous - again, you cannot show me any good prevalence studies, also have you red the conclusion of your study regarding Beighton?

@Hip was asking you to do your own work here. Granted, little has been found regarding the etiology and treatment of ME/CFS, but there's certainly plenty on the epidemiology of the illness. Even if you take into account the controversies regarding diagnostic criteria, you can't say there isn't plenty of research in this area. FYI, this is list of about 40 publications on the "prevalence of CFS" from "ME-Web" (which took me about 5 minutes to find on a web search).

• Bates D.W., Schmitt W., Lee J., Kornish R.J., Komaroff A.L. (1991) Prevalence of fatigue and chronic fatigue syndrome in a primary care practice. Clinical Research., 39, A571-A571.
  • Bates, D.W., Schmitt, W., Buchwald, D., et al. (1993). Prevalence of fatigue and chronic fatigue syndrome in a primary care practice. Archives of Internal Medicine.,153, 2759-2765.
  • Bazelmans, E., Vercoulen, J.H., Galama, J.M., van Weel, C., van der Meer, J.W. & Bleijenberg, G. (1997). Prevalence of chronic fatigue syndrome and primary fibromyalgia syndrom in The Netherlands. Ned. Tijdschr. Geneeskd., 141, 1520-1523.
  • Buchwald, D., Umali, P., Umali, J., Kith, P., Pearlman, T. & Komaroff, A. L. (1995). Chronic fatigue and the chronic fatigue syndrome: prevalence in a Pacific Northwest health care system. Ann. Intern. Med., 123 (2), 81-88.
  • Calder, B. D., Warnock, P. J., McCartney, R. A. & Bell, E. J. (1987). Coxsackie B viruses and the post-viral syndrome: a prospective study in general practice. J. R. Coll. Gen. Pract., 37 (294), 11-14.
  • David, A., Pelosi, A. & McDonald, E. (1990). Tired, weak or in need of rest: fatigue among general practice attenders. British Medical Journal, 301, 1199-1222.
  • Gunn, W. J., Connell, D.B. & Randall, B. (1993). Epidemiology of chronic fatigue syndrome: the Centers for Disease Control Study. Ciba Foundation Symposium, 173, 83-93.
  • Hickie, I.B., Hooker, A.W., Hadzi-Pavlovic, D., Bennett, B.K., Wilson, A.J. & Lloyd, A.R. (1996). Fatigue in selected primary care settings; sociodemographic and psychiatric correlates. Med. J. Aust., 164, 585-588.
  • Ho-Yen, D.O. (1988). The epidemiology of postviral fatigue syndrome. Scot. Med. J., 33, 368-369.
  • Ho-Yen, D.O. & McNamara, I. (1991). General practitioners´ experience of the chronic fatigue syndrome. Br. J. Gen. Pract., 41, 324-326.
  • Jason, L.A., Taylor, R., Wagner, L., et al. (1995). Estimating rates of chronic fatigue syndrome from a community-based sample: a pilot study. Am. J. Community Psychol., 23, 557-568.
  • Jason, L. A., Wagner, L., Rosenthal, S., Goodlatte, J., Lipkin, D., Papernik, M., Plioplys, S. & Plioplys, A. V. (1998). Estimating the prevalence of chronic fatigue syndrome among nurses. American Journal of Medicine, 105 (3A), 91-93.
  • Jason, L. A., Richman, J. A., Rademaker, A. W., Jordan, K. M., Plioplys, A. V., Taylor, R. R., McCready, W., Huang, C. F. & Plioplys, S. (1999). A community-based study of chronic fatigue syndrome. Arch. Intern. Med., 159 (18), 2129-2137.
  • Kawai, K. & Kawai, A. (1992). Studies on the relationship between chronic fatigue syndrome and Epstein-Barr virus in Japan. Intern. Med., 31 (3), 313-318.
  • Kawakami, N., Iwata, N., Fujihara, S. & Kitamura, T. (1998). Prevalence of chronic fatigue syndrome in a community population in Japan. Tohoku J. Exp. Med., 186, 33-41.
