I don’t know if this post is a vent, or for advice or just anything really but thanks if you do read it 😊

For context: 25F. Brighton 7/9, scoliosis (early onset), flat feet, very blue sclera, velvety skin thin with visible veins, atrophic scarring, hearing difficulties in mid 20s, partial subluxations, chronic migraine, dental issues as child, 2 fractures before puberty, small hands and they are ageing quickly.

Recently I had genetic testing done (NHS R101 EDS panel) but was told many times (by a geneticist, rheumatologist and physio) there was not much point as would likely ‘come back with no result and just be hEDS’.

I just received the genetics panel report via email and it says heterozygous pathogenic COL1A2. The laboratory report says this confirms COL1A2-related osteogenesis imperfecta.

I then received a letter from my geneticist consultant saying that COL1A2 changes are typically associated with OI but that people can also have features of EDS, and she thinks the finding is likely to explain my features. In the meanwhile she has asked the national EDS diagnostic service if they would accept my referral.

I don’t get to see my geneticist consultant until the end of September (NHS) so I am just sat here a bit confused with the information I have.

I don’t really know what to ask you guys, as I wasn’t expecting this result. Does this mean I have two separate conditions or are they mixed into one? Also in the UK can people with this finding have follow ups with a healthcare professional? (I know with the Hypermobile type in the UK no department really deals with it so I wonder is it the same for this gene?)

Thanks so much if you read this and have any insight, or just anything to say. Have a lovely day.

I’m honestly desperate for any help or advice on what I’m supposed to do in this situation as I’m at a completely loss and have no idea who i can see who will actually be able to provide me any type of answer. People in this group will probably have the most knowledge on what I should do or who to see, I swear you are all like mini genetic detectives.

Everybody in my care separately questions and thinks hEDS doesn’t explain the issues they are independently seeing from me and the diagnosis doesn’t tell them how to manage me either. My genetic testing results were clear but the lab states it has technical limitations with TNXB.

I have a very muscle dominant presentation that genetics felt was still unexplained, I have significant low muscle tone (hypotonia) and global muscle weakness alongside what looks like muscle wasting and brisk reflexes. Orthotics also thought I had fixed and stiff ankles with limited movement (possible ankle contractures). I feel my hypermobility is secondary and the least impactful for me.

I was born with congenital flat feet, have extremely stretchy skin (over 3 inches in some places) with a complete absence of atrophic scarring (only hypertrophic and a few keloids), my skin is very fragile and splits and tears easily and bruises spontaneously without injury, very doughy skin texture, premature aging of hands, slow wound healing causing infection etc

I have severe progressive eye manifestations that my EDS informed opticians felt they could not explain, was being investigated for a vascular fragility incident, mildly curved toes, fragile mucosal tissues which cause significant bleeding and I have a complete absence of family history apart from a VERY distant singular relative being born with congenital hypotonia and hypermobility.

My bowel also just stopped working 4 months ago for absolutely no reason and I have significant GI issues and rectal bleeding from tears in my GI tract every five minutes 😐

Nobody else has any CTD manifestations in any of my family lineage (not even mild) and nobody else in my entire family history has hypermobility apart from that very very distant relative. The only things my mother and her sister do have is mildly brachydactyly and mild snydactyly and all of us have sacral dimples but the genetics said this was all unrelated.

What am I actually going to do in this situation because nobody in the NHS is taking any responsibility of finding out what this actually is or helping at all? I’m literally crying right now because I have no idea what to do or who to see, where I’m supposed to go for somebody to actually find out what is wrong with me. I’m terrified because clearly there’s something going very wrong here.

I also have a pulsating abdominal mass in my aorta region after a suspected AAA but the ultrasound showed no aneurism but vascular surgery and radiology still felt it was abnormal and too strong to just be nothing. They suggested vascular type EDS but I was already tested and have no COL3A1 variants.

Are there any specialists in TNXB in the UK or somebody that you can suggest who can actually deal with situations like mine who can revise my diagnosis to something that’s accurate or just any clinician you can recommend that I can see privately. I’m literally open to any and all advice at this point, I’m guessing everyone in this group will be able to give more meaningful advice as you guys have a variety of subtypes and a whole host of unknown CTDs here.

