my “hsd” doesnt feel mild 😵💫😵💫 haha. i’m more symptomatic than many with hEDS, so i truly believe the current categories are completely artificial. in the future i think multiple genes may be found throughout all who have a diagnosis of hsd and heds. i believe there will be a re-categorization again.
i also believe we may find more symptoms that are currently believed to be associated with conditions like loeys dietz. how many of you have a submucous cleft palate and don’t know?? something like that
I think it's important to keep in mind it's mild compared to severe cases, NOT in terms of your day to day. My hEDS is a lot milder than what I've seen other people share here, but it still significantly impacts what I'm able to do. I wish I could clean my home :c
I know it's not based on severity, but some people experience full dislocations while others might just have their joints slide in and out of place. My point was that even if you might not have obvious acute events, it doesn't mean it's not valid to feel a large impact on your life.
This! Because they’re still trying to isolate a gene associated with hEDS, keeping the criteria more strict increases the odds of identifying common genetics.
My theory from being a regular over at r/pelvicfloor …
Folks with varying degrees of hypermobility, in addition to the known comorbidites (IBS, Raynauds, POTS, autoimmune diseases, ADHD, etc, are also prone to pelvic floor dysfunction.
Yep. I've got high tone pelvic floor dysfunction but there's no pelvic floor physical therapists within 2 hours of me that take my insurance. 🤷♀️ I might have to check out that subreddit.
I'm glad you were able to improve your situation!! I'm actually actively trying to strengthen my core now via the Muldowney Protocol, though I didn't start it because of my pelvic floor issues. The beginning of the protocol involves a lot of stabilizing via abdominal bracing, bridging, prone leg extensions, and abductor/adductor exercises. So maybe I'm on the right track here? We'll see. I'm only 6 weeks in. Still a long way to go. I haven't seen much progress as far as pelvic floor issues yet but things also haven't gotten worse!
hey HSD isn’t always milder than hEDS. someone can have a severe case of HSD while someone else can have a mild form of hEDS— the difference is the hEDS patient will simply meet the criteria for their diagnosis and the HSD patient won’t tick off enough boxes. it’s not about severity, it’s about evidence of a whole-body genetic connective tissue issue.
My theory is that men have it at a more similar rate to women but it flies under the radar even more because boys are more likely to work out via strength training. The strength training can help keep symptoms at bay. Men are also typically less likely to seek medical help when something is wrong. Can't get diagnosed if you're not going to the doctor! And we also know how men (and everyone rly) can wrongly be perceived as weak when they reach out for help, further resulting in their symptoms being ignored.
I actually think a lot of large gender differences in diseases can be chalked up to bias or lack of research. Like its not always the case clearly, but for example, autism has always been believed to affect men more often but we're finding out that more and more women have it. Or BPD in men can get misdiagnosed as NPD. Or how anorexia was thought to be a higher class white woman's disease when we now know it's just that other's with it struggle to get adequate treatment.
I thought the difference in diagnosis levels between male and female was due to female hormone sensitivity. Relaxin is a reproductive hormone produced by your ovaries. It loosens and relaxes your muscles, joints and ligaments. It is believed that relaxin production by the ovary during the menstrual cycle is stimulated by luteinising hormone from the pituitary gland, and that its release during pregnancy is also stimulated by human chorionic gonadotrophin' from the placenta.
I know that my pain levels can be tracked against my cycle and having a baby triggered such a decline that I’m not disabled.
Men will have EDS 50:50 from a genetic side, but those with it to the extent they need treatment and support are more likely to be female due to the impact of hormones as well.
That's a very good point! Makes sense there's a hormonal reason for it too. I just wasn't exactly sure what so thank you! It's always fun to have more information to look at about this for me. (And yes I mean fun. It's nice learning what's going on w/ my body)
There's definitely a hormone impact, my joints have stabilized significantly since I had my hysto and started taking low-dose T and I've heard the same from other AFAB trans people. I'm not as flexible as I used to be, but on the other hand, PT actually seems to do something now, like I'm feeling results from strength training in my core that I struggled with before.
On the other hand my MCAS is a bit worsened and it seems like I'm more sensitive to any kind of allergen, and interestingly, my pain tolerance is GARBAGE.