  • Kenter, E.G. & Okkes, I.M. (1999). Patients with fatigue in family practice: prevalence and treatment. Ned. Tijdschr. Geneeskd., 143, 796-801.
  • Klein Rouweler, E. Severens J.L., Bleijenberg, G (1999). Prevalentie-rapport. University Hospital Nijmegen, The Netherlands
  • Lawrie, S.M. & Pelosi, A. J. (1995). Chronic fatigue syndrome in the community. Prevalence and associations. British Journal of Psychiatry, 166, 793-797.
  • Lawrie, S.M., Manders, D.N., Geddes, J.R. & Pelosi, A. (1997). A population-based incidence study of chronic fatigue. Psychol. Med., 27, 343-353.
  • Lloyd, A.R., Hickie, I., Boughton, C.R., Spencer, O. & Wakefield, D. (1990). Prevalence of chronic fatigue syndrome in an Australian population. Med. J. Aust., 153, 522-528.
  • Lloyd, A.R., Pender, H. (1992). The economic impact of chronic fatigue syndrome. Med. J. Aust., 157, 599-601.
  • McDonald, E., David, A. S., Pelosi, A. J. & Mann, A. H. (1993). Chronic fatigue in primary care attenders. Psychol. Med., 23 (4), 987-998.
  • Minowa, M. & Jiamo, M. (1996). Descriptive epidemiology of the chronic fatigue syndrome based on a nationwide survey in Japan. J. Epidemiol., 6, 75-80.
  • Murdoch, J.C. (1988). The myalgic encephalomyelitis syndrome. Fam. Pract., 5, 302-306.
  • Nisenbaum, R., Jones, A., Jones, J. & Reeves, W. (2000). Longitudinal analysis of symptoms reported by patients with chronic fatigue syndrome. Ann. Epidemiol., 10 (7), 458.
  • Price, R.K., North, C.S., Wessely, S. & Fraser, V.J. (1992). Estimating the prevalence of chronic fatigue syndrome and associated symptoms in the community. Public Health Rep., 107, 514-522.
  • Reeves, W.C. (1999) Prevalence of chronic fatigue syndrome. Update Reyes et al., 1998 Transcript CFSCC Meeting, April 21-22, 1999.
  • Reyes M., Nisenbaum. R., Hoaglin D., Reeves W.C. (1998) Prevalence of chronic fatigue syndrome. CDC Executive Summary, October 10, 1998.
  • Shefer, A., Dobbins, J.G., Fukuda, K., Steele, L., Koo, D., Nisenbaum, R. & Rutherford, G.W. (1997). Fatiguing illness among employees in three large state office buildings, California, 1993: was there an outbreak? J. Psychiatr. Res., 31, 45-50.
  • Steele, L., Dobbins, J.G., Fukuda, K., Reyes, M., Randall, B., Koppelman, M. & Reeves, W.C. (1998). The epidemiology of chronic fatigue in San Francisco. American Journal of Medicine, 105, 83-90.
  • Versluis, R.G., de Waal, M.W., Opmeer, C., Petri, H. & Springer, M.P. (1997). Prevalence of chronic fatigue syndrome in 4 family practices in Leiden. Ned. Tijdschr. Geneeskd., 141, 1523-1526.
  • Wagner, L.I. and Jason L.A. (1997). Outcomes of occupational stressors on nurses: Chronic fatigue syndrome-related symptoms. Nursing connections, 10, 41-49.
  • Wessely, S., Chalder, T., Hirsch, S., Wallace, P., & Wright, D. (1997). The prevalence and morbidity of chronic fatigue and chronic fatigue syndrome: a prospective primary care study. Am. J. Public Health, 87(9), 1449-1455.

I can bend every finger on this planet beyond 90 degrees,

No, you cannot bend any of my fingers beyond 90º, at least not without me punching you for breaking my fingers! I score 6/9 on the Beighton scale sometimes, and sometimes 5, and I'm 57 years old, but I cannot bending either pinky finger back past 90º. Maybe I could have as a child, but no way now. Maybe that's because I have a lot of joint stiffness in my hands since becoming ill.