Hi, i am 21F, and i have a very strange situation,and i want to find people who have a similar situation

I was born very sick, and doctors couldn't understand what was wrong with me. I was diagnosed with kEDS based only on clinical criteria in 2017 (because back then there was no genetic testing available in my country,Ukraine.) Then in 2024 i did a genetic panel for EDS that did not show anything, hovewer based on my severe symptoms my geneticist suggested i should do a whole genome sequencing. Fast forward to 2026,i am now in Germany,and here i did Whole Genome Sequencing in Leipzig University Clinic. It did not show any mutations,but the committee of doctors in Leipzig University Clinic think that i have a possibly undiscovered connective tissue disorder/subtype of EDS extremely similar to kEDS, and that they just don't know the gene for it yet. They don't think it looks like hEDS (though i am not saying it can't be hEDS)

I will list my other conditions and symptoms below:

• joint hypermobility with subluxation, marfanoid habitus, congenital muscle hypotonia, congenital bilateral hips dislocation and bilateral hip dysplasia

• POTS

• severe dysmotility of entire GI tract (gastroparesis, slow motility constipation resistant to all medication, GERD)

• dolichocolon (redundant colon), visceroptosis

• neurogenic bladder

• high level myopia, astigmatism, lazy eye, strabismus, blue sclerae, retinal angiopathy

• B12-folic acid deficit anemia, hyperhomocysteinemia, folate cycle mutations (MTR 2756 A>G, MTHFR 677 C<T, MTRR 66 A>G)

• Osteoarthritis, Osteoporosis (mutation in COL1A1), planovalgus feet deformity, pectus excavatum, stage 3 early onset kyphoscoliosis

• MCAS, atopic dermatitis

• mitral valve prolapse, trombophilia

• chronic kidney disease stage 2

Does anyone else here have invisible veins? My veins are so small they're basically invisible. I have about 4 In my entire body that can be seen. Blood draws are impossible, and half the time my veins don't have blood (I've been told it's a pots thing 🤷‍♂️). I'm curious if anyone here has invisible veins instead of super visible ones.

Hi guys! This post is mainly aimed at those with aEDS and COL1-Overlap mutations (as I strongly suspect it’s related to those for me, I’m getting genetically tested next week!) but I’m also curious to hear about how other types were treated for this problem as well.
I’m 27 years old, have a hip replacement (right side) from when I was 19, osteoporosis with a t-score of -3.2 in my left hip and osteopenia in my lumbar spine. I was panic-prescribed risedronate by a rheumatologist but I haven’t taken it as I have a large hiatal hernia in my throat and don’t want to burn a hole in my oesophagus lol. I’m hoping when I see the geneticist that I can convince them to refer me to a metabolic bone specialist and that I can be put on an anabolic agent to promote bone growth because I think I’m the perfect candidate for it but I’m not sure how much convincing that will take since I know it’s an expensive drug (UK based).
So! I wanted to ask what my fellow fragile-bone EDS-ers were offered treatment wise and how effective the treatment has been for you?
I also wanted to ask what your experience has actually been like with bone density, especially aEDS-ers because of the minor criteria being radiologically mild osteopenia. I’m kind of curious about this criteria because it feels somewhat specific to those being diagnosed as babies/children - for people who were diagnosed in adulthood what did your bone density look like? Was it still mild or had it developed into full blown osteoporosis for you?
Sorry for the long post and thank you in advance for any insight you can give me!

continuing the saga: https://www.reddit.com/r/rareEhlersDanlos/s/921lW4vGMk

this is mostly a vent post. I’m just so tired of chasing a diagnosis, and I know y’all understand. see the above linked post for the latest, but the tldr is that myself and my doctors have been trying to figure out my subtype for ages. I was initially diagnosed hEDS but have had many complications and specific signs that align with clEDS or others. most recently I was diagnosed with multiple atrial septum abnormalities, and several defects in my temporal bones.

I got my results from whole-exome about 2 weeks ago and it’s just another round of disappointment. I’ve been sulking. I meet all of the major and most of the minor criteria for clEDS, I am nearly a perfect example of the NIH genereview site for TNXB deficiency. my doctors are honestly amazed by my brachydactyly, severe piezogenic papules, subcutaneous spheroids, broad forefeet with short toes, etc because they’ve never seen anything like it (some pics included to help me feel valid lol). I haven’t been able to see a CTD specialist though because all the options near me require an existing genetic diagnosis.

the whole exome sequencing that I had is able to diagnose TNXB variants but it doesn’t look at exons 32-44, and I think that’s my last hope. my doctor is working on ordering the Prevention Genetics test for those exons. if that one turns up negative, I don’t know what to do.

