The Fundamental Distinction: Food Allergy vs Food Intolerance vs Food Sensitivity
The relationship between food intolerance and chronic inflammatory skin conditions — atopic dermatitis, psoriasis, seborrheic dermatitis, contact dermatitis, urticaria — food is a driver that is never investigated. The standard dermatological model treats skin in isolation: topical steroids, antifungals, immunosuppressants. The gut-skin relationship is acknowledged in research but rarely assessed in clinical practice. The result is a cycle of suppression and recurrence that continues for years while the dietary and immunological triggers that sustain the inflammation are never identified.
This post covers the evidence for food intolerances as drivers of skin disease — including the critical distinction between IgE allergy and IgG-mediated delayed food reactions, the role of gut barrier disruption and intestinal permeability, how specific foods affect the microbiome and mucosal immune response, what functional markers like calprotectin and lactoferrin measure, and how a systematic investigation and elimination approach can resolve presentations that topical management has repeatedly failed.
Can food intolerances cause skin conditions? Yes — through multiple, well-characterised immune and barrier mechanisms. IgG-mediated delayed food intolerance reactions (occurring up to 48–72 hours after exposure) drive chronic low-grade systemic inflammation that worsens atopic dermatitis, psoriasis, urticaria, and seborrheic dermatitis. These reactions are distinct from IgE-mediated allergy, are not detected by standard allergy testing, and are frequently missed. Simultaneously, food-driven gut dysbiosis and intestinal permeability impair the mucosal immune barrier, allowing food antigens and bacterial endotoxins to cross into systemic circulation — amplifying the inflammatory load that manifests in the skin.1,2,3
The Fundamental Distinction: Food Allergy vs Food Intolerance vs Food Sensitivity
One of the most consequential errors in clinical practice is conflating food allergy with food intolerance. They are distinct immunological processes with different mechanisms, timelines, severity profiles, and clinical implications for skin disease.
| Parameter | IgE-Mediated Allergy | IgG-Mediated Sensitivity | Non-Immune Intolerance |
|---|---|---|---|
| Immune mechanism | Type I hypersensitivity — mast cell degranulation | Type III hypersensitivity — immune complex formation | No immune involvement — enzymatic or metabolic |
| Onset of reaction | Immediate — minutes to 2 hours | Delayed — 2 to 72 hours after exposure | Variable — often hours to days |
| Detectable by standard testing | Yes — skin prick test, serum IgE | Not by standard IgE panel — requires IgG testing | No — clinical history and elimination diet |
| Dose dependency | Threshold-based — trace amounts can trigger | Dose-dependent — cumulative load drives severity | Dose-dependent |
| Common skin manifestations | Urticaria, angioedema, acute eczema flare | Chronic eczema, psoriasis, urticaria, seborrheic dermatitis | Urticaria, flushing, non-specific rash |
| Reversibility | Avoidance essential — tolerance rarely develops spontaneously | Often reversible with elimination and gut repair | Dose-dependent management |
The clinical implication is direct: a negative IgE panel does not rule out food intolerance as a driver of skin disease. IgE negativity is not food clearance. The majority of food-driven skin presentations are mediated by IgG immune complexes and non-immune mechanisms — neither of which appear on standard allergy testing.4 A patient told their allergy test was negative may have never been tested for the mechanism actually driving their skin condition.
Why the 48-Hour Delay Matters Clinically
The defining feature of IgG-mediated food sensitivity is the delay between consumption and reaction. Where IgE allergy presents within minutes — making the trigger obvious — IgG reactions take 2 to 72 hours to manifest symptoms. This delay is the reason most patients and clinicians fail to connect food consumption to skin flares. The patient who eats dairy on Monday and develops a worsening eczema flare on Wednesday does not intuitively link the two events.
