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Nutrition and diet in ethnic atopic dermatitis
*Corresponding author: Trashita Hassanandani, Department of Dermatology, Venerology and Leprosy, Amaltas Institute of Medical Sciences, Dewas, Madhya Pradesh, India. htrashita@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Hassanandani T, Dhakad JS. Nutrition and diet in ethnic atopic dermatitis. Indian J Skin Allergy. doi: 10.25259/IJSA_27_2025
Abstract
Atopic dermatitis (AD) is a chronic, inflammatory, eczematous skin disorder that more frequently affects children. The disease is mainly mediated by Th2 cells and has skin barrier impairment in genetically predisposed individuals as the main underlying etiological factor. The role of diet and nutrition has been well understood in the functioning of the immune system, but the role of dietary factors in the pathogenesis of AD is still a topic of debate. Various studies have shown the role of certain nutrients, including Vitamins (D, C, E, A), minerals (zinc, iron, magnesium, selenium, copper), fatty acids polyunsaturated fatty acids, prebiotics, and probiotics, in the pathogenesis and progression of the disease. However, certain food materials such as cow’s milk and eggs may predispose the infants to develop AD, and studies evaluating the exclusion of these food items from the diet have been conducted. Various differences are seen in the food habits, dietary requirements, availability of food items, and local practices in different ethnicities. In this article, we have reviewed the role of supplementation and exclusion diets, which can help us in managing and preventing the progression of the disease.
Keywords
Atopic dermatitis
Diet and nutrition
Elimination diet
INTRODUCTION
Atopic dermatitis (AD) is a common, chronic, inflammatory, eczematous disease with an incidence of 15–30% in childhood and 3–5% among adults.[1-3] Over one half of children with AD develop the lesions in 1st year of life, and 90% of children with AD develop lesions by age five.[4] Diet has been suggested as an important factor in the management of AD. Various studies have indicated the role of dietary triggers such as cow’s milk, eggs, gluten, junk food, and nightshades in the aggravation of AD. Studies also indicate that the addition of vegetables, fish oil, organic foods, and fruits has a beneficial role and leads to improvement of AD. In an open pilot study conducted on Indian patients, dietary elimination in 100 children showed significant improvement in AD.[5] Werfel et al. compiled the results of eight studies and found the prevalence of food allergy (FA) to be 33–63%.[6] In a study of Japanese nursery school children, increased serum immunoglobulin E (IgE) levels, maternal history of atopy, and FA were linked to developing AD in children <6 months of age.[7] On the contrary, there are few studies with no temporal association of FA and AD.[8] However, more robust data are required to make strong recommendations regarding elimination diets and dietary interventions in AD patients. A comprehensive narrative review of literature was conducted by searching articles published in PubMed and Google Scholar databases using the keywords “atopic dermatitis,” “nutrition,” “diet,” “pediatric,” and “ethnic.” This review included original articles, review articles, case reports, and other relevant publications.
PATHOGENESIS OF AD
The skin barrier plays an important role in the prevention of exposure to various antigens and sensitization. The development of AD depends on a multifactorial etiology including genetic predisposition, impaired skin barrier function, and exposure to environmental triggers, such as allergens, irritants, microorganisms, and diet. Certain nutrients, such as Vitamin D, Vitamin A, gamma-linolenic acid (GLA), eicosapentaenoic acid, probiotics, and zinc, might play an important role in the pathogenesis of AD.
The defective skin barrier allows penetration of allergens and microorganisms, leading to contact (of allergens and microorganisms) with the Langerhans cells, which can lead to sensitization (immediate type-I or delayed type-IV reaction) in the lymph nodes. This contact can then lead to immune activation and inflammation (elicitation). The inflammatory response is characterized by increased production of IL-4, elevated levels of IgE levels, and eosinophilia. These factors contribute to the activation of helper T cells, particularly Th2 and Th17, leading to the various cytokines such as interleukin (IL)-2, IL4, IL5, IL8, IL10, IL13, and IL17a, along with tumor necrosis factor-a and interferon gamma (IFN-g). IFN-g in particular has been implicated in exacerbating skin barrier dysfunction by suppressing the expression of structural proteins such as filaggrin and intercellular adhesion molecules such as claudin-1.[9]
The barrier dysfunction leads to sensitization to various antigens found in the environment or in food. AD can lead to the development of the “atopic march,” where there is a progression of allergic disorders from early AD to FA, allergic rhinitis, and finally asthma.[10] Bacteria in the gastrointestinal tract have an important role in food digestion, xenobiotic metabolism, and maintenance of immune homeostasis.[11] It helps in the absorption of iron, magnesium, and calcium, and also regulates fat storage.[12] The bacteria have also been associated with the production of short-chain fatty acids such as acetate and butyrate, which help in the regulation of the immune response.[11] A disruption in the balance of human gut microbiota (dysbiosis) in early childhood may prove to be a risk factor for AD. In a study, Clostridia colonization of the infant intestine in early life has been shown to be associated with an increased risk of developing AD in the following 6 months of life.[13] It has also been observed that colonization of the gut with Lactobacillus lactic acid bacilli (Lactobacillus rhamnosus, Lactobacillus casei, Lactobacillus paracasei) and Bifidobacterium adolescentis in early life has been associated with a lower incidence of AD during the first 2 months of life.[14] Reduced relative quantities of potentially immunomodulatory intestinal bacteria have been associated with excessive production of pro-inflammatory cytokines, which may increase the likelihood of the development of eczema.
