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Dermatitis Herpetiformis: Food-First Dietary Approach#

Medical Disclaimer

This content is for informational purposes only. It is not medical advice. Read the full disclaimer.

Compiled: February 14, 2026

Philosophy: Every mechanism targeted by the supplements in Natural & Dietary Analogs can be partially or fully addressed through whole foods. This document maps specific foods to the same pharmaceutical mechanisms, prioritizing dietary sources over supplementation wherever evidence supports it.

Important: This does not replace a strict gluten-free diet or dapsone for active disease. These are adjunctive dietary strategies that target the same pathways as both pharmaceutical and supplement interventions.


Table of Contents#

  1. Regulatory T-Cell (Treg) Promotion
  2. Gut Barrier Restoration
  3. Neutrophil / MPO Inhibition
  4. Butyrate Production via Resistant Starch
  5. Microbiome Restoration via Fermented Foods
  6. Anti-Inflammatory Omega-3s from Fatty Fish
  7. Food-to-Mechanism Master Map
  8. Daily Meal Template
  9. What Food Can't Cover

1. Regulatory T-Cell (Treg) Promotion#

Pharmaceutical analogs: KAN-101, TPM502, engineered Tregs

Tregs are the immune cells that tell your body "this is harmless, stand down." In DH/celiac, Treg function is insufficient to suppress the gluten-driven immune cascade. Two foods stand out for directly promoting Treg differentiation through distinct epigenetic and metabolic pathways.

Raw / Unprocessed Milk#

Mechanism: Milk is a postnatal epigenetic imprinting system that stabilizes FoxP3 expression (the master transcription factor for Tregs) through at least six signaling pathways:

  1. Exosomal TGF-beta transfer — Milk exosomes carry TGF-beta, which induces SMAD2/SMAD3-dependent FoxP3 expression directly
  2. FoxP3 promoter demethylation — Milk exosomal microRNAs attenuate DNA methyltransferase (DNMT) expression, promoting demethylation of the Treg-specific demethylated region (TSDR). This is the same epigenetic mechanism that makes Tregs stable and long-lived.
  3. IL-10 delivery — Raw milk contains bioactive IL-10, a key anti-inflammatory cytokine that supports Treg function
  4. Lactoferrin — Modulates dendritic cell function toward tolerogenic phenotype

Evidence quality: Published in Clinical and Translational Allergy. Farm milk consumption in early life is epidemiologically associated with reduced atopic and autoimmune disease. The epigenetic mechanisms are well-characterized at the molecular level.

Practical notes: - Raw (unpasteurized) milk retains the exosomal microRNAs and bioactive TGF-beta that pasteurization destroys - Legal access varies by state/country; "herd share" programs exist in many US states - If raw milk is unavailable, minimally pasteurized (vat/batch pasteurized at 145F) retains more bioactives than ultra-pasteurized - Kefir made from raw milk may provide dual benefit (Treg promotion + fermented food microbiome effects) - Caution: Raw milk carries infection risk (Salmonella, Listeria, E. coli). Source from tested, reputable farms.

How much: 1-2 cups daily

Sources: PMC - Milk: Postnatal Imprinting System Stabilizing FoxP3, Clinical and Translational Allergy

Beef Liver (and Other Organ Meats)#

Mechanism: Liver is the most concentrated food source of preformed retinol (vitamin A), which the body converts to retinoic acid — the molecule directly required for Treg differentiation in the gut.

The pathway: Retinol (from liver) -> Retinal -> Retinoic acid (RA)

CD103+ dendritic cells in the gut use retinoic acid to convert naive CD4+ T cells into FoxP3+ regulatory T cells. Without adequate vitamin A, this conversion is impaired. Retinoic acid combined with TGF-beta (present in raw milk) is the most potent known natural Treg differentiation signal.

