Iodine and Dermatitis Herpetiformis: Deep Dive#

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Compiled: February 14, 2026

Purpose: This document examines the relationship between dietary iodine and dermatitis herpetiformis (DH) in detail, including the molecular mechanism of iodine-triggered flares, dose-response evidence, high-iodine food data, and a conflict analysis with the food-first dietary recommendations in Food-First Dietary Approach. This is directly relevant because several foods we recommend (oysters, sardines, salmon, raw milk) are meaningful iodine sources.

Table of Contents#

Mechanism of Iodine-Triggered DH Flares
Dose-Response Relationship
High-Iodine Foods: Comprehensive Table
Conflict Analysis with Food-First Recommendations
Iodine Restriction Studies in DH
Practical Guidance
Key Takeaways

1. Mechanism of Iodine-Triggered DH Flares#

Historical Context#

The observation that iodine compounds can trigger or worsen DH dates to 1891 -- making it one of the oldest known environmental triggers of any autoimmune skin disease. For decades before direct immunofluorescence became available, the potassium iodide (KI) patch test was used as a diagnostic tool for DH. Applying 50% potassium iodide solution to the skin of DH patients would provoke a local inflammatory reaction mimicking the disease.

Sources: Haffenden et al., 1980 - KI Patch Test in DH (British Journal of Dermatology), PubMed - On Iodine Sensitivity in Duhring's DH (1954)

The KI Patch Test Evidence#

Haffenden et al. (1980) studied the KI patch test in 26 DH patients, finding:

5/5 patients with active, untreated disease had a positive test
2/6 patients on a gluten-free diet were positive
1/8 patients on dapsone were positive
0/3 patients in full remission were positive
0/2 patients with linear IgA disease (a different condition) were positive

This established two critical findings: (1) iodine sensitivity is specific to DH and correlates with disease activity, and (2) iodine sensitivity diminishes as the disease comes under control via GFD or dapsone.

Source: Haffenden et al. - KI Patch Test (PubMed)

Molecular Mechanism: TG3 Enzymatic Activation by Iodide#

The best-characterized mechanism, established by Zone and colleagues at the University of Utah, works as follows:

Step 1 — Baseline DH pathology (gluten-driven):

Gluten ingestion triggers the formation of IgA antibodies against tissue transglutaminase 2 (TG2) in the gut.
These antibodies cross-react with epidermal transglutaminase 3 (TG3), which is structurally homologous to TG2. (Sardy et al. established TG3 as the autoantigen in DH.)
TG3-IgA immune complexes deposit in the papillary dermis of the skin, either by: (a) circulating complexes depositing from the bloodstream, or (b) TG3 released from keratinocytes binding to circulating IgA locally.
These deposits recruit neutrophils via Fc IgA receptor binding, complement activation, and fibrinogen activation. Neutrophils release proteases that cleave the dermal-epidermal junction, producing the characteristic blisters.

Step 2 — Iodide amplification:

The critical finding is that TG3 within the IgA aggregates in DH skin retains enzymatic activity, and this enzymatic activity is dramatically increased in the presence of iodide. Specifically:

TG3 is normally expressed as an inactive 77 kDa zymogen requiring proteolytic activation into two fragments (44 kDa and 30 kDa), of which the N-terminal fragment carries catalytic activity.
Once activated, TG3 catalyzes the formation of isopeptide bonds between glutamine and lysine residues via an enzyme-substrate thioester intermediate.
Iodide ions appear to enhance this catalytic activity when TG3 is complexed with IgA in the skin.
The enzymatically active TG3-IgA complexes bind and activate soluble fibrinogen at the tips of the papillary dermis.
Fibrinolysis from this activation directly contributes to blister formation and also acts as a chemoattractant for neutrophils, T-cells, and macrophages -- amplifying the inflammatory cascade.

In essence: iodide does not initiate DH. It amplifies an already-primed immune reaction by increasing the enzymatic activity of TG3 within pre-existing immune complexes in the skin.

