The Connective IssueThe Fascia Institute & Treatment Center Journal
A weekly report from the corner of fascia medicine — where pain, performance, and getting back in are decided.
Two scorecards. One was wrong about you for years. The other never got filled in.
The sentence we hear most often in clinic is said apologetically: I can’t touch my toes, so how can I have hypermobility? Here is the part nobody explained.
The flexibility exam checks five places on your body, on one afternoon, in one decade of your life. Hypermobility is a whole-body connective tissue trait. Those are not the same thing — and the literature has known it for years. It is why more than half the people already carrying a confirmed hEDS diagnosis would fail the screening test today. If you have been turned away because you were not bendy enough, you were measured with the wrong ruler. That is this week’s lead, and it runs to 44 references.
And second, because it earned the space: last Saturday in Midland, Texas, Victor “Jalapeño” Hernandez won the WBC USA featherweight title. He put Conrad Martinez down three times, and the fourth ended it in the second round — so the judges’ scorecards never got filled in. Ten months ago he was retired, at 15-0 with thirteen knockouts and ranked twelfth in the world at 126 pounds, because of myofascial pain. The full return-to-sport case study is now published, and it is the more useful document, because it walks through what we actually did and where the evidence for each step runs out.
Victor is our patient, and The Fascia Institute is a sponsor of his professional boxing career. His name, story, and treatment details appear with his written authorization. That is a real conflict of interest, and a win makes it a bigger one, not a smaller one. It should change how skeptically you read what we say about him.
Two things we are deliberately not publishing: which part of his body was treated, and the workup he had already been through before he reached us. Those are his to share, not ours.
And the limit that matters more than the disclosure: one athlete getting better over ten months, across nine treatments, while also training, resting, and changing how he loaded — cannot tell you which of those things did it. We did not clear him to fight. Clearance for a professional bout belongs to the athletic commission.
Also this week: a self-score you can do at the kitchen table, why a loose body feels tight, the most under-recognized group in this entire condition (men), and a book I hand to patients.
Inside This Issue
- I’m not flexible — so how can I have hypermobility or EDS?Main Event
- Score yourself: nine points and five questionsTale of the Tape
- Stuck, not stiff — why a loose body feels tightBetween Rounds
- The signal that isn’t flexibility at allScouting Report
- Men, testosterone, and a ten-to-one gapOpen Scoring
- Victor wins the WBC USA featherweight titleChampion’s Corner
- CoreSalt™ — built for the standing problemCorner Bucket
- What I’m handing patients: LesondakSpeed Bag
Gloves up. Round one.
I’m not flexible — so how can I have hypermobility or EDS?
You can be hypermobile and stiff at the same time. In connective tissue those are not opposites, and the literature has known it for years.
Hypermobility describes how much passive give a joint has when someone else takes it to its end range. Stiffness is what you feel when you try to move it yourself — and that sensation is produced by muscle, fascia, joint surfaces, scar, pain, and your nervous system’s willingness to let the joint travel. A ligament can be lax while every layer stacked on top of it is guarding, gripping, densified, or arthritic.
So the honest answer has four parts, and each one is documented:
The exam is narrow
The Beighton score samples five sites for nine points. It does not look at your jaw, neck, shoulders, ribs, hips, pelvis, wrists, ankles, or feet. A critical review in Rheumatology International found it consistently failed to identify hypermobility in joints outside its own scoring system, and concluded it should never be used alone to exclude generalized hypermobility.
The exam is a snapshot
Measured hypermobility falls with age — enough that the diagnostic threshold has to move with it. A 2026 meta-analysis pooling 46 studies and roughly 23,000 adults found data-driven cut-offs that decline steadily across the lifespan.
Things get layered on top
Arthritis, old sprains, surgical scar, muscle guarding, and fascia that no longer glides all reduce the range you can actually reach. If you are hypermobile you have probably had more sprains, more subluxations, more repairs and more time in a brace than your peers. Each episode quietly takes range away.
Most of the condition isn’t flexibility at all
Dysautonomia, mast cell reactivity, gut dysmotility, chronic pain, fatigue. None of it is measured by how far your thumb bends.