It's also important to note that there are specifics to the way the Beighton scale should be applied. It's not as simple as just bending a certain joint so far. Here are the precise details (from here).

"PLEASE NOTE: When reading about this in professional textbooks the formal language used is as follows:​

​

(A) With the palm of the hand and forearm resting on a flat surface with the elbow flexed at 90°, if the metacarpal-phalangeal joint of the fifth finger can be hyperextended more than 90° with respect to the dorsum of the hand, it is considered positive, scoring 1 point.​

(B) With arms outstretched forward but hand pronated, if the thumb can be passively moved to touch the ipsilateral forearm it is considered positive scoring 1 point.​

(C) With the arms outstretched to the side and hand supine, if the elbow extends more than 10°, it is considered positive scoring 1 point.​

(D) While standing, with knees locked in genu recurvatum, if the knee extends more than 10°, it is considered positive scoring 1 point.​

(E) With knees locked straight and feet together, if the patient can bend forward to place the total palm of both hands flat on the floor just in front of the feet, it is considered positive scoring 1 point."​

Furthermore, there's more to a diagnosis of Ehlers Danlos Syndrome than a diagnosis of hypermobile joints. Each of the 13 subtypes has specific diagnostic criteria as established by The International EDS Consortium in 2017. Here is a link to the criteria for all of the subtypes (of which hypermobile EDS or hEDS is the most common): EDS Diagnostics 2017. Here's a link to a handy PDF form for diagnosing hEDS: "Diagnostic Criteria for Hypermobile Ehlers-Danlos Syndrome (hEDS)".

Here's a nice summary of the diagnostic criteria for hEDS (from here).

"The clinical diagnosis of hEDS needs the simultaneous presence of criteria 1 and 2 and 3. This is a complex set of criteria, and there is much more detail than presented in this overview; please see the page for hypermobile EDS [see link above].​

​

1. Generalized joint hypermobility (GJH); and​

2. Two or more of the following features must be present (A & B, A & C, B & C, or A & B & C):​

Feature A—systemic manifestations of a more generalized connective tissue disorder (a total of five out of twelve must be present)​

​

Feature B—positive family history, with one or more first degree relatives independently meeting the current diagnostic criteria for hEDS​

​

Feature C—musculoskeletal complications (must have at least one of three); and​

​

3. All these prerequisites must be met: absence of unusual skin fragility, exclusion of other heritable and acquired connective tissue disorders including autoimmune rheumatologic conditions, and exclusion of alternative diagnoses that may also include joint hypermobility by means of hypotonia and/or connective tissue laxity."​

And very important to this discussion is the following caveat to consider when diagnosing hEDS [Italics mine]:

"There is a range of conditions which can accompany hEDS, although there is not enough data for them to become diagnostic criteria. While they’re associated with hEDS, they’re not proven to be the result of hEDS and they’re not specific enough to be criteria for diagnosis. Some of these include sleep disturbance, fatigue, postural orthostatic tachycardia, functional gastrointestinal disorders, dysautonomia, anxiety, and depression. These conditions may be more debilitating the joint symptoms; they often impair daily life, and they should be considered and treated." (from here)​

​

So, people with hEDS may have many symptoms that overlap with those of ME/CFS, but those symptoms are neither necessary or sufficient for a hEDS diagnosis, while they are essential to an ME/CFS diagnosis (depending on which criteria is used this could include e.g. fatigue, sleep disturbance, orthostatic intolerance, GI disorders, and cognitive problems). Here's an excellent resource for the 5 diagnostic criteria for ME/CFS used in research: Open Medicine Foundation: Diagnosis of ME/CFS.

 

[Oliver3]

@Hip was asking you to do your own work here. Granted, little has been found regarding the etiology and treatment of ME/CFS, but there's certainly plenty on the epidemiology of the illness. Even if you take into account the controversies regarding diagnostic criteria, you can't say there isn't plenty of research in this area. FYI, this is list of about 40 publications on the "prevalence of CFS" from "ME-Web" (which took me about 5 minutes to find on a web search).