NUTRITION AND DIET IN AD
The role of diet in AD is not well defined. Earlier, it was recommended to delay the exposure of food, but now, it is recommended to do the opposite in certain situations. In fact, delaying exposure to certain types of food can increase the likelihood of food allergies.[9] The latest American Academy of Pediatrics (AAP) guidelines emphasize a balanced approach to managing AD, focusing on effective topical treatment, hydration, and avoidance of irritants rather than solely relying on restrictive diets unless a FA is present. Although dietary interventions have a role in managing AD symptoms, their effectiveness may vary among different populations due to differences in age, dietary habits, and immune health. There are a considerable number of studies investigating probiotic and prebiotic supplementation in the pediatric population. This highlights a strong interest in using gut health and microbial modulation as early-life interventions for AD. Almost all studies focused on two particular genera (Lactobacillus and Bifidobacterium) and their beneficial role in AD. Three separate studies demonstrated that prebiotic supplementation has effective long-term protective effects on AD and is associated with a reduction in plasma levels of total IgE.[15]
The role of various nutrients in AD and the corresponding studies are discussed below.
Vitamin D
It plays an important role in immune regulation and cellular differentiation. Notably, it promotes keratinocyte production of antimicrobial peptides, which have a central role in the pathogenesis of AD. Vitamin D can be obtained from ultraviolet-induced synthesis in the skin or from food materials such as cod liver oil, salmon, tuna, egg yolk, and fortified foods. Various observational studies have demonstrated that inadequate vitamin D exposure during pregnancy correlates with a significantly increased risk of AD in infants (Jones et al.), and the deficiency of Vitamin D during early childhood may predispose children to the development of AD (Chiu et al.).[16,17]
Vitamin C
It aids in ceramide synthesis within the epidermis and the reduction of cellular oxidative stress.[18-20] Dietary sources rich in vitamin C are citrus fruits, berries, green leafy vegetables, sweet potatoes, tomatoes, bell peppers, et cetera. Research by Shin et al. found an inverse association between serum vitamin C levels and the severity of AD, as measured by the SCORing Atopic Dermatitis (SCORAD) index.[21] Hoppu et al. further reported that higher levels of vitamin C in breast milk were associated with reduced risk of atopy in infants.[22]
However, the literature remains inconclusive, with varying findings regarding the dietary Vitamin C intake, its levels in breast milk, serum levels in infants, and risk of developing AD.