More than half of already-diagnosed patients fail the flexibility test
An Italian reference center re-examined 327 patients from 213 families, all previously diagnosed with hypermobile Ehlers-Danlos syndrome under the earlier Villefranche and Brighton criteria. Applying the current age-adjusted Beighton threshold, only 43.12% — 141 of 327 — still met it. These were not borderline cases; they were patients a specialist center had already diagnosed. The authors concluded the 2017 criteria “should be made less stringent.”
Ritelli M, et al. Am J Med Genet A. 2024. PMID 37774134. Single tertiary referral center, retrospective — and the authors are openly arguing for looser criteria, so read the direction of their conclusion accordingly.
A separate analysis of more than 2,000 clinically diagnosed hEDS patients reached the same place from the other direction: Beighton scores were of little use for characterizing how much illness a patient was actually carrying. How bendy you are does not tell anyone how sick you are.
Nine points, five questions, two minutes at your kitchen table
Most patients have never been walked through the thing they are being judged on. Here it is.
The Beighton score — nine points
- Little fingers — passive bend backward past 90°. One point each side.
- Thumbs — fold down to touch the forearm. One point each side.
- Elbows — hyperextend past 10°. One point each side.
- Knees — hyperextend past 10°. One point each side.
- Forward bend — palms flat on the floor with knees straight. One point.
| Age group | Threshold in the 2017 criteria |
|---|---|
| Prepubertal children and adolescents | 6 of 9 |
| Pubertal adults, up to age 50 | 5 of 9 |
| Adults over 50 | 4 of 9 |
The five historical questions — two or more “yes” is positive
This is the provision most patients are never told about. Published in 2003, validated against clinical diagnosis in two cohorts at roughly 84% sensitivity and 89% specificity. Note the tense — four of the five ask what you could do, not what you can do today.
- Can you now, or could you ever, place your hands flat on the floor without bending your knees?
- Can you now, or could you ever, bend your thumb to touch your forearm?
- As a child, did you amuse your friends by contorting your body into strange shapes, or could you do the splits?
- As a child or teenager, did your shoulder or kneecap dislocate on more than one occasion?
- Do you consider yourself “double-jointed”?
Read this before you draw a conclusion. Neither of these is a diagnosis, and the historical questionnaire is narrower than the internet suggests: in the 2017 criteria it substitutes for the Beighton score when your current score is one point below your age cut-off, plus separately when range has been lost to surgery, amputation, or wheelchair use. It is not a general “I was bendy as a kid” pathway to an hEDS diagnosis. What a low score does mean is that the conversation is not over — it moves to the historical questions, to the hypermobility spectrum categories below, and to the systemic picture. Independent replications of the questionnaire also report weaker specificity than the original, around 62–75%: it is a good rule-out and a mediocre rule-in.
And there is already a name for your situation
Alongside the 2017 classification, a companion paper set out four categories of hypermobility spectrum disorder — not one. Read the fourth.
| Category | What it means |
|---|---|
| G-HSD · Generalized | Positive Beighton score plus musculoskeletal consequences. The version most clinicians are looking for. |
| P-HSD · Peripheral | Hypermobility limited to hands and feet. Your fingers are loose; your hamstrings were never long. Both can be true. |
| L-HSD · Localized | A single joint or region — one shoulder that will not stay in, one unstable ankle, one hypermobile jaw. |
| H-HSD · Historical | Self-reported past generalized hypermobility with a currently negative Beighton score, plus consequences. The framework has a named diagnosis for the person who used to be bendy and no longer is. |
This matters for treatment, not just labeling. HSD and hEDS are managed along the same lines and carry a comparable burden. Which box you land in is largely a research and communication convenience.
Stuck, not stiff — why a loose body feels bound
Your tissue is not the wrong kind of hypermobile. Things have been layered on top of it.
Fascia that has stopped sliding
Deep fascia is built to glide: adjacent fibrous layers are separated by loose connective tissue rich in hyaluronan, and that hyaluronan is what lets the layers move on one another. When it shifts to a more packed conformation, the sliding of the fascia and the muscle beneath it is compromised — the mechanism described as densification.
