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Year : 2021  |  Volume : 22  |  Issue : 1  |  Page : 21-28

Role of Elimination Diet in Atopic Dermatitis: Current Evidence and Understanding

1 Department of Dermatology, KPC Medical College and Hospital, India
2 Consultant Dermatologist, Belle Vue Clinic, Kolkata, West Bengal, India

Date of Submission22-May-2020
Date of Decision09-Jun-2020
Date of Acceptance14-Jul-2020
Date of Web Publication31-Dec-2020

Correspondence Address:
Anupam Das
“Prerana”, 19, Phoolbagan, Kolkata - 700 086, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpd.IJPD_88_20

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Atopic dermatitis (AD) is a fairly common dermatosis of childhood. In many cases, parents are concerned that food allergy plays a role in their child's symptoms and they ask whether practicing elimination diets would help in controlling the symptoms. In this review, we try to provide concise answers to the questions raised by the parents, apart from addressing the myths associated with elimination diets in AD and provide scientific evidence in favor of or against the common notions. A comprehensive English-language literature search for the role of elimination diet in AD across multiple databases (PubMed, EMBASE, MEDLINE, and Cochrane) for keywords (alone and in combination) was performed. MeSH as well as non-MeSH terms such as “AD,” “diet elimination,” “treatment,” “prevention,” “evidence,” “blanket elimination,” and “specific exclusion diet” were taken into consideration. There is level I evidence to support specific exclusion diets in preselected and screened patients, but there is insufficient evidence to recommend strict (blanket) elimination diets.

Keywords: Atopic dermatitis, diet, elimination, evidence

How to cite this article:
Das A, Panda S. Role of Elimination Diet in Atopic Dermatitis: Current Evidence and Understanding. Indian J Paediatr Dermatol 2021;22:21-8

How to cite this URL:
Das A, Panda S. Role of Elimination Diet in Atopic Dermatitis: Current Evidence and Understanding. Indian J Paediatr Dermatol [serial online] 2021 [cited 2021 May 6];22:21-8. Available from: https://www.ijpd.in/text.asp?2021/22/1/21/305818

  Introduction Top

The saga of association of food allergy and eczema dates back to early 20th century case reports of eczema improvement after dietary elimination of specific foods.[1] At the outset, we would like to highlight the subtle differences between food sensitivity and food allergy. Food sensitivity or intolerance is referred to a situation where a patient is unable to digest certain food items and presents with bloating, indigestion, diarrhea and abdominal pain. On the other hand, food allergy is an immunological reaction, wherein multiple organs of the body are affected, often leading to a life-threatening condition. However, it is prudent to accept that this compartmentalization of food sensitivity and food allergy into two different boxes does not hold true in patients with atopic dermatitis (AD). Approximately 40% of infants and young children with moderate to severe AD and 8% of the general population of children will manifest a specific immunoglobulin E (IgE)-based food allergy. Some of the common foods which have been thought to precipitate allergy and AD include cow's milk, egg, gluten, sugar, nightshades, food-coloring agents, food additives, and preservatives.[2],[3],[4],[5],[6] It should be remembered that if someone is allergic to a particular food item, that can trigger the exacerbation of AD and in such situations, avoidance of the trigger leads to improvement of the condition of patients. However, those who do not have a clear allergy to a food item, blanket elimination has failed to demonstrate any significant improvement for these patients.[5],[7]

According to the guidelines from the American Academy of Dermatology (AAD), children younger than 5 years who have intractable AD or known food-induced reactions should be tested for food allergies. As per the guidelines, avoidance of food items is recommended if true IgE-mediated allergy is documented (strength of recommendation: A).[8]

We do not have proper evidence in favor of statistically significant benefits of elimination of cow's milk and eggs from the diet in patient with AD. Some evidence suggests that egg elimination might be helpful in children who are suspected of having allergy to eggs and those who are sensitized to eggs; however, extensive research is needed in this group of children to come to a convincing conclusion.[5] We would like to mention that prolonged elimination diets (which are not clinician-guided) put patients at risk of nutritional deficiencies, apart from actually initiating the phenomenon of “clinical food allergy.”[9],[10]

Food elimination is increasingly common these days. The first documentation of food allergy leading to provocation of AD, dates back to 1915.[11] This cannot be completely ruled out because it is true that food allergy is more common in children with AD-30% of them are affected (in comparison to 4%–10% in the general pediatric population).[12] However, it is to be noted that epidermal barrier dysfunction (the backbone of pathogenesis of AD) might be the initiating step towards penetration of food proteins and subsequent sensitization. Therefore, it would be prudent to mention that AD precedes the development of food allergy, instead of believing that consumption of allergic food items exacerbates AD.

