Food Sensitivities & Allergic Response

Food Sensitivities & Allergic Response

1. Definition and Classification

Adverse food reactions include immune-mediated food allergies and non-immune-mediated intolerances. These two broad categories are frequently conflated in popular discourse, yet they arise through fundamentally distinct biological mechanisms and carry different clinical implications.

A true food allergy is a disorder in which ingestion of a small amount of food elicits an abnormal immunologically mediated clinical response. Food allergy is an abnormal immune response to a food protein mediated by immunoglobulin E (IgE), non-IgE, or mixed IgE/non-IgE immunological mechanisms.

Food allergy, a subset of food hypersensitivity, denotes an immune response to food proteins categorized into IgE-mediated or non-IgE-mediated reactions. Conversely, food intolerance refers to non-immunological reactions in which the human body cannot properly digest certain foods or components, leading to gastrointestinal discomfort and other non-immune-related symptoms.

Non-IgE-mediated immune-mediated food reactions include celiac disease and gluten sensitivity. Non-immune-mediated reactions encompass different categories such as disorders of digestion and absorption, inborn errors of metabolism, as well as pharmacological and toxic reactions.

The principal classification scheme, as summarised in the peer-reviewed literature, recognises four major categories:

• IgE-mediated food allergy — rapid-onset (typically within minutes to two hours), driven by cross-linking of allergen-specific IgE antibodies on mast cells and basophils, triggering degranulation and the release of histamine and other mediators.
• Non-IgE-mediated food allergy — delayed reactions (hours to days) involving T-cell and eosinophil-mediated pathways; examples include food protein-induced enterocolitis syndrome (FPIES) and food protein-induced proctocolitis.
• Mixed IgE- and cell-mediated disorders — eosinophilic gastrointestinal diseases (EoGD) share a complex pathogenesis triggered by foods in which an IgE-mediated component is integrated with T cell-mediated immunological mechanisms, characterised by a predominant eosinophilic infiltration of the gastrointestinal tract.
• Non-immune food intolerances — non-allergic food intolerance may be due to pharmacological, metabolic, and toxic causes. Pharmacological causes may provoke anaphylactoid reactions, flushing, hypotension, and urticaria — as with foods high in histamine content (e.g., scombroid fish). Tyramine in cheese or red wine may provoke or exacerbate migraine. Monosodium glutamate may provoke flushing, headache, and abdominal symptoms. Lactase deficiency is an example of non-allergic food intolerance due to a metabolic cause, manifesting as abdominal symptoms and chronic diarrhoea after ingestion of milk.

Food intolerances are estimated to affect up to 20% of the population, but complete understanding of diagnosis and management is complicated given the variability in presentation and the non-immunological mechanisms involved.

2. Prevalence and Epidemiology

Food allergy has become an important public health burden in the past few decades, particularly in developed countries. The prevalence of food allergies is now estimated at 5–10% of the population in developed countries. Recent epidemiological data in North America showed that the prevalence of food allergy in children has increased.

The prevalence of food-challenge-defined allergies for common food allergens has been reported to be: 0.6% to cow's milk, 0.2% to egg, 0.1% to wheat, 0.3% to soy, 0.2% to peanut, 0.5% to tree nuts, 0.1% to fish, and 0.1% to shellfish.

The most common food allergens in the United States include egg, milk, peanut, tree nuts, wheat, crustacean shellfish, and soy. The Food Standard Agency identifies a broader set of 14 major allergens regulated in the European Union. These include celery, gluten-containing cereals (wheat, rye, barley, and oats), crustaceans, eggs, fish, lupin, milk, mollusks, mustard, peanuts, sesame, soybeans, sulfur dioxide and sulfites, as well as tree nuts (cashew nuts, almonds, and hazelnuts).

3. Mechanisms and Body Systems Involved

3.1 IgE-Mediated (Type I Hypersensitivity)

Immunologically mediated hypersensitivity to foods is defined as food allergy, mainly due to immunoglobulins of class E (IgE) triggering immediate reactions (type I hypersensitivity) with possible involvement of mucosa, skin, airways, intestinal tract, and the vascular system.