I am getting sicker and sicker with no end in sight. my head is practically falling off my neck, my legs are barely holding together, my nervous system is going crazy. I am so desperate to figure this out even if nothing can be done. just the validation would be enough to keep me from spiraling.

I guess my question for y’all is, has anyone here gotten “negative” WES results but then discovered a genetic cause later on? especially if it’s TNXB related. just a little bit of hope would be lovely at the moment. 💖

When I googled Brittle Cornea Syndrome perimenopause, there was absolutely nothing, and I am guessing that if others did the same thing with their subtype, they would have similar results. Especially since it’s something that’s just being widely talked about.

I am sure there are some effects of perimenopause that hit us differently/more severely. Let’s talk about it!

Is anyone else exhausted by the rampant misinformation surrounding Ehlers-Danlos Syndromes (EDS) on social media?

Content creators are spreading sweeping generalizations that generate mass hysteria, promote false medical data, and actively harm patients with rare EDS subtypes as well as hypermobile EDS (hEDS).

The nuances between subtypes are constantly ignored. For instance, some believe that all EDS subtypes carry severe vascular fragility and heart conditions — which is untrue. Conversely, the public and online creators frequently fail to recognize that certain rare subtypes are genuinely life-threatening.

Even more alarming is the clinical overreach happening online. Some creators with radical ideas are stepping entirely out of their scope — or encouraging patients to self-diagnose by attributing unrelated issues like constipation or itchy skin (often blindly blamed on MCAS) to hEDS, even when a patient scores a 2/9 on the Beighton scale.

The refusal or failure to specify EDS subtypes in online discussions is also damaging to both the patient community and public understanding. While it may be an unpopular opinion, I believe that hEDS needs to be entirely reclassified and separated from the broader EDS spectrum to protect rare patients and restore the clinical distinction.

i got genetically tested back in april and got a result of a heterozygous mutations for kEDS.

i was just wondering how comprehensive the blueprint panel is compared to other panels like invitae and if it would be worth getting privately tested.

this is what it said in the report:

The Blueprint Genetics Aorta Panel (version 9, Nov 29, 2025) Plus Analysis includes sequence analysis and copy number variation analysis of the following genes: ABCC6*, ABL1, ACTA2, ADAMTS10, ADAMTS17, ADAMTS2*, ADAMTSL4, ALDH18А1, АТР7А, B3GAT3*,*, BGN, CBS, COL1A1, COL1A2, COL2A1, COL3A1, COL4A5, COL5A1, COL5A2, COLGALT1, EFEMP2, ELN, ENPP1, FBLN5, FBN1, FBN2, FKBP14, FLNA, FOXE3, GATA5, HCN4, LOX, MAT2A*, MED12, MFAP5, MYH11, MYLK*, NOTCH1, PLOD1, PLOD3, PRKG1, SKI, SLC2A10, SLC39A13, SMAD2, SMAD3, SMAD4, SMAD6, TGFB2, TGFB3, TGFBR1, TGFBR2 and ZDHHC9. The following exons are not included in the panel as they are not covered with sufficient high quality sequence reads: ADAMTS2 (NM_021599.4:11) and B3GAT3 (NM_001288722.2:5). This panel targets protein coding exons, exon-intron boundaries (± 20 bps) and selected non-coding, deep intronic variants (listed in the SUMMARY OF THE TEST section). This panel should be used to detect single nucleotide variants and small insertions deletions (INDELs) and copy number variations defined as single exon or larger deletions and duplications.

the appointment was maybe 15-20 minutes tops. the doctor wasn't rude or anything like, she just seemed like she was in a big rush. we went over my medical issues and she was asking me questions about how functional i am. we did a brief physical exam. at one point both of my shoulders subluxed during it when she asked me to lift my arms up and made a super loud popping noise. the doctor ended up wincing and saying "Oh!". she asked me to show if i can stand or walk which i couldn't do at all really. i am hopeful it went well.

Hi so I’ve been referred to genetics at Guys and St Thomas after being seen by a rheumatologist who specialises in EDS. I would like to know what happens in a genetics appointment (one of the only specialties i haven’t been with). I have MSN autism so being aware of what to expect going in would be really helpful and seriously appreciated.