Sources: Taylor et al. - TG3 in IgA Aggregates Is Enzymatically Active (J Invest Dermatol, 2015), Sardy et al. - TG3 Is the Autoantigen of DH (PMC), Zone et al. - DH Sera Transferred to Human Skin-Grafted Mice (J Immunol, 2011), StatPearls - Dermatitis Herpetiformis

Neutrophil Pathway Details#

The downstream neutrophil activation that iodide amplifies works through:

Fc IgA receptor binding — Both circulating and skin-resident neutrophils in DH highly express Fc IgA receptors. When disease is active, circulating neutrophils show increased CD11b expression and enhanced IgA-binding capacity.
Neutrophil migration — Cutaneous IgA deposits function as a ligand for neutrophil migration and attachment.
Protease release — Neutrophils bound to IgA aggregates release proteases that cleave the dermal-epidermal junction, causing blistering.
Fibrinolysis — TG3-activated fibrinogen at the dermal papillae undergoes fibrinolysis, which both directly damages tissue and attracts more neutrophils (positive feedback loop).

By increasing TG3 enzymatic activity, iodide accelerates the fibrinogen activation step, intensifying the entire downstream cascade.

Sources: Frontiers in Immunology - DH Novel Perspectives (2019), Bonciani et al. - From Genetics to Skin Lesions (PMC)

Additional Hypothesized Mechanisms#

Several other mechanisms have been proposed but are less well-established:

Direct neutrophil chemotaxis — Iodide may directly increase neutrophil migration independent of TG3, though this is not well-proven in DH specifically.
Hofmeister anion effect — A 1954 German study proposed that the KI patch test reaction was a nonspecific example of the Hofmeister anion effect (ions affecting protein stability and solubility), rather than a DH-specific mechanism. This has been largely superseded by the TG3 enzymatic activation model but has not been definitively ruled out as a contributing factor.
Mucosal involvement — Patinen et al. (2002) challenged DH patients with iodine and gliadin on buccal mucosa and found the oral mucosa less responsive than skin, suggesting the mechanism is primarily cutaneous rather than mucosal.

Sources: PubMed - Hofmeister Anion Effect (1954), Patinen et al. - Iodine and Gliadin Challenge on Oral Mucosa (Acta Derm Venereol, 2002)

Why Iodide Matters Only in DH (Not Plain Celiac)#

This is a key distinction. Iodide worsens DH but is not a concern for celiac patients without skin involvement because:

The TG3-IgA complexes in the papillary dermis are specific to DH -- they do not exist in celiac disease without DH.
Without pre-existing dermal immune complexes, there is no TG3 for iodide to activate.
Celiac patients without DH may have circulating anti-TG3 antibodies, but without dermal deposition, iodide has no relevant substrate to act on.

This means iodine sensitivity is a marker of active dermal disease, not of celiac disease per se.

2. Dose-Response Relationship#

The Central Problem: No Controlled Dose-Response Studies Exist#

There are no published randomized controlled trials establishing a precise iodine dose threshold for DH flares. What we have instead is:

Expert clinical opinion from leading DH researchers
Case reports documenting flares at specific intake levels
The KI patch test data (topical, not dietary)
Inference from disease activity state

What the Experts Say#

Dr. John J. Zone, Professor and Dermatology Chair at the University of Utah and the leading US researcher on DH, states:

"There is little question that ingestion of large amounts of iodine dramatically worsens DH. However, small amounts of iodine found in vitamin pills and most foods are not a problem."

He further clarifies that iodine restriction "need only be considered if patients are consuming excessive iodide in the form of vitamin pills, kelp, or seafood."

Source: Celiac Disease Foundation - DH and Iodine Exposure (2015)