Food allergy reactions may be of two types: immediate and late. Noneczematous IgE-mediated food reactions develop immediately after ingestion of allergic foods, while eczematous reactions are usually thought to be “late events,” occurring 2–6 h after ingestion. Eczematous reactions are encountered less frequently in comparison to noneczematous ones. In 1983, Sampson demonstrated the role of food allergies in eczema with double-blind placebo-controlled food challenges (DBPCFC).[13] It is to be noted that clinically relevant food allergy does not have a good correlation with history and reporting by the parents. In most of the cases, the eczematous reactions (late onset) are inappropriately correlated with food intake by the parents. Sicherer and Sampson reported in 1999 that one-third of children with AD reacted to food allergies.[14] This was corroborated by an interesting study conducted on 64 children with AD who visited a German OPD, where in the positive predictive value (PPV) of parental history for immediate reactions was found to be 85%. On the other hand, PPV for eczematous reactions was only 33%.[15] Thus, in the first half of 2000s, standard texts suggested: “A rational approach in evaluating children with AD and suspected food allergies is to screen them using skin-prick test for the most common offending foods, including eggs, milk, soy, wheat, fish, peanut, walnut (or cashew), and selected foods as suggested by history.”[16]

Isolated eczematous reactions, in the absence of an immediate reaction, are very uncommon in patients with AD. In a study by Rowlands et al., only one eczematous food reaction was observed amongst a total of 58 DBPCFC.[17] In another study by Breuer et al., 64% of the children were reported to have a positive reaction to at least one type of food, but isolated eczematous reaction (in the absence of immediate reaction) was documented in only six per cent of all challenges. A combination of immediate type reaction followed by eczematous reaction was observed in 21% of the challenges.[15] Another study by Celik-Bilgili et al. found reported that 45% of the challenge attempts culminated in a clinically relevant allergic reaction, but again, an exclusive eczematous reaction was observed in only six per cent of all challenges, and combined reactions were observed in seven per cent only.[18]

For better understanding, we discuss the evidences in favor of/against dietary elimination under the following sections:

  1. Role of specific exclusion diets
  2. Role of general elimination diet
  3. Role of tailored elimination diet
  4. Role of strict elimination diet
  5. Role of calorie restrictions and other dietary interventions.

  Role of Specific Exclusion Diets Top

Cow's milk and eggs have been anecdotally found to be the two food items which are blamed to be responsible for childhood allergies, and therefore, these have been the easy targets when it comes to elimination diets (irrespective of history of allergy). The role of elimination of cow's milk and eggs from the diet in the management of AD remains elusive.

In a study by Armenio et al., two demographically similar groups of children with AD (78 and 84 patients) were placed on an egg-and cow's milk–free diet (followed by a general elimination diet for those who did not respond to the initial diet), and it was found that 53% of children in the first group and 27% in the second group had statistically significant improvement in clinical severity scores with either of the diet strategies.[19] Another study was conducted on 59 children (4-week elimination diet of cow's milk, eggs, or both), wherein, clinical improvement was noted in 80% of the patients.[20] In a double-blind randomized controlled crossover trial by Atherton et al., patients were put on a 4-week washout period with a normal diet, followed by a 4-week trial of the intervention (soymilk substitute or placebo). The authors observed that empirical elimination of milk and egg in children with eczema resulted in improvement in 14 out of 20 patients and thus, concluded that dietary manipulation can play a role in the treatment of AD. The study also concluded that skin prick tests do not provide information of therapeutic relevance.[21]