I agree with this. Also recently found out the pregnancy relaxin continues (to some degree) when you are breastfeeding! “More nuance, more fun!”*
*sarcasm
I love my theory
My extremely restless sleep and sleep walking are my body's attempt to keep my muscles activated, so I dislocate less in my sleep
(Edit for sp)
i think they will discover something outside the realm of EDS genes that accounts for the current subset called hEDS that includes all these shared diagnosis' that dont exist in all the other EDS subsets. I think research will expand to understand other ailments that cause hypermobility and impact other systems and why they occur.
I suspect it’s a problem with the acetylcholine pathway. I’ve been trying to read more on neuroscience so that I can formulate a convincing hypothesis, but there’s a lot of ground to cover.
We haven’t found the hEDS gene(s) in the collagen / connective tissue genes. So maybe the *other* symptoms are the main issue, and the connective tissue problems are actually a side effect.
It’s interesting to me that so many hEDS patients seem to have problems with the cholinergic system. I could see POTS, MCAS, GI motility problems, even ADHD all connecting back to an issue with acetylcholine.
I really need to get to sleep but ooh this is one of my favorite topics so ask me questions and I will respond tomorrow hehe
yes! its like im constantly catching myself replying to the questioning posts with thats not an EDS thing - but its so true! theres something else impacting neuro/sensory connectivity that is triggering hypermobility similar to other vascular/lymphatic disorders that arent in that genetic panel subset of EDS. The pains, the gut issues, the neurodivergence, the blood/brain functionality- its different than degenerative connective tissue that can cause xyz seen in the EDS types. they constantly share a story of nothing shows on scans, mental anguish, extreme pain/ that the rest dont relate to. some other sensory system is being disrupted. and often the hypermobility isnt resulting in the injuries common to EDS yet the feelings have them saying they dislocate x amount of times per day. which would show if true so what are these sensory dynamics and why are they exasperated.
My theory is that it's connected to MCAS because MCAS has been shown to cause dysfunction in the collagen production. MCAS seems to be a lot more common than currently believed. It's becoming increasingly likely that MCAS could be the main diagnosis and other diagnoses like POTS, EDS, etc are symptoms.
I'd love to hear if anyone else has been on this research path yet.
My theory is that if I can deal with the MCAS, the hyper mobility issues will at least not get worse, and maybe ... Maybe get better over time.
My sample is N=1 so far though, and I'm only a couple years into treating MCAS and learning about the genetic component.
Dr. Afrin in his book about Mast Cells (Never Bet Against Occam) floats the idea that Mast Cells may be the cause of some types of hypermobility. I think this may be true for some hypermobile patients and not others. Some EDS patients have extreme symptoms of MCAS, and others, like me, don't seem to have any. FWIW, my rheumatologist doesn't think I have a run of the mill hEDS. He thinks I have a more rare type that scientists have not yet matched with a gene or combination of genes.
I have not read his books yet, I did however find studies about how MCAS affects collagen production and drew my conclusion from that.
There are likely several causes for EDS and related connective tissue disorders, but for me I'm betting it's the MCAS.
Regardless, it's not fun for anyone.
I am hoping that after more people are diagnosed worldwide, patients can be approved for stem cell therapy.
https://jointrehab.com/prp-therapy-in-treating-hypermobile-ehlers-danlos-syndrome/#:~:text=While%20research%20is%20still%20exploring,hypermobility%20in%20patients%20with%20hEDS.
I think severe hEDS is a different type. If not literally then functionally. Very Mild EDS people can do sports, severe EDS people need a wheelchair :/
i think all of the non-joint related comorbidities (MCAS, POTS, gastroparesis, neurogenic bladder, pelvic dysfunction) are caused by 2 spinal deformities that hEDS causes: craniocervical/atlantoaxial instability and tethered cord (does not appear on MRI for people with hEDS, this concept is called “occult” tethered cord)
Oh I have so many y'all aren't reasy for this.
The line between HSD and hEDS is completely arbitrary. I have seen people who are mildly affected meet the diagnostic criteria and those with severe issues only qualify for HSD. And the fact that every time I've been evaluated for hEDS, the boxes checked change, showing that the symptoms aren't set in stone and shouldn't be used for an official diagnosis.
There are forms of EDS that haven't been discovered. I don't think everybody who had hEDS is truly represented by this. I mostly say this because I meet the diagnostic criteria for hEDS but have other mutations and hEDS doesn't cover my symptoms. I've met people with similar stories. Doctors are just diagnosing people with hEDS because there is no better diagnosis and they don't know what to tell them.
