- Three things have to be present at once for autoimmunity to switch on: a genetic susceptibility, an environmental trigger, and increased intestinal permeability.
- You cannot change the first one. You can very often change the other two — and that is the whole basis of root-cause autoimmune care.
- Antibody levels are highly modifiable. How many antibodies you carry over the coming decades determines how much tissue you lose.
- Around seventy percent of your immune system lives in the gut lining, which is why intestinal permeability sits in the model at all.
- We work alongside your rheumatologist, never instead of them. This is additive care, and your specialist should know exactly what you are doing.
The three-part triad
The model that changed how I think about autoimmunity came from Dr. Alessio Fasano's work at Harvard, and it is the clearest framework I know for explaining why this happens to some people and not others.
Fasano's proposal is that three components must be present simultaneously for autoimmune disease to develop.
One: genetic susceptibility. Certain HLA gene variants predispose you. This is fixed, and it explains why autoimmunity clusters in families. It is also, importantly, not destiny — plenty of people carry the genes and never develop the disease.
Two: an environmental trigger. A viral infection, a specific food protein, a chemical exposure, a period of severe stress, or in many women a pregnancy. Something has to start it.
Three: increased intestinal permeability. The junctions between intestinal cells loosen, allowing partially digested proteins and bacterial fragments to reach immune tissue that was never meant to see them.
What makes this framework so useful clinically is the arithmetic. One of the three is fixed. Two of the three are modifiable. And in my experience, addressing those two changes what happens to a person over the following decades.
The triad, in one picture
Only the first box is fixed. Everything to the right of it is something we can measure and change — which is why antibody levels respond to proper root-cause work.
Why the gut keeps coming up
Patients sometimes find it strange that a thyroid or joint problem leads to a conversation about their intestines. Here is why it does.
Roughly seventy percent of your immune tissue sits in the lining of your gut. That is not incidental — it is where your body does most of its deciding about what is friend and what is foe, because it is where the outside world comes closest to the inside.
When the barrier is intact, that decision-making works. When it is not, proteins that should have been fully digested cross into circulation partially intact. Your immune system sees them, mounts a response, and if one of those proteins structurally resembles your own tissue — a phenomenon called molecular mimicry — the response can turn on you.
The best-documented example is the resemblance between gliadin, a wheat protein, and thyroid tissue, which is part of why coeliac disease and Hashimoto's occur together far more often than chance would predict.
The testing that finds the drivers
The ten levers that lower autoimmune activity
Ranked by how much difference they make and how consistently the driver sits there.
Repair the Gut Barrier
The third leg of the triad and the one most directly modifiable. Comprehensive stool testing first, then remove what is driving permeability, then rebuild the lining with L-glutamine, zinc carnosine and collagen peptides. This is where autoimmune work either succeeds or stalls.
What the evidence showsAutoimmunity requires genetic susceptibility, an environmental trigger and increased intestinal permeability — the three-factor model described by Fasano. Two of the three are modifiable.Get Vitamin D to 50–80
Vitamin D is required for regulatory T-cell function — the cells whose entire job is telling your immune system what not to attack. Deficiency is nearly universal in the autoimmune patients we test, and correcting it is inexpensive.
What the evidence showsZonulin regulates tight junction permeability and is elevated across multiple autoimmune conditions. Fasano's work established the mechanistic link between barrier function and autoimmune onset.Identify and Remove Your Triggers
Gluten first, because of the molecular mimicry evidence, but dairy, corn, soy, eggs and nightshades all matter for some people. A structured elimination and reintroduction identifies yours. IgG panels frequently do not.
What the evidence showsVitamin D is required for regulatory T cell function and immune tolerance. Deficiency is associated with higher prevalence and greater activity across multiple autoimmune conditions.Address Chronic Infection
Epstein-Barr is implicated across multiple autoimmune conditions, and reactivation is common in people under sustained stress. Where titres suggest it, addressing that changes the immune picture rather than just the marker.
What the evidence showsEpstein-Barr virus is associated with multiple autoimmune conditions, and a large longitudinal cohort published in Science established EBV infection as a likely necessary precursor for multiple sclerosis.Correct Selenium and Zinc
Selenium reduces thyroid antibodies in randomised trials and supports glutathione peroxidase throughout the immune system. Zinc is required for regulatory T-cell function. Both measured, because the ceiling on selenium is closer than people expect.
What the evidence showsMolecular mimicry — structural resemblance between pathogen or food proteins and self tissue — is a well-characterised mechanism for the initiation of autoimmune responses.Lower Inflammatory Load
Omega-3s at genuine therapeutic doses, polyphenols, and curcumin all act on inflammatory signalling. hs-CRP gives us a number to track, so this is measured rather than assumed.
What the evidence showsSelenium supports regulatory T cell function and reduces thyroid autoantibodies in randomised trials. Omega-3 fatty acids reduce inflammatory eicosanoid production and have trial evidence in rheumatoid arthritis.Regulate the Stress Response
Sustained stress raises intestinal permeability directly and suppresses regulatory T-cell function. Nearly every patient can date their first flare to a period of genuine difficulty, and this is not a coincidence.