Case Report Evidence: Known Trigger Doses#

Case	Estimated Iodine Intake	Outcome	Source
Kelp supplement (Microplex VMZ, doTERRA)	Kelp contains 16-8,165 mcg/g; supplement dose unknown but likely several hundred to thousands mcg/day	Dapsone-resistant DH. Patient on 400 mg/day dapsone + GFD with persistent disease. Cleared within 2 months of stopping kelp supplement. Remained clear for 4 years.	PMC - Dapsone-Resistant DH Due to Dietary Iodide
12 eggs per day	~312 mcg/day from eggs alone (26 mcg/egg x 12) = 204% of RDA	Previously well-controlled patient on GFD + sulfasalazine developed crusted erythematous macules and erosions on face, arms, and legs.	PMC - DH Flare After Excess Egg Ingestion
Iodinated contrast media (CT scan)	15,000-75,000 mcg (typical contrast dose range)	DH flare following diagnostic imaging.	PubMed - DH Triggered by Iodine Contrast Media
Triiodomethane dental packing	Continuous topical iodine exposure from iodoform strips	Refractory DH flare that resolved after removal of iodoform material.	PMC - DH Flare from Triiodomethane Dental Strips

Interpreting the Dose Data#

Key reference points:

RDA for iodine: 150 mcg/day for adults
Tolerable Upper Intake Level (UL): 1,100 mcg/day (healthy adults)
Egg case report: Flare at ~312 mcg/day from eggs alone (2x RDA), but patient was also getting iodine from other dietary sources. Total daily intake was likely 400-500+ mcg.
Kelp case report: Likely thousands of mcg/day. This patient was resistant to 400 mg/day dapsone -- an extraordinarily high dose -- suggesting extreme iodine overload.

The practical threshold appears to be somewhere above the RDA (150 mcg) but varies by:

Disease activity — Active, untreated DH patients are maximally iodine-sensitive. Patients in remission on GFD may tolerate normal dietary iodine without issue (as shown by the KI patch test data, where remission patients tested negative).
GFD compliance — The GFD reduces TG3-IgA complex formation over time. Less substrate in the skin means less for iodide to activate.
Individual variation — Some patients are exquisitely sensitive (the kelp case), while many tolerate normal dietary iodine without issue.
Cumulative exposure — Chronic moderate intake may be different from acute large doses. The egg case was chronic (daily for a period), while contrast media cases are acute boluses.

Are DH Patients More Sensitive Than Celiac Patients Without Skin Involvement?#

Yes, by definition. Celiac patients without DH do not have TG3-IgA deposits in their skin, so iodide has no relevant target. Iodine sensitivity is a DH-specific phenomenon. A celiac patient without skin involvement has no reason to restrict iodine.

3. High-Iodine Foods: Comprehensive Table#

Iodine Content Per Serving#

All values from USDA/FDA/ODS-NIH Iodine Database unless otherwise noted. RDA is 150 mcg/day for adults.

Food	Serving Size	Iodine (mcg)	% of RDA	Risk Tier for DH
Seaweed / Kelp
Kombu (dried)	1 g	~2,276	1,517%	AVOID
Oarweed (dried)	1 g	~7,800	5,200%	AVOID
Sugar kelp (dried)	1 g	~4,469	2,979%	AVOID
Nori (dried, sushi)	1 sheet (~2.5g)	58-232	39-155%	HIGH CAUTION
Wakame	1 g	~42	28%	Moderate caution
Fish
Cod (baked)	3 oz (85g)	99	66%	Moderate
Haddock (baked)	3 oz (85g)	~192	128%	Moderate-High
Salmon (wild)	3 oz (85g)	~15	10%	LOW
Salmon (farmed)	3 oz (85g)	~13	9%	LOW
Sardines (canned)	3 oz (85g)	~30	20%	LOW
Tuna (canned)	3 oz (85g)	17	11%	LOW
Shellfish
Oysters (cooked)	3 oz (85g)	~93	62%	Moderate
Lobster (cooked)	3 oz (85g)	185	123%	Moderate-High
Shrimp	3 oz (85g)	35	23%	Low-Moderate
Blue crab (canned)	3 oz (85g)	~38	25%	Low-Moderate
Dairy
Cow's milk (1 cup)	8 fl oz	56-85	37-57%	Moderate
Yogurt (plain)	1 cup	~75	50%	Moderate
Cheese (cheddar)	1 oz	~12	8%	Low
Eggs
Egg (hard-boiled)	1 large	~26	17%	Low (normal intake)
Eggs (12 per day)	12 large	~312	208%	HIGH (case report)
Salt
Iodized salt	1/4 tsp (1.5g)	~45-50	30-33%	Moderate
Sea salt (non-iodized)	1/4 tsp	<1	<1%	Negligible
Bread
White bread (with iodate dough conditioner)	2 slices	~296	197%	HIGH
White bread (without iodate conditioner)	2 slices	~10-15	7-10%	Low
Whole wheat bread (with iodate conditioner)	2 slices	~273	182%	HIGH