In hEDS specifically, ultrasound of the iliotibial tract measured interfascial shear strain — how much the layers slide on each other — at roughly 46% in hEDS versus about 121% in pain-free controls, with lower-limb pain patients in between.
That study had nine subjects in total across all three groups. Quote the direction, not the precision — the effect size is implausibly large for that sample and it needs replication. And note what the same group’s elastography work found: hEDS tissue trending toward abnormal softening, not hardening, with increased deep fascial thickness at the sternocleidomastoid but no significant difference at the iliotibial tract or iliac fascia. The whole tissue-mechanics literature in this population is about four studies.
So the accurate statement is not your fascia is stiff. It is your fascia is stuck — the layers have stopped sliding, and a body whose layers do not slide feels bound and restricted no matter how lax the ligaments underneath are. That distinction changes treatment: stretching a stuck interface harder does not restore glide. Restoring the plane between the layers does.
Weak muscles working overtime
The intuitive version is that hypermobile people clamp down to hold unstable joints together. The evidence is more specific and more sobering. Mild-to-moderate muscle weakness was documented in 85% of patients across EDS types, along with hypotonia, myalgia and easy fatigability. In girls with generalized hypermobility, knee co-activation ratios were higher than controls — but partly because of reduced hamstring drive rather than harder antagonist firing, and other studies of walking and postural tasks found no difference or even less activity.
Taken together this is a control problem more than a tension problem: muscles that are weaker and less well coordinated, asked to stabilize a joint the passive tissue is not stabilizing, working near their limit most of the day. That state does not feel loose. It feels tight, tired and braced.
Joints that are harder to locate in space
A meta-analysis of five studies and 254 participants found significantly poorer lower-limb joint position sense and a higher threshold for detecting joint movement in hypermobility, with finger proprioception also affected — and shoulder position sense not significantly different. If your nervous system cannot reliably tell where a joint is, guarding it is a sensible strategy. Guarding, sustained for years, is experienced as stiffness.
Arthritis, scar, and a body that learned movement hurts
Once a joint develops osteoarthritis its range drops in step with radiographic severity. Arthrofibrosis — the fibrotic response to injury, surgery, infection or immobilization — lays down excess matrix and adhesions that mechanically prevent normal motion. A knee that hyperextended at sixteen can measure frankly stiff at forty-five, and the Beighton point it used to earn is simply gone. Kinesiophobia is measurably elevated in hypermobility and correlates with fatigue severity — though notably not with pain intensity, so this is not about how much pain someone can tolerate.
An honest caveat on arthritis. You will read that hypermobility causes early osteoarthritis. The population data are genuinely mixed and some of the largest studies point the other way — in the Johnston County cohort, generalized joint hypermobility was inversely associated with hand and knee OA. What is not in doubt is the downstream half: where arthritis is present, that joint loses range. We do not need the causal claim to explain why you feel stiff.
The signal that isn’t flexibility at all
Hypermobility travels with a cluster of systemic conditions, and in a patient who does not look bendy that cluster is the louder signal.
A third of a gastroenterology waiting room, carrying an unrecognized connective tissue diagnosis. The field has responded: a 2025 American Gastroenterological Association practice update now advises gastroenterologists seeing gut-brain interaction disorders to ask about joint hypermobility and to strongly consider the Beighton score as a screening tool.
If you get lightheaded standing, if your heart races in the shower, if you flush or react to foods you used to tolerate, if you were given a fibromyalgia label that never explained the dislocations or the fainting — those are the threads worth pulling. A fibromyalgia diagnosis and a hypermobility diagnosis are not mutually exclusive; in that 733-patient cohort they were the most common combination.
Why we are careful with these numbers. Nearly all of them come from specialty and referral clinics, so they describe people who were already sent somewhere — not the general population. The 2017 expert review on autonomic dysfunction in hEDS says plainly that true incidence and prevalence remain unquantified. And on mast cell activation: reported prevalence depends almost entirely on which criteria are applied — in one 2025 cohort of young patients with orthostatic intolerance the figure moved from 2% to 37% to 87% depending on the definition. A 2025 systematic review found no studies that diagnosed mast cell disorders alongside POTS or EDS using prespecified validated criteria. Our position: these conditions demonstrably travel together, we treat what we find, and we do not claim to know that one causes another.