Food allergens are derived from common naturally-occurring food proteins of plant and animal origin. The proteins in the food are initially broken down by hydrolytic enzymes in the gastrointestinal tract during the digestive process. It is hypothesised that food allergens can be modified into different forms and different structures, which can be processed by antigen-presenting cells, exhibited on the major histocompatibility complex class II molecules, and subsequently recognised by antigen-specific T cells.

Upon re-exposure to the allergen, cross-linking of bound IgE on mast cells and basophils triggers rapid degranulation and systemic release of histamine, prostaglandins, and leukotrienes. During desensitisation, mast cell and basophil activation are decreased through an unclear mechanism, and a shift occurs from the predominance of T helper 2 (TH2) cells to that of allergen-specific regulatory T (Treg) cells, which in turn may lead to the observed shift in allergen-specific antibodies from the IgE to the IgG4 isotype.

3.2 Non-IgE-Mediated and Mixed Pathways

The adverse immune response in food allergy consists of IgE-mediated immediate hypersensitivity reactions, non-IgE-mediated reactions, and disorders with mixed IgE-mediated and cell-mediated immune reactions. In non-IgE-mediated reactions, T-lymphocytes, eosinophils, and mucosal immune cells predominate, with symptoms typically delayed and confined predominantly to the gastrointestinal tract.

3.3 Oral Tolerance and Its Breakdown

Although oral tolerance is the normal physiologic response to ingested antigens, a breakdown in this process appears to have occurred in the past two decades, leading to an increasing prevalence of sensitisation to food allergens.

Ingested food proteins may cause allergic immune responses leading to food allergy, but how these proteins become immunogenic and cause food allergies is not completely understood. Tolerance to food is mainly acquired by dendritic cells, epithelial cells in the gut, and the gut microbiome. A subset of CD103+ dendritic cells is capable of inducing T regulatory cells (Treg cells) that express anti-inflammatory cytokines. Anergic T cells also contribute to oral tolerance by reducing effector cells. Regulatory B cells (Breg cells) suppress effector T cells and contribute to immune tolerance to food allergens.

3.4 The Epithelial Barrier and Transcytosis of Allergens

Intestinal epithelial barrier dysfunction in sensitised intestines involves enhanced transcytotic rates of allergens. Recent studies demonstrate that food allergens are transported across the epithelium and avoid lysosomal degradation by binding to cell surface IgE and the low-affinity receptor CD23/FcεRII.

Loss of epithelial barrier integrity can be caused by allergens, infectious agents (e.g., bacteria, fungi, and viruses), injury, environmental substances (e.g., particulate matter, microplastics, detergents), or genetic predisposition (e.g., filaggrin, claudin-1).

3.5 Body Systems Affected

Food-allergic responses can engage multiple organ systems simultaneously or sequentially:

• Gastrointestinal system: The spectrum of GI symptoms such as abdominal pain, bloating, abdominal distension, flatulence, and diarrhoea is prevalent and very common in food intolerance and non-IgE-mediated allergy.
• Cutaneous system: Urticaria, angioedema, and atopic dermatitis are frequent manifestations of IgE-mediated food allergy, particularly in children.
• Respiratory system: Rhinitis and asthma can be triggered or worsened by food allergens, particularly in those with concomitant atopy.
• Vascular/systemic: Anaphylaxis represents the most severe systemic manifestation, involving the cardiovascular system through IgE-mediated mast cell and basophil activation.
• Immune system: Biologics blocking TSLP, IL-33, IL-4 and IL-13, or IgE may help dampen the type 2 immune response central to food allergy.

4. Contributing and Associated Factors

4.1 Genetic Factors

This systematic review and meta-analysis of 2.8 million participants in 190 studies identified the following largest and most certain risk factors associated with the development of food allergies in children: prior allergic conditions (atopic march/diathesis), atopic dermatitis, increased skin transepidermal water loss, filaggrin gene sequence variations, delayed solid food introduction, infant and intrapartum antibiotic exposure, male sex, being firstborn, family history of allergy, parental migration, self-identification as Black, and caesarean delivery.