- Step 1 — Barrier disruption: Increased intestinal permeability allows incompletely digested food peptides to cross the gut epithelium into the lamina propria and systemic circulation.3
- Step 2 — IgG antibody production: The immune system produces IgG antibodies specific to food antigens — including dairy casein, egg albumin, gluten gliadin, soy protein, and peanut proteins — that would normally remain in the gut lumen.4
- Step 3 — Immune complex formation: Food antigens bind IgG antibodies to form circulating immune complexes. These are deposited in tissues — including skin — and activate complement, triggering local inflammation.1,4
- Step 4 — Delayed cutaneous manifestation: The complement activation and cytokine release (TNF-α, IL-6, IL-1β) at the tissue level drives the chronic, low-grade inflammation that presents as eczema flares, psoriatic activity, urticaria, or seborrheic dermatitis worsening — typically 24–72 hours after the triggering meal.2,3
Intestinal Permeability: The Gateway Mechanism
Intestinal permeability — colloquially known as "leaky gut" — is the mechanistic link between food consumption and systemic immune activation. The gut epithelium is a single-cell-layer barrier separating the external environment (food, microbes, toxins) from the internal immune and circulatory systems. Its integrity depends on tight junction proteins — occludin, claudin, and zonulin-regulated structures — that seal the intercellular spaces.
When tight junctions are disrupted — by dysbiosis, chronic stress, NSAIDs, alcohol, certain food antigens, and infections — paracellular permeability increases. Food antigens that would normally remain in the gut lumen gain access to the lamina propria and portal circulation. The immune response that follows is the origin of IgG food antibody development.4
In 111 adults with and without gastrointestinal symptoms, food-specific IgG antibody titers were significantly and positively associated with intestinal permeability biomarkers — specifically anti-LPS (lipopolysaccharide) and anti-occludin IgG and IgA antibodies. The strength of the association was greatest when wheat, dairy, and egg reactions were simultaneously present — suggesting cumulative multi-food IgG burden correlates with greater barrier disruption. The findings support the interpretation that IgG food antibodies are indicators of impaired intestinal barrier function, not merely dietary exposure markers.4
In 50 adult atopic dermatitis patients and 25 controls, food sensitization was significantly more prevalent in the AD group. Critically, atopic dermatitis severity scores (EASI, SCORAD) correlated with the number of positive food-specific IgEs and with leaky-gut biomarkers (LBP, syndecan-4) and inflammatory cytokines (IL-10, IL-22). Higher food sensitization was also associated with lower short-chain fatty acid (SCFA) concentrations — key anti-inflammatory microbial metabolites — and higher indoxyl levels. The findings establish a direct link between food sensitisation, gut barrier impairment, microbiome disruption, and AD severity in adults.2
The Microbiome Connection: How Food Shapes Gut Ecology and Skin Inflammation
The gut microbiome is not a passive bystander in food intolerance — it is a central mediator. Microbiome composition directly influences both the development of food tolerance and the severity of the immune response to food antigens. The same dietary patterns that trigger food reactions also reshape microbial ecology, creating a self-perpetuating inflammatory cycle.
In 102 clinically diagnosed atopic dermatitis patients and matched controls, microbial diversity declined markedly in AD patients (Shannon index −20%, p<0.001), with reductions in Firmicutes and Bacteroidota — the primary short-chain fatty acid producers — and enrichment in inflammatory Actinobacteriota. In the corresponding mouse AD model, gut induction of AD caused dose-dependent increases in serum IgE (up to 3.0-fold). Dietary patterns in AD patients showed lower refined grain intake but these shifts strongly correlated with microbiome remodelling and reduced carbohydrate and energy metabolism capacity. The study confirmed a diet–microbiota–immune axis driving AD pathogenesis.6
The key microbiome pathways that connect food intolerance to skin inflammation include:
- SCFA depletion: Loss of butyrate-producing bacteria (Faecalibacterium prausnitzii, Roseburia, Akkermansia) from dysbiosis reduces SCFA production — impairing tight junction integrity, reducing regulatory T-cell activity, and increasing systemic inflammatory tone.2
- LPS translocation: Gram-negative bacterial cell wall components (LPS/endotoxin) cross the disrupted gut barrier and activate TLR4 receptors on immune cells — driving TNF-α, IL-6, and IL-1β production that amplifies cutaneous inflammation.4
- Th2 immune skewing: Dysbiosis reduces regulatory T-cell activity and promotes Th2-dominant immune responses — the same pathway that drives atopic dermatitis, allergic urticaria, and food sensitisation.3
