The Connective IssueThe Fascia Institute & Treatment Center Journal
A weekly report from the line of scrimmage of fascia medicine — where grit, recovery, and getting back in the game meet.
New season, new field.
The World Cup went back in the case, and so did our soccer theme. This week The Connective Issue laces up for the other football — and it turns out the gridiron is exactly the right place to talk about what we do.
American football is a sport of misdirection — the play that looks like one thing and is really another. Pain works the same way. So for our first Gridiron edition, we’re leading with one of the great fakes in medicine: leg pain that everyone calls sciatica but that’s often coming from somewhere else entirely — the glutes and their fascia.
From there, a genuinely proud day for our whole team — one of our athletes, Kendall Hagedorn, just signed with the Milwaukee Brewers — and a remarkable letter that traveled more than five thousand miles: a reader in Argentina with Ehlers-Danlos syndrome who found our research and, in her words, “got out of bed” because of it.
Three stories, one theme: read the play before you commit to it. Let’s kick off.
In This Issue
- Is It Sciatica — or Your Glutes? Highlight Reel
- Kendall Hagedorn Signs With the Milwaukee Brewers Draft Day
- A Letter From Argentina: Folate, MTHFR & EDS The Playbook
- Stalled After Surgery? Come Get Mapped Two-Minute Drill
Is it sciatica — or your glutes?
Pain that starts in the buttock and shoots down the leg gets one label almost reflexively: sciatica. But a great deal of it isn’t a pinched nerve in the spine at all — it’s referred pain from the gluteal muscles and fascia. And telling the two apart changes everything about how you fix it.
True sciatica is irritation or compression of a nerve root where it exits the lower spine — often from a disc. The pain tends to travel a specific nerve path, and it can come with numbness, tingling, or weakness down the leg. It’s real, and when that’s the problem, it deserves to be treated as such.
The catch is that the deep gluteal muscles and the fascia around them — piriformis, the gluteus medius and minimus, the thoracolumbar fascia — can refer pain into the buttock and down the leg in a pattern that looks and feels like sciatica, with no nerve-root problem behind it at all. Sometimes the sciatic nerve itself is being irritated not in the spine but as it passes through tight, adhered fascia in the deep gluteal space. Same symptom, entirely different source.
That’s why the distinction matters so much. Here’s the quick tell — though only a proper evaluation can confirm it:
Looks like true sciatica
Pain follows a clear nerve path down the leg, often past the knee, and may bring numbness, pins-and-needles, or weakness. Frequently traces back to the lumbar spine and a nerve root — and behaves like a nerve problem on exam.
Acts like referred gluteal pain
Deep, achy buttock pain that can radiate down the leg but doesn’t track a tidy nerve line. Tender, restricted spots in the gluteal fascia reproduce it; it worsens with sitting or direct pressure and eases when the tissue is freed. The spine imaging often reads “clean.”
How we sort it out is by looking at the tissue itself. A careful history and exam, paired with high-resolution ultrasound and Fascial Mapping™, let us watch the gluteal fascia and the sciatic nerve move in real time — so we can see whether the pain is coming from a restricted, adhered soft-tissue plane or from a genuine nerve-root problem in the spine. When it’s fascial, it’s often very treatable: targeted soft-tissue work, and where a nerve is entrapped in sticky fascia, hydrodissection to free it.
The point isn’t that sciatica isn’t real — it very much is. It’s that “sciatica” has become a catch-all for almost any leg pain, and the label can send you down a spine-focused path for a problem that was never in your spine. If you’ve been treated for sciatica and it never quite added up, that’s worth a second, tissue-level look.
Not all leg pain is fascial, and not all is sciatica — results vary and a clinical evaluation is required to determine the source. Educational information only, not medical advice.
Congratulations, Kendall Hagedorn.
Every so often you get to watch an athlete’s hard work meet the moment it was built for. This is one of those days — Kendall Hagedorn has signed with the Milwaukee Brewers organization.