In another double-blind randomized controlled trial (RCT) with a crossover phase, 40 patients completed a 6-week egg and cow's milk exclusion diet with soy substitute.[22] There were no statistically significant differences in skin area affected, itching, or topical steroid use between the treatment diet and normal diet or control diet. It was concluded that exclusion diets can provide negligible benefit in unselected children. In an open pilot study conducted by Dhar and Banerjee, patients were advised to strictly adhere to a diet excluding milk and milk products, all kinds of nuts and nut-containing foods, egg and egg-containing foods, sea fish and prawns, brinjal, and soybean for a period of 3 weeks. A statistically significant reduction in AD severity score was noted, after dietary elimination alone.[23] A 2008 Cochrane review (which included 9 randomized controlled trials) on egg and cow's milk exclusion, however, did not support the use of dietary eliminations. The review categorically mentioned that there is no additional prolonged benefit of excluding cow's milk or eggs from the diet of children with AD.[24] Thus, the Expert Panel of the 2010 National Institute of Allergic and Infectious Diseases guidelines for the management of food allergy acknowledged the controversy of whether food allergy can exacerbate AD, and the lack of high-quality evidence to support elimination diets in the management of AD.[25] It is worth recalling here that as early as in 1976, May had reported that in patients with eczema demonstrating sensitization to foods with positive skin tests, food challenges to these foods were often negative, indicating the poor specificity of food testing in patients with eczema.[26]

In a study by Aoki et al., an egg elimination diet was prescribed for 213 patients younger than 3 years and their breastfeeding mothers in egg-allergic and nonallergic children determined by a positive (RAST) Radioallergosorbent test or (SPT) Skin Prick Test. Clinical improvement was significantly associated with egg allergy in the 3-to 6-month-old cohort that was breastfeeding.[27] One of the studies reported benefit in egg-sensitized infants, when treated with an egg exclusion diet for 4 weeks.[28] In another single-blind crossover RCT (amino acid–based elemental formula vis-à-vis cow's milk–based formula), authors did not find any statistically significant difference in AD severity score, and global health scores during the active or placebo phase.[29]

In a recently published controlled crossover study from Kerala, patients (1–15 years of age) were randomized into trial period (egg and cow's milk exclusion diet) or control period (egg and cow's milk inclusion diet). Patients in the trial arm were advised to avoid milk, egg, and all food items containing milk and egg for 3 weeks, and those in the control arm, were to take egg and cow's milk daily for 3 weeks. In the next 3 weeks, patients resumed their normal diet to minimize any carryover effect. In the last 3-week period, the arms (trial and control) were crossed over. The difference in mean SCORAD and mean absolute eosinophil count was statistically not significant. The authors could not confirm the beneficial effects of an allergen avoidance diet in AD, reiterating the fact that elimination of diet has poor scientific evidence in the management of AD.[30] Similar to the results of a systematic review,[31] this Indian study pointed out that AD precedes the development of food sensitization and allergy. Moreover, findings from another two trials suggest that dietary elimination of cow's milk in patients with a positive DBPCFC improves AD.[32],[33]

  Role of General Elimination Diet Top

A general elimination diet (all food items being eliminated except for a predetermined set of 12–20 foods generally suspected to be hypoallergenic (e.g., lamb, chicken, rice, carrots, potato etc.) is commonly employed because of the ease of implementation. In a study by Caffarelli et al., general elimination diet led to reduction of AD severity score in approximately 70% in 60% of patients.[34] In another study by Van Asperen et al., a 2-week elimination diet showed statistically significant improvement in mean itch score and total area affected by eczema.[35] However, we would not recommend general elimination diet, because of the small sample size in aforementioned trials, apart from fallacies in the study design.

  Role of Tailored Elimination Diet Top

Identification and elimination of the suspected food items has its own advantages by providing the patients, a degree of dietary freedom. Moreover, this seems to be more rational and practical. A 3-year prospective study of 100 children with AD had positive results with an elimination diet based on positive DBPCFCs.[36] There was statistically significant improvement in mean SCORAD scores, apart from reduction in mean topical corticosteroid use and total serum IgE levels. In another study, tailored elimination diets resulted in moderate to marked improvement in 40 of 44 patients.[37] The results were similar to another trial, where a tailored elimination diet based on history and SPT resulted in statistically significant improvement in clinical skin scores in 49 of 66 patients who completed the trial.[38] Based on the evidences, and the glaringly positive results of these studies, the trend of advising tailored elimination diets as a treatment for AD, has become popular.