- Histamine dysregulation: Dysbiotic overgrowth of histamine-producing bacteria (certain Lactobacillus species, Morganella morganii) combined with reduced diamine oxidase (DAO) activity from gut mucosal damage impairs histamine clearance — contributing to urticaria, flushing, and dermatographic responses.7
Key Food Triggers: Dairy, Eggs, Nuts, and Soy — What the Evidence Shows
Dairy (Cow's Milk)
Casein and whey proteins are among the most prevalent IgG food antigens. Dairy consumption drives intestinal inflammation through multiple routes: casomorphin peptides directly increase gut permeability; A1 beta-casein increases inflammatory cytokines; lactose malabsorption promotes dysbiosis. In atopic dermatitis, dairy elimination is consistently among the most impactful single interventions. Elevated calprotectin is frequently observed in patients with undiagnosed dairy sensitivity.5,6,8
Eggs (Hen's Egg)
Egg albumin (ovalbumin) and ovomucoid are the primary sensitising proteins. Both IgE and IgG egg reactions are well-documented in atopic dermatitis — with children placed on egg elimination diets showing measurable improvements in eczema severity and reduced affected surface area in clinical trials. Egg sensitivity is closely associated with skin barrier disruption: filaggrin gene variants increase both egg sensitisation risk and barrier permeability simultaneously.5,6
Peanuts & Tree Nuts
Peanut and tree nut (walnut, cashew, almond) sensitivity is characterised by low rates of resolution and high persistence. Ara h proteins in peanut are highly stable food antigens that resist digestion and cross the compromised gut barrier intact. IgG-mediated nut reactions are consistently among the highest-reactivity findings on food sensitivity panels in patients with chronic urticaria and psoriasis. Elimination of IgG-reactive nuts — distinct from IgE allergy — has been documented to reduce psoriasis severity in case reports.9
Soy
Soy is both a frequent IgG sensitiser and a microbiome disruptor. Soy phytoestrogens (genistein, daidzein) alter gut microbial composition, particularly affecting Firmicutes:Bacteroidetes ratios. Soy isoflavones may also exacerbate hormonal-driven skin conditions (acne, seborrheic dermatitis) by modulating androgen receptor sensitivity. Soy-based dairy alternatives are frequently consumed by patients eliminating dairy — but can themselves be reactive foods in the same patients.7
Calprotectin, Lactoferrin, and Functional Gut Markers: What They Measure
One of the most powerful aspects of a functional investigation into food-driven skin disease is the ability to objectively measure intestinal inflammation and barrier disruption — providing objective evidence that gut pathology is contributing to skin disease, and a baseline against which dietary and therapeutic interventions can be tracked.
Faecal Calprotectin
Calprotectin is a calcium- and zinc-binding protein comprising approximately 60% of the cytosolic protein of neutrophils. During intestinal inflammation, neutrophils infiltrate the gut mucosa and release calprotectin into the intestinal lumen — where it is excreted in faeces at concentrations six times higher than in plasma. Faecal calprotectin (FC) is the most validated non-invasive marker of mucosal intestinal inflammation available.10
Normal faecal calprotectin is defined as <50 μg/g. Levels of 50–200 μg/g indicate mild-to-moderate mucosal inflammation; levels above 200 μg/g indicate significant active intestinal inflammation. A meta-analysis established a cut-point of 250 μg/g as optimal for detecting endoscopically confirmed mucosal inflammation. Calprotectin is stable in stool at room temperature for up to one week, making home sample collection clinically feasible. It can be measured from a teaspoon-sized stool sample by quantitative ELISA. Crucially, calprotectin reflects local gut inflammation — unlike CRP, which reflects systemic inflammation — making it specific to the mucosal environment where food antigen reactions occur.10,11
Faecal Lactoferrin
Lactoferrin is an iron-binding glycoprotein present in secondary granules of mature neutrophils. During intestinal inflammation, neutrophilic infiltration of the mucosa markedly increases lactoferrin excretion into faeces. Normal lactoferrin is <7.25 μg/g. It exhibits similar diagnostic performance to calprotectin for intestinal inflammation, correlating better than CRP with mucosal inflammation observed on endoscopy.11
In clinical practice, the combination of elevated faecal calprotectin and lactoferrin in a patient with chronic skin disease — in the absence of a confirmed IBD diagnosis — is a meaningful signal of subclinical mucosal inflammation that warrants dietary investigation. It provides the objective bridge between gut and skin that many patients have been seeking for years of unexplained skin reactivity.