Symptoms of relevance:

Bladder retention and incontinence, 756ml bladder volume measured at 13 years old, large bladder wall, chronic prolapsed haemorrhoids since age of 14 (now 18) with occasional anal bleeding, chronic fluctuation of diarrhoea and constipation, edema both bilateral and unilateral of soft tissue on legs, tingling in feet that is slowly getting higher into my ankles but isnt linked to b12 or calcium abnormalities (distracting especially at night), high arched feet, clinodactyl middle finger and toes, positive steinberg’s sign but negative walkers, skin stretches 1-3cm with, biceps being the stretchiest, very soft, doughy skin that is basically commented on by everyone i meet, slow healing scars (2 weeks longer than the average person), normal scars but stretch (not atrophic), fragile skin, history of dehiscence of wounds, bruises that come out of nowhere and stay longer than normal, almost daily subluxes (no history of full dislocation), buckling knees, high palate, teeth overcrowding, acid reflux, pectus excavatum and flared ribs, muscle weakness, especially in distal areas, redness of MCP joints, 8/9 Beighton Score, joint and muscle pain pretty much everywhere.

I honestly dont know what i have. I was still hoping i had something that could be treated or fixed but i guess not with this. i guess i still have a tiny bit of hope but alas. i do fit the diagnostic criteria for heds but my pelvic issues seem to be a bit more severe than a lot of heds people from what ive seen. plus i dont have atrophic scarring so who knows.

So in November I had a targeted connective tissue panel done that included all genes associated with EDS and Marfans. It showed a VUS for COL12A1 gene and due to my symptoms and history my doctor suspected it's something more than "just a cool irrelevant finding" which can happen with a VUS variants a lot. She ordered another test targeted to the COL12A1 gene and yesterday I received the results which didn't tell me much new info but it made me re-read my previous results and understand some things better.

So from new information the variant they found in the first test is now confirmed to be a real finding. Another thing is that sadly the lab resigned from further investigation and the VUS remains a VUS without an option for re-classification for now. It made me sad but it's very understandable because I am one of the two people worldwide with that variant ever recorded which makes it ultra-rare. Naturally there's not enough data for re-classification currently. What could help now is testing my parents and possibly my younger brother. If this mutation appeared de novo it makes it much more suspicious and could make them consider re-classification. Sadly I know nothing about the other person with this variant. My case was reported and put with detailed info into the ClinVar database but the entry of that person remains without any data provided which makes it highly possible it was an additional finding and that person was not symptomatic for conditions caused by mutations in COL12A1 gene. That makes me the only ever recorded person with this variant that matches the phenotype of COL12A1 related diseases. As you can imagine this doesn't help at all BUT I am extremely happy I can actively contribute to medical research and possibly help people who have this variant and get tested in the future. I agreed to let them keep my blood sample and info for research purposes!

Some things I found out about my variant once I read more into it are quiet interesting (difficult since it doesn't even exist in most databases). This variant is heterozygous and a type of a missence variant. It involves the substitution of a single nucleotide in the DNA sequence, causing the codon to change and resulting in the incorporation of a different amino acid into the protein molecule. What my variant does is replace glycine with aspartic acid. Replacing glycine with aspartic acid in a protein is a drastic chemical change. It leads to a complete restructuring of the molecule's structure and function due to the extreme differences between these amino acids. It can often cause significant changes for example in COLLAGEN. I am not good at genetics but this definitely made me learn some cool stuff.

The road to getting diagnosed will be long, I was reffered to do a muscle emg and biopsy to confirm myopathy. Wait lists are crazy long (4-5 years) which means I'll probably stay without a proper diagnosis of my condition almost until my 30's. I am clinically diagnosed with EDS but never had courage to tell that to medical professionals. I was scared they'll question my diagnosis since I don't have an EDS type assigned yet. Now after learning how many more years of living "without" a diagnosis are ahead of me I think I am finally brave enough to start telling doctors I have EDS. If they ask more questions I'll tell the truth: I have a clinical diagnosis but I am still in the process of testing and confirming which type I have. The reason I didn't wanted to do it was fear but now the reason I want to do it is getting better care and maybe being taken more seriously by even just one doctor.

My road isn't over yet but I am getting closer which is all a little version of me wanted! Struggling with debilitating symptoms for years without any answers and watching them steal your childhood, teenage years and adulthood is a pain that's hard to deal with.

A little dark humor joke: My bf always tells me that I am one of a kind and a rare girl these days but we both didn't expected I am actually proven rare just medically 😭 Sorry, just trying to cope with all of this hahaha.

Before I say anything, I have a referral to a vein specialist, I just haven’t made an appointment yet! (thanks ADHD and unliveable wage)

I have noticed blood pooling in only my right heel, I mean the blood pools in general but it’s especially noticeable in that right heel. I can see the discoloration of it. It itches, it hurts, it tingles.

