Updated: Sep 19, 2018
In contrast to popular belief, eczema is not just a 'random' occurrence. It is an external manifestation of a systemic error or dysfunction in the immune system, and can be reversed through appropriate dietary and lifestyle interventions. This article will outline some of the potential underlying root causes of eczema, and then will provide some basic recommendations to support this condition.
Atopic eczema is an inflammatory skin condition characterised by skin barrier dysfunction, lesions, and itching. Interestingly, patients with eczema have frequently been found to have elevated serum immunoglobulin E (Dokmeci & Herrick, 2008). Immunoglobulin E is a type of immune cell involved in allergic reactions, rhinitis, food allergies, and asthma, and around 50% of kids with eczema go on to develop these conditions.
Underlying processes involved in eczema
People with eczema typically exhibit overactive immune responses to external antigens such as environmental chemicals, foods (usually milk, peanuts, eggs, wheat), and inhalants such as mold toxins. Through coming into contact with these substances, there is an excessive release of innate chemicals such as histamine and prostaglandins which are involved in inflammatory processes featured in eczema.
Furthermore, imbalances in the bacteria populating the skin are also found in eczema. Healthy skin is ordinarily populated by a wide variety of different species of bacteria, and these help to maintain the skin barrier whilst fighting off pathogenic organisms. However, imbalances in these bacteria can lead to problems. Two kinds of bacteria involved in eczema are Staphylococcus Aureus and Staphylococcus Epidermis. When there are overgrowths in these bacterial species, they release toxins called "enterotoxins" which can contribute to the inflammation in these cases (redness, itching, scaling).
The digestive tract is filled with bacteria, and these are extraordinarily important for maintaining overall health. They help to regulate the immune and nervous systems, facilitate proper digestion, absorption, and excretion of nutrients, and also protect the body against pathogenic infection (amongst many other things). Healthy people have been shown to have great diversity in gut bacteria, whilst practically every disease is correlated with lower diversity and overabundance in certain pathogenic strains.
It turns out that people with eczema have consistently been shown to have lower diversity in their gut bacteria (Wang et al., 2008). Systemic antibiotic use, which disrupts the gut bacteria, is also strongly correlated with eczema development (Tsakok et al, 2013).
Skin alkalinity and external chemicals
The skin should ideally be relatively acidic. This acidity helps maintain the health of the skin. Elevated skin pH is present in eczema, which means that it becomes more alkaline than usual.
Throughout our evolutionary history, the skin did not evolve with exposure to the vast quantities of the chemicals we come into contact with. Environmental agents such as soap and detergents increase skin pH and emulsify surface lipids, and therefore may contribute to barrier dysfunction that is found. Exposure to wifi and mobile-phone radiation has also been shown to disrupt the bacteria living on the skin, and for more information you can read THIS article.
Potential causes of eczema
Defective histamine metabolism and "histamine intolerance"
Elevated plasma histamine concentrations (Ionescu and Kiehl, 1988) found in eczema potentially indicate the presence of “histamine intolerance”, a condition characterised by poor histamine metabolism resulting in excess histamine. Symptoms of histamine intolerance might include:
headaches or migraines.
nasal congestion or sinus issues.
irregular menstrual cycle.
One enzyme responsible for effective histamine degradation is called diamine oxidase (DAO). Reduced DAO activity can contribute to histamine elevations (Maintz and Novak, 2007), which may exacerbate eczema symptoms (Worm et al., 2009). Indeed, reduced serum DAO was reported in a subpopulation of people with eczema (Maintz et al., 2006).
Testing for serum DAO activity may be a useful diagnostic marker for histamine intolerance (Music et al., 2011). Despite this, DAO activity is normal in some symptomatic patients (Pinzer et al., 2017), indicating that the clinical utility of this test may be of limited value. In addition, high interassay variability was found (Schnoor et al., 2013), suggesting poor reliability of test results.
