“Thanks to Your Research,
I Was Able to Get Out of Bed”

A reader in Argentina living with Ehlers-Danlos syndrome — someone we have never met and never treated — wrote to tell us what changed after she found our work on MTHFR, folate, and hypermobility.

Every so often a message arrives that reminds us why we publish our research in the open. This one came from a follower in Argentina — more than 5,000 miles from our Beverly Hills clinic. We have never met her. She has never been our patient. 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.

“Thank you. 🇦🇷 Thanks to you, I was able to get out of bed. I have Ehlers-Danlos syndrome (EDS), 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 all of that from my diet and taking methylated folate instead, I’m doing much better. And today, it’s time to cheer for Messi!”

We share this not as a promise of what treatment can do — it is one person’s experience, and everyone is different — but because of what it represents. A woman on the other side of the world read the research, recognized herself in it, and worked with her own clinicians to do something about it. That is the whole reason we publish.

We can’t independently verify that 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.

At our New Orleans flagship, Dr. Jacques Courseault and his research team noticed something unexpected while screening patients with hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD): many of them had high levels of unmetabolized folate on their labs, and those high levels tracked with common variants in a gene called MTHFR.

MTHFR makes an enzyme that converts folic acid and dietary folate into the active, usable form your body runs on (often called L-methylfolate or 5-MTHF). When common MTHFR variants slow that enzyme down, synthetic folic acid can pile up without being converted. Working with neuroscientist Dr. Gregory Bix, the team proposed a mechanism — published in the journal Heliyon in 2023 — linking this altered folate metabolism to the way the body maintains collagen and the extracellular matrix (the scaffolding that holds connective tissue together), by way of proteins such as MMP-2 and decorin. Their hypothesis: this could help explain both the joint laxity and the fascial pain and thickening that so many hypermobile patients live with.¹

A follow-up study in ACR Open Rheumatology (2024) looked at how often MTHFR variants show up in a hypermobility clinic population, building the case that folate metabolism deserves a closer look in this group.² The idea even made headlines — Tulane University and Ehlers-Danlos News both covered it.

Important: this is an emerging, research-stage model — not an established, universally accepted diagnosis. It doesn’t replace the genetic and clinical evaluation of Ehlers-Danlos syndrome. It’s a promising line of inquiry that we’re actively studying.

This is the part that deserves nuance, because it is easy to hear “folic acid” and “methylated folate” and draw the wrong conclusion.

For the general population, folic-acid fortification is one of the great public-health wins of the last century. Adding folic acid to flour dramatically reduces neural-tube birth defects, and the U.S. Centers for Disease Control and Prevention is explicit that a common MTHFR variant is not a reason to avoid folic acid — anyone who could become pregnant should still get 400 mcg of folic acid daily.³ Please don’t read this reader’s story as “folic acid is bad.” It isn’t.

The narrower question our research explores is different: for a specific subset of people who have MTHFR variants and connective-tissue symptoms, does the active (methylated) form of folate work better than the synthetic form their body struggles to convert? For that subset, switching to methylated folate — which is FDA-recognized and widely available — is a reasonable thing to discuss with a clinician, ideally guided by lab testing. That is very different from a blanket recommendation for everyone.

Two facts make her message especially interesting. First, common MTHFR variants are widespread across Latin American populations — some of the highest frequencies of the C677T variant in the world are found in the Americas.⁵ Second, since Ley 25.630 took effect in 2002, Argentina has required wheat flour to be fortified with synthetic folic acid — a policy that measurably cut folate deficiency across the country.⁴

So you have a population where MTHFR variants are common, layered on top of a food supply deliberately enriched with folic acid. For most people, that combination is exactly what fortification was designed to do — and it works. For the small group whose biology matches the folate-dependent hypermobility picture, it raises a genuine question worth investigating with their doctors. Our reader lived inside that question, tested it with her clinicians, and told us the difference she felt.

That is the honest frame: fortification is good policy and individual biology varies. Both things are true at once.

None of these is a diagnosis on its own — but together they’re the pattern that makes us look at folate metabolism:

If that sounds familiar, the next step isn’t to self-treat — it’s to get a proper look. Our hypermobility & EDS evaluation and our FIT GPS genomic screen are built for exactly this kind of question, and Fascial Mapping can pinpoint where the fascial pain is actually coming from. Learn more about the tissue itself in What Is Fascia?

Ask the folate question with a team that studies it

If hypermobility, unexplained pain, and folate metabolism sound like your story, we can help you evaluate it properly — and treat the fascial pain that so often comes with it.

Book an Evaluation →
Hypermobility & EDS Care

The Fascia Institute and Treatment Center of LA · 415 North Crescent Drive, Suite 130, Beverly Hills, CA 90210 · (424) 378-3488 · Telehealth available for patients in California

What is folate-dependent hypermobility syndrome (FDHS)?

It’s a proposed subtype of hypermobility described by Dr. Courseault and colleagues in Heliyon (2023). The model suggests that in some people, common MTHFR variants alter folate metabolism in a way that affects how the body maintains collagen and connective tissue — potentially contributing to joint laxity and fascial pain. It’s an emerging, research-stage idea, not an established diagnostic category.

Does having an MTHFR variant mean I should stop taking folic acid?

No. The CDC says common MTHFR variants are not a reason to avoid folic acid, and anyone who could become pregnant should still get 400 mcg daily to help prevent neural-tube defects. Any change to how you take folate should be made with your own clinician.

Can methylated folate cure Ehlers-Danlos syndrome?

No. EDS is a genetic connective-tissue disorder with no cure. Some patients with folate-related hypermobility report symptom improvement on methylated folate, but this is individualized, still under study, and should be guided by lab testing and a clinician. Results vary.

I don’t live in Los Angeles — can you still help?

Our published research is freely available so you can bring it to your own doctors — exactly what this reader in Argentina did. Hands-on evaluation happens at our Beverly Hills clinic and our New Orleans flagship; telehealth consultations are available for patients located in California.

1. Courseault J, et al. Folate-dependent hypermobility syndrome: A proposed mechanism and diagnosis. Heliyon. 2023;9(4):e15387. PMID: 37095957.
2. Courseault J, et al. Prevalence of MTHFR Polymorphisms in Patients With Hypermobile Ehlers-Danlos Syndrome and Hypermobile Spectrum Disorders in a US Hypermobility Clinic. ACR Open Rheumatol. 2024. doi:10.1002/acr2.11667. PMID: 38523329.
3. Centers for Disease Control and Prevention. MTHFR gene variant and folic acid facts. cdc.gov.
4. Food Fortification Initiative. Argentina — mandatory wheat-flour fortification with folic acid (Ley 25.630, 2002). ffinetwork.org/argentina.
5. Ethnogeographic prevalence and implications of the MTHFR 677C>T variant (review). PMC6630484.

The research & the flagship — New Orleans: Read the model this reader found: Folate-Dependent Hypermobility Syndrome at The Fascia Institute, our Hypermobility & EDS Clinic in New Orleans, and Dr. Jacques Courseault, who leads the work.

Living with EDS? Our dedicated Hypermobility and Ehlers-Danlos Clinic and its EDS blog — including Ehlers-Danlos Syndrome 101 — are a good place to start.