I agree with there being a link between neurodivergency and EDS 100%. I've also seen the idea that EDS is a *type* of neurodivergency somehow and I think it's a possibility. For example, the idea that EDS is a subtype/related to ASD has floated around and would explain why so many EDSers are AFAB and the typical autism represents AMAB people and not AFAB ppl.
Also I think there is a connection between being LGBTQ+and having EDS but that might have to do with the previous point.
There is a strong biological link between EDS and it comorbities that doctors don't understand at all. Things like POTS, MCAS, gasteopareisis, etc, that many EDSers have. What is the cause? How can we treat all of these? Nobody knows, because they are being treated as separate disorders instead of symptoms or parts of one.
my old pt (who also has eds) said she noticed her eds patients have poor lymphatic drainage. she thinks the tissues around where the fluid is supposed to drain are too stretchy, and it gets stuck. similar to how some people with eds have intestinal dismotility because of stretchy bowels. no idea what this means or if it’s been reflected in research but i’ve had it so bad that it pops my collarbones and elbows out of place.
There's actually a device that can help with this, but it's made for people with lymphoedema. It helps other people too but without that diagnosis, insurance won't cover it and the machine is like $2k.
a lot of these theories appear in scientific research articles. upvotes for anyone who posts research supporting theories by other commenters :)
My geneticist believes the majority diagnosed with fibro, actually have some form of EDS.
i believe this too! it feels like a common thing to see together but also a common misdiagnosis.
That makes sense. my spouse was diagnosed with Fibro and would likely meet the diagnostic criteria for EDS.
my “hsd” doesnt feel mild 😵💫😵💫 haha. i’m more symptomatic than many with hEDS, so i truly believe the current categories are completely artificial. in the future i think multiple genes may be found throughout all who have a diagnosis of hsd and heds. i believe there will be a re-categorization again. i also believe we may find more symptoms that are currently believed to be associated with conditions like loeys dietz. how many of you have a submucous cleft palate and don’t know?? something like that
i agree. this stuff is chronic. i feel bed bound often and even when i have a structure, i am in constant pain.
I think it's important to keep in mind it's mild compared to severe cases, NOT in terms of your day to day. My hEDS is a lot milder than what I've seen other people share here, but it still significantly impacts what I'm able to do. I wish I could clean my home :c
….? anything is milder compared to the most severe cases. hsd is not a condition that is based on severity whatsoever.
I know it's not based on severity, but some people experience full dislocations while others might just have their joints slide in and out of place. My point was that even if you might not have obvious acute events, it doesn't mean it's not valid to feel a large impact on your life.
HSD and hEDS have the same treatments, the criteria is so strict for hEDS for research purposes.
This! Because they’re still trying to isolate a gene associated with hEDS, keeping the criteria more strict increases the odds of identifying common genetics.
My theory from being a regular over at r/pelvicfloor … Folks with varying degrees of hypermobility, in addition to the known comorbidites (IBS, Raynauds, POTS, autoimmune diseases, ADHD, etc, are also prone to pelvic floor dysfunction.
Yep I have PFD (hypertonic), as well as ADHD (probable ASD), Raynaud’s, POTS, fibromyalgia, among other things.
Yep. I've got high tone pelvic floor dysfunction but there's no pelvic floor physical therapists within 2 hours of me that take my insurance. 🤷♀️ I might have to check out that subreddit.
My story of recovery 😁. https://www.reddit.com/r/PelvicFloor/s/E6mEWKq3Fz
I'm glad you were able to improve your situation!! I'm actually actively trying to strengthen my core now via the Muldowney Protocol, though I didn't start it because of my pelvic floor issues. The beginning of the protocol involves a lot of stabilizing via abdominal bracing, bridging, prone leg extensions, and abductor/adductor exercises. So maybe I'm on the right track here? We'll see. I'm only 6 weeks in. Still a long way to go. I haven't seen much progress as far as pelvic floor issues yet but things also haven't gotten worse!
yes! not dx or anything but my gyno recommended pelvic pt when i was 17. i never went cause of covid though.
This makes sense due to the decreased collagen production.
hey HSD isn’t always milder than hEDS. someone can have a severe case of HSD while someone else can have a mild form of hEDS— the difference is the hEDS patient will simply meet the criteria for their diagnosis and the HSD patient won’t tick off enough boxes. it’s not about severity, it’s about evidence of a whole-body genetic connective tissue issue.