  Role of Strict Elimination Diet Top

In this section, we touch upon two extreme forms of diet namely, six food diet and few foods diet. The Six Food diet permits only six foods for consumption, and the Few Foods diet may consist of anywhere from 1 to 19 foods (with most ultimately including 5–9). In both, permitted foods are selected from a list of foods which are thought to be hypoallergenic (similar to general elimination diets). Elemental diets lie on the furthest end of this spectrum, comprising of the essential components of foods, i.e., amino acids, glucose, vitamins, minerals, and oils. Some of the trials have shown positive results, but smaller sample size and lack of a control group, questions the external validity of the results of the study.[39],[40],[41],[42] On the other hand, unsatisfactory results were found in some of the other studies, which were again flawed, in terms of methodology and study design.[43],[44],[45] To summarize, on account of lack of properly designed trials, we do not recommend strict elimination diets as a strategy in the management of AD.

  Role of Calorie Restrictions and Other Dietary Interventions Top

It is believed that calorie restriction can lead to improvement of AD, because undernutrition (without malnutrition) can have a beneficial effect on inflammatory disorders including AD. The results of some of the studies and isolated case reports look promising and encouraging, but the poor quality of the study design limit our ability to draw a conclusion in favor of calorie restriction as a therapeutic option in AD.[46],[47],[48]

Moreover, relationship between metal sensitivity and the etiology and aggravation of AD is yet to be clearly described. Some of the studies evaluating the role of low-metal (nickel) diets show promising results and we believe that low-metal diets in those with metal allergies may be an area worthy of future investigation.[49],[50]

  Investigations Top

Some of the routine investigations advised in patients with suspected food allergies and AD is IgE levels (and skin prick tests). We would like to firmly state that positive results of so called “allergy tests” in children with AD might not have any clinical relevance at all. It is to be noted that approximately 80% of children with AD have elevated food-or pollen-specific IgE levels, but; hardly 35%–40% of these children will have clinical signs and symptoms of food allergy (as documented by double-blind, placebo-controlled food challenge studies).[51] The negative predictive value of serum-specific IgE levels and skin-prick test results in excluding food allergy is higher than 95%, but the PPV for diagnosing food allergy is 30%–50% for skin-prick tests and 20%–60% for food-specific IgE levels.[12] The aforementioned numbers clearly indicate the fallacies of falling for these “allergy tests.” Together, serum IgE and skin prick tests can confirm sensitization to an allergen, but neither alone can reliably ascertain a food allergy.

Estimation of IgA and IgG have been often used as surrogate markers of food allergy, but evidence suggests that IgG and IgA levels do not have a good correlation with the clinical parameters of AD.[52] Estimation of levels of serum eosinophil and eosinophil cationic protein has been attempted, but results have not found to be of clinical significance.[12]

We would strongly recommend that double-blind, placebo controlled oral food challenge should be considered as the gold standard investigation for diagnosis delayed eczematous reactions.[10],[53] Ideally, patients who do not respond to first line therapy in AD (emollients and anti-inflammatory drugs) should be evaluated for identification of triggering factors (including allergies). The panel of investigations includes IgE-mediated allergies (serology and skin prick test) and delayed-type hypersensitivity allergies (patch test). If certain food items are tested to be positive, they should be strictly eliminated from diets. However, if there is no conclusive evidence (positivity) of allergy, sequential elimination of food items may be done (one at a time and for a limited period of time before being introduced into the diet).[54]