Vitamin E
Vitamin E is well known for its antioxidant and anti-inflammatory properties. It has been shown to modulate immune responses by inhibiting prostaglandin synthesis, and supplementation has been shown to lower serum IgE levels in AD patients. Major dietary sources of vitamin E are nuts, seeds, vegetable oils, and green leafy vegetables. Jaffary et al. demonstrated that low-dose vitamin E supplementation served as an effective adjunctive therapy for AD. Nevertheless, maternal serum levels did not correlate significantly with infant AD severity, indicating a complex relationship requiring further exploration.[23-25]
Vitamin A
The active metabolite of Vitamin A, retinoic acid (RA), produced by dendritic cells, is integral to immune tolerance. RA facilitates the differentiation of naïve T-cells into regulatory T-cells. It also helps in modulating allergic inflammation by suppressing IgE production and antagonizing innate lymphoid cells type 2 (ILC2) activity.[26]
Dietary sources rich in vitamin A are liver (chicken, fish, or beef), dairy products, carrots, sweet potatoes, spinach, pumpkin, egg yolk, et cetera. Experimental studies by Yang et al. revealed more severe eczema in vitamin A-deficient mice, and clinical data suggest an association between lower serum vitamin A levels and higher SCORAD index in children.[27]
Zinc
It serves as a cofactor in cellular growth, proliferation, and regeneration, and possesses anti-inflammatory effects.[28] Oysters, crab, lobster, red meat, poultry, legumes, nuts and seeds, and dairy products are rich sources of dietary zinc. Various studies have consistently reported lower serum and erythrocyte zinc levels in AD patients compared to healthy controls, as evidenced by David et al. and Karabacak et al., respectively, pointing toward a potential deficiency-related immune dysregulation in AD.[29,30]
Iron and copper
They exhibit contrasting roles in oxidative stress and inflammation. Excess free iron in the blood can generate reactive oxygen species, which increases oxidative stress within the cells.[31] Copper acts as a cofactor for enzymatic functions and has a role in cell and tissue growth.[32] Red meat, poultry, fish and seafood, legumes, green leafy vegetables, and fortified cereals are rich sources of iron, while shellfish, nuts and seeds, legumes, organ meats, and whole grains are rich in copper. David et al. found elevated serum copper and decreased serum ferritin in children with AD, suggesting altered trace element homeostasis.[33] Di Toro et al. further corroborated these findings, reporting increased hair copper levels in AD patients, hinting at a possible link to atopic risk.[34]
Selenium
It acts as a potent antioxidant and can reduce oxidative stress associated with inflammatory diseases like AD.[35] Dietary sources of selenium are brazil nuts, fish and seafood, meat, eggs, brown rice, whole wheat, et cetera. Yamada et al. identified selenium deficiency as a significant risk factor for the development of AD, reinforcing the element’s role in maintaining the balance in immune responses.[36]
Magnesium
It has an important role in cellular proliferation and differentiation, while its deficiency has been associated with heightened inflammatory responses.[37] Magnesium-containing food materials are green leafy vegetables, nuts and seeds, legumes, whole grains, fish, dark chocolates, et cetera. Toyran et al. conducted a study measuring various trace elements in AD and demonstrated that serum magnesium levels were significantly reduced in individuals with AD as compared to controls, supporting the hypothesis that magnesium status influences immune-mediated skin conditions.[38]
Polyunsaturated fatty acids (PUFAs)
Most of the dietary PUFAs, particularly linoleic and GLA, cannot be synthesized by mammals but have immunomodulatory functions. Arachidonic acid, derived from linoleic acid, integrates into immune cell membranes and, upon activation, is converted into leukotrienes that promote Th2-mediated cytokine production, including IL-4, IL-5, and IL-13.[39] Fatty fish, fish oil supplements, flaxseeds, chia seeds, walnuts, nuts, and seeds are rich sources of PUFAs. Various studies have been conducted on supplementation using PUFA-rich oils such as evening primrose and borage oil have shown a reduced prevalence of AD, especially in infancy.[40]
The role of prebiotics and probiotics in modulating the gut-skin immune axis is increasingly being recognized. Probiotics improve intestinal barrier integrity and favorably alter the gut microbiota, enhancing Treg cell activity and anti-inflammatory cytokine production, such as IL-10 and TGF-b in mesenteric lymph nodes, thus playing an important anti-inflammatory role. Prebiotics have been shown to expand and stabilize iTreg populations and promote intestinal IgA secretion.[39] Meta-analyses of randomized controlled trials (RCTs) suggest a preventive benefit of probiotics in the development of AD when administered in pre- and postnatal periods. However, another meta-analysis reported that probiotics produced preventive effects only when given to both pregnant mothers and infants rather than sole administration to infants.[39,40]
Table 1 summarizes the various nutrients and their roles in AD.