Zonulin
Zonulin is a protein that regulates tight junction permeability — increasing paracellular passage when elevated. Elevated serum or stool zonulin is used as a marker of intestinal permeability and has been correlated with food-specific IgG antibody titers, systemic inflammatory markers, and skin disease severity in several observational studies. It provides mechanistic confirmation that barrier disruption — rather than coincidental dysbiosis — is driving food antigen translocation.4
Types of Dermatitis and Their Relationship to Food
Atopic Dermatitis (Eczema)
Atopic dermatitis has the strongest and best-documented relationship with food. Food sensitisation is significantly more prevalent in adult AD patients than controls — and AD severity correlates directly with the number of reactive foods, leaky gut biomarkers, and degree of microbiome disruption.2 The AAAAI Best Practices document (2022) confirms that both IgE-mediated and non-IgE-mediated food reactions can exacerbate AD, with non-IgE reactions particularly presenting with delayed flares that are diagnostically difficult without systematic investigation.5
Psoriasis
Psoriasis is increasingly recognised as a condition with significant food-environment interactions mediated through the gut-skin axis. The bidirectional relationship between metabolic syndrome and psoriasis is partly mediated by dietary-driven gut dysbiosis and intestinal permeability — the same pathways through which IgG food reactions perpetuate systemic inflammation. A documented case series demonstrated near-complete resolution of psoriasis patches in a patient following IgG-guided elimination of reactive foods (wheat, egg, bell peppers, cashews), with sustained remission maintained over months of follow-up.9
Seborrheic Dermatitis
As I cover in detail in my post on Malassezia yeast and seborrheic dermatitis, high-glycaemic foods and inflammatory dietary patterns directly promote Malassezia overgrowth through sebum dysregulation. Beyond this, dairy and gluten sensitivity can amplify the systemic inflammatory environment that enables Malassezia pathogenic transition — particularly in patients where gut dysbiosis is a co-driver of sebaceous gland dysfunction.
Chronic Urticaria
Chronic idiopathic urticaria has documented associations with food-specific IgG reactions, histamine intolerance, and intestinal permeability. The role of IgG-guided elimination diets in urticaria management is supported by observational data and case reports showing improvement in hive frequency and severity following food panel-guided elimination — in patients where standard allergy testing was negative.7
Contact Dermatitis and Perioral Dermatitis
While primarily driven by topical triggers, contact dermatitis can be perpetuated by systemic food reactions — particularly in patients with combined gut barrier disruption. Perioral dermatitis specifically has documented associations with dairy consumption and gut microbiome disruption, with dairy elimination a recognised clinical intervention alongside addressing fluoride and topical steroid exposure.
The Clinical Investigation Protocol: From Suspicion to Resolution
Step 1 — Baseline functional testing
Faecal calprotectin and lactoferrin establish whether mucosal inflammation is present. Serum zonulin confirms intestinal permeability. A food-specific IgG panel (minimum 96–200 foods) identifies the specific antigens generating an immune response. Stool microbiome analysis identifies dysbiosis patterns, including loss of SCFA producers and presence of pathobionts. This combination provides the objective evidence base for a targeted elimination protocol.4,10,11
Step 2 — Guided elimination phase (4–8 weeks)
Foods with high IgG reactivity are eliminated for a minimum of 4 weeks — typically 6–8 weeks for skin disease, which has a slower resolution trajectory than gut symptoms. The elimination must be complete: trace exposure to IgG-reactive foods continues to drive immune complex formation and skin inflammation. During this phase, most patients experience an initial 1–2 week period of unchanged or worsened symptoms before improvement emerges as immune complex burden reduces.8,9
Step 3 — Gut repair concurrent with elimination
Elimination alone does not repair the gut barrier. Concurrent mucosal repair — targeting tight junction integrity through probiotic recolonisation, SCFA restoration, anti-inflammatory botanicals, and elimination of dysbiosis drivers — is essential to prevent reactivation of food sensitivities on reintroduction. Without barrier repair, the cycle recommences.2,4
Step 4 — Structured reintroduction
Foods are reintroduced sequentially, one at a time, over 3–5 days per food, monitoring for both immediate and delayed reactions. This process establishes which foods represent true ongoing sensitivities versus those where tolerance has been restored by gut repair. The goal is the widest possible dietary breadth consistent with symptom resolution — not permanent elimination of multiple food groups, which carries nutritional and microbiome diversity risks.5,8
Step 5 — Repeat markers at 12 weeks
Repeat faecal calprotectin and lactoferrin at 12 weeks provide objective confirmation of mucosal improvement. Reduction in calprotectin from elevated baseline levels is one of the most clinically satisfying markers of gut-driven skin disease resolution — it documents that the intestinal inflammation generating the systemic immune activation has been meaningfully reduced.