According to multivariate statistical analysis, loss-of-function variants in the FLG gene represent a risk factor for the onset of severe manifestations of food allergy (OR = 8.9; CI: 3.1–28.3). Peanut and hazelnut were identified as high-risk foods in patients with FLG mutations. This study demonstrates that atopic children carrying FLG mutations represent a high-risk population due to their predisposition to develop severe food allergy reactions, such as anaphylaxis.

Celiac disease is a systemic immunological disorder triggered by the intake of gluten and related prolamins in genetically at-risk individuals, i.e., those bearing HLA-DQ2 or HLA-DQ8 haplotypes.

4.2 The Dual Allergen Exposure Hypothesis and Skin Barrier Disruption

The Lack dual-allergen exposure theory was originally proposed as a hypothesis but is now widely regarded as an established theory supported by multiple randomised controlled trials. It proposes that sensitisation primarily occurs through a disrupted, inflamed skin barrier, particularly in infants with eczema, whereas early oral exposure promotes tolerance.

Severity of atopic dermatitis played a significant role in food allergy risk, with each 5- to 10-point increase on the Scoring Atopic Dermatitis scale associated with a 1% risk increase. Elevated skin transepidermal water loss showed a 10% risk difference, and filaggrin gene loss-of-function variations carried a 4.2% risk difference.

4.3 Gut Microbiome and Dysbiosis

Increasing evidence suggests that the balance of human gut microbiota and the integrity of the intestinal barrier may play roles in the development of food allergy. Environmental factors, including industrialisation and consumption of highly processed food, can contribute to altering the gut microbiota and the intestinal barrier, increasing the susceptibility to allergic sensitisation.

One of the mechanisms by which the gut microbiome promotes tolerance is through induction of regulatory T-cells, which can be achieved through microbial production of short-chain fatty acids, such as butyrate. The intestinal microbiota may also prevent allergic sensitisation to foods via induction of IL-22 production by immune cells, leading to decreased intestinal epithelial permeability and reduced interaction of the immune system with the allergen.

Environmental factors including a low-fibre/high-fat diet, caesarean delivery, antiseptic agents, lack of breastfeeding, and drugs can induce gut microbiome dysbiosis and have been associated with food allergy.

Altered faecal microbiomes were associated with food allergies in infants, with specific food allergy subtypes associated with increased incidence in infants; reduced bacterial diversity at the 1-month and 12-month mark was inversely associated with allergic sensitisation, as evidenced by increased peripheral eosinophils and allergic rhinitis symptoms.

4.4 Intestinal Permeability ("Leaky Gut")

Increased permeability of the gut barrier allows the translocation of allergenic molecules, triggering Th2 immune responses. The gut barrier encompasses several interactive, physical, and functional components, such as the gut microbiota, the mucus layer, the epithelial layer, and the gut mucosal immunity. All these contribute to homeostasis in a well-regulated manner. Nevertheless, this frail balance might be disrupted by westernised dietary habits, infections, pollution, or exposure to antibiotics, thus diminishing protective immunity and leading to the onset of chronic diseases.

4.5 Timing of Food Introduction and the Hygiene Hypothesis

Delayed introduction of allergenic foods significantly increased food allergy risk. Introducing peanuts after 12 months was associated with a 6.8% risk increase (OR 2.55), while delayed introduction of fish, eggs, and fruits showed similar patterns.

A study found that infants who were introduced to peanut before 12 months of age after cessation of breastfeeding had a 66% reduced risk of sensitisation at 5 years compared to those who were not. Furthermore, if mothers introduced peanut early while they were breastfeeding and were also regularly consuming peanut themselves, this risk was further reduced, suggesting that maternal peanut consumption in addition to breastfeeding at the time of peanut introduction during infancy may help decrease the risk of peanut sensitisation.

The epithelial barrier hypothesis and hygiene hypothesis highlight how pollution, westernised diets, smaller family size, and reduced microbial exposure may further explain rising food allergy prevalence.

4.6 Antibiotic Exposure

Antibiotic exposure was a major modifiable factor, with the strongest association when administered in the first month of life and smaller effects for prenatal or later infancy exposure.