And this is why it took so long
Among 505 patients with clinically confirmed hEDS, the average time to diagnosis was 10.4 years. They saw an average of 15.6 clinicians — nearly a quarter saw twenty or more — and collected an average of 10.45 alternative diagnoses along the way, most commonly anxiety, depression and migraine. A global survey of 3,906 people reported a mean delay of 22.1 years for hEDS and 17.5 years for HSD.
Those are not numbers about patient resilience. They are numbers about a system that has been screening for a whole-body condition with a five-joint test. Both figures come from self-selected patient surveys with retrospective recall, which inflates delay estimates — attribute them to patient-reported data, not chart review.
Men, testosterone, and a ten-to-one gap
If you are a man wondering whether this is even on the table for you, look at the arithmetic.
hEDS follows an autosomal dominant inheritance pattern, which predicts a roughly equal split between men and women. That is not remotely what the clinics see.
A condition inherited in an autosomal dominant pattern does not affect ten women for every man. Something is happening between having the trait and being diagnosed with it, and the most parsimonious explanation is that men are not being counted — not that men do not have it. Worth stating plainly: the evidence does not show men are diagnosed later than women. It shows they are diagnosed far less often.
Where testosterone likely fits
Androgens change connective tissue, and they change it in the direction of less measured give. A meta-analysis of 32 studies found human tendon stiffness significantly higher in males. Tendon collagen synthesis at rest and after exercise is roughly twice as high in men, and habitual loading enlarges the patellar tendon in men but not women. An authoritative review notes that testosterone can enhance tendon stiffness through increased collagen turnover and content — and, importantly here, has been linked to reduced responsiveness to relaxin, the hormone most associated with ligamentous laxity.
The most direct test of the mechanism is an animal study and should be read as one: in ovariectomized female rats, three days of testosterone significantly reduced knee passive range of motion and downregulated both relaxin receptor isoforms, an effect abolished by blocking the androgen receptor. Elegant mechanism. No human study has shown that testosterone lowers a Beighton score.
Where the evidence pushes back on our own argument. The largest synthesis available found no statistically significant sex difference in Beighton scores at any threshold across roughly 23,000 adults — all p-values at or above 0.17. So “men are simply less flexible” does not carry the argument. Which is the more interesting point: the gap in measured hypermobility between the sexes is small and inconsistent, while the gap in diagnosed hypermobility is roughly ten to one. Testosterone plausibly explains why a hypermobile man presents differently — bulkier, stiffer-feeling, complaining of tight hamstrings and a bad back rather than of bendiness. It does not explain the diagnostic gap. Nobody looking is what explains that.
Two corrections to claims that circulate online. This is not about collagen cross-linking — human patellar tendon biopsies found cross-link density comparable between men and women and unchanged by resistance training, even though men’s tendons were larger and stiffer; the stiffness comes from size and geometry. And laxity does not reliably swing with the menstrual cycle the way it is often described: a 2025 meta-analysis of 54 studies found no effect of the menstrual cycle on knee laxity or anterior tibial translation.
One more thing, because this is where the topic goes wrong. Stiffer is not healthier. Testosterone therapy has been associated with increased tendon rupture and repair rates in observational data — the proposed mechanism being tissue that is mechanically stiff yet less able to accommodate repeated loading or repair microdamage. Testosterone is not a treatment for hypermobility or hEDS, and we do not use it that way.
Ten months ago he was retired. Saturday it lasted two rounds.
The case study is published — and the useful part of it is where the evidence runs out.
Victor “Jalapeño” Hernandez was 15-0 with thirteen knockouts and ranked twelfth in the world at 126 pounds when he walked away in November 2025. Not because someone caught him. Because of myofascial pain — the kind that does not appear on an MRI, does not have a name most people recognize, and does not get better because you want it to.