Does Food Intolerance Testing Actually Work? The Evidence
IgG-guided elimination diets have demonstrated clinical benefit in IBS, asthma, migraines, and inflammatory skin conditions across multiple prospective trials and case series, though the mainstream medical position on IgG testing remains cautious. The debate centres not on whether IgG food antibodies correlate with symptoms — multiple studies confirm they do — but on whether elevated IgG represents pathological sensitivity or normal immune exposure. In practice, the clinical evidence of benefit from IgG-guided elimination in patients with chronic inflammatory conditions, combined with the objective resolution of mucosal inflammation markers, provides a functional justification for the approach that precedes the mechanistic debate being fully resolved.4,9
A patient with chronic plaque psoriasis underwent IgG food antibody panel testing revealing high-reactivity foods including wheat, egg, bell peppers, vanilla, cashews, mustard, and winter squash. Following conservative management and complete elimination of all high-IgG-reactive foods, the patient's psoriasis patches nearly completely disappeared within months. The case illustrates both the unexpected breadth of IgG-reactive foods (extending well beyond the standard dairy/gluten/egg triad) and the clinical potential of panel-guided rather than assumption-guided elimination in chronic skin disease.9
Does everyone with eczema have food intolerances?
No — but a clinically significant proportion do, and they are the patients most likely to be managed with ongoing topical steroids or immunosuppressants without resolution. In adult atopic dermatitis, food sensitisation affects a substantial proportion of patients — the precise figure varying by study design and severity cohort. The patients most likely to have a food-driven component are those with: flares that follow no identifiable topical trigger, persistent disease despite barrier repair, concurrent GI symptoms (bloating, altered stool, abdominal pain), a history of antibiotic use or known gut dysbiosis, and symptoms that wax and wane without obvious external correlation. None of these is diagnostic — but together they represent a pattern that justifies functional investigation.2,5,6
Can you have a food intolerance without gut symptoms?
Yes — and this is one of the most clinically underappreciated aspects of food-driven inflammation. Vita et al. (2022) specifically found that food-specific IgG titers and intestinal permeability biomarkers were elevated in both symptomatic and asymptomatic participants — and critically, the difference between the two groups was not statistically significant.4 This means intestinal inflammation and barrier disruption can be present and driving systemic immune activation (including skin manifestations) in the complete absence of gut symptoms. The absence of bloating, diarrhoea, or abdominal pain does not exclude gut-mediated food intolerance as a driver of skin disease.
Frequently Asked Questions: Food Intolerances and Skin
Is IgG food testing reliable?
IgG food testing is a functional clinical tool — not a diagnostic gold standard. Elevated IgG to a food indicates immune exposure and sensitisation, which correlates with intestinal permeability and symptom burden in research settings. Its clinical utility lies in guiding a structured elimination protocol that can then be objectively validated by symptom response and repeat mucosal markers (calprotectin, lactoferrin). It should not be interpreted in isolation as a definitive allergy diagnosis.4,9
How long does it take for skin to improve after food elimination?
For IgG-mediated reactions, skin improvement typically follows a different timeline to gut symptom improvement. Gut symptoms often improve within 1–2 weeks of elimination. Skin changes — particularly eczema and psoriasis — typically require 4–8 weeks of complete elimination before meaningful improvement is visible. This reflects both the time required for immune complex clearance and the slower turnover of cutaneous inflammatory processes compared to gut mucosa.8,9
What is calprotectin and why does it matter for skin conditions?
Faecal calprotectin is a neutrophil-derived protein released into the gut lumen during mucosal inflammation. It is the most validated non-invasive marker of intestinal inflammation available. In the context of skin disease, elevated calprotectin (>50 μg/g, and particularly >200 μg/g) indicates that gut mucosal inflammation is present and generating the systemic inflammatory load that may be manifesting in the skin. It provides objective evidence of the gut-skin connection and a baseline against which dietary and therapeutic interventions can be tracked.10,11
Do I need to eliminate dairy and gluten even if my allergy test was negative?