4.7 Western Dietary Pattern

Dietary patterns characterised by high fibre, rich in antioxidants and healthy fats (such as the Mediterranean diet) show potential protective effects against food allergies by promoting intestinal flora balance, maintaining intestinal barrier integrity, and regulating immune responses. In contrast, the "Western diet" pattern characterised by high saturated fat, high sugar, low fibre, and highly processed foods is associated with an increased risk of food allergies.

Within the PUFAs category, omega-3 may reduce inflammation, whereas omega-6 PUFAs are generally considered to have a proinflammatory effect. Recent evidence highlights an imbalance in the ω-3:ω-6 ratio with an increased intake of ω-6 as a consequence of the shift towards a westernised diet.

5. Nutrients, Herbs, and Natural Ingredients Studied in Relation to Food Sensitivities

The following entries separate traditional use from scientific evidence and characterise the strength of available evidence.

5.1 Quercetin

Traditional Use

Quercetin is a polyphenolic flavonoid found widely in onions, apples, capers, and buckwheat. Its consumption as part of plant-rich diets has been an intrinsic component of traditional cuisines across Mediterranean, East Asian, and Middle Eastern food cultures for millennia, where these foods were understood — without formal mechanistic knowledge — to support general health and reduce inflammatory complaints.

Scientific Evidence

Quercetin inhibits mast cell degranulation, reduces the production of histamine and pro-inflammatory cytokines, and restores homeostasis of the immune system by modulating the Th1/Th2 and Treg/Th17 balances. Additionally, its antioxidant properties help to dampen oxidative stress, a critical factor in the pathophysiology of allergic diseases.

In vitro studies have consistently demonstrated quercetin's ability to suppress allergic reactions. In vivo studies, particularly in murine models of allergic rhinitis, have confirmed its efficacy in relieving symptoms (such as nasal itching, sneezing, rhinorrhoea, and congestion) and dampening type 2 mucosal inflammation. Preclinical evidence also supports its therapeutic potential in asthma, conjunctivitis, atopic dermatitis, and food allergies.

However, human studies are still scarce, as only two clinical trials investigated quercetin as a monotherapy. Both studies reported promising results, including symptom reduction and improved quality of life, though larger, randomised trials are needed to validate these findings.

Quercetin stabilises mast cells, inhibits Lyn/PLCγ pathways, and improves rhinitis symptoms in small randomised trials using bioavailable formulations.

Evidence strength: Robust mechanistic and preclinical data; human clinical evidence is preliminary and limited to small trials. Robust randomised controlled trials in food-allergic populations specifically are lacking.

5.2 Omega-3 Polyunsaturated Fatty Acids (EPA & DHA)

Traditional Use

High consumption of fatty fish (herring, mackerel, salmon, sardines) is a long-established feature of coastal and Northern European, Inuit, and Japanese traditional diets, where it was historically associated with robust health. Traditional medicine systems in Scandinavia and East Asia empirically used fish and fish-liver oils for a range of inflammatory and respiratory conditions.

Scientific Evidence

Omega-3 fatty acids modulate Th2 responses, promote regulatory T cells, and generate specialised pro-resolving mediators, with modest clinical benefits observed in pregnancy and early life.

One RCT administered omega-3 fatty acids during pregnancy and breastfeeding in high-risk mothers and found a decrease in food allergy. A systematic review reported reduced sensitisation to peanut and egg in the infant and/or child if omega-3 fatty acids were administered during pregnancy and/or lactation.

A systematic review and meta-analysis of 10 prospective cohort studies and 5 randomised clinical trials on omega-3 intakes during pregnancy and outcomes of childhood allergic disease found inconsistent results. Although firm conclusions could not be drawn due to heterogeneity of studies, the overall findings were "suggestive" of a protective association between higher maternal intakes of long-chain omega-3s or fish and incidence of allergic disease symptoms in the offspring. The authors of a Cochrane review concluded that there is limited evidence to support the use of omega-3 supplements by women during pregnancy and/or lactation for reducing the risk of allergic disease.

Clinical studies results are still conflicting about the best timing and dosages of supplementation and which individuals are most likely to benefit; therefore, it is still not possible to draw firm conclusions. With regard to food-allergic children, it is still debated whether PUFAs could slow disease progression or not, since consistent data are lacking. More data on the effects of ω-3 PUFA supplementation alone or in combination with other nutrients are warranted.