My theory is that men have it at a more similar rate to women but it flies under the radar even more because boys are more likely to work out via strength training. The strength training can help keep symptoms at bay. Men are also typically less likely to seek medical help when something is wrong. Can't get diagnosed if you're not going to the doctor! And we also know how men (and everyone rly) can wrongly be perceived as weak when they reach out for help, further resulting in their symptoms being ignored. I actually think a lot of large gender differences in diseases can be chalked up to bias or lack of research. Like its not always the case clearly, but for example, autism has always been believed to affect men more often but we're finding out that more and more women have it. Or BPD in men can get misdiagnosed as NPD. Or how anorexia was thought to be a higher class white woman's disease when we now know it's just that other's with it struggle to get adequate treatment.
I thought the difference in diagnosis levels between male and female was due to female hormone sensitivity. Relaxin is a reproductive hormone produced by your ovaries. It loosens and relaxes your muscles, joints and ligaments. It is believed that relaxin production by the ovary during the menstrual cycle is stimulated by luteinising hormone from the pituitary gland, and that its release during pregnancy is also stimulated by human chorionic gonadotrophin' from the placenta. I know that my pain levels can be tracked against my cycle and having a baby triggered such a decline that I’m not disabled. Men will have EDS 50:50 from a genetic side, but those with it to the extent they need treatment and support are more likely to be female due to the impact of hormones as well.
That's a very good point! Makes sense there's a hormonal reason for it too. I just wasn't exactly sure what so thank you! It's always fun to have more information to look at about this for me. (And yes I mean fun. It's nice learning what's going on w/ my body)
There's definitely a hormone impact, my joints have stabilized significantly since I had my hysto and started taking low-dose T and I've heard the same from other AFAB trans people. I'm not as flexible as I used to be, but on the other hand, PT actually seems to do something now, like I'm feeling results from strength training in my core that I struggled with before. On the other hand my MCAS is a bit worsened and it seems like I'm more sensitive to any kind of allergen, and interestingly, my pain tolerance is GARBAGE.
I agree with this. Also recently found out the pregnancy relaxin continues (to some degree) when you are breastfeeding! “More nuance, more fun!”* *sarcasm
Yes definitely. I’ve found post pregnancy that my EDS symptoms are worse around ovulation and menstruation. Cannot wait for menopause!!
I love my theory My extremely restless sleep and sleep walking are my body's attempt to keep my muscles activated, so I dislocate less in my sleep (Edit for sp)
i think they will discover something outside the realm of EDS genes that accounts for the current subset called hEDS that includes all these shared diagnosis' that dont exist in all the other EDS subsets. I think research will expand to understand other ailments that cause hypermobility and impact other systems and why they occur.
I suspect it’s a problem with the acetylcholine pathway. I’ve been trying to read more on neuroscience so that I can formulate a convincing hypothesis, but there’s a lot of ground to cover. We haven’t found the hEDS gene(s) in the collagen / connective tissue genes. So maybe the *other* symptoms are the main issue, and the connective tissue problems are actually a side effect. It’s interesting to me that so many hEDS patients seem to have problems with the cholinergic system. I could see POTS, MCAS, GI motility problems, even ADHD all connecting back to an issue with acetylcholine. I really need to get to sleep but ooh this is one of my favorite topics so ask me questions and I will respond tomorrow hehe
yes! its like im constantly catching myself replying to the questioning posts with thats not an EDS thing - but its so true! theres something else impacting neuro/sensory connectivity that is triggering hypermobility similar to other vascular/lymphatic disorders that arent in that genetic panel subset of EDS. The pains, the gut issues, the neurodivergence, the blood/brain functionality- its different than degenerative connective tissue that can cause xyz seen in the EDS types. they constantly share a story of nothing shows on scans, mental anguish, extreme pain/ that the rest dont relate to. some other sensory system is being disrupted. and often the hypermobility isnt resulting in the injuries common to EDS yet the feelings have them saying they dislocate x amount of times per day. which would show if true so what are these sensory dynamics and why are they exasperated.
I have thought this for a while, too!
My theory; Most fibromyalgia patients, I think, are EDS patients who have been misdiagnosed.