Vitamin A content: - Beef liver: ~20,800 mcg retinol per 100g (~6,000 mcg per 3 oz serving) - This is approximately 6-7x the daily RDA in a single serving - Grass-fed liver has higher retinol content than grain-fed

Practical notes: - 3 oz (85g) of beef liver 1-2x per week provides more than adequate retinol - Chicken liver is also excellent (~3,300 mcg retinol per 3 oz) - Liver pate, liverwurst, or desiccated liver capsules for those who dislike the taste - Do not eat liver daily — vitamin A is fat-soluble and accumulates. 1-2 servings per week is the sweet spot. - Pairs synergistically with raw milk: liver provides retinoic acid, milk provides TGF-beta. Together they drive the strongest Treg differentiation signal.

How much: 3-4 oz, 1-2x per week

Sources: NIH - Vitamin A Fact Sheet, PubMed - Vitamin A and Retinoic Acid in T Cell Immunity, Linus Pauling Institute - Vitamin A

Why These Two Foods Together#

Liver + raw milk is arguably the most potent food-based Treg promotion stack available:

Component Source Role in Treg Differentiation
Retinoic acid (from retinol) Liver Required substrate for CD103+ DC-mediated Treg conversion
TGF-beta Raw milk exosomes Induces SMAD2/3-dependent FoxP3 expression
Exosomal miRNAs Raw milk Demethylate FoxP3 promoter (TSDR), stabilizing Treg identity
IL-10 Raw milk Anti-inflammatory cytokine supporting Treg function

This combination hits three of the four requirements for stable Treg generation: the antigen-presenting cell signal (retinoic acid), the cytokine signal (TGF-beta), and epigenetic stabilization (TSDR demethylation). The only thing it can't provide is antigen-specificity — you can't make gluten-specific Tregs with food, which is what TPM502 and KAN-101 attempt.


2. Gut Barrier Restoration#

Pharmaceutical analog: Larazotide acetate (zonulin antagonist)

Bone Broth (Long-Simmered)#

Mechanism: Bone broth provides the key amino acids that intestinal epithelial cells need to maintain tight junctions and repair damage:

  • L-Glutamine — Primary fuel for enterocytes. Promotes epithelial cell proliferation, regulates tight junction proteins directly, and suppresses NF-kB signaling. Research indicates glutamine can reduce intestinal permeability by up to 40%.
  • Glycine — Anti-inflammatory amino acid that protects intestinal cells from oxidative injury. Reduces the local inflammatory load that drives permeability, breaking the damage-permeability cycle.
  • Proline — Supports collagen synthesis for mucosal structural integrity
  • Arginine — Promotes intestinal cell growth and wound healing
  • Minerals — Calcium, phosphorus, potassium, magnesium, zinc — all support epithelial function

A 2025 review in Digestive Diseases and Sciences confirmed that bone broth nutrients fortify the gut barrier in both health and disease, resolving long-standing questions about whether the traditional remedy had clinical backing.

Practical notes: - Simmer bones for 12-24 hours (beef) or 6-12 hours (chicken) to maximize amino acid extraction - Add 1-2 tbsp apple cider vinegar during simmering to draw minerals from bones - A cup of broth contains roughly 2-6g of glutamine and 1-3g of glycine (varies by preparation) - Commercially available bone broths vary widely in quality; homemade is more reliable - Can be used as a base for soups, for cooking grains, or consumed straight

How much: 1-2 cups daily

Sources: PubMed - Bone Broth Benefits: Gut Barrier in Health and Disease, Springer - Bone Broth Nutrients Fortify Gut Barrier

Zinc-Rich Foods#

Mechanism: Zinc induces tight junction remodeling and increases ZO-1 expression. Intracellular zinc in intestinal epithelial cells is essential for maintaining the tight junction barrier.

Top whole-food sources (per serving): | Food | Zinc per serving | Notes | |------|-----------------|-------| | Oysters (6 medium) | ~32 mg | Richest food source of zinc by a wide margin | | Beef liver (3 oz) | ~4.5 mg | Also provides retinol (dual benefit) | | Beef (3 oz) | ~5-7 mg | Red meat in general is zinc-dense | | Pumpkin seeds (1 oz) | ~2.2 mg | Plant source; phytates reduce absorption | | Crab (3 oz) | ~6.5 mg | Excellent bioavailable source |

How much: Aim for 15-30 mg/day from food (RDA is 8-11 mg; higher end for gut barrier support). Oysters 1-2x per week plus regular red meat covers this easily.