Evidence strength: Mechanistic evidence is well-established; clinical evidence in the context of food allergy is mixed and heterogeneous. Epidemiological associations are suggestive but not conclusive.

5.3 Vitamin D

Traditional Use

Cod liver oil — a traditional remedy across Scandinavian, Northern European, and Scottish coastal communities — was used historically for general immunity and winter health, though its vitamin D content was not understood until the 20th century. Sun exposure as a health-promoting practice is documented across many ancient cultures, from Ayurveda (heliotherapy) to Greek medicine.

Scientific Evidence

Within the innate and adaptive immune systems, the vitamin D receptor and enzymes in monocytes, dendritic cells, epithelial cells, T lymphocytes, and B lymphocytes mediate the immunomodulatory actions of vitamin D. Vitamin D insufficiency/deficiency early in life has been identified as one of the risk factors for food allergy.

Vitamin D has been shown to affect several mechanisms that promote immunologic tolerance, including T regulatory cell function and the induction of tolerogenic dendritic cells.

Several studies have observed an association between increasing latitude and food allergy prevalence, plausibly linked to lower ultraviolet radiation (UVR) exposure and vitamin D synthesis in the skin.

In a large-scale cohort study in Australia, comparing data of 5,276 children, infants with vitamin D deficiency were over twice as likely to suffer from multiple food allergies compared with ordinary infants; vitamin D-deficient children's probability of food allergy was 6 times that of ordinary children, and they were more likely to have peanut and egg allergies.

It has been suggested that vitamin D deficiency might impair epithelial barrier integrity, leading to increased and inappropriate mucosal exposure to food antigens and a pro-sensitisation immune imbalance that compromises immunological tolerance. Consequently, early correction of vitamin D deficiency might promote mucosal defence, maintain healthy microbial ecology and allergen tolerance, and decrease risk of food allergies in children.

A systematic review indicated that vitamin D supplementation in pregnancy and/or lactation and/or early life feeding was not associated with offspring food allergies. There is currently no evidence to support vitamin D supplementation during pregnancy or lactation for food allergy prevention. Many clinical studies believe that vitamin D supplementation can improve infants' and children's food allergy; however, some show negative results or opposite results.

Evidence strength: Strong epidemiological and mechanistic associations with vitamin D status and food allergy risk; however, supplementation trials are heterogeneous and do not yet support firm recommendations, particularly in the prenatal context.

5.4 Probiotics

Traditional Use

Fermented foods — including yoghurt, kefir, miso, tempeh, kimchi, and sauerkraut — are traditional dietary staples across Eurasian, East Asian, and Middle Eastern cultures, consumed for centuries for digestive health and general wellbeing. The concept that fermented foods support immunity predates the germ theory of disease in many folk medical traditions.

Scientific Evidence

Preclinical and clinical studies have highlighted the potential of probiotics, prebiotics, and postbiotics in the prevention and treatment of food allergy through enhancing gut barrier function and promoting the restoration of healthy gut microbiota.

Lactobacillus species, particularly L. rhamnosus and L. plantarum, influence both local and systemic immunity by enhancing regulatory T cell activity, promoting anti-inflammatory cytokines such as IL-10, and improving epithelial barrier function. Their impact on the gut–lung and gut–skin axes highlights the central role of the microbiome in allergic disease modulation.

Administration of defined Clostridia, or bacteria-derived short-chain fatty acids (SCFA) to germ-free mice induced an increase in Treg cell numbers and reduced allergic response.

The human clinical trial evidence for probiotics in allergic disease is growing but remains strain-specific and context-dependent. The observed improvements in disease markers and clinical outcomes suggest that probiotic supplementation could offer a preventive and therapeutic benefit; however, larger randomised trials are needed to validate these findings.

Evidence strength: Preclinical evidence is compelling. Human trials show benefit for specific strains in atopic dermatitis and allergic rhinitis; evidence specifically for food allergy prevention remains mixed and strain-dependent.