  Risk of Elimination Diets Top

Blanket elimination of food items in suspected cases of food allergy, can lead to some unwanted consequences. In most of the cases, parents tend to eliminate plenty of food items (in the absence of a recommendation from clinician) and eventually, the children land up with nutritional deficiencies. If dietary restriction is initiated in pregnancy, reduced birth weight of babies can be a complication.[55] In an interesting series reported by Liu et al., 12 cases of kwashiorkor in children (1–22 months of age) were reported in 7 tertiary referral centers across the United States.[56] Christie et al. documented that 25% of children on strict elimination diets, actually consume <67% of the recommended daily intake of vitamins and minerals including calcium, phosphorus, iron, Vitamin K, Vitamin D, zinc, Vitamin A, B1, B2, B6, niacin, cholesterol, and Vitamin C. Moreover, those who eliminated more than 2 types of food were shorter in comparison to those who eliminated only 1 type of food (statistically significant).[57],[58]

Moreover, we should remember that excessive intake of vegetables in individuals with extensive food allergies can lead to development of carotenemia.[59] Protein-restricted diets from use of rice milk or dietary protein restriction can lead to protein energy malnutrition (kwashiorkor and marasmus).[60],[61],[62]

In this context, we would like to mention about an important concept. Early low-dose cutaneous exposure to food allergens leads to allergic sensitization, and early oral consumption of food proteins induces immune tolerance. This is referred to as “dual allergen-exposure hypothesis.” Tolerance pathways in sensitized individuals seem to require continued consumption of the food allergen. Avoidance may result in the loss of tolerance and increase the risk of developing immediate-type hypersensitivity to the avoided food.[63] Over the past three decades, there have been multiple reports of children with AD managed on elimination diets, whose clinical reaction patterns to the foods they were avoiding changed from exclusive dermatologic symptoms to severe IgE-mediated reactions including anaphylaxis, with one report of fatal anaphylaxis.[64],[65],[66],[67] It is to be remembered that prolonged elimination of food items from diet might actually lead to clinically relevant food allergy in future. In a double-blind, placebo-controlled oral cow's milk challenge conducted by Flinterman et al., 11 children with AD was evaluated. All of them were put on prolonged cow's milk elimination diet. Interesting to note, all the children developed immediate allergic reactions, despite having tolerated cow's milk before elimination; however, none of them were found to develop eczematous reactions.[68]

In a fairly recent study by Chang et al., the main risk factor for the development of new immediate-type reactions to a food was found to be avoidance of that food. The authors concluded that the patients would need anticipatory guidance when these avoided foods are reintroduced into their diets with preparation for possible allergic reactions including anaphylaxis. They hypothesized that instead of complete avoidance of the food, there may be a threshold dose of tolerated food for eczema management that prevents the development of immediate-type food hypersensitivity.[69]

Savage et al. reported a peanut-tolerant 50-year-old female who stopped eating peanut for 3 years because of the peanut-IgE level of 0.69 kU/L, who subsequently experienced lower respiratory tract symptoms on food challenge to peanut.[70] It has also been reported that 8% of peanut allergic children passing oral peanut challenges, who continue to limit peanut consumption, experience relapse of their peanut allergy.[71] It is worthwhile citing the landmark learning early about peanut allergy (LEAP) trial in this regard. The LEAP trial randomized 530 infants (age 4–11 months) to peanut-avoidant vis-à-vis peanut-exposed diets for 5 years. The results showed statistically reduced (1/12th of the risk) peanut allergy even in infants known to be sensitized (approximately 1/3rd of the risk), thus reinforcing the hypothesis that early introduction of food items actually prevents the development of allergic manifestations in the long run.[72] In fact, multiple studies in the past decade show that delayed introduction of foods (milk, egg, wheat, and peanut) increases the risk of developing allergies to those foods.[73] A review of food allergy and AD advises clinical corroboration of food allergy testing with a 4-to 6-week elimination diet followed by office food challenge.[74] Patients with eczema and their families will benefit from more careful monitoring and frequent follow-up, optimized dermatologic management, and from the reassurance that the natural history of pediatric eczema is resolution from age 1–7 years for most children, whereas acquired food hypersensitivities may be long lasting.[75]

  Role of Synbiotics Top

Probiotics and prebiotics have been hypothesized to work by reducing the severity of inflammation in AD, but they have not been recommended in the AAD guidelines. Prenatal and postnatal (maternal and child) supplementation of Lactobacillus rhamnosus has shown promising results.[76],[77],[78]

In the context of elimination of diet, we would like to briefly mention about synbiotics. These appear to be a promising adjunctive therapeutic option in AD. Synbiotics are a combination of probiotics (which contain live, beneficial microbes) and prebiotics (which support the growth of beneficial microbes). In a meta-analysis evaluating the randomized controlled trials of synbiotics in the management of AD, use of these supplements for at least 8 weeks with mixed-strain bacterial species led to a statistically significant improvement in SCORAD index.[79] However, larger studies are required to comment on the specific formulations of prebiotics and probiotics, which can be beneficial to the patients of AD.

