AUTOIMMUNITY

Partners in Leaky Gut Syndrome: Intestinal Dysbiosis and Autoimmunity

The article explores how an imbalance in gut bacteria (dysbiosis) and a compromised intestinal barrier (leaky gut syndrome) may contribute to autoimmune diseases like type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and celiac disease. Normally, the gut lining acts as a barrier, preventing harmful substances from entering the bloodstream. However, when this barrier weakens, it allows bacteria and their by-products to leak into the body, triggering inflammation and immune system overactivity. The article discusses how certain immune cells and molecules, such as IL-22, play roles in maintaining or disrupting this barrier. It also highlights that the gut microbiota influences immune responses, and disruptions in its composition can lead to systemic inflammation and autoimmune conditions.

Fight them or feed them: how the intestinal mucus layer manages the gut microbiota

This article explains how the mucus layer in our intestines acts like a protector and caretaker for the bacteria living there. It keeps harmful germs away from our gut wall while feeding the good bacteria by providing nutrients. The types of bacteria and the mucus work together to keep the gut healthy. But if the mucus gets damaged—like from a poor diet—it can let bad bacteria in, which might cause gut problems and inflammation.

Opposing microbiome signatures in autoimmunity vs cancer (Microbiome, 2022).
By re-analyzing many published datasets, the authors showed that gut communities tend to shift in predictably different directions in autoimmune diseases compared with cancers—almost like mirror-image patterns of immune tone. This cross-disease lens suggests that “which microbes are up or down” aligns with how the immune system is skewed (over-reactive in autoimmunity, under-reactive in some cancers). The work supports using microbiome profiles as disease-class fingerprints rather than single-disease quirks.

Leaky gut and autoimmunity: mechanistic overview (Int. J. Mol. Sci., 2020).
Here, the authors unpack tight-junction biology (the “zippers” between gut cells), the regulator zonulin, and how increased permeability exposes the immune system to molecules it shouldn’t see. They connect this to a range of autoimmune conditions, arguing that permeability is not just a side effect but a plausible driver. The review also surveys early therapeutic angles—from diet to probiotics—that aim to reseal the barrier and rebalance microbes.

Microbiome in rheumatoid arthritis—state of the science (Rheumatology Advances in Practice, 2023).
A comprehensive review summarizing evidence that RA-linked dysbiosis can precede joint symptoms and may shape autoantibody development and mucosal inflammation. It also evaluates periodontitis-oral–gut connections, Prevotella expansion, and diet, and calls for interventional trials testing microbe-targeted strategies.

Gut microbiota and autoimmune thyroid disease—meta-analysis (Frontiers in Endocrinology, 2021).
Pooling data across studies, patients with Graves’ disease or Hashimoto’s thyroiditis showed reduced microbial diversity and reproducible shifts in specific taxa versus controls. The authors propose microbiome-influenced bile acids, SCFAs, and immune signaling as routes to thyroid autoimmunity, and they encourage rigorous trials of diet/probiotics as adjuncts to endocrine care.

Exploring the role of gut microbiota in autoimmune thyroid disease (Frontiers in Endocrinology, 2023).
This review pulls together human and animal evidence showing that people with Hashimoto’s thyroiditis and Graves’ disease often share a recognizable “microbial fingerprint”: lower overall diversity, fewer butyrate-producing (anti-inflammatory) species, and shifts in bile-acid and tryptophan-related metabolism. It explains plausible mechanisms—how dysbiosis can increase gut permeability, alter immune tolerance, and nudge B-cells toward making thyroid autoantibodies—and translates that into practical levers (dietary fiber, fermented foods, targeted probiotics, and prebiotics). The authors are careful to note that while associations are strong, interventional trials are still catching up, so microbiome support is best considered an adjunct to, not a replacement for, conventional endocrine care.