Sources: PMC - Zinc Induces Tight Junctional Remodeling


3. Neutrophil / MPO Inhibition#

Pharmaceutical analog: Dapsone

Quercetin-Rich Foods (Especially Capers)#

Mechanism: Quercetin directly inhibits myeloperoxidase (MPO)-mediated HOCl formation (75% inhibition at 10 micromolar), reduces neutrophil extracellular trap release, and decreases both elastase and MPO release from stimulated neutrophils. This is mechanistically the closest natural analog to dapsone's primary mechanism.

Critical advantage of food-form quercetin: Quercetin from food has dramatically better bioavailability than quercetin supplements. Absorption from isoquercetin-rich onions is 52%, compared to 24% from standard quercetin supplements. Onion skin extract shows a 3.6-fold higher peak blood concentration than quercetin capsules. The food matrix — particularly dietary fats and fiber consumed alongside quercetin — approximately doubles bioavailability.

Quercetin content by food source:

Food Quercetin (mg/100g) Notes
Capers (pickled) 180-520 Richest known food source. Pickling converts rutin to quercetin, increasing content.
Capers (raw) Up to 323 Still the highest raw source
Red onions 30-40 Onion quercetin glycosides have superior absorption (52%)
Yellow onions 13-20 Still significant with high bioavailability
Kale 7-23 Varies by variety
Cranberries 15 Modest but consistent
Blueberries 5-8 Lower but consumed in larger quantities
Broccoli 3-4 Modest but part of a varied diet
Cherries 2-3 Minor contributor

Why capers are exceptional: Capers grow in arid regions with poor, rocky soils and have developed unusually high polyphenol levels to protect their flower buds from UV radiation, heat, and drought. This stress adaptation produces quercetin concentrations 5-15x higher than any other common food.

Practical notes: - 1 tablespoon of capers (~8.5g) provides roughly 15-44 mg of quercetin — equivalent to eating a medium-large red onion - Eat capers with fat (olive oil, fish, meat) to further boost absorption - Red onions are the best high-volume quercetin source for daily cooking - Eating quercetin-rich foods with fat is important — dietary fat approximately doubles quercetin absorption via micelle incorporation

How much: 1-2 tbsp capers daily + liberal use of red onions in cooking

Sources: PubMed - Quercetin Inhibits MPO-Mediated HOCl, PubMed - Bioavailability of Quercetin and Food Matrix, ScienceDirect - Quercetin Bioavailability

Turmeric (Whole Root or Powder)#

Mechanism: Curcumin in turmeric inhibits NF-kB (master inflammatory switch), reduces IL-8 (primary neutrophil chemoattractant in DH), modulates JAK/STAT pathway, and inhibits leukotriene synthesis.

Practical notes: - Curcumin is 2-8% of turmeric by weight; you need meaningful amounts - Black pepper (piperine) increases curcumin bioavailability by 2,000% — always combine - Fat also increases absorption — traditional curries with oil/ghee and black pepper are optimal delivery - Golden milk (turmeric + black pepper + fat from coconut or whole milk) is an efficient daily vehicle - Fresh turmeric root can be grated into cooking; stronger than dried powder

How much: 1-2 tsp turmeric powder daily (with black pepper and fat), or 1-inch piece of fresh root


4. Butyrate Production via Resistant Starch#

Pharmaceutical analog: Tributyrin supplements / engineered SCFA-producing probiotics

Mechanism: Resistant starch (RS) passes through the upper GI tract intact and is fermented by colonic bacteria into short-chain fatty acids, predominantly butyrate. Butyrate is a triple-mechanism compound:

  1. Gut barrier — Preferred fuel for colonocytes; maintains tight junction integrity
  2. Treg promotion — Inhibits histone deacetylase (HDAC), directly promoting FoxP3+ Treg induction
  3. Anti-inflammatory — Enhances retinoic acid production by CD103+ dendritic cells, promoting tolerogenic immune responses

Resistant starch from potatoes produces the greatest increase in butyrate compared to other RS sources tested.