What the evidence showsChronic stress and cortisol dysregulation impair regulatory T cell function and shift cytokine balance toward inflammatory phenotypes, and stressful life events precede autoimmune onset in a substantial proportion of cases.Prioritise Sleep
Immune regulation is substantially a night-time process, and short sleep raises inflammatory signalling measurably. This is unglamorous and it is frequently the difference between a protocol that works and one that stalls.
What the evidence showsGut microbial composition shapes regulatory T cell development through short-chain fatty acid production, particularly butyrate. Dysbiosis is documented across autoimmune conditions.Investigate Environmental Exposure
Mold and biotoxin illness, heavy metals and chemical exposures all drive immune dysregulation. Where the history points at one — water damage, occupation, a specific timeline — this deserves proper testing rather than assumption.
What the evidence showsSeveral environmental exposures including mercury, silica and solvents are associated with increased autoimmune prevalence in occupational and population studies.Use Advanced Therapies Where They Help
Ozone modulates rather than stimulates immune function, which is the property that matters in autoimmunity. HOCATT and red light support the inflammatory and stress side. These are additive, and they work best once the eight above are handled.
What the evidence showsOzone and hyperbaric therapies modulate rather than suppress immune signalling, shifting cytokine profiles toward regulation — mechanistically distinct from immunosuppressive pharmacotherapy.What patients commonly experience under our care
When patients receive the proper guidance, here is what they commonly experience under our care.
- Weeks 2–4 — energy and digestion. Removing genuine triggers and supporting digestion produces a change patients often describe as a weight lifting. Bloating settles and the post-meal fatigue eases.
- Weeks 4–8 — joint and skin symptoms. As inflammatory load drops, the aching and the skin manifestations that patients had stopped mentioning begin to settle. Flare frequency typically reduces before flare severity does.
- Weeks 8–12 — the inflammatory panel moves. hs-CRP falling. ESR coming down. Ferritin normalising as the inflammatory drive settles. This is the objective evidence that the immune load has genuinely changed.
- Months 6–12 — antibodies. The slowest and most meaningful marker. Antibodies fall gradually when the drivers underneath are properly addressed, and that is the change that alters where this condition goes over a lifetime.
If you have been given a diagnosis and a prescription and nobody has asked why your immune system started attacking your own tissue, schedule a consultation. My team will work through the triad properly, alongside your specialist, and find what is actually driving it. We will not stop until the root cause of every one of your health issues has been found and addressed.
The antibody panel, permeability markers, comprehensive stool analysis and the nutrient status that immune tolerance depends on.
Common questions
Can autoimmune disease be reversed?
In many cases we have seen antibodies fall substantially and symptoms resolve, and we have seen this consistently in our clinic. The genetic susceptibility does not go away, but the genetic component is only one of three required parts. Address the trigger and the intestinal permeability and you change what the disease does over your lifetime, which is what matters most.
What causes autoimmune disease?
The best framework is Dr. Alessio Fasano's three-part model: a genetic susceptibility, an environmental trigger, and increased intestinal permeability — all three present at once. Genetics is fixed. The trigger and the permeability are both modifiable, which is where the entire opportunity sits.
Is there a functional medicine doctor for autoimmune disease near Nashville?
Yes. We are at 329 S. Royal Oaks Blvd in Franklin, Tennessee, about twenty minutes south of downtown Nashville. We work alongside your rheumatologist or specialist rather than instead of them, and we focus on the drivers underneath the diagnosis rather than only on symptom control.
Do I have to go gluten free with an autoimmune condition?
Not necessarily, but a proper trial is worth doing. The structural resemblance between gliadin and several human tissues is well described, and coeliac disease occurs alongside other autoimmune conditions far more often than chance predicts. We screen for coeliac first, because removing gluten beforehand invalidates that test.
Will this replace my rheumatologist?
No, and it should not. We work alongside your specialist and we want them to know exactly what you are doing. Medication decisions belong with your prescribing physician. What we add is the investigation into why the immune system switched on in the first place, which is a question that often goes unasked.
- Fasano A. Leaky gut and autoimmune diseases. Clinical Reviews in Allergy & Immunology. 2012;42(1):71–78. PMID 22109896
- Fasano A. All disease begins in the (leaky) gut: role of zonulin-mediated gut permeability. F1000Research. 2020;9:F1000. PMC6996528
- Aranow C. Vitamin D and the immune system. Journal of Investigative Medicine. 2011;59(6):881–886. PMC3166406
- Houen G, Trier NH. Epstein-Barr virus and systemic autoimmune diseases. Frontiers in Immunology. 2021;11:587380.
- Huwiler VV, et al. Selenium supplementation in patients with Hashimoto thyroiditis: a systematic review and meta-analysis. Thyroid. 2024;34(3):295–313. PMC10951571
This article is educational and reflects the published literature as of August 2026. It is not a diagnosis or a treatment recommendation for any individual, and any decision about your care belongs in a conversation with a licensed practitioner who has seen your history and your labs.