5.5 Curcumin (from Curcuma longa, Turmeric)

Traditional Use

Turmeric has been used for over 4,000 years in Ayurvedic and Traditional Chinese Medicine as an anti-inflammatory and digestive remedy. In South Asian culinary and medicinal tradition, it was prepared as a paste, decoction, or incorporated into foods, and applied both topically and internally for inflammatory conditions, skin complaints, and digestive disorders. Turmeric milk (haldi doodh) is a well-documented traditional preparation in India.

Scientific Evidence

Curcumin inhibits NF-κB/MAPK signalling, enhances barrier function, and improves allergic rhinitis and dermatitis despite limited bioavailability.

The capacity of curcumin to inhibit the production of antigen-specific IgE in a dose- and time-dependent manner has been well documented in in vitro and in vivo studies.

Numerous studies using animal models of food allergy have considered the impact of various polyphenols including curcumin on the immune response, showing their potential to ameliorate food hypersensitivity and allergy symptoms in sensitised mice.

Evidence strength: Strong preclinical evidence; limited bioavailability constrains clinical translation. Small human studies report benefit in allergic rhinitis and dermatitis; large, well-powered RCTs in food-allergy populations are lacking.

5.6 Epigallocatechin Gallate (EGCG) from Green Tea (Camellia sinensis)

Traditional Use

Green tea has been consumed in China for over 2,000 years and in Japan for more than 1,000 years, valued in traditional medicine for its purported ability to clear heat, support digestion, and promote general vitality. Japanese Benifuuki green tea — a cultivar particularly rich in methylated catechins — has been cultivated specifically for its reported anti-allergic properties.

Scientific Evidence

EGCG stabilises mast cells, attenuates FcεRI signalling, and reduces airway inflammation in preclinical models, though clinical data are scarce.

Tea catechins such as epigallocatechin (EGC) and epigallocatechin gallate (EGCG) are effective in inhibiting mast cell activation, specific IgE, and Th2 cytokine production, and reduce the degree of pathological changes in the intestine in a mouse model sensitised by αs1-casein milk protein.

Evidence strength: In vitro and animal data are supportive. Clinical data in humans are scarce; one study in Benifuuki green tea showed benefit for cedar pollen allergy, but food-allergy-specific human trials are lacking.

5.7 Stinging Nettle (Urtica dioica)

Traditional Use

Stinging nettle has a long history of use in European herbalism, recorded in texts as far back as Roman antiquity (Pliny the Elder) and prominently in medieval European materia medica. It was used internally as a tea or decoction and externally, both for rheumatic complaints and for respiratory and allergic symptoms including hay fever and urticaria. Traditional preparations included teas brewed from dried leaves, and nettle soup as a spring tonic food.

Scientific Evidence

A randomised, double-blind, placebo-controlled clinical trial of Urtica dioica root extract in allergic rhinitis patients was published in the Iranian Journal of Pharmaceutical Research. Forty patients completed the trial. A significant improvement in clinical symptom severity was observed in both groups. A statistically significant reduction in mean nasal smear eosinophil count was observed after treatment with nettle. However, the current study showed certain positive effects of nettle in the management of allergic rhinitis on controlling the symptoms, though similar effects were demonstrated by the placebo group as well, indicating the results must be interpreted cautiously.

Evidence strength: Preliminary. One small RCT with a strong placebo response; evidence is insufficient to support firm conclusions. The NCCIH has reviewed this herb, and the overall evidence base for its use in food allergy specifically remains weak.

5.8 Bromelain (from Ananas comosus, Pineapple)

Traditional Use

Pineapple and its stem extracts have been used in folk medicine in Central and South America as digestive aids and for anti-inflammatory purposes. Bromelain as an isolated enzyme complex has been used in traditional naturopathic practice in the 20th century to reduce mucous membrane inflammation in allergic conditions and sinusitis.

Scientific Evidence

Bromelain is an enzyme found in pineapple that may help reduce inflammation and improve respiratory symptoms. Animal research has demonstrated anti-inflammatory effects in murine models of asthma. However, bromelain does not have solid evidence to suggest that it is helpful for allergy symptoms in well-powered human trials, and human data specific to food allergic reactions are minimal.

Evidence strength: Mostly preclinical. Human clinical evidence for bromelain in food allergy or food sensitivity is lacking.