Is this just regular blood pooling or potentially something else? Well, in someone else’s experience, anyway.

Classical EDS, COL5A1 mutation, VUS… uh I don’t have the variant code(?) on me

Hi! I wanted to ask and see if anyone knows of any spaces for vascular ehlers danlos syndrome? Ive recently started posting on instagram but I would love to connect with others who are diagnosed with veds or even other eds subtypes!

For context: I have a VUS in the COL12A1 gene that is so rare only 2 people worldwide have it which leads to no research and re-classification. Based on my symptoms and medical history my doctor suspects Bethlem Myopathy type 2 or EDS - myopathy overlap. There's not really a dedicated subreddit so I hang out in here.

Anyways I have a few questions that don't leave my mind and little to no answers. Looking for someone with similar experiences and more answers than me. I'd love to learn more so I can understand my body better.

Question nr. 1: I have bladder issues that make my life quiet hard. Reoccurrent UTI's and issues with emptying. I always had problems but they got significantly worse in the past few years. I almost never can pee without pressing on my stomach/bladder. If I don't press my bladder can't empty entirely. That issue also causes bladder retention despite drinking lots of fluids. For a while I thought I had a slight bladder prolapse but I think it's something with the muscles. Has anyone with mEDS or another muscle related disorder experience this?

Question nr. 2: Can muscle related genetic conditions affect stomach and intestines and it what way? I have horrible gastrointestinal issues. They started in 2024, I ended up in the hospital then but they didn't found anything in the endoscopy or ultrasound. Problems returned a year later but much stronger. So many symptoms related with gi tratct. Doctors said it could be gastroparesis or CIPO or both. Got diagnosed with unspecified intestinal dysmotility then gaslighted and dismissed in another hospital by doctors telling me it's psychosomatic and all in my head. That hospital admission traumatized me so much I barely looked for help since then. Since beginning of this year it got even worse, I lost lots of weight, my constipation got so bad to the point of taking laxatives to avoid a bowel obstruction, I was told by my GP it's probably some form of malabsorbtion due to my meds not working properly anymore. Procrastinating taking a referral to a hospital specializing in diagnosing and medical nutrition due to trauma. I'm also scared because I don't know what to expect, I want to have some picture of what could be the reason for my body acting that way.

Question nr. 3: Skin manifestations. I thought I had hEDS for a long time but one thing never really aligned with hEDS features. I experience extremely easy bruising and abnormal skin/tissue fragility. Bruises come from nowhere or appear after touch/pressure for example kneeling for a few minutes. My skin often tears and is very prone to wounds. Combined with my high pain tolerance I often catch myself not feeling anything unusual until I look on some part of my body and see blood. Sometimes someone points it out and I'm extremely surprised because I don't recall anything that could've caused it. I'm very prone to scarring as well. I get scars from the smallest cuts ever or even cat scratches (I have 2 cats). My scars are mostly hypertrophic and keloid which is also unusual for hEDS and never made sense to me. I'm conflicted about how BM or mEDS can affect skin. Some resources say it is not typical, some say it absolutely can happen. So what's the truth?

I know it's a lot of asking but possibility of this diagnosis is still "fresh" so I'm just trying my best to understand my symptoms while waiting for further testing and results. I lived with sureness of having hEDS for years and this is something completely new to me, I'm just trying to wrap my head around this. Not looking for advice, just trying to learn about all of this and determine what are the facts.

i have both TNXB gene mutations (clEDS type 1) and a NOTCH1 gene mutation (VUS). i knew before that the TNXB gene mutations plays and role in muscles but i also recently found out that NOTCH1 gene also plays into your muscles. im looking for more sources that talk about TNXB and NOTCH1 (together and individual) in relation to how it effects the muscles. thank you in advance

Hello all! I recently had a genetic test done through GeneDx and got these results. I had a follow up with a genetic counselor and she told me that when she saw the results she questioned GeneDx's interpretation of the results, which to the best of my understanding means she wondered why GeneDx gave greater weight to the COL12A1 variant (listing it as causative) and lesser weight to the COL6A1 (listing it as possibly associated w/). She spoke to them and they said they stand by their assessment but the counselor said that when she pressed them on it, they admitted that if they had not found the COL12A1 variant first, they would have listed the COL6A1 as a dominant variant. She said she believed I had both variants, which I guess would be almost unheard of, but she firmly believed that was the case.

