A tangled mess: addressing the knots of autoimmune conditions
Think of an autoimmune condition as a bundle of knotted yarn. Most people take one look and think, “I don’t want to touch that.” In functional medicine, untangling knots is what we do — and the more you look, the more the mess makes sense.
In my first two articles on autoimmunity, I talked about how researchers are learning more about what sets these conditions off. Here, I want to walk through the triggers I see most often — the knots, if you will — and how we tease them apart.
For some patients, we can methodically find the loose end and start untangling. For others, the bundle has been rolling around the knitting bag for years, and the knots take patience and care to work through. Those cases ask more of both patient and doctor. Either way, the yarn never looks quite the same again, and it can re-tangle if it isn’t handled well going forward — but by addressing root issues and watching their triggers, most people can live an abundant life.
Why these cases get missed
Autoimmune conditions are elusive to anyone not used to working with them — they’re complex and multifactorial, which is exactly why they’re missed so often. Cleaning up your diet and taking a few gut supplements can bring real improvement, but on their own they leave a lot on the table. Below are the pieces I look for in nearly every autoimmune patient.
And one honest note up front: you can never truly cure an autoimmune condition. What you can reach is remission — and for the autoimmune patient, remission is a sweet place to be.
1. It starts with your genes
The triggers we’ll get to — environment, gut, infections — tend to create the specific condition you’re already genetically prone to. That’s why family history is so helpful: if Hashimoto’s runs in your family, that may be where you land if the right triggers show up. Two gene variations I see a lot:
- HLA — makes it harder to detox from mold, and tends to leave people inflamed by all sorts of catalysts (mold, Lyme, other toxins, gluten). It’s linked to rheumatoid arthritis, lupus, type 1 diabetes, celiac disease, and multiple sclerosis.
- MTHFR — also affects how well you detox, plus hormone balance and immune function. It’s been associated with fibromyalgia, Hashimoto’s, and lupus.
These are only two of many. There are hundreds of genetic panels that can help map your individual picture — and once we know what we’re working with, we can support it for a better outcome.
2. What’s in your environment
- Mold. Mold can dysregulate the immune system — especially in genetically susceptible people — leading to a loss of tolerance that shows up as food allergies, sensitivities, and chemical sensitivities. Over time, that lost tolerance can tip into autoimmunity.
- Toxins. Many are suspected to contribute — mercury, iodine, vinyl chloride, organic solvents,1 hydrazines, tartrazines, cadmium,2 formaldehyde,3 trichloroethylene, and asbestos,4 among others. They hide in everyday things: household cleaners, personal-care and cosmetic products, building materials, pesticides, and processed foods.
You can’t avoid toxins entirely in the modern world, but you can be intentional — about the products you bring home, what you put on your skin, and what you eat. A high-quality air purifier at home or work helps, too; in our office we use and recommend Austin Air purifiers.
3. What’s happening in your gut
Gut health is one of the biggest levers we have, both for preventing and for calming autoimmune conditions.5,6,7 These problems can drive autoimmunity — or be a result of it:
- Dysbiosis (poor diet). Every food you eat feeds either good or bad bacteria. When the balance tips, pathogenic bugs take over — and that imbalance can trigger autoimmune disease.8
- Leaky gut. The intestinal lining should be tightly sealed. When it becomes permeable (from food sensitivities, stress, poor diet, or infections), undigested food and bacteria slip into the bloodstream and trigger reactions.
- SIBO. Small intestinal bacterial overgrowth is connected to conditions like IBS, scleroderma, celiac disease, and Hashimoto’s.9
- Food allergies & sensitivities. Eating foods your body reacts to keeps you in a constant inflammatory state. Celiac disease is the clearest example, with gluten as the trigger.10
4. Hidden infections
Infections can be a huge driver — and interestingly, certain ones tend to steer autoimmunity toward particular tissues. Knowing which infection is in play can point us toward what to screen for.
- Epstein-Barr virus (EBV). The “mono” virus. It goes dormant after infection but can reactivate and trigger lupus,11 partly by switching on autoimmunity-linked genes.12 It’s also tied to MS, rheumatoid arthritis, IBD, celiac, and type 1 diabetes.
- HHV-6. Associated with MS, connective-tissue diseases, and Hashimoto’s — often through molecular mimicry, where the virus imitates your own cells so your body attacks both.13
- Lyme disease. If the infection lingers or goes undetected, long-term exposure to the bacteria can provoke inflammatory and immune reactions that trigger autoimmunity.14
- Herpes simplex (HSV-1). Once you have it, it stays dormant until something reactivates it15 — and like HHV-6, it can trigger autoimmunity through molecular mimicry.16
- H. pylori. A very common stomach infection — more than half the world has it. It’s linked to immune thrombocytopenia (where the immune system attacks platelets),17 and patients often improve once it’s addressed.18
- Fusobacterium. Normally part of gut, oral, and genital flora, but some species turn opportunistic and may play a role in autoimmunity — specifically Crohn’s disease.19
Common questions
References (19) ▾
- Environmental/occupational chemical exposures and autoimmunity. PubMed. https://pubmed.ncbi.nlm.nih.gov/10970167/
- Cadmium and other metals in autoimmunity. PubMed. https://pubmed.ncbi.nlm.nih.gov/10970167/
- Formaldehyde exposure and immune/autoimmune effects. PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3496812/
- Environmental triggers of autoimmunity (asbestos and other exposures). PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4290643/
- The gut microbiome in autoimmune disease. J Immunol Res. 2019;2019:7546047. https://www.hindawi.com/journals/jir/2019/7546047/
- The gut microbiome in autoimmune disease. J Immunol Res. 2019;2019:7546047. https://www.hindawi.com/journals/jir/2019/7546047/
- National Institutes of Health. Gut microbe drives autoimmunity. NIH Research Matters. https://www.nih.gov/news-events/nih-research-matters/gut-microbe-drives-autoimmunity
- Dysbiosis and the development of autoimmune disease. PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742538/
- Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterol Hepatol (NY). 2007;3(2):112-122. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/
- Gluten as the trigger in celiac disease. PubMed. https://pubmed.ncbi.nlm.nih.gov/9196849/
- Epstein-Barr virus and systemic lupus erythematosus. PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395176/
- National Institutes of Health. Epstein-Barr virus protein can “switch on” risk genes for autoimmune diseases. NIH News Releases. https://www.nih.gov/news-events/news-releases/epstein-barr-virus-protein-can-switch-risk-genes-autoimmune-diseases
- Human herpesvirus-6 (HHV-6) and autoimmune disease. PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825270/
- Lyme borreliosis and autoimmunity. PubMed. https://pubmed.ncbi.nlm.nih.gov/15214872/
- Nicoll MP, Proença JT, Efstathiou S. A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation. J Gen Virol. 2015;96(Pt 7):1581-1602. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635449/
- HSV and molecular mimicry in autoimmunity. PubMed. https://pubmed.ncbi.nlm.nih.gov/9478893/
- Helicobacter pylori and immune thrombocytopenia. PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3643302/
- Helicobacter pylori eradication and autoimmune outcomes. Biomed Pharmacother. https://www.sciencedirect.com/science/article/abs/pii/S0753332212000443
- Fusobacterium and Crohn’s disease. Front Microbiol. 2016;7:1081. https://www.frontiersin.org/articles/10.3389/fmicb.2016.01081/full
We specialize in the tangled cases — finding the genetic, environmental, gut, and infectious threads others miss, and working them loose toward remission.