Other supplements and interventions have been found to show promising results in murine models include Lithospermum erythrorhizon, Platycodon grandiflorus, Hypsizygus marmoreus, fortified ginseng extract, polyunsaturated fatty acids, and galacto-oligosaccharides.[80],[81],[82],[83],[84],[85]

  Role of Food Additives in Atopic Dermatitis Top

Parents are often found to associate the exacerbation of the disease in their children, to food additives (colorants, sweeteners and preservatives).[86] This question must be addressed appropriately, because carmine and tartrazine have been documented to be associated with AD. Carmine (red dye) is often added as a food colorant to cheese, fruit and vegetable preparations, jams, chewing gum, breakfast cereals, meat products (salami, sausages), processed fish, fishery products etc. Two studies have reported carmine as a cause of intermittent flares of AD in children.[87],[88] Similarly, tartrazine (aniline dye) is added to cheese, canned or bottled fruit or vegetables, soups, processed fish or fishery products, pickles, desserts, sauces, seasonings, etc. It has been frequently linked with recurrent flares of AD in children.[89]

  Role of Diet in Prevention of Atopic dermatitis Top

Keeping in mind, the dysbiosis which is observed in AD, it has been proposed that probiotics may have a beneficial role in the prevention of AD. The mechanism is not clear, but it is thought that probiotics may lead to an increase in the diversity of intestinal microflora, inhibit the attachment of Staphylococcus aureus, inhibit Th2 response, stimulate Th1 response, upregulate regulatory T-cells, and enhance the skin barrier.[90] Recent meta-analyses of perinatal use of probiotics have suggested a diminution of incidence of AD (20%–24%) and a preventative role, especially when the probiotics are given during the last 2 weeks of pregnancy and first 3–6 months of life. However, the long-term effects are not well understood.[91]

Similarly, Pelucchi et al.[92] and Panduru et al.[93] demonstrated a 20%–24% reduction in the chances of development of AD with the use of probiotics (both prenatal and postnatal), particularly Lactobacillus and Bifidobacterium, but long-term benefits are yet to be proven. Moreover, the beneficial role of prebiotics (32% reduction in AD) in early infancy have been documented by the use of galacto-oligosaccharide and fructo-oligosaccharide combination, but long-term data are absent.[94]

  Conclusion Top

According to current evidence, strict dietary elimination is unscientific, irrational and it is not recommended, while avoiding proven food allergens in AD could be permitted in the management of AD in children who are previously sensitized to those food items. The current state of evidence seems to indicate that the acquisition and maintenance of tolerance to foods in atopic children requires both early introduction and continued consumption of those foods. With the increasing evidence that early introduction promotes tolerance in the young child, and that food elimination may result in loss of tolerance with subsequent development of immediate-type food hypersensitivity and anaphylaxis, patients and families need to be aware of the possible unintended consequences of prolonged food avoidance and elimination diets. Avoidance of a particular food should be advised only on the basis of a sound history and diagnosis of food allergy. If there is consistent correlation of food intake and exacerbation of symptoms, a diagnostic elimination diet for approximately 4–6 weeks with the suspected food item may be tried. If there is a significant improvement of the symptoms during the period of elimination diet, a double blind placebo controlled food challenge test should be considered.[95] Those children who are prescribed elimination diets need to be educated on recognizing the signs and symptoms of immediate-type reactions including anaphylaxis, and have available self-injectable epinephrine. Therefore, the role of nutrition counseling in patients with allergy and/or AD holds paramount importance. Until future studies indicate more precise relationships between food allergy, AD and the immunologic pathways determining tolerance and immediate hypersensitivity, clinical decision-making for food elimination diets must be evidence based and err on the side of caution.

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