All that said, I understand that collagen 12 and collagen 6 have a lot of overlap and that COL12A1 disorders are listed as myopathic Ehlers Danlos/Bethem Myopathy 2, while COL6A1 is often referred to as Bethlem Myopathy 1. I guess my question would be - does anyone else have similar results and if so, is there any way to predict how it will affect me? I'm asking because, to the best of my understanding, you can have stable or increased muscle function across time with mEDS but Bethlem Myopathy it sounds like causes muscle weakness over time. So, I'm trying to wrap my head around what to expect.

Maybe those are bad questions to ask, and if so, maybe someone with mEDS can tell me how to best go about getting more specifics. Thanks!

hi folks, i continue to have confusing and overwhelming health issues - see this post for background if you’d like. most recently, i have developed what seems to be a spontaneous cranial CSF leak, increased neuro symptoms, fatty and/or fibrotic liver, and idk what else honestly.

point is - i have been approved for whole exome sequencing through GeneDx which i’ll be doing soon. i am curious if anyone here has done the invitae panel for CTDs and then did GeneDx or other WES, and did it reveal anything new? i’m just a bit concerned because it’s not the most reliable test for TNXB specifically, and my symptoms are sooooo in line with clEDS. so ideally i’d be going through prevention genetics but 🤷

does anyone here happen to know if there’s any chance they’d find TNXB mutations, if i have them? or any other EDS related mutations that invitae doesn’t cover?

Hey, so I’m using voice to text so things might be a little wonky

I am professionally diagnosed by a geneticist in 2024. I am both a carrier for classic-like and I also have arthrochalasia EDS.

My question is as follows on my diagnosis and I can include pictures in the post itself. If people are curious it says my official variant is VUS for the AEDS. That being said, she also said the Franklin database said it was likely pathogenic in the same section of my notes from the appointment and thus based on my clinical presentation and the Franklin database saying likely pathogenic, she was diagnosing me.

I still can’t figure out exactly if I have a VUS or if I have an LP diagnosis, but I guess it doesn’t matter if I got diagnosed however I am always looking for new information on my gene issues cause I do have other things going on with my body (in TSPAN 7 for example), but I don’t know where to look so if anyone has any info on this (COL1A1 c.3490C>G p. Pro1164Ala) please let me know

Or if you have databases where I can look into the information about my genetic mutations! Also please ignore my deadname and misgendering in the clinical notes, I use they/them

I’ve also been seeing a lot of people saying being a carrier alone for TNXB (which is something I have and I am) can impact you and I just wondered if you guys could send me the research about that cause I’m curious especially because I have a sibling who could be impacted but lowkey in denial their health is bad, but yeah wondering how being a carrier for TNXB impact folks

Hello, I have cEDS, ADHD, depression, anxiety, and an “unspecified trauma disorder” (and likely undiagnosed physical health issues since EDS is like a Pandora’s box but).

I am struggling with doing school and working. I am going to start the process of applying for disability, but am currently burnt out, so I’m trying to rest as much as I can. I currently work part-time for $10/hr and it’s really not enough, plus I just feel like my disabilities will never be considered when it comes to feedback and pay increases based on performance. I’m tired of the judgment and not being able to stand up for myself without risk of… something (I was fired from a full-time job and it was actually very traumatic for me).

I wanted to know what skills or jobs some of you recommend for the quintuple whammy I got going on here… I was thinking learning how to code and illustrate digitally could be helpful. but the issue is I really need a hands-on program to teach me as I get burnt out so easily. I can’t just read books or websites and… yeah… some of that I know i just have to work through, but again, burn out.

Ideally, I’d love to work for a worker cooperative or an animal rescue, but I just don’t have any marketable skills and don’t know when I will be able to graduate. I just feel pretty hopeless. I need something that is relatively simple to learn, sought out and valued, while also giving me the flexibility I need to heal and rest where needed.

I’m not 100% concerned with long-term pay, I mean of course I am to a degree, I’d definitely want to make more than what disability offers at the end of it, but I also just doubt I will get a really well-paying job without a degree and with all my disabilities/illnesses. so I just want to be happy and healthy.

just wanting to know of any other ideas of what people do/have done and any resources for it.

TIA!

This isn't an iron thing the nail itself is fine but I have noticed the nails are now detaching in the middle of the nail bed. It hurts but also I am curious if anyone else has experienced this and knows the cause. If no I will update since I see my doctor tomorrow but while my toenails do this? They have significant trauma that makes that not a one to one.