You're at a rheumatology appointment. The doctor flips through your chart, pauses, and says, "You know, we don't see many men with this."
If you're a guy with Ehlers-Danlos syndrome, you've probably heard some version of that. A geneticist. Maybe it was a physical therapist. The ER doc who looked at your chart like it was written in another language Most people skip this — try not to..
Here's the thing: that comment isn't wrong. But it's not right either.
What Is Ehlers-Danlos Syndrome
EDS isn't one condition. It's a group of thirteen (last count) inherited connective tissue disorders. They all share a common thread — faulty collagen. Collagen is the scaffolding that holds your skin, joints, blood vessels, and organs together. When the recipe is off, things stretch too far, tear too easily, or just don't hold Which is the point..
Most people who get diagnosed have hypermobile EDS (hEDS). So no genetic test exists for it yet. Diagnosis is clinical — Beighton score, family history, a checklist of systemic features. The other twelve types? Think about it: those have identified gene mutations. Classical. Vascular. Kyphoscoliotic. The list goes on.
But the question people actually ask — the one that brought you here — is simpler. Do men get this less? Or do they just get diagnosed less?
The Short Answer: No, But It's Complicated
Genetically speaking, most EDS types are autosomal dominant or recessive. Which means a father with classical EDS passes it to sons and daughters at the same rate. Your biological sex doesn't change the odds of inheriting it. That means the mutated gene sits on a numbered chromosome, not a sex chromosome. Same for a mother Nothing fancy..
So strictly speaking? Men aren't less likely to have the mutation.
But walk into any EDS support group, scroll any forum, look at any clinic's patient roster — and you'll see women outnumbering men by a lot. Some studies put the ratio at 3:1. Others say 9:1 for hEDS specifically.
That gap isn't genetics. It's everything else.
Why It Feels Like Women Get It More
Diagnostic Bias Is Real
Let's start with the uncomfortable truth. Medicine has a long history of taking women's pain less seriously — but also of looking for certain conditions in women more aggressively. EDS got labeled a "women's disease" decades ago, partly because hypermobility is more visible in female bodies (estrogen increases ligament laxity) and partly because... well, doctors expected to see it in women.
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Men with the same symptoms often get different labels. Consider this: " "Old football injury. Think about it: " "Clumsy. In real terms, " "Double-jointed. Think about it: "Growing pains. " "Just tight hamstrings — stretch more Worth keeping that in mind..
I've talked to men who spent twenty years being told their chronic shoulder dislocations were "instability from weak rotator cuffs" before someone finally connected the dots. Because of that, twenty years. Same mutation. Different starting assumption Turns out it matters..
Hormones Change How Symptoms Show Up
Estrogen and progesterone affect collagen. They make it more elastic. That's why many women notice symptom flares around their period, during pregnancy, or postpartum. It's also why hypermobility is often more obvious in women — the Beighton score captures passive range of motion, and hormones give women a natural boost there.
Not the most exciting part, but easily the most useful.
Men don't get that hormonal fluctuation. Their collagen stiffness is more stable. They might have the same genetic defect, but their joints don't "perform" hypermobility the same way on exam day. They fail the Beighton test not because they're not hypermobile — but because their baseline stiffness masks it That's the part that actually makes a difference. Surprisingly effective..
Counterintuitive, but true Not complicated — just consistent..
The "Bendy Girl" Stereotype
Pop culture doesn't help. The contortionist. Think about it: the yoga teacher. The dancer who ties herself in knots. These images are overwhelmingly female. So when a teenage boy can't touch his toes but dislocates his kneecap walking down stairs, nobody thinks "connective tissue disorder." They think "awkward growth spurt Simple, but easy to overlook..
The stereotype becomes a self-fulfilling prophecy. And girls get screened. Boys get shrugged off.
What the Genetics Actually Say
Autosomal Inheritance Means Equal Odds
Let's be precise. Now, classical EDS (COL5A1/COL5A2), vascular EDS (COL3A1), kyphoscoliotic EDS (PLOD1/FKBP14) — these follow autosomal patterns. Think about it: if a parent has the mutation, each child has a 50% shot (dominant) or 25% shot (recessive, if both parents carry it). Sex doesn't enter the equation That's the part that actually makes a difference. Practical, not theoretical..