Gut microbiota dysbiosis in ankylosing spondylitis: systematic review & meta-analysis (Frontiers in Cellular and Infection Microbiology, 2024).
Pooling dozens of studies, this meta-analysis confirms that ankylosing spondylitis (axSpA/AS) is consistently linked with a less diverse gut ecosystem and specific taxonomic shifts (loss of beneficial commensals, enrichment of pro-inflammatory taxa). Beyond taxonomy, the paper highlights functional themes—reduced short-chain-fatty-acid (SCFA) potential and altered tryptophan metabolism—both of which can skew immune cells toward inflammation at the gut–joint interface. Clinically, the message is that dysbiosis isn’t a one-off finding; it replicates across cohorts, strengthening the case for trials that target microbial function (dietary fiber, resistant starch, postbiotics).

Leaky gut and autoimmunity: mechanistic review (International Journal of Molecular Sciences, 2020).
This review gets granular about barrier biology. It explains how tight-junction proteins (occludin, claudins) and modulators like zonulin shape what gets through the gut wall, and how stress, infections, NSAIDs, alcohol, and ultra-processed diets can push permeability higher. It then links this to antigen mimicry and bystander activation pathways that may break tolerance in genetically susceptible people. Practical implications include focusing on barrier-supportive nutrition (adequate protein, zinc, omega-3s, diverse fibers), minimizing gut-irritants where appropriate, and recognizing that barrier repair and dysbiosis correction likely need to happen together.

Gut microbiome metagenomics suggests a functional model for type 1 diabetes autoimmunity (PLOS ONE, 2011).
One of the earlier metagenomic studies in children at risk for type 1 diabetes found that changes in gut microbial function—particularly reduced diversity and diminished SCFA-related capacity—could be detected around the time autoantibodies first appeared, sometimes before clinical diagnosis. While small and exploratory by today’s standards, the study was influential because it suggested the microbiome might mark (and possibly modulate) the transition from genetic risk to active autoimmunity. It paved the way for larger longitudinal cohorts and interventional ideas like fiber enrichment and SCFA-focused strategies in at-risk populations.

The enemy within: Gut bacteria drive autoimmune disease

Yale researchers discovered that a gut bacterium called Enterococcus gallinarum can leave the intestines and migrate to organs like the liver, spleen, and lymph nodes, where it triggers inflammation and autoimmune antibodies—especially in genetically susceptible individuals. They reproduced this effect in mice and human liver cells, and even found E. gallinarum in liver tissue from patients with autoimmune diseases. Remarkably, they also showed that either an antibiotic or a vaccine specifically targeting this bacterium could suppress the autoimmune response, offering a promising new treatment approach for conditions such as lupus and autoimmune liver disease.

How to Cure Multiple Sclerosis - Dr. Terry Wahls

Dr. Terry Wahls, diagnosed with secondary progressive multiple sclerosis, reversed her severe symptoms—facial pain, vision loss, and mobility issues—through a nutrient-dense paleo diet, mitochondrial supplements, and lifestyle changes after conventional treatments failed. By prioritizing leafy greens, sulfur-rich vegetables, and organ meats, she regained her ability to walk and bike, highlighting the role of diet and environmental factors in managing autoimmune diseases. Now, she advocates for these approaches and conducts clinical trials to prove diet’s impact on MS, aiming to transform standard care.

Dr Terry Wahls on Reversing Multiple Sclerosis

Dr. Terry Wahls, a clinical professor and MS patient, transformed her health from wheelchair-bound to walking and jogging by adopting a nutrient-dense paleo diet, mitochondrial supplements, and electrical muscle stimulation. Facing progressive MS, she researched dietary interventions, leading to significant improvements in fatigue, mobility, and quality of life. Her work, in

itially met with skepticism, has gained recognition, with ongoing clinical trials comparing ketogenic and modified paleo diets to standard care in MS patients, aiming to demonstrate diet’s impact on brain volume loss and overall health, potentially reshaping MS treatment standards.