How to Create Resistant Starch (Retrograded Starch / RS3)#

When starchy foods are cooked then cooled, the amylose chains retrograde (recrystallize) into a form resistant to digestion. This is called RS type 3.

Food Method RS Content
Potatoes Boil/bake, then refrigerate 12-24h High (highest butyrate yield)
White rice Cook, then refrigerate overnight Moderate-high
Green bananas Eat unripe (naturally high RS2) High (no cooking needed)
Legumes (lentils, beans) Cook, then cool Moderate
Oats (if tolerated) Cook, then refrigerate overnight Moderate

Practical notes: - Reheating does NOT destroy all the resistant starch — cooled-then-reheated potatoes and rice retain significant RS3 - Potato salad, cold rice dishes, and overnight oats are natural RS3 delivery vehicles - Green (unripe) bananas can be sliced into smoothies - Cooked-and-cooled potatoes in bone broth soup = dual mechanism (RS3 + glutamine/glycine) - Oat tolerance note: Most DH patients tolerate gluten-free certified oats, but ~5% react to avenin. Introduce cautiously and monitor.

How much: 1-2 servings of cooked-cooled starchy foods daily

Sources: PMC - Resistant Starch and Gut Microbiome, Healthline - Cooling Foods Increases Resistant Starch, CSIRO - Resistant Starch Facts


5. Microbiome Restoration via Fermented Foods#

Pharmaceutical analog: Engineered probiotics, FMT

Sauerkraut, Kimchi, Kefir#

Mechanism: Fermented foods introduce diverse Lactobacillus and Bifidobacterium species that: - Produce butyrate and other SCFAs - Modulate dendritic cell function toward tolerogenic phenotypes - Support Treg differentiation

A December 2025 human study using single-cell RNA sequencing found that kimchi dietary intervention directly modulated CD4+ T cell differentiation. Trajectory analysis revealed accelerated differentiation toward regulatory phenotypes, while CD8+ T cells, B cells, and NK cells remained stable — indicating targeted immunomodulation rather than broad immune suppression.

Separately, kefir has been shown in animal models to increase Treg and IL-10 levels while attenuating neutrophil activity and CXCL1 (a neutrophil chemoattractant).

Key foods: | Food | Key Organisms | Notes | |------|--------------|-------| | Sauerkraut (raw, unpasteurized) | Lactobacillus plantarum, L. brevis | Must be refrigerated/raw; shelf-stable versions are pasteurized (dead bacteria) | | Kimchi | L. plantarum, L. brevis, Leuconostoc | Human clinical data for Treg modulation (Dec 2025 study) | | Kefir (milk or water) | 30-50+ species including Lactobacillus, Bifidobacterium | Most diverse probiotic food; raw milk kefir = Treg + microbiome dual benefit | | Natto | Bacillus subtilis | Also provides nattokinase (fibrinolytic enzyme) | | Fermented vegetables | Various Lactobacillus species | Pickles (naturally fermented, not vinegar), fermented carrots, beets |

Practical notes: - Raw/unpasteurized is essential — pasteurized fermented foods contain no live organisms - Look for "live cultures" and refrigerated products - Homemade sauerkraut and kimchi are easy, cheap, and contain more diverse organisms than commercial products - Raw milk kefir combines Treg-promoting exosomes from milk with probiotic organisms from fermentation - Start slowly (1-2 tbsp) and increase — introducing large amounts of fermented foods can cause temporary bloating

How much: 2-4 tbsp of fermented vegetables daily + kefir if tolerated

Sources: Nature - Kimchi Modulates CD4+ T Cells (2025), PMC - Anti-Inflammatory Properties of Fermented Plant Foods, PMC - Gut Microbiota-Targeted Diets Modulate Immune Status


6. Anti-Inflammatory Omega-3s from Fatty Fish#

Pharmaceutical analog: Resolvin/protectin pathways (endogenous), Treg engineering