All of us at The Fascia Institute are thrilled for Kendall. It’s a milestone earned by years of work, and his talent, discipline, and work ethic earned this opportunity — full stop. We’re simply proud to have played a small part in keeping his body ready to perform at the level his game demands.
Optimized on ultrasound
High-level baseball asks the body to do explosive, repeatable, asymmetric work. To keep an athlete at his ceiling, you have to understand his soft tissue in detail — not guess at it. With diagnostic ultrasound and fascial mapping, we evaluate how fascia, muscle, and connective tissue actually move and load in real time — turning “something feels off” into a specific, treatable finding.
Fueling the athlete
Even dedicated athletes commonly run low on the nutrients that drive energy, recovery, and connective-tissue health. Through personalized supplementation, targeted labs, and our genomic performance screen, we identify and correct the specific deficiencies that quietly hold athletes back — so the body recovers faster and performs longer.
Baseball is a soft-tissue sport — the throw, the rotational power of the swing, the sprints and slides all load the connective tissue that ties the body together. The Fascia Institute is built to evaluate, treat, and prevent the shoulder, elbow, oblique, and lower-body injuries that most affect ballplayers, so athletes don’t just come back — they come back better protected.
A letter from Argentina — folate, MTHFR & EDS.
Every so often a message arrives that reminds us why we publish our research in the open. This one came from a reader in Argentina — someone we’ve never met and never treated — living with Ehlers-Danlos syndrome.
She found our published work on folate-dependent hypermobility syndrome, brought it to her own doctors, and acted on it in her own country. Here, in her words — translated from Spanish — is what she wanted us to know.
“Thanks to your research, I was able to get out of bed.”
“I have Ehlers-Danlos syndrome, and because of your research, I became the first person in Argentina to be diagnosed with an MTHFR mutation and to start taking methylated folate. In Argentina there’s a law requiring foods to be fortified with synthetic folic acid. After removing that from my diet and taking methylated folate instead, I’m doing much better.”
— A reader in Argentina living with EDS, shared publicly on Facebook. We’re keeping her anonymous.
Here’s the science she found. While screening patients with hypermobile EDS and hypermobility spectrum disorders, Dr. Courseault’s team noticed many had high levels of unmetabolized folate — and those levels tracked with common variants in a gene called MTHFR. MTHFR makes the enzyme that converts folic acid into the active form the body runs on. When common variants slow that enzyme, synthetic folic acid can pile up unconverted. The team’s hypothesis, published in Heliyon (2023) and followed up in ACR Open Rheumatology (2024), links this altered folate metabolism to how the body maintains collagen and connective tissue — potentially contributing to both joint laxity and fascial pain.
The careful version
For the general population, folic-acid fortification is one of the great public-health wins of the last century — it dramatically reduces neural-tube birth defects, and the CDC is explicit that a common MTHFR variant is not a reason to avoid folic acid. Please don’t read this as “folic acid is bad.” The narrower question our research explores is whether a specific subset of people — those with MTHFR variants and connective-tissue symptoms — do better on the active (methylated) form. Don’t start or stop any folate supplement on your own; bring the question, and your labs, to your own clinician — especially during pregnancy.
We can’t independently verify she was truly the first person in Argentina diagnosed this way — but her message captures something real. Outside a handful of clinics, folate-dependent hypermobility is still a very new idea, and many people are meeting it for the first time through research they find online. That is the whole reason we publish.
Folate-dependent hypermobility is an emerging area of research and does not replace evaluation and diagnosis of Ehlers-Danlos syndrome. Educational information only, not medical advice.
Pain that never added up? Come get mapped.
A “sciatica” that won’t quit, a diagnosis that never fit, or an injury that stalled — the first move is the same: find out where the pain is actually coming from before you treat it.
The fastest way to do that is Fascial Mapping™ — a high-resolution ultrasound diagnostic that watches your tissue while it moves and pinpoints exactly where fascia and nerves are restricted, even when other imaging reads “clean.” From there, treatments like neurofascial hydrodissection restore glide at the source.
Missed last week? Revisit the Fascia Cup run — migraines and fascia, the “restless legs” case report, and our EDS care. This week we’re on a new field, same mission.