• Bates D.W., Schmitt W., Lee J., Kornish R.J., Komaroff A.L. (1991) Prevalence of fatigue and chronic fatigue syndrome in a primary care practice. Clinical Research., 39, A571-A571.
  • Bates, D.W., Schmitt, W., Buchwald, D., et al. (1993). Prevalence of fatigue and chronic fatigue syndrome in a primary care practice. Archives of Internal Medicine.,153, 2759-2765.
  • Bazelmans, E., Vercoulen, J.H., Galama, J.M., van Weel, C., van der Meer, J.W. & Bleijenberg, G. (1997). Prevalence of chronic fatigue syndrome and primary fibromyalgia syndrom in The Netherlands. Ned. Tijdschr. Geneeskd., 141, 1520-1523.
  • Buchwald, D., Umali, P., Umali, J., Kith, P., Pearlman, T. & Komaroff, A. L. (1995). Chronic fatigue and the chronic fatigue syndrome: prevalence in a Pacific Northwest health care system. Ann. Intern. Med., 123 (2), 81-88.
  • Calder, B. D., Warnock, P. J., McCartney, R. A. & Bell, E. J. (1987). Coxsackie B viruses and the post-viral syndrome: a prospective study in general practice. J. R. Coll. Gen. Pract., 37 (294), 11-14.
  • David, A., Pelosi, A. & McDonald, E. (1990). Tired, weak or in need of rest: fatigue among general practice attenders. British Medical Journal, 301, 1199-1222.
  • Gunn, W. J., Connell, D.B. & Randall, B. (1993). Epidemiology of chronic fatigue syndrome: the Centers for Disease Control Study. Ciba Foundation Symposium, 173, 83-93.
  • Hickie, I.B., Hooker, A.W., Hadzi-Pavlovic, D., Bennett, B.K., Wilson, A.J. & Lloyd, A.R. (1996). Fatigue in selected primary care settings; sociodemographic and psychiatric correlates. Med. J. Aust., 164, 585-588.
  • Ho-Yen, D.O. (1988). The epidemiology of postviral fatigue syndrome. Scot. Med. J., 33, 368-369.
  • Ho-Yen, D.O. & McNamara, I. (1991). General practitioners´ experience of the chronic fatigue syndrome. Br. J. Gen. Pract., 41, 324-326.
  • Jason, L.A., Taylor, R., Wagner, L., et al. (1995). Estimating rates of chronic fatigue syndrome from a community-based sample: a pilot study. Am. J. Community Psychol., 23, 557-568.
  • Jason, L. A., Wagner, L., Rosenthal, S., Goodlatte, J., Lipkin, D., Papernik, M., Plioplys, S. & Plioplys, A. V. (1998). Estimating the prevalence of chronic fatigue syndrome among nurses. American Journal of Medicine, 105 (3A), 91-93.
  • Jason, L. A., Richman, J. A., Rademaker, A. W., Jordan, K. M., Plioplys, A. V., Taylor, R. R., McCready, W., Huang, C. F. & Plioplys, S. (1999). A community-based study of chronic fatigue syndrome. Arch. Intern. Med., 159 (18), 2129-2137.
  • Kawai, K. & Kawai, A. (1992). Studies on the relationship between chronic fatigue syndrome and Epstein-Barr virus in Japan. Intern. Med., 31 (3), 313-318.
  • Kawakami, N., Iwata, N., Fujihara, S. & Kitamura, T. (1998). Prevalence of chronic fatigue syndrome in a community population in Japan. Tohoku J. Exp. Med., 186, 33-41.
  • Kenter, E.G. & Okkes, I.M. (1999). Patients with fatigue in family practice: prevalence and treatment. Ned. Tijdschr. Geneeskd., 143, 796-801.
  • Klein Rouweler, E. Severens J.L., Bleijenberg, G (1999). Prevalentie-rapport. University Hospital Nijmegen, The Netherlands
  • Lawrie, S.M. & Pelosi, A. J. (1995). Chronic fatigue syndrome in the community. Prevalence and associations. British Journal of Psychiatry, 166, 793-797.
  • Lawrie, S.M., Manders, D.N., Geddes, J.R. & Pelosi, A. (1997). A population-based incidence study of chronic fatigue. Psychol. Med., 27, 343-353.
  • Lloyd, A.R., Hickie, I., Boughton, C.R., Spencer, O. & Wakefield, D. (1990). Prevalence of chronic fatigue syndrome in an Australian population. Med. J. Aust., 153, 522-528.
  • Lloyd, A.R., Pender, H. (1992). The economic impact of chronic fatigue syndrome. Med. J. Aust., 157, 599-601.
  • McDonald, E., David, A. S., Pelosi, A. J. & Mann, A. H. (1993). Chronic fatigue in primary care attenders. Psychol. Med., 23 (4), 987-998.
  • Minowa, M. & Jiamo, M. (1996). Descriptive epidemiology of the chronic fatigue syndrome based on a nationwide survey in Japan. J. Epidemiol., 6, 75-80.
  • Murdoch, J.C. (1988). The myalgic encephalomyelitis syndrome. Fam. Pract., 5, 302-306.
  • Nisenbaum, R., Jones, A., Jones, J. & Reeves, W. (2000). Longitudinal analysis of symptoms reported by patients with chronic fatigue syndrome. Ann. Epidemiol., 10 (7), 458.
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No, you cannot bend any of my fingers beyond 90º, at least not without me punching you for breaking my fingers! I score 6/9 on the Beighton scale sometimes, and sometimes 5, and I'm 57 years old, but I cannot bending either pinky finger back past 90º. Maybe I could have as a child, but no way now. Maybe that's because I have a lot of joint stiffness in my hands since becoming ill.