Salmon, Sardines, Mackerel, Anchovies#

Mechanism: EPA and DHA from fatty fish: - Limit T-cell proliferation and guide differentiation toward Tregs — directly promoting regulatory phenotype - Generate specialized pro-resolving mediators (resolvins, protectins, maresins) that actively resolve inflammation rather than just suppressing it - Reduce TNF-alpha, IL-6, and IL-1beta - Modulate B-cell activation (relevant to IgA production)

Fatty fish also provides vitamin D — another Treg promoter. Wild-caught salmon contains 600-1,000 IU vitamin D per 3 oz serving, contributing to the same Treg pathway supported by liver and raw milk.

EPA + DHA content by fish source: | Fish | EPA+DHA per 3 oz serving | Notes | |------|--------------------------|-------| | Atlantic mackerel | ~2,500 mg | Highest common source | | Salmon (wild) | ~1,500-2,000 mg | Also high in vitamin D | | Sardines | ~1,400 mg | Also high in zinc and calcium (bones) | | Anchovies | ~1,200 mg | Excellent in small doses (capers + anchovies = MPO + omega-3) | | Herring | ~1,700 mg | Pickled herring is also fermented | | Oysters | ~600 mg | Also the richest zinc source (dual benefit) |

Practical notes: - Wild-caught > farmed for omega-3 content and lower contaminant load - Small fish (sardines, anchovies) have lower mercury than large predator fish - Canned sardines and mackerel are affordable, shelf-stable, and retain omega-3 content - Sardines eaten with bones provide calcium + zinc + omega-3 in one food - Anchovies + capers on a GF cracker or vegetable = combined MPO inhibition (quercetin) + anti-inflammatory (omega-3)

How much: 3-4 servings of fatty fish per week (aim for 2-3g total EPA+DHA daily from food)

Sources: Wiley - Immunomodulatory Effects of Omega-3 Fatty Acids, NIH - Omega-3 Fatty Acids Fact Sheet, PMC - Dietary Omega-3 and Inflammation


7. Food-to-Mechanism Master Map#

DH Pathogenic Step Pharmaceutical Food Analog Key Compounds
Gut barrier breakdown Larazotide Bone broth, oysters, liver Glutamine, glycine, zinc, retinol
TG2 deamidates gliadin ZED1227 (No strong food analog)
T-cell activation / Treg deficit KAN-101, TPM502, Treg therapy Liver + raw milk, fatty fish, fermented foods Retinoic acid, TGF-beta, exosomal miRNAs, EPA/DHA, vitamin D
B-cell produces anti-TG3 IgA APRIL inhibitors (No food analog)
IgA-TG3 deposits in skin (No pharmaceutical) (No food analog)
Complement activation Avacopan (Weak: quercetin foods, turmeric) Quercetin, curcumin (indirect)
Neutrophil / MPO activation Dapsone Capers, red onions, turmeric Quercetin, curcumin
Inflammation amplification JAK inhibitors, biologics Fatty fish, turmeric EPA/DHA, resolvins, curcumin
Microbiome dysbiosis Engineered probiotics / FMT Sauerkraut, kimchi, kefir Live Lactobacillus, Bifidobacterium
Low butyrate / SCFA Butyrate supplements Cooked-cooled potatoes, rice, green bananas RS3 -> butyrate via fermentation

Coverage Assessment#

Strong food coverage (comparable to supplement stack): - Gut barrier restoration - Treg promotion - Butyrate production - Microbiome restoration - Anti-inflammatory / omega-3

Moderate food coverage (weaker than supplements): - MPO / neutrophil inhibition (quercetin from food is better absorbed but lower dose than supplements) - NF-kB / JAK-STAT modulation (turmeric is potent but curcumin content is low per serving)

No food coverage (requires pharmaceutical or supplement intervention): - TG2 inhibition (glucosamine supplement is only natural option) - IgA-specific reduction (no natural analog exists) - Dermal IgA clearance (no natural analog exists) - Gluten enzyme degradation (AN-PEP enzyme supplement for accidental exposure)


8. Daily Meal Template#

This template incorporates all the food-first mechanisms into a realistic daily eating pattern. All items are gluten-free.