Sources: USDA/FDA/ODS-NIH Iodine Database Release 3, NIH ODS - Iodine Fact Sheet, PMC - Commercially Available Kelp and Seaweed Products, PMC - Iodine Content of Wild and Farmed Seafood

Critical Observation: Kelp is in a Category by Itself#

The iodine content of kelp and brown seaweeds is orders of magnitude higher than any other food source. A single gram of oarweed contains 52x the RDA. Compare this to salmon, where an entire 3 oz serving provides only 10% of the RDA. Kelp is the clear outlier that deserves outright avoidance for DH patients, while most other foods exist in a reasonable range.

Variability Warning#

Iodine content in food is highly variable due to: - Dairy: Iodine in milk depends on iodine-supplemented animal feed, iodophor sanitizers used in dairy processing, and season (winter milk tends to be higher due to more supplemented feed use) - Seafood: Varies by species, geography, season, and water conditions - Bread: Entirely depends on whether the manufacturer uses iodate dough conditioners (about 20% of US bread products do; check ingredient labels for potassium iodate or calcium iodate)

4. Conflict Analysis with Food-First Recommendations#

The Foods in Question#

Our Food-First Dietary Approach recommends the following iodine-containing foods:

Recommended Food	Frequency	Primary Mechanism	Iodine per Serving	Daily Iodine Contribution
Oysters	1-2x/week	Zinc (gut barrier)	~93 mcg per 3 oz	~13-27 mcg/day (averaged)
Sardines	Part of 3-4x/week fish rotation	Omega-3 (Treg, anti-inflammatory)	~30 mcg per 3 oz	~13-17 mcg/day (averaged)
Salmon	Part of 3-4x/week fish rotation	Omega-3 + vitamin D	~15 mcg per 3 oz	~6-9 mcg/day (averaged)
Raw milk / kefir	Daily (1-2 cups)	TGF-beta, exosomal miRNAs (Treg)	~56-85 mcg per cup	~56-170 mcg/day
Bone broth	Daily (1-2 cups)	Glutamine, glycine (gut barrier)	Negligible	~0 mcg/day
Beef liver	1-2x/week	Retinol (Treg via retinoic acid)	Negligible	~0 mcg/day

Estimated Total Daily Iodine from Our Recommendations#

A rough daily average across a week following our meal template:

Source	Estimated Daily Average
Raw milk (1-2 cups)	56-170 mcg
Fatty fish (3-4x/week, averaged daily)	10-25 mcg
Oysters (1-2x/week, averaged daily)	13-27 mcg
Eggs (1-2/day, assumed)	26-52 mcg
Iodized salt (if used)	45-100 mcg
Other foods	10-30 mcg
Total estimated range	~160-400 mcg/day

This puts a DH patient following our full dietary recommendations at roughly 1-2.5x the RDA for iodine.

Risk Assessment by Food#

Salmon and Sardines: LOW RISK#

Verdict: These are safe for DH patients. No modification needed.

Salmon is among the lowest-iodine fish at ~15 mcg per 3 oz serving (10% RDA). Sardines are also low at ~30 mcg (20% RDA). These are well below the levels implicated in any case report. There are no published case reports of DH flares from moderate fish consumption at normal serving sizes. The case reports involve kelp, high-dose supplements, excessive eggs (12/day), and medical contrast dye -- not normal fish intake.

For comparison, cod (99 mcg/3 oz) and haddock (~192 mcg/3 oz) are significantly higher in iodine than salmon or sardines. If a DH patient wanted to minimize iodine exposure from fish while maximizing omega-3 intake, salmon and sardines are actually among the best choices.

Oysters: MODERATE RISK, LIKELY ACCEPTABLE#

Verdict: Probably fine at recommended frequency (1-2x/week). Worth monitoring.

