Controversy of food impact on eczema: some evidence from the research

eczema-foodsLately, I’ve frequently found myself digging into a myriad of medical references published in peer-reviewed journals and available on PubMed looking for the evidence of assertions we know to be true in functional medicine.  Spurred by what seems to be a challenge by conventional peers (physicians not practicing from a functional medicine framework), my goal is to collect and present data to them to disarm the seemingly hostile denial that there is a link.  The latest challenge has come in the form of the connection between diet and eczema, also known as atopic dermatitis.  From a functional medicine perspective, we know that an allergy like reaction to foods can be mediated both by IgE (histamine based immune response) AND IgG mediated immune response (a delayed hypersensitivity reaction).  Below is a review article discussing the evidence for the impact of diet on atopic dermatitis.

Though atopic dermatitis is frequently seen in young children, similar allergy-like responses, such as hives can start at any time in one’s life even well into adult hood as a response to inflammatory reactions to foods in the presence of leaky gut.  The scope of this article limits the discussion of these details, but bottom line is, consider food reactions in the case of chronic or recurring itchy skin rashes.  Some of the most common culprits are dairy, eggs, gluten, soy and peanuts.  An elimination diet of a removing all of these foods simultaneously for a minimum of 4 weeks is a good place to start to see how food may be playing a role in your or your child’s skin rash.

Lastly, there is also some evidence that supplementing with specific probiotics can help reduce symptoms of eczema in children.  That article can be found here:

Excerpt about atopic dermatitis (eczema) included below.

From PubMed article:
Year : 2010 | Volume : 76 | Issue : 2 | Page : 103-115
Diet in dermatology: Revisited

Sowmya Kaimal, Devinder Mohan Thappa
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry – 605 006, India

Role of diet in AD

Diet in dermatology: Revisited

Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry – 605 006, India

The role of diet in the cause and treatment of AD is very controversial. Pediatricians and allergologists are convinced of the causative role of food in the onset of AD, while dermatologists are convinced of the contrary. [6] Arguments in favor of the role of diet in AD include the fact that some foods provoke AD, an elimination diet can heal AD, diet manipulation can prevent allergy in newborns at risk for atopy, presence of specific serum immunoglobulin (Ig) E for food allergens (positive radioallergosorbent test [RAST]), positive prick tests to foods and the presence of intestinal mast cell degranulation and IgE, tumor necrosis factor (TNF)-a, eosinophil chemotactic protein and alpha-1 antitrypsin (a1-AT) in the feces. The corresponding arguments against the hypothesis that foods aggravate AD are the fact that AD can persist despite elimination diets and diet manipulation can delay but not prevent allergy in newborns at risk for atopy, positive RAST and prick test results may be irrelevant or unrelated to AD and gastrointestinal symptoms are absent in spite of the presence of various proinflammatory cytokines in the feces. [6]

The mechanisms of aggravation of AD by food are:

  • Increased binding of antigen to immature gut microvillus, along with increased intestinal permeability in small children (and AD), can initiate and perpetuate prompt immune responses in atopic patients with primarily altered antigen transfer. [7]
  • The role of pathogenic bacteria in the gut may be similar to the role of Staphylococcus aureus in the skin of AD patients, both as an infectious agent as well as a super antigen. [8]

Clinical features of food allergy

Clinical manifestations of food allergy can remain localized at the site of the primary direct contact, i.e. the oropharynx (oral allergy syndrome) or the gastrointestinal tract (isolated gastrointestinal food allergy); however, after ingestion, resorption and hematogenous transport of food allergens to the various target organs, other symptoms can occur. The skin is the most frequently affected organ. The spectrum of cutaneous adverse reactions to food includes urticaria and angioedema, induction or flare of AD, contact urticaria, protein contact dermatitis and allergic contact dermatitis. Non-dermatologic manifestations of food allergy include vomiting, diarrhea, abdominal pain, rhinitis, asthma and, also, anaphylaxis. [9]