| Nutrients | Role in AD | Sources |
|---|---|---|
| Vitamin D | Regulates immune response, boosts Treg cells, improves the skin barrier, and promotes keratinocyte production of AMP | Cod liver oil, fatty fish, fortified dairy products, egg yolks, sunlight |
| Vitamin C | Supports the skin barrier through collagen production, ceramide synthesis, and offers antioxidant protection | Citrus fruits, bell peppers, strawberries, broccoli, guava, tomatoes, et cetera. |
| Vitamin E | Reduces oxidative stress and inflammation | Nuts (almonds, hazelnuts), seeds, vegetable oils, spinach |
| Vitamin A | Supports skin cell differentiation and barrier integrity. It boosts Treg cells and inhibits inflammation | Carrots, sweet potatoes, leafy greens, liver, orange/yellow vegetables |
| Zinc | Mediates cellular growth, proliferation, and regeneration along with anti-inflammatory properties | Meat, shellfish, legumes, nuts, seeds, whole grains |
| Iron and copper | The evidence is not strong enough to define their roles clearly | Iron: Red meat, legumes, leafy greens; Copper: seafood, nuts, seeds |
| Selenium | It provides antioxidant protection | Brazil nuts, fish, eggs, sunflower seeds, seafood, brown rice, whole wheat |
| Magnesium | Deficiency associated with a heightened inflammatory response | Green leafy vegetables, whole grains, legumes, fish, dark chocolate |
| PUFA | Help maintain lipid barrier integrity and have anti-inflammatory effects | Fatty fish (salmon, mackerel), flaxseed, walnuts, evening primrose oil, borage oil, flaxseeds, chia seeds, nuts |
| Prebiotics and probiotics | Promotes growth of Bifidobacterium and Lactobacillus in gut | Prebiotics: (Galacto-oligosaccharide) Human breast milk, (Fructo-oligosaccharides) onion, garlic, banana, asparagus, wheat Probiotics: Yogurt, fermented foods, or specific probiotic supplements |
AD: Atopic dermatitis, AMP: Antimicrobial peptides, PUFA: Polyunsaturated fatty acids
MATERNAL DIET DURING PREGNANCY
Maternal nutrition and dietary diversity are important aspects in the development of a child. Numerous studies have highlighted the importance of the first 1000 days post conception, which have their impact on the development of various allergic conditions.[41] The colonization of the gut, airways, and skin by beneficial microbiota during the initial life plays a crucial role in determining susceptibility toward various immune-mediated disorders later in life.
Dietary guidelines from various countries, such as Australia, Germany, and the United Kingdom, recommend the inclusion of fatty fish in the maternal diet.[42] A study conducted by Beckhaus et al. showed that supplementation of the maternal diet with Vitamin C, D, and E decreased the incidence of wheezing in early childhood, but their protective effect did not extend to other allergic conditions.[43] A systematic review conducted in 2019 reported no significant association between maternal diverse Mediterranean diet and atopic outcomes in offspring.[42]
These findings highlight the requirement for further studies to better elucidate the association between maternal dietary intake and long-term allergic disease risk outcomes in children.
ROLE OF FORMULA FEEDING
Several specialized formula feeds, such as elemental cow’s milk formulas, soy-based formulas, and hydrolyzed cow’s milk formulas, are frequently prescribed to prevent allergic conditions in infants. However, the effectiveness of these in the prevention of allergy remains inconclusive. Various studies have been conducted on both partially and extensively hydrolyzed protein formulas to investigate their role in reducing the risk of allergic conditions. However, findings from two RCTs indicated no significant difference in outcomes between these two. Contrastingly, Oldaeus et al. reported a lower incidence of AD in infants fed with casein-based hydrolyzed formula as compared to those who received standard cow’s milk formula.[44]
ROLE OF EXCLUSION DIET
Dietary food allergens have been found in breast milk, peanuts, eggs, and cow milk protein. Several previous AAP publications have advised lactating mothers with infants at high risk of developing AD to avoid peanuts, tree nuts, eggs, cow’s milk protein, and egg from their diet. However, it was summarized in the Cochrane review 2006 that there is no protective effect of a maternal exclusion diet (including cow’s milk and egg) during pregnancy on the development of AD in infants. In a recently published study from Kerala, patients were randomized into 2 groups. Group 1 was instructed to avoid milk, egg, and related food products for three weeks, while Group 2 was advised to consume cow’s milk and eggs during the same period. In the following three weeks, all participants resumed their regular diets, with the interventions crossed over between the groups. The difference in mean SCORAD and mean absolute eosinophil count was not statistically significant.[44] Although food elimination is beneficial in one subset of AD, it has its own risks. It may lead to nutritional deficiency, delayed growth and development of the child, social isolation, and the risk of anaphylaxis following reintroduction of restricted food.[45] Food allergies usually decrease with age, except for nuts. This may be due to the immunological tolerance to restricted food when reintroduced to the diet after restriction for 6–12 months.[46] It is also important to ensure that complementary foods rich in nutrients are added to the diet if an elimination diet is followed. It is also recommended that children under five years with intractable AD should be tested for food allergies, and then, the exclusions should be made accordingly.
CONCLUSION
The role of diet and nutrition in AD is like a double-edged sword. Careful considerations must be made regarding the exclusions and supplementations by the healthcare provider, and this approach should be customized according to the patient’s health, disease activity, availability of food items, and social practices. Parents should be counselled about the risks of food elimination, correct supplementation, and the myths about various dietary practices.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent is not required as there are no patients in this study.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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