Oysters provide ~93 mcg per 3 oz serving (62% RDA). This is a meaningful amount of iodine but far below the levels in documented flare cases. At 1-2 servings per week, averaged daily contribution is modest (~13-27 mcg/day).

The zinc benefit (32 mg per 6 oysters) is extraordinary and difficult to replicate from other foods. The risk-benefit calculation favors keeping oysters in the protocol for most patients. However, during active disease flares, temporarily reducing oyster consumption is reasonable.

No case reports exist of DH flares from oyster consumption at moderate frequency.

Raw Milk: MODERATE RISK, NEEDS ATTENTION#

Verdict: The highest iodine contributor in our protocol. Warrants awareness but not elimination.

At 1-2 cups daily, raw milk contributes 56-170 mcg of iodine -- potentially the single largest dietary iodine source in our recommendations. Milk iodine content is highly variable (dependent on feed, season, and processing) and is difficult to predict precisely.

However, there are important caveats:

No case reports link moderate dairy consumption to DH flares. All published flare cases involve kelp, supplements, excessive eggs, contrast media, or dental materials.
Raw milk from small, grass-fed farms may have lower iodine content than conventional dairy because conventional operations use more iodine-containing sanitizers and iodine-supplemented feed.
The Treg-promotion benefit (TGF-beta, exosomal miRNAs, FoxP3 demethylation) is mechanistically one of the strongest interventions in our entire protocol. Removing it to reduce iodine would sacrifice a major therapeutic mechanism.

Bread (if consumed): POTENTIALLY HIGH RISK (HIDDEN SOURCE)#

Verdict: Check labels. Avoid breads with iodate dough conditioners.

This is not a food we specifically recommend, but DH patients following a GFD are increasingly finding gluten-free bread products. About 20% of US bread products use potassium iodate or calcium iodate as dough conditioners, which can add up to 296 mcg per 2 slices -- nearly 200% of the RDA from a single food. This is a hidden source that many patients and clinicians overlook. GF breads should be checked for these conditioners.

Is There Evidence of Fish or Dairy Triggering DH via Iodine?#

No. After extensive search, I found no published case reports or clinical evidence of DH flares caused by: - Normal fish consumption (at typical serving sizes and frequency) - Normal dairy consumption (1-2 cups of milk per day)

All documented iodine-triggered DH flares involve: - Kelp/seaweed supplements (concentrated iodine, often thousands of mcg) - Extreme dietary patterns (12 eggs/day) - Medical iodine (contrast media, dental iodoform) - Iodine-containing supplements

This is an important distinction. The literature consistently implicates concentrated or excessive iodine sources, not normal dietary patterns that happen to include fish and dairy.

5. Iodine Restriction Studies in DH#

Formal Clinical Trials#

There are no published randomized controlled trials of low-iodine diets in DH. The evidence base consists of:

Case reports (kelp, eggs, contrast media) showing improvement after removing a high-iodine source
The KI patch test studies showing reduced iodine sensitivity with GFD and dapsone
Expert clinical experience (Zone, Reunala, and others)
Mechanistic studies (TG3 enzymatic activity)

What the Case Evidence Shows#

Case 1: Kelp supplement (2019) - Patient: Woman with DH, on GFD + dapsone 400 mg/day (4 mg/kg -- an extremely high dose). Disease uncontrolled. Also tried sulfapyridine without improvement. - Discovery: Taking doTERRA Microplex VMZ (containing kelp) and marine oil supplement. - Intervention: Discontinued kelp-containing supplement only. - Outcome: Dramatic improvement over 2 months. Stopped developing new lesions. Remained clear for 4 years on GFD + dapsone 50 mg twice daily. - Significance: Demonstrates that a single concentrated iodine source can render even high-dose dapsone ineffective, and that removing it alone (without further diet change) restored disease control.

Source: JAAD Case Reports - DH Resistant to Dapsone Due to Dietary Iodide

Case 2: Egg overconsumption (2022) - Patient: Man with previously well-controlled DH on GFD + sulfasalazine 3g daily. - Trigger: Consuming 12 eggs per day (~312 mcg iodine from eggs alone). - Presentation: Crusted erythematous macules and erosions on face, arms, legs. - Intervention: Provided list of high-iodine foods to avoid; instructed to decrease egg consumption. - Significance: First reported case of DH flare from excessive egg consumption, attributed to iodine content.