Morning#

  • Bone broth (1 cup) — glutamine, glycine, zinc for gut barrier
  • Raw milk kefir (1 cup) — TGF-beta, exosomal miRNAs for Treg + probiotics
  • Cooked-cooled potato hash (reheated from fridge) — resistant starch for butyrate
  • Turmeric golden milk (turmeric + black pepper + raw milk or coconut milk) — curcumin + Treg support

Midday#

  • Sardines or salmon over greens with red onion and capers — omega-3 (Treg/anti-inflammatory) + quercetin (MPO inhibition)
  • Sauerkraut (2-3 tbsp as side) — live Lactobacillus for microbiome
  • Dress with olive oil — fat improves quercetin + curcumin absorption

Evening#

  • Beef liver (3 oz, 1-2x per week) or other protein — retinol for retinoic acid -> Treg differentiation
  • Cooked-cooled rice (made day before, reheated) — resistant starch
  • Kimchi (2-3 tbsp as side) — Treg modulation + microbiome diversity
  • Vegetables cooked in bone brothadditional glutamine/glycine

Snacks / Extras#

  • Green banana slices — resistant starch (RS2)
  • Oysters (when available, 1-2x per week) — zinc (32mg per 6 oysters) + omega-3
  • Raw milk (additional cup if tolerated)

Weekly Frequency Guide#

Food Frequency Primary Mechanism
Bone broth Daily (1-2 cups) Gut barrier
Raw milk / kefir Daily (1-2 cups) Treg promotion
Capers Daily (1-2 tbsp) MPO inhibition
Red onions Daily (in cooking) MPO inhibition
Fermented vegetables Daily (2-4 tbsp) Microbiome
Cooked-cooled starch Daily (1-2 servings) Butyrate
Turmeric + black pepper Daily (1-2 tsp) Anti-inflammatory
Fatty fish 3-4x per week Treg + anti-inflammatory
Beef liver 1-2x per week Treg (retinoic acid)
Oysters 1-2x per week Zinc (gut barrier)

9. What Food Can't Cover#

These mechanisms have no meaningful food-based analog and require either supplements or pharmaceuticals:

Gap Why Food Falls Short Minimum Intervention
TG2 inhibition No food inhibits tissue transglutaminase. Glucosamine (supplement) is the only natural option. Glucosamine sulfate 1500 mg/day
Gluten enzyme protection No food degrades immunogenic gluten peptides fast enough to prevent immune activation from accidental exposure. AN-PEP enzyme (OTC) with meals
IgA reduction No food or supplement specifically reduces pathogenic IgA production. This requires APRIL inhibitors (sibeprenlimab) or similar. Pharmaceutical only
Dermal IgA clearance Once IgA-TG3 complexes deposit in the papillary dermis, nothing — not food, supplements, or any current drug — actively clears them. They dissipate slowly over years on strict GFD. Time + strict GFD (up to 10 years)
Acute neutrophil suppression While quercetin-rich foods inhibit MPO, the dose achievable through food alone is unlikely to match dapsone's rapid (1-3 day) neutrophil suppression during active flares. Dapsone for acute disease; food-based quercetin for maintenance/prevention

The Realistic Picture#

Food-first approaches are strongest for: - Prevention (maintaining remission, supporting the GFD) - Upstream modulation (Treg promotion, gut barrier, microbiome) - Long-term immune environment shaping

Food-first approaches are weakest for: - Acute disease control (active flare with blistering) - Specific molecular targets (TG2, IgA, complement) - Dose-dependent effects (where therapeutic concentrations exceed what food provides)

The ideal approach combines a food-first foundation with targeted supplements (glucosamine, AN-PEP enzyme) for the gaps, and pharmaceutical intervention (dapsone, GFD) as the clinical backbone.


Document compiled from PubMed, PMC, Nature, Springer, Clinical and Translational Allergy, CSIRO, NIH ODS, Linus Pauling Institute, and other peer-reviewed sources. February 2026.