5.9 Butterbur (Petasites hybridus)

Traditional Use

Butterbur was used in European herbalism since at least the Middle Ages, recorded by herbalists such as Lobelius (16th century) and in various German and Swiss folk medicine traditions as a remedy for fevers, respiratory complaints, and pain. The common name derives from the traditional use of its large leaves to wrap butter in warm weather. It was used as an infusion or decoction for coughs and respiratory allergy.

Scientific Evidence

Butterbur (Petasites hybridus) has been studied in clinical trials for allergic rhinitis, where its petasin and isopetasin compounds appear to act as leukotriene inhibitors. Randomised controlled trials comparing butterbur extract (ZE339) to cetirizine and fexofenadine for seasonal allergic rhinitis have demonstrated comparable efficacy in symptom reduction. However, the raw plant contains pyrrolizidine alkaloids (PAs), which are hepatotoxic; only PA-free certified extracts are used in research and are considered relevant for any application.

Evidence strength: The strongest human clinical evidence of the herbs listed here for allergic rhinitis, though not specifically food allergy. Use of non-PA-free preparations carries hepatotoxicity risk.

5.10 Polyphenols: Rosmarinic Acid and Other Dietary Compounds

The capacity to inhibit the production of antigen-specific IgE in a dose- and time-dependent manner has been well documented in in vitro and in vivo studies for a number of polyphenols such as curcumin, rosmarinic acid, quercetin, ferulic acid, tea catechins (EGCG, ellagitannins, and gallic acid), and red grape polyphenols.

Chinese sweet tea polyphenols, particularly ellagitannins and gallic acid, have been demonstrated as a potent inhibitor of hen egg ovalbumin-induced allergic response in mice by modulating the Th1/Th2 balance, increasing the percentage of Treg subtype, and enhancing intestinal IgA secretions, which clinically manifested as a reduction in scratching behaviour and other allergic symptoms.

Evidence strength: Animal and in vitro data are consistent and mechanistically informative; robust human RCT data in food allergy are lacking for most individual polyphenols other than quercetin.

5.11 Ginger (Zingiber officinale)

Traditional Use

Ginger has been used as both a food and medicine in South and East Asia for over 2,000 years, documented in Sanskrit texts, Chinese pharmacopoeias (Shennong Bencao Jing), and later in Unani and Ayurvedic traditions. It was used for digestive complaints, respiratory congestion, and as a general anti-inflammatory remedy, typically as a decoction, fresh juice, or dried powder.

Scientific Evidence

Ginger constituents ([6]-gingerol and [6]-shogaol) modulate Th1/Th2 balance, mast-cell activity, and oxidative stress, with early clinical evidence in rhinitis and asthma.

Evidence strength: Preclinical mechanistic data and very early clinical signals in respiratory allergy; food-allergy-specific human trials are absent.

6. Dietary and Lifestyle Factors

6.1 Mediterranean Dietary Pattern

The Mediterranean diet (MD), which includes a lot of fruits and vegetables, whole grains, legumes, nuts, olive oil, and fish, has been linked to a variety of health benefits, including a lower risk of chronic and allergic disease.

The MD is rich in polyphenols and polyunsaturated fatty acids (PUFAs), particularly omega-3 fatty acids, and evidence suggests that these compounds may play a role in lowering the risk of developing food allergies.

A 2023 systematic review published in Nutrients (PMC10420808) identified nine relevant studies. In human studies, when the Mediterranean diet intervention was given during pregnancy and lactation, a beneficial effect was observed. When the intervention was given during pregnancy and until birth or to the infant for six months, no effect was observed.

A 2025 MEDALLION cohort study found that higher maternal adherence to the Mediterranean diet was associated with reduced odds of food allergy in offspring during both pregnancy (adjusted OR 0.94, 95% CI 0.89–1.00) and lactation (adjusted OR 0.94, 95% CI 0.88–1.00).

An earlier systematic review and meta-analyses involving 62 articles found weak evidence that vitamins A, D, and E; zinc; fruits and vegetables; and a Mediterranean diet are associated with protection against asthma, but not other allergic diseases including food allergy. This underscores the need for caution in over-interpreting dietary pattern data.

