Food and Immunity: How Diet Changes the Course of Autoimmune Diseases

Autoimmune diseases are becoming one of the most “silent” epidemics of the 21st century: they affect about 4% of the population and are more common in women. A new editorial review in Nutrients sums up the results of the special issue “Nutrition and Autoimmune Diseases” and formulates a simple conclusion: nutrition is not a peripheral factor, but a full-fledged module of the immune system and the integrity of the intestinal barrier. And it is from this position that we should look at prevention, accompanying therapy and the quality of life of patients.

Background of the study

Autoimmune diseases (AIDs) - from thyroiditis and rheumatic diseases to inflammatory bowel diseases and multiple sclerosis - are growing in prevalence, especially in women and in industrialized countries. The mechanics of their onset are multifactorial: genetic predisposition and epigenetics are superimposed on external triggers - infections, stress, diet composition, vitamin D deficiency, changes in microbiota and integrity of barrier tissues. The "Western" dietary pattern (excess of ultra-processed foods, sugar, saturated and ω-6 fats, salt; lack of fiber, ω-3, polyphenols and trace elements) is associated with dysbiosis, increased intestinal permeability and a shift in the immune response towards pro-inflammatory axes (Th1/Th17), while diets rich in fiber and ω-3 increase the production of short-chain fatty acids, support T-regulators and the "tightness" of the epithelium.

Against this background, nutrition has ceased to be a secondary "background" of therapy. It affects three pathogenesis contours at once:

• Barrier (tight junctions, mucous layer, permeability);
• Microbiota (composition and metabolites such as butyrate, propionate);
• Immunomodulation (cytokine balance, Treg/Th17, innate immunity).

In autoimmune thyroid diseases, fine-tuning with iodine and selenium is important; in IBD, correction of deficiencies (iron, vitamin D, protein), exclusion of individually triggering foods and support of an anti-inflammatory dietary pattern; in neuroimmunology, the role of ω-3, polyphenols, antioxidants and metabolic pathways (e.g., via SCFA and activation of T-regulators) is studied. However, most of the data are observational: they set the direction, but do not replace randomized trials with “hard” outcomes (risk of onset, frequency of exacerbations, need for hospitalizations/biologics).

Hence the need for a consolidated, interdisciplinary view: what can already be recommended as a standard of care (general dietary patterns such as the Mediterranean), where personalization is needed (thyroid antibody status, gender, BMI, microbiota, deficiencies, concomitant medications), and which inexpensive, safe nutraceuticals have biological plausibility and require testing in RCTs. The special issue of Nutrients closes this “gap” between biology and practice, collecting clinical and preclinical signals to move the conversation about nutrition in AIDs from the realm of general slogans to algorithms suitable for everyday medicine.

Why Nutrition Is About Immunity, Not Just Calories

• It forms physical barriers (skin, intestinal mucosa) and affects the “tightness” of tight epithelial junctions.
• Sets the tone for the intestinal microbiota, which trains and disciplines the immune system.
• Modulates the innate and adaptive response: from macrophage activity to the balance of T-regulators and Th1/Th17.
• The relationship is two-way: chronic inflammation alters appetite, absorption, and nutritional needs, complicating patient management.

The editors have collected six outstanding papers, ranging from clinical observations to preclinical immunology. Together, they form a “framework” for conversations about nutrition: where we already have practical supports, and where there are careful hints that require RCTs.

Six Special Issue Materials - What Was Shown and Why You Should Know It

• Hashimoto's and quality of life (cross-sectional study, 147 women).
  Most participants ate less than ideally, but a simple gradation of "low vs. average diet quality" did not explain differences in nutritional status and quality of life - fatigue, anxiety and depression were elevated in many. Conclusion: interventions and a more refined, "Hashimoto's-specific" dietary assessment tool are needed.
• Mediterranean diet (MD) - "double benefit" for rheumatic and thyroid autoimmune diseases (review).
  Antioxidants, omega-3, polyphenols and fiber reduce systemic inflammation and oxidative stress - exactly what accelerates autoimmunity. MD - a complementary strategy to basic therapy.
• Iodine and autoimmunity in Chinese children/adolescents after 20 years of universal salt iodization.
  Overall iodine status is adequate, but thyroid autoantibodies still occur; risk subgroups have been identified (e.g., boys with low iodine/creatinine ratios are more likely to be TgAb positive; seronegatives are at risk of subclinical hypothyroidism with high BMI and iodine). Personalized iodine strategies that take into account antibody status are needed.
• Yerba mate and a model of autoimmune encephalomyelitis (mouse EAE).
  The drink alleviated symptoms, reduced immune cell infiltration into the CNS and demyelination, and most importantly, increased the number and function of T-regulators. Potentially a cheap immune modulator that is worth further study.
• Diet and risk of onset of multiple sclerosis (UK Biobank).
  Protective signals from moderate consumption of fatty fish and… weekly alcohol; trend in favour of DM is still statistically “borderline”, but biologically plausible. Large-scale confirmation and mechanistic detail are needed.
• Sepsis outside the intensive care unit - how nutrition can influence survival.
  The review systematizes metabolic breakdowns in sepsis, approaches to assessing nutritional status and targeted supplements (including working with microbiota). The practical focus is to standardize nutrition routes in regular hospitals, not only in the intensive care unit.

What does this change right now for patients and doctors?

• Integrate nutrition into your AID management plan - at least at the level of basic patterns (DM, fiber, fish, olive oil), and not individual “superfoods”.
• Thyroid ≠ hormones only. In autoimmune thyroid diseases, it is advisable to discuss diet, antioxidant saturation and individual iodine (including with different antibody profiles).
• Neuroimmunity and food. On the horizon are nutraceuticals with Treg modulation (example: yerba mate components). This is still preclinical, but the direction is promising.
• Comorbidities and hospital practice. Nutritional management protocols, from screening to targeted supplements, are needed for sepsis outside the ICU.

Now, a (useful) spoonful of skepticism. Most dietary signals are observational: they set hypotheses, but do not replace RCTs. Even where the picture is convincing (SD), the question of “how much and for how long” remains open; the same goes for doses, forms, and “targets” for nutraceuticals. But the general trajectory is clear: nutrition has ceased to be “background” and should be included in the routing standards along with drugs and monitoring.

Where should science go?

• Large randomized trials of “dietary pattern → clinical outcomes” in rheumatology, neuroimmunology and thyroiditis.
• Personalization by biomarkers: antibody status, polymorphisms of metabolic/signaling pathways, microbiota, barrier function markers.
• Research into cheap, accessible immune modulators (plant matrices with polyphenols and Treg triggers) - from dosages to safety.

Conclusion

Eating is a controlled "twist" of immunity. And although we still lack ideal RCTs, it is already reasonable to shift the emphasis towards the Mediterranean pattern, precise work with iodine and the search for low-cost, safe nutraceuticals - especially where drug options are limited.

Source: Ruggeri RM, Hrelia S, Barbalace MC Nutrition and Autoimmune Diseases. Nutrients 2025;17(13):2176. Special issue “Nutrition and Autoimmune Diseases”. https://doi.org/10.3390/nu17132176