Source: JAAD Case Reports - DH Flare After Excess Egg Ingestion

The KI Patch Test as a Proxy for Iodine Sensitivity Over Time#

The Haffenden (1980) study provides indirect evidence about iodine restriction effects:

Patient Group	KI Patch Test Positive	Interpretation
Active disease, untreated	5/5 (100%)	Maximum iodine sensitivity
On GFD alone	2/6 (33%)	GFD reduces but does not eliminate sensitivity
On dapsone	1/8 (13%)	Dapsone suppresses the neutrophil cascade that iodide amplifies
Full remission	0/3 (0%)	Complete resolution of dermal immune complexes eliminates sensitivity

This suggests that iodine restriction is most important during active disease and becomes less critical as GFD and treatment reduce the dermal TG3-IgA substrate.

Expert Consensus Position#

The Celiac Disease Foundation, Gluten Intolerance Group of North America, and Dr. John Zone all converge on the same position:

A blanket low-iodine diet is NOT recommended for DH patients.
Avoid concentrated/excessive iodine sources (kelp, seaweed supplements, excessive seafood).
Normal dietary iodine from most foods is not problematic.
Iodine restriction becomes unnecessary once the rash clears (months to years on GFD).
Inadequate iodine intake carries its own health risks (goiter, hypothyroidism).

Sources: Celiac Disease Foundation - DH and Iodine Exposure, GIG - Iodine and DH, Gluten.org - DH Fact Sheet

6. Practical Guidance#

Tiered Approach Based on Disease Activity#

Tier 1: Active, Uncontrolled DH (New Diagnosis or Flare)#

This is when iodine sensitivity is at its maximum. The dermal TG3-IgA complexes are abundant and enzymatically primed.

Recommendations: - Eliminate: Kelp, seaweed, seaweed-containing supplements, iodine supplements - Avoid: High-iodine fish (cod, haddock, lobster), excessive dairy, excessive eggs - Limit to 1x/week or less: Oysters, shellfish - Safe to continue: Salmon, sardines, 1-2 eggs/day, moderate dairy (1 cup/day), non-iodized salt - Check labels: Avoid bread products with iodate dough conditioners - Alert medical providers: Request non-iodinated contrast if imaging is needed; inform dentists about iodoform sensitivity - Estimated target: Keep total dietary iodine near or slightly below the RDA (~150 mcg/day) without going into deficiency

Tier 2: DH Controlled on GFD + Dapsone (Stable but Not in Remission)#

Disease is managed but dermal immune complexes likely still present. Moderate iodine sensitivity may persist.

Recommendations: - Eliminate: Kelp, seaweed supplements - Limit: High-iodine shellfish to 1-2x/week - Safe to resume: Normal fatty fish intake (salmon, sardines 3-4x/week), moderate dairy (1-2 cups/day), normal egg consumption (1-2/day) - Monitor: If unexplained flares occur despite strict GFD, evaluate total dietary iodine intake before assuming gluten contamination - Estimated target: RDA range (150-300 mcg/day) is likely tolerable

Tier 3: DH in Remission (Rash Cleared on GFD, IgA Deposits Resolving)#

KI patch test data suggests iodine sensitivity resolves with disease remission. The dermal substrate is largely gone.

Recommendations: - No iodine restrictions necessary beyond general health guidelines - Still avoid kelp as a general precaution (it exceeds the UL for healthy people too) - Resume normal dietary patterns including all foods in our protocol - Continue monitoring skin for any recurrence