X-linked inheritance does exist in connective tissue land — think Fabry disease, or some forms of osteogenesis imperfecta. But EDS? Not the main types.
So a man with classical EDS has the same chance of passing it to his son as his daughter. His father had the same chance of passing it to him as to his sister. The mutation doesn't care Still holds up..
But Expression Isn't Always Equal
Here's where it gets interesting. Penetrance (whether you show symptoms at all) and expressivity (how bad they are) can vary by sex. Hormones. Muscle mass. Even so, activity patterns. Occupational wear and tear. A mutation expresses itself inside a whole body — and male bodies are different environments.
Some researchers suspect androgen protection. Testosterone increases collagen cross-linking and muscle bulk. More muscle = more dynamic joint stability. A hypermobile guy who lifts weights might function better than a hypermobile woman who doesn't — same mutation, different outcome And it works..
But "functioning better" isn't the same as "not having it." It just means the diagnosis gets missed longer.
Do Men Present Differently?
Joint Hypermobility Scores
The Beighton scale is the gatekeeper. So nine points. But the scale favors certain joints — thumbs, pinkies, elbows, knees, spine. Also, five or more (adults) = generalized joint hypermobility. It doesn't capture ankles, hips, shoulders, jaw, cervical spine well.
Men often score lower on Beighton despite clear hypermobility elsewhere. Broad shoulders hide scapular
scapular instability and reduced thoracic mobility, which can masquerade as simple postural strain or overuse injury. When a male patient reports chronic shoulder dislocations, recurrent acromioclavicular sprains, or unexplained scapular winging, clinicians may attribute these findings to athletic trauma rather than an underlying connective‑tissue vulnerability. The Beighton maneuver, which emphasizes thumb-to‑forearm apposition and fifth‑finger extension, fails to capture the laxity that often resides in the glenohumeral joint, the sternoclavicular articulation, or the cervical spine — areas where men frequently experience symptomatic hypermobility.
Beyond the upper girdle, men with EDS may present with early‑onset degenerative changes in weight‑bearing joints. Hip labral tears, premature osteoarthritis of the knees, and chronic ankle instability are reported more often in male carriers than the classic “flexible‑finger” picture suggests. These manifestations tend to emerge after repetitive loading — such as manual labor, military training, or high‑impact sports — leading to a diagnostic odyssey that spans orthopedics, physiotherapy, and pain clinics before a genetic etiology is considered.
Hormonal milieu also shapes the phenotypic expression. Androgen‑mediated increases in collagen cross‑linking and muscle mass can temporarily compensate for ligamentous laxity, allowing affected males to maintain higher functional scores on standard mobility tests well into adulthood. Still, this compensatory reserve is not infinite; as age‑related sarcopenia sets in or when activity levels decline, the latent instability becomes clinically evident, often precipitating a sudden cascade of joint pain, subluxations, and soft‑tissue injuries.
Recognizing these sex‑specific nuances requires a shift in screening strategy. A thorough family history remains indispensable; even when a male proband appears only mildly affected, identifying a similarly affected parent or sibling can raise the index of suspicion. Now, clinicians should supplement the Beighton score with joint‑specific assessments that target the shoulders, hips, ankles, and cervical spine — such as the hypermobility questionnaire, the Brighton criteria, or targeted ultrasound evaluation of joint laxity. Genetic testing for COL5A1, COL5A2, COL3A1, PLOD1, FKBP14, and other EDS‑related genes should be pursued when the clinical picture fits, irrespective of sex‑based expectations Which is the point..
The short version: the belief that Ehlers‑Danlos syndrome is predominantly a “female” condition obscures a substantial subset of men whose hypermobility manifests in less‑captured joints, is masked by muscular compensation, or presents as early degenerative joint disease. By broadening our diagnostic lens beyond the Beighton scale and appreciating the influence of sex‑dependent modifiers, we can prevent prolonged misdiagnosis, institute timely surveillance for vascular or visceral complications, and provide appropriate multidisciplinary care for all individuals living with EDS, regardless of gender Simple as that..
