From Tulane to a Melbourne Podcast
The Research Behind Folate-Dependent Hypermobility

A clinical concept that has changed how thousands of hypermobile patients are evaluated and treated did not start in a Beverly Hills clinic or a London hospital. It started at Tulane University School of Medicine in New Orleans, in the practice of Assistant Professor Jacques Courseault, MD — the founder of The Fascia Institute and Treatment Center^®. In 2023, that work made its way across the Pacific when Dr. Courseault was invited onto Lateral Think — The Melbourne Athletic Development Podcast to discuss his publication exploring the relationship between hypermobility syndromes and dietary micronutrient intake.

The conversation is a useful summary of the work — and a reminder that the framework now used in our Hypermobility & EDS Clinic in New Orleans is grounded in published research, not opinion.

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Assistant Professor Jacques Courseault — Lateral Think Podcast

Melbourne Athletic Development · Aug 20, 2023 · 58 min

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Dr. Courseault’s research starts with a clinical observation made repeatedly in the New Orleans patient population: a significant subset of patients meeting criteria for hypermobile Ehlers-Danlos syndrome (hEDS) or Hypermobility Spectrum Disorder (HSD) showed lab patterns — and clinical patterns — consistent with impaired folate metabolism. Many were carriers of MTHFR polymorphisms. Many had elevated histamine-related symptoms. Many responded clinically to methylated folate supplementation in ways that the standard “lax-ligaments-and-PT” model could not account for.

The hypothesis that emerged is what we now call folate-dependent hypermobility: a connective tissue presentation driven not by a primary collagen gene defect, but by inefficient one-carbon metabolism affecting collagen quality, mast cell stability, neurotransmitter regulation, and tissue repair. It is a meaningful refinement of how hypermobility is understood — and it has practical, measurable implications for treatment.

Louisiana sits in the middle of a hypermobility care desert. Patients across the Gulf South — from New Orleans to Baton Rouge, Lafayette to the North Shore — routinely travel out of state to find clinicians who understand connective tissue disorders. The folate-dependent hypermobility framework changes what is possible at the local level in three important ways.

It introduces testable biology.

Hypermobility has historically suffered from a “diagnosis of exclusion” reputation. Methylation testing, MTHFR variant analysis, serum folate, B12, and homocysteine measurement provide objective, measurable data points that anchor the clinical picture in physiology.

It opens a non-structural treatment lever.

For patients whose symptoms are partially driven by impaired methylation, targeted methylated folate and B12 supplementation — at clinically appropriate doses, paired with the correct cofactors — can produce changes in joint stability, energy, autonomic regulation, and inflammatory tone that physical therapy alone could not.

It improves the response to structural treatment.

When the methylation environment is corrected, the same prolotherapy, Hydrofascia Release™, and physical therapy that previously plateaued begin to produce durable results. The biology comes online and the structural work finally compounds.

The mechanism is well established in the broader medical literature, even if its application to hypermobility is new. Methylation depends on a chain of enzymatic conversions that turn dietary folate into 5-methyltetrahydrofolate (5-MTHF), the active form your body actually uses. Variants in the MTHFR gene — particularly C677T — reduce that conversion efficiency. Antoniades and colleagues (2009) documented the functional consequences for one-carbon metabolism, and a substantial subsequent literature has extended the implications across multiple body systems.

In the hypermobile patient, reduced methylation capacity affects several pathways at once: collagen lysyl oxidase activity (cross-linking quality), histamine N-methyltransferase activity (mast cell modulation), catecholamine processing (autonomic regulation), and DNA methylation patterns that govern fibroblast behavior. It is a multi-system effect — which is exactly why hypermobile patients present as multi-system patients.

At The Fascia Institute and Treatment Center^® in New Orleans, hypermobility evaluations go beyond the standard joint-laxity exam and Beighton score. Patients in the Hypermobility & EDS Clinic protocol typically include functional methylation testing, MTHFR variant status, and a personalized supplementation plan that pairs the right form of folate and B12 with the cofactors needed for the cycle to actually run.

That biochemical layer sits underneath the structural work — high-resolution musculoskeletal ultrasound, ultrasound-guided prolotherapy, Hydrofascia Release™, Fascial Mapping®, and coordinated physical therapy. The two layers are not redundant. They address different biological problems, and the combination is what produces the meaningful changes our patients have come to expect.

“This is the framework Dr. Courseault discusses on the podcast. It is also the framework that has been refined across thousands of patient encounters in our New Orleans clinic.”

The Lateral Think episode runs 58 minutes and covers the publication itself, the clinical patterns that motivated it, and how this research is changing the way hypermobility is evaluated. If you or someone in your life carries a hypermobility diagnosis, has been told their symptoms are “just stress,” or has cycled through specialists without a coherent plan, the episode is worth your time.

When you are ready to bring that knowledge to a clinical visit, our Hypermobility & EDS Clinic in New Orleans was built to receive it.