A negative IgE allergy test does not exclude dairy or gluten as drivers of skin disease. Standard allergy testing only detects IgE-mediated reactions — the immediate hypersensitivity type. IgG-mediated delayed reactions to dairy (casein, whey), gluten (gliadin), eggs, and soy are an entirely different immune mechanism that does not appear on standard allergy panels. If your allergy test was negative but your skin condition is chronic and responds inconsistently to topical management, IgG food testing combined with intestinal permeability markers is the appropriate next investigation.1,4
Can improving gut health resolve chronic skin conditions?
Evidence consistently supports that addressing gut dysbiosis, restoring intestinal barrier integrity, and eliminating IgG-reactive foods can produce significant and sustained improvement in atopic dermatitis, psoriasis, urticaria, and seborrheic dermatitis — particularly in patients where conventional management has provided only temporary relief. The key is simultaneity: gut repair, elimination, and skin treatment together produce outcomes that each approach alone does not. I discuss the broader gut-skin axis in my posts on rosacea and the gut-skin axis and the skin microbiome.2,4,6
A functional investigation — calprotectin, lactoferrin, IgG food panel, intestinal permeability markers, and microbiome analysis — can identify the gut-mediated drivers most patients with chronic skin disease have never had tested.
Further Reading & Trusted Sources
- Vita, Zwickey & Bradley (2022) — IgG Food Antibodies and Intestinal Permeability Biomarkers — open access, Frontiers in Nutrition.
- Sherwood & Walsham (2012) — Faecal Calprotectin and Lactoferrin: Measurement and Clinical Utility — open access, Clin Exp Gastroenterol.
- Nutrients (2022) — The Role of Nutrition in Immune-Mediated Inflammatory Skin Disease — open access, Nutrients.
- PMC12445428 (2024) — Food Sensitization, Atopic Dermatitis Severity, Leaky Gut and Gut Metabolites — open access.
References
- Turnbull JL, Adams HN, Gorard DA. Review article: the diagnosis and management of food allergy and food intolerances. Aliment Pharmacol Ther. 2015;41(1):3–25. doi:10.1111/apt.12984.
- Kunkusova L, et al. Food sensitization is associated with atopic dermatitis severity, gut-derived metabolites and leaky gut in adults. J Eur Acad Dermatol Venereol. 2024. PMC12445428.
- Leaky Gut Review — Camilleri M. Leaky gut: mechanisms, measurement and clinical implications in humans. Gut. 2019;68(8):1516–1526. doi:10.1136/gutjnl-2019-318427.
- Vita R, Zwickey H, Bradley R. Associations between food-specific IgG antibodies and intestinal permeability biomarkers. Front Nutr. 2022;9:962093. PMC9485556.
- AAAAI Work Group Report. Atopic dermatitis and food allergy: best practices and knowledge gaps. J Allergy Clin Immunol Pract. 2022. doi:10.1016/j.jaip.2021.12.027.
- Huang Y, et al. Dietary modulation of gut microbiota and its role in atopic dermatitis. Nutrients. 2024. PMC12545045.
- Schnedl WJ, Lackner S, Enko D, et al. Evaluation of symptoms in non-celiac gluten sensitivity, histamine intolerance, and fructose malabsorption. Nutr Res. 2019;71:81–88.
- Yoon JY, et al. Eczema food triggers: eggs, dairy, gluten and diet strategies. Review of dietary interventions in atopic dermatitis (104 studies, 7 dietary categories). 2024.
- Virdee K, et al. Food-specific IgG antibody-guided elimination diets followed by resolution of asthma symptoms. Glob Adv Health Med. 2015;4(1):62–66; and: Utilization of IgG testing to significantly reduce psoriasis symptoms — case report. J Contemporary Chiropractic. 2024.
- Walsham NE, Sherwood RA. Fecal calprotectin in inflammatory bowel disease. Clin Exp Gastroenterol. 2016;9:21–29. PMC3724198.
- D'Inca R, et al. Calprotectin and lactoferrin in the assessment of intestinal inflammation and organic disease. Dig Liver Dis. 2007;39(10):957–962; and: Fecal biomarkers: calprotectin and lactoferrin. PubMed. 2016. PMID:26982329.
- Bunyavanich S, et al. The gut microbiome in food allergy. Ann Allergy Asthma Immunol. 2019;122(3):276–282.