Specific Guidance for Our Food-First Protocol#

Food	Active DH	Controlled DH	DH in Remission
Salmon (3-4x/week)	Continue as recommended	Continue as recommended	Continue as recommended
Sardines (3-4x/week)	Continue as recommended	Continue as recommended	Continue as recommended
Raw milk (1-2 cups/day)	Reduce to 1 cup/day; consider sourcing from small farms (lower iodine)	Resume 1-2 cups/day	No restriction
Oysters (1-2x/week)	Reduce to 1x/week or biweekly	Resume 1-2x/week	No restriction
Beef liver	No iodine concern	No iodine concern	No iodine concern
Bone broth	No iodine concern	No iodine concern	No iodine concern
Fermented vegetables	No iodine concern	No iodine concern	No iodine concern
Capers, turmeric	No iodine concern	No iodine concern	No iodine concern

What NOT to Do#

Do not eliminate iodine entirely. Iodine deficiency causes goiter, hypothyroidism, and cognitive impairment. The goal is to avoid excess, not achieve zero.
Do not assume iodine is the problem when gluten is more likely. Gluten drives DH. Iodine amplifies it. A patient with persistent DH should first verify strict GFD compliance before restricting iodine.
Do not conflate kelp with fish. The iodine in a serving of kelp can be 100-500x the iodine in a serving of salmon. These are categorically different exposures.
Do not restrict iodine indefinitely. Once DH rash clears (months to years on GFD), iodine sensitivity resolves. Unnecessary long-term restriction creates nutritional risk with no benefit.

Non-Dietary Iodine Sources to Watch#

Source	Iodine Exposure	Action
CT contrast media	15,000-75,000 mcg (single dose)	Request non-iodinated contrast when possible; alert radiology to DH diagnosis
Iodoform dental packing	Continuous topical exposure	Alert dentist; request alternative packing materials
Povidone-iodine (Betadine)	Variable topical exposure	Use alternative antiseptics (chlorhexidine) for wound care
Amiodarone (cardiac drug)	~75,000 mcg iodine per 200 mg tablet	Discuss alternatives with cardiologist if DH is active
Thyroid medications (Lugol's iodine)	Variable	Coordinate with endocrinologist

7. Key Takeaways#

Iodine amplifies DH; it does not cause it. Iodide increases the enzymatic activity of TG3 within pre-existing IgA complexes in the skin. Without gluten-driven immune complex deposition, iodine is irrelevant.
Sensitivity is proportional to disease activity. Active, untreated DH = maximum sensitivity. Remission = no sensitivity. This is the most important variable.
There is no precise safe threshold. The evidence suggests that intakes near the RDA (150 mcg/day) are tolerable for most patients, while intakes exceeding 2-3x the RDA from concentrated sources carry risk during active disease.
Kelp/seaweed is the only food that warrants outright avoidance. Its iodine content (thousands of mcg per gram) is orders of magnitude above all other dietary sources.
Our food-first recommendations (salmon, sardines, oysters, raw milk) are compatible with DH management. Salmon and sardines are among the lowest-iodine fish. Oysters and raw milk contribute meaningful but moderate iodine that is well below case-report thresholds. No published case reports implicate normal fish or dairy consumption in DH flares.
The main actionable risk in our protocol is cumulative. No single recommended food is dangerous, but a DH patient eating oysters + raw milk + eggs + iodized salt daily during active disease could reach the upper range. Awareness of total intake matters during flares.
Iodine restriction is a temporary measure during active disease, not a permanent lifestyle change. It becomes unnecessary once DH enters remission on GFD.

Recommended Update to food-first-dietary.md#

Based on this analysis, consider adding a brief note to the food-first document:

Iodine Note for Active DH: Several foods in this protocol (oysters, raw milk, fatty fish) contain iodine, which can amplify DH flares during active disease by increasing TG3 enzymatic activity in the skin. Salmon and sardines are low-iodine and safe at all disease stages. During active flares, consider reducing oyster frequency and raw milk volume. Avoid kelp, seaweed, and iodine supplements entirely. See Iodine Deep Dive for full analysis. Iodine restriction becomes unnecessary once the rash clears on GFD.

Document compiled from PubMed, PMC, JAAD Case Reports, Journal of Investigative Dermatology, Journal of Immunology, British Journal of Dermatology, Acta Dermato-Venereologica, Frontiers in Immunology, NIH Office of Dietary Supplements, USDA Iodine Database, Celiac Disease Foundation, and Gluten Intolerance Group. February 2026.