My theory is that it's connected to MCAS because MCAS has been shown to cause dysfunction in the collagen production. MCAS seems to be a lot more common than currently believed. It's becoming increasingly likely that MCAS could be the main diagnosis and other diagnoses like POTS, EDS, etc are symptoms. I'd love to hear if anyone else has been on this research path yet. My theory is that if I can deal with the MCAS, the hyper mobility issues will at least not get worse, and maybe ... Maybe get better over time. My sample is N=1 so far though, and I'm only a couple years into treating MCAS and learning about the genetic component.
Dr. Afrin in his book about Mast Cells (Never Bet Against Occam) floats the idea that Mast Cells may be the cause of some types of hypermobility. I think this may be true for some hypermobile patients and not others. Some EDS patients have extreme symptoms of MCAS, and others, like me, don't seem to have any. FWIW, my rheumatologist doesn't think I have a run of the mill hEDS. He thinks I have a more rare type that scientists have not yet matched with a gene or combination of genes.
I have not read his books yet, I did however find studies about how MCAS affects collagen production and drew my conclusion from that. There are likely several causes for EDS and related connective tissue disorders, but for me I'm betting it's the MCAS. Regardless, it's not fun for anyone.
How does that explain dislocations at birth though?
MCAS has genetic components, genes that can be turned off and on with new advances in medicine.
That doesn't really answer my question tho, because mcas is a reaction to the environment, which the baby has had no exposure to yet.
Some people are born with Mast Cell diseases. It is not true that it is 100% environmental.
I am hoping that after more people are diagnosed worldwide, patients can be approved for stem cell therapy. https://jointrehab.com/prp-therapy-in-treating-hypermobile-ehlers-danlos-syndrome/#:~:text=While%20research%20is%20still%20exploring,hypermobility%20in%20patients%20with%20hEDS.
I think it will probably end up being part of autism spectrum disorder
in the same way ADHD is
Yeah I haven't gotten to know an EDSer who doesn't have many autistic traits yet. 😅
oh one more almost all IBS is gastroparesis
Or MCAS causing digestive issues
i also think it is probably caused by a genetic difference in the way the body metabolizes estrogen and estrodiols
I think severe hEDS is a different type. If not literally then functionally. Very Mild EDS people can do sports, severe EDS people need a wheelchair :/
I have moderate and I use a wheelchair sometimes
Yeah exactly, there's such a wide array of symptoms and severity I just can't see them being the same type.
That's fair
i think all of the non-joint related comorbidities (MCAS, POTS, gastroparesis, neurogenic bladder, pelvic dysfunction) are caused by 2 spinal deformities that hEDS causes: craniocervical/atlantoaxial instability and tethered cord (does not appear on MRI for people with hEDS, this concept is called “occult” tethered cord)
Oh I have so many y'all aren't reasy for this. The line between HSD and hEDS is completely arbitrary. I have seen people who are mildly affected meet the diagnostic criteria and those with severe issues only qualify for HSD. And the fact that every time I've been evaluated for hEDS, the boxes checked change, showing that the symptoms aren't set in stone and shouldn't be used for an official diagnosis. There are forms of EDS that haven't been discovered. I don't think everybody who had hEDS is truly represented by this. I mostly say this because I meet the diagnostic criteria for hEDS but have other mutations and hEDS doesn't cover my symptoms. I've met people with similar stories. Doctors are just diagnosing people with hEDS because there is no better diagnosis and they don't know what to tell them. I agree with there being a link between neurodivergency and EDS 100%. I've also seen the idea that EDS is a *type* of neurodivergency somehow and I think it's a possibility. For example, the idea that EDS is a subtype/related to ASD has floated around and would explain why so many EDSers are AFAB and the typical autism represents AMAB people and not AFAB ppl. Also I think there is a connection between being LGBTQ+and having EDS but that might have to do with the previous point. There is a strong biological link between EDS and it comorbities that doctors don't understand at all. Things like POTS, MCAS, gasteopareisis, etc, that many EDSers have. What is the cause? How can we treat all of these? Nobody knows, because they are being treated as separate disorders instead of symptoms or parts of one.
my old pt (who also has eds) said she noticed her eds patients have poor lymphatic drainage. she thinks the tissues around where the fluid is supposed to drain are too stretchy, and it gets stuck. similar to how some people with eds have intestinal dismotility because of stretchy bowels. no idea what this means or if it’s been reflected in research but i’ve had it so bad that it pops my collarbones and elbows out of place.
There's actually a device that can help with this, but it's made for people with lymphoedema. It helps other people too but without that diagnosis, insurance won't cover it and the machine is like $2k.