It's also important to note that there are specifics to the way the Beighton scale should be applied. It's not as simple as just bending a certain joint so far. Here are the precise details (from here).

"PLEASE NOTE: When reading about this in professional textbooks the formal language used is as follows:​

​

(A) With the palm of the hand and forearm resting on a flat surface with the elbow flexed at 90°, if the metacarpal-phalangeal joint of the fifth finger can be hyperextended more than 90° with respect to the dorsum of the hand, it is considered positive, scoring 1 point.​

(B) With arms outstretched forward but hand pronated, if the thumb can be passively moved to touch the ipsilateral forearm it is considered positive scoring 1 point.​

(C) With the arms outstretched to the side and hand supine, if the elbow extends more than 10°, it is considered positive scoring 1 point.​

(D) While standing, with knees locked in genu recurvatum, if the knee extends more than 10°, it is considered positive scoring 1 point.​

(E) With knees locked straight and feet together, if the patient can bend forward to place the total palm of both hands flat on the floor just in front of the feet, it is considered positive scoring 1 point."​

Furthermore, there's more to a diagnosis of Ehlers Danlos Syndrome than a diagnosis of hypermobile joints. Each of the 13 subtypes has specific diagnostic criteria as established by The International EDS Consortium in 2017. Here is a link to the criteria for all of the subtypes (of which hypermobile EDS or hEDS is the most common): EDS Diagnostics 2017. Here's a link to a handy PDF form for diagnosing hEDS: "Diagnostic Criteria for Hypermobile Ehlers-Danlos Syndrome (hEDS)".

Here's a nice summary of the diagnostic criteria for hEDS (from here).

"The clinical diagnosis of hEDS needs the simultaneous presence of criteria 1 and 2 and 3. This is a complex set of criteria, and there is much more detail than presented in this overview; please see the page for hypermobile EDS [see link above].​

​

1. Generalized joint hypermobility (GJH); and​

2. Two or more of the following features must be present (A & B, A & C, B & C, or A & B & C):​

Feature A—systemic manifestations of a more generalized connective tissue disorder (a total of five out of twelve must be present)​

​

Feature B—positive family history, with one or more first degree relatives independently meeting the current diagnostic criteria for hEDS​