On Saturday, September 12, in Midland, Texas, he fought Conrad Martinez for the WBC USA featherweight title — the same opponent he had been matched with before he walked away. He put Martinez on the canvas three times, and the fourth knockdown ended it in the second round. Ten months of care, and the fight itself took under six minutes. He is still undefeated.
We are going to say the obvious thing about that, because somebody should: a two-round stoppage is a thrilling result and it is not clinical evidence. It says nothing about whether the pain is gone, whether it stays gone, or whether any of this would work for you. What it tells you is that a man who could not plan around his own body ten months ago was able to plan around it on Saturday.
The return-to-sport case study walks through the four stages, and the order matters more than the list: find it (Fascial Mapping®, a physician ultrasound exam that scores tissue quality and glide side-to-side while the athlete contracts, relaxes and rotates); change the tissue (Hydrofascia Release™, ultrasound-guided fascial hydrodissection, and dextrose prolotherapy where tissue is lax rather than stuck); turn it down (shockwave, TECAR, red light, PEMF, microcurrent); and reload — the stage that decides whether any of the rest holds.
You cannot release tissue you have not located, and a release will not hold if the athlete never loads it.
What a single case cannot tell you. Nine treatments across ten months, alongside training, rest, changed loading and a great deal of time. One person getting better cannot tell you which of those things did it, and it does not predict anyone else’s course. There are no published clinical trials on the devices themselves — the evidence supports the training principles, not the hardware brand. And on Fascial Mapping: it is a clinical exam, not a validated test with published sensitivity and specificity. We say that in the case study too.
The standing problem has a name, and it is not “drink more water”
Built because my patients kept quitting their electrolytes— not because the science was wrong, because the powder was undrinkable
More than half the POTS patients in one 91-person series were hypermobile. If you are in that overlap, electrolytes are not a wellness accessory — sodium loading is standard first-line advice for orthostatic intolerance. The problem was never the advice. It was that patients with hypermobility, POTS, or jobs in the Louisiana heat would try a flavored powder for two weeks and stop, because of the taste, the sweeteners, or a stomach that already does not cooperate.
So I built a taste-free capsule: sodium, magnesium and potassium, plus tyrosine, taurine, and ginger so it sits easy. No fillers, no artificial sweeteners or colors, made in an NSF-certified facility. Nothing to drink and nothing to taste — which is the entire point, because the version you actually keep taking is the one that works.
Plainly: CoreSalt™ is our own product, formulated by Dr. Courseault — so this is a house advertisement, not a neutral comparison. Read it that way. CoreSalt™ is a dietary supplement and is not intended to diagnose, treat, cure, or prevent any disease. Sodium loading is not appropriate for everyone — talk with your physician first, particularly if you have high blood pressure, heart failure, or kidney disease.
One book, if you want to understand the tissue this is all about
Fascia: What It Is and Why It Matters
David Lesondak · Handspring Publishing · second edition
Patients ask me what to read, and almost everything in this field is either a textbook or a blog post. Lesondak’s book is the rare thing in between: a full-colour primer written so that a non-clinician can actually follow it, by a structural integrator at the UPMC Center for Integrative Medicine. It is the book I point to when someone wants to understand why we keep talking about layers that slide.
A note on what it is not: it is a primer, not a treatment manual, and it will not tell you what to do about your own shoulder. For clinicians who want the deeper version, he also co-edited Fascia, Function, and Medical Applications with Angeli Maun Akey, MD (CRC Press, second edition 2025) — that one is a genuine medical textbook and reads like it. We have no financial relationship with the author or publisher.
Hypermobility is a body type — high-performance and high-maintenance
A Ferrari, not a lemon. It becomes disordered when it is not cared for properly, and a great deal of what makes people miserable in this population is not the laxity itself but what accumulated on top of it. Much of that is treatable.
One last piece of context, because it is the honest state of the field: the 2017 criteria are being revised. The International Consortium on EDS and HSD has announced a new classification for publication on December 1, 2026, and has indicated the Beighton score is likely to be revised or supplemented with additional joint assessments. The ruler everyone has been measuring you with is itself under review.
You do not have to be bendy to be believed.
Know someone who has been told they are not flexible enough to have this? Send them this issue. That is genuinely how most of our hypermobility patients found us.