The most common manifestation is acute urticaria (with or without angioedema), accounting for 40-60% of patients with IgE-mediated food allergy. In the case of pruritus, erythema or urticaria, the subsequent scratching can worsen the skin conditions and exacerbate pre-existing AD (dual reaction). Worsening of the eczema occurring 6-48 h after food provocation without an immediate reaction is rarely observed (late reaction). The pathogenesis of such late reactions is unclear. Among the mechanisms discussed are a late phase, IgE-dependent mechanism with formation of leukotrienes and other substances of the arachidonic acid cascade, a type III reaction with circulating IgE or IgG immune complexes that activate the complement system and delayed-type hypersensitivity mediated by T cells and activated eosinophils. [9] The role of food allergy in the pathogenesis of AD is still controversial; however, there is no doubt that, particularly in infants and young children, food allergens can induce AD or aggravate skin lesions. In adults, food allergy as a cause or a trigger of AD is very rare. However, in food-allergic patients with AD, the ingestion of the food item can provoke the whole spectrum of IgE-mediated symptoms, from oral allergy syndrome to severe anaphylaxis. [9]

Food allergy plays a role in 20% of children under the age of 4 years with AD. A direct effect on eczema is observed in four of 10 children with AD and proven food allergy. [10] Ninety percent of food allergy is caused by six foods such as wheat, milk, soy, fish, eggs and peanut. [11]

Evaluation of food hypersensitivity

It is very important to use appropriate procedures to evaluate food hypersensitivity. Misdiagnosis of food allergy and implementation of highly restrictive diets can lead to severe malnutrition. The methods of testing to confirm food allergy are the skin prick test, skin application food test (SAFT), RAST and the oral challenge test. The skin prick test is the test of first choice for investigating immediate IgE-mediated reaction. The SAFT has been developed by Oranje et al. on the basis of the mechanism of the contact urticaria syndrome. [12] In the SAFT test, the food, in the same state as it is consumed, is applied on the back of the patients using large Finn chambers and the test is read after 10, 20 and 30 mins. Skin tests may be performed with commercially available extracts of foods or fresh foods, although fresh foods give a better result and are preferred. Ideal and final proof of the diagnosis of food allergy is obtained only by (double-blind and placebo-controlled) oral challenge. However, the SAFT is a reliable and child-friendly skin test for evaluating (suspected) food allergy in children younger than 4 years with AD. [13]

Dietary interventions in AD

A recent Cochrane review of nine randomized controlled trials of food allergy in patients with AD showed that there appears to be no benefit of an egg and milk-free diet in unselected participants with atopic eczema. [14]

There appears to be little benefit in eliminating cow’s milk from the diet or using an ‘elemental’ (liquid diet containing only amino acids, carbohydrates, fat, minerals and vitamins) or ‘few foods diet’ for improving atopic eczema in people who have not undergone any form of testing (for specific IgE to food allergens). There may be some benefit in using an egg-free diet in infants with suspected egg allergy who have positive specific IgE to eggs. This is important, particularly since some children with AD show impaired physical development, secondary to gastrointestinal involvement. Although strict elimination diets may be impractical, there is evidence to show that a strict antigen avoidance regimen may be associated with improvement of refractory widespread AD where conventional treatments have failed. [15] Having said this, it must be remembered that a very strict diet can lead to nutritional deficiency.

With regard to preventive diets, high-risk infants may benefit from maternal diet during lactation, although there is no documented beneficial effect of maternal diet during pregnancy. [10]

Treatment of AD can be supported by supplementation of ‘probiotic’ intestinal bacteria. [16] A probiotic is currently defined as a live microbial food supplement with an established beneficial effect on human health. [17]

Probiotics are selected from members of the normal healthy intestinal microbiota, most of them belonging to Lactobacillus or Bifidobacterium. The aims of intervention are to avert deviant microbe development, strengthen the immature or impaired gut barrier function and alleviate abnormal immune responsiveness.

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