​

Feature C—musculoskeletal complications (must have at least one of three); and​

​

3. All these prerequisites must be met: absence of unusual skin fragility, exclusion of other heritable and acquired connective tissue disorders including autoimmune rheumatologic conditions, and exclusion of alternative diagnoses that may also include joint hypermobility by means of hypotonia and/or connective tissue laxity."​

And very important to this discussion is the following caveat to consider when diagnosing hEDS [Italics mine]:

"There is a range of conditions which can accompany hEDS, although there is not enough data for them to become diagnostic criteria. While they’re associated with hEDS, they’re not proven to be the result of hEDS and they’re not specific enough to be criteria for diagnosis. Some of these include sleep disturbance, fatigue, postural orthostatic tachycardia, functional gastrointestinal disorders, dysautonomia, anxiety, and depression. These conditions may be more debilitating the joint symptoms; they often impair daily life, and they should be considered and treated." (from here)​

​

So, people with hEDS may have many symptoms that overlap with those of ME/CFS, but those symptoms are neither necessary or sufficient for a hEDS diagnosis, while they are essential to an ME/CFS diagnosis (depending on which criteria is used this could include e.g. fatigue, sleep disturbance, orthostatic intolerance, GI disorders, and cognitive problems). Here's an excellent resource for the 5 diagnostic criteria for ME/CFS used in research: Open Medicine Foundation: Diagnosis of ME/CFS.

The point is the criteria for both diseases are clumsy and non specific. Hence doctor Ron looking for biomarkers that are testable. I saw an EDS specialist and he said there is so little known about the disease and there are likely other undiagnosed forms such as spine hypermobility, mitral valve prolapse, vein weakness etc etc. The Beighton scale is so basic, so primitive, all it's shows is outside manifestations of the disease. Heds doesn't even have a genetic basis found yet. the research is just rudimentary.


Autism, epsecially in women has been overlooked in terms of prevalence. There are many factors and biases that go into creating a 'disease'. Social, economic and scientific knowledge and awareness. The 19th and 20th century model of chopping the body into various mechanical parts to create a disease is obviously not helpful anymore. Is depression a lack of serotonin in the brain. First doctors said it was weak charachter, thenThe drug companies said it was serotonin based...then came more understanding that there was a second gut in the brain. Then came further understanding that it may be systemic inflammation getting into the brain and that pathogens and the vagus nerve may be responsible.
You have to keep an open mind. And a global view. Why is there so much overlap between these conditions? As you say when does something become pathologic? we don't know but the beighton score is a pathetic way of understanding EDS. Its almost like taking someone;s high temperature and trying to find out what virus they have.
CFS ,as of as yet an unacknowledged form of EDS should deffo be explored , after all as i said before, both Dr Ron Davies and his daughter have EDS. I don't think theyve been able to assess Whitney, but a bit of a coincidence don't you think?
Again i'd just like to point out no one knows but this seems like an obvious path of investigation to take

 

[rel8ted]

No you don't You can have seized up as you age. The Beighton scale is just an incomplete very primitive test. As the article in health rising says:

The criteria are such that at some point you needed to meet the hyper mobility requirements. At the time of my dx 6 months ago, I was less bendy than I am now due to some extra pounds I was carrying. As those disappear, I am realizing that I am still as hyper mobile as ever. The criteria are to exclude people who are flexible, but not hyper mobile. Also, there are other criteria in addition that must be met in order to get a dx.

FWIW, if someone wants to pursue a dx & cannot find a local geneticist , www.atwalclinic.com does do televisores & he has an interest in EDS.

. I saw an EDS specialist and he said there is so little known about the disease and there are likely other undiagnosed forms such as spine hypermobility, mitral valve prolapse, vein weakness etc etc. The Beighton scale is so basic, so primitive, all it's shows is outside manifestations of the disease. Heds doesn't even have a genetic basis found yet. the research is just rudimentary

I do believe that there may be other undiscovered subtypes. When I was dx, I was told that hEDS dx supersedes my fibro dx. In other words, he feels that I was misdiagnosed with fibro and really it was hEDS all along. That was no surprise to me. My rheumatologist later told me she always thought it was hEDS, but it’s not a big deal so she didn’t dx it. She told me I had fibro & inflammatory arthritis. The med she had me on can cause vision issues. But, at least she didn’t call it hEDS, right?