6.2 Dietary Fibre and Short-Chain Fatty Acids

Evidence has shown promise that a diet rich in fibre and diverse plant-based foods can foster a healthy gut microbiome, promoting immune tolerance and reducing the risk of food allergy.

Short-chain fatty acids (SCFAs) produced from bacterial fermentation of dietary fibre — particularly butyrate — are mechanistically linked to Treg induction. One of the mechanisms by which the gut microbiome promotes tolerance is through induction of regulatory T-cells, which can be achieved through microbial production of short-chain fatty acids, such as butyrate.

6.3 Early Allergen Introduction as a Dietary Strategy

Although there are limited data with respect to other major food allergens and whether early introduction may prevent allergy development, there is no need to delay the introduction of these allergens into the infant diet.

The primary intervenable risk factor identified to date is avoiding delay in introduction of common allergens early in life.

6.4 Breastfeeding

The relationship between breastfeeding and food allergy risk is complex. Breastfeeding is generally encouraged for its many health benefits, and there is some evidence that exclusive breastfeeding may support the maturation of gut immunity. However, a Cochrane review concluded that maternal avoidance diets in pregnancy were unlikely to reduce risk of atopic disease in childhood. More recent data suggest that breast milk consumed simultaneously with infant allergen exposure may potentiate tolerance induction.

6.5 Elimination Diets for Diagnosis and Symptom Management

Food allergy diagnostic procedures include skin prick testing, food-specific IgE measurement, and elimination diets, with the gold standard being a double-blind, placebo-controlled food challenge. Assuming that certain foods are suspected to be the cause of an allergic disorder, they can be eliminated from the patient's diet to alleviate symptoms and confirm the diagnosis.

There is a discrepancy between the perceived versus actual prevalence of immune-mediated food allergies and non-immune reactions to food. The risk of an inappropriate approach to their correct identification can lead to inappropriate diets with severe nutritional deficiencies.

6.6 Nutritional Consequences of Food Allergy Management

Elimination of common food allergens — including milk, egg, wheat, soy, and multiple tree nuts — carries significant nutritional implications. The risk of an inappropriate approach to correct identification of adverse food reactions can lead to inappropriate diets with severe nutritional deficiencies. Close attention to nutrient adequacy, particularly for calcium, vitamin D, iron, zinc, and essential fatty acids, is warranted in the context of medically supervised elimination diets.

6.7 Environmental and Lifestyle Factors

The increase in food allergy prevalence is attributed to genetic predisposition, air pollution, climate change, lack of physical activity, and alterations in eating habits.

Psychological stress and mast cell activity may also play a role in gut barrier defects and intestinal sensitisation.

Environmental factors including the rise in caesarean sections, antibiotic use, a diet full of saturated fats and low fibre, and reduced omega-3 fatty acids and vitamin D have all been identified as contributing to gut dysbiosis.

7. Current State of Evidence: Summary Table

• Quercetin: Robust preclinical data; two small human RCTs show promise; insufficient for firm clinical recommendations in food allergy.
• Omega-3 fatty acids (EPA/DHA): Consistent mechanistic and preclinical data; mixed human trial results; possible modest benefit when administered perinatally in high-risk populations.
• Vitamin D: Strong epidemiological and mechanistic associations; supplementation trial results are heterogeneous; no established preventive benefit yet confirmed in RCTs for food allergy.
• Probiotics: Compelling preclinical data; growing human evidence for specific strains (e.g., L. rhamnosus GG) in atopic conditions; strain and timing specificity limit generalisable recommendations.
• Curcumin: Well-characterised anti-inflammatory mechanisms; bioavailability limitations; small human studies support benefit in rhinitis and dermatitis; food allergy RCTs are absent.
• EGCG (green tea): Mechanistically plausible mast-cell stabilisation; limited human clinical data; no food allergy-specific RCTs.
• Stinging nettle: Preliminary evidence from one small RCT with a strong placebo effect; insufficient evidence for food allergy.
• Bromelain: Animal models supportive; solid human clinical evidence absent.
• Butterbur: Best-evidenced herb for allergic rhinitis in RCTs; PA-free preparations essential; not studied in food allergy specifically.
• Ginger bioactives: Early mechanistic and limited clinical data for respiratory allergy; no food-allergy-specific trials.

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