I believe my mom had hEDS (girlies sign, mitral valve, lots of hand contortions, digestive issues) as did my paternal grandfather (he was super bendy in his 80s, keloid scarring, crowded teeth, digestive issues). I was doomed by both sides (hypermobile, high palate, crowded teeth, stretchy scars).
My dental hygienist has actually asked a billion questions about hEDS as she is somewhat of a zebra (different rare problem) and wants to be able to help catch it. She asked for info about the dental implications. We need more people like her in medicine & dentistry.

Whitney, but a bit of a coincidence don't you think

@Janet Dafoe (Rose49) has been working diligently and tirelessly on getting Whitney an MRI. So, they obviously have a hunch & a plan in mind bc it has been no small feat. Whitney is always in my prayers. They are an amazing family that has given so much to this community when they could have chosen to focus solely on their own son

 

[Oliver3]

The criteria are such that at some point you needed to meet the hyper mobility requirements. At the time of my dx 6 months ago, I was less bendy than I am now due to some extra pounds I was carrying. As those disappear, I am realizing that I am still as hyper mobile as ever. The criteria are to exclude people who are flexible, but not hyper mobile. Also, there are other criteria in addition that must be met in order to get a dx.

FWIW, if someone wants to pursue a dx & cannot find a local geneticist , www.atwalclinic.com does do televisores & he has an interest in EDS.


I do believe that there may be other undiscovered subtypes. When I was dx, I was told that hEDS dx supersedes my fibro dx. In other words, he feels that I was misdiagnosed with fibro and really it was hEDS all along. That was no surprise to me. My rheumatologist later told me she always thought it was hEDS, but it’s not a big deal so she didn’t dx it. She told me I had fibro & inflammatory arthritis. The med she had me on can cause vision issues. But, at least she didn’t call it hEDS, right?

I believe my mom had hEDS (girlies sign, mitral valve, lots of hand contortions, digestive issues) as did my paternal grandfather (he was super bendy in his 80s, keloid scarring, crowded teeth, digestive issues). I was doomed by both sides (hypermobile, high palate, crowded teeth, stretchy scars).
My dental hygienist has actually asked a billion questions about hEDS as she is somewhat of a zebra (different rare problem) and wants to be able to help catch it. She asked for info about the dental implications. We need more people like her in medicine & dentistry.


@Janet Dafoe (Rose49) has been working diligently and tirelessly on getting Whitney an MRI. So, they obviously have a hunch & a plan in mind bc it has been no small feat. Whitney is always in my prayers. They are an amazing family that has given so much to this community when they could have chosen to focus solely on their own son

I'll say it again. The criteria for the Beighton test are inaccurate or rather lack precision. The test can only capture what you have deemed is part of the illness....can we agree that may be a possibility?

For example look at this. Would the Beighton test have picked this up: https://www.ehlers-danlos.com/a-new-type-of-ehlers-danlos-syndrome-discovered/

The point being, we don't know if we have to expand the parameters of what we believe is EDS to incorporate what we call CFS. If there are new types to be found, are we looking at EDS beingthe real cause of CFS but one that doesn't have the Beighton score at the centre of the assessment criteria as it wouldn't pick thesepeople up? It needs to be looked at.

Good to know they are trying to find ways to assess Whitney for these issues.

 

[bread.]

around 50% of the severely ill (like myself) patients in the Davis-Stanford study have EDS.

THIS IS NO OFFICIAL STUDY RESULT YET

 

[Oliver3]

around 50% of the severely ill (like myself) patients in the Davis-Stanford study have EDS.

THIS IS NO OFFICIAL STUDY RESULT YET.

Interesting but not a suprise. Where did you hear this or are you trolling lol!?

 

[bread.]

it is true, I think they probably even said it somewhere on a public forum.

 

[Oliver3]

Now i know youre trolling lol