Another factor implicated in impaired histamine metabolism is gut dysbiosis. The amino acid L-histidine (found in dietary proteins) is converted into histamine by certain strains of gut bacteria (Thomas et al., 2012) which wer efound to be elevated in atopic conditions (Barcik et al., 2016). When your gut bacteria produce excess histamine, this can be absorbed and contribute to the overall histamine load.
Lower bacterial diversity, moderate gut inflammation, and dysbiosis are also associated with eczema (Zheng et al., 2016). Broad-spectrum antibiotic exposure can reduce microbial diversity in the gut, and lower bacterial diversity is associated with immune dysfunction (Langdon, 2016). Furthermore, early life exposure to antibiotics was found to increase the risk of developing eczema by 41% in one study (Tsakok et al., 2013).
Together, these findings support a link between imbalanced commensal flora and eczema pathogenesis.
Comprehensive stool analysis testing may be utilised in this context to help identify dysbiosis and guide further therapeutic intervention. Genova Diagnostics’ “GI Effects” test appears suitable for this purpose.
Food intolerance and immune system dysfunction
Zonulin is a protein responsible for modulating the "leakiness" of the gut. One primary trigger of zonulin release gliadin, a protein found in cereal grains. Leaky gut may lead to immunoglobulin-G (IgG) mediated food hypersensitivities, which can result in elevated pro-inflammatory cytokines and immune system dysregulation (Karakuła-Juchnowicz et al., 2016). Elevated zonulin levels (Sheen et al., 2018), leaky gut (Rosenfeldt et al. 2004), and gliadin (gluten) IgG antibiodies (Finn et al., 1985) have all been reported in patients with eczema, suggesting that food sensitivities may be implicated.
T-regulatory immune cell (Treg) homeostasis in the gut is also influenced by resident gut flora (Zeng and Chi, 2015). Tregs are responsible for maintaining immune tolerance and modulating immune system. Research suggests that gut dysbiosis (imbalance of gut bacteria) may contribute to immune dysfunction (Levy et al., 2017), a characteristic feature of eczema
Vitamin D and A deficiency
Another important factor governing immune cell function is vitamin D. Vitamin D promotes regulatory immune cell differentiation, reduces skin inflammation, and may directly regulate circulating IgE (immune cells involved in inflammation) levels (James, 2016).
Patients with eczema were shown to have low serum vitamin D levels (Pacheco-Gonzalez et al,. 2015), and sunlight exposure, which facilitates vitamin D synthesis, is inversely correlated with symptom flare-ups. Additionally, for vitamin D to promote immune system regulation, it needs access to enough vitamin A.
Eczema patients were found to have reduced vitamin A in both affected and non-affected skin sites (Mihály et al., 2011). Jointly, these findings point to potential vitamin D and vitamin A deficiencies driving eczema.
Serum vitamin is a cheap and easily accessible test for the general public, and is considered the best biomarker of vitamin D status in most individuals (Jones, 2014).
Involved in immune cell differentiation, wound healing, and maintaining epidermal barrier integrity.
Blood cell zinc deficiency is positively correlated with eczema severity (Karabacak et al., 2016).
Exerts an antagonistic effect on zinc, and excess copper may negatively impact zinc status.
Patients with eczema were found to have imbalanced copper-zinc ratios (Hon et al., 2010).
Heavy metal toxicity
Additionally, exposure to heavy metals including lead and mercury is also a risk factor for ezema (Hon et al., 2010). Both metals can exert pro-inflammatory, cytotoxic, and immune-disrupting effects, and serum levels or mercury and lead are positively correlated with symptom severity in eczema (Weidinger et al., 2004).
To test the above minerals and metals, I would opt for Quicksilver Scientific’s “Blood Metals Panel”.
Chemicals found in cosmetic and personal care products containing fragrance and cinnamic aldehyde are common triggers for hypersensitivity reactions, and sodium lauryl sulfate found in shampoos and soaps was found to induce dose-dependent transepidermal water loss, a characteristic feature of eczematous lesions (di Nardo et al., 1996). Preservatives including formaldehyde, parabens, and isothiazolinones are associated with inflammation and skin itching in sensitive individuals (Overgaard et al., 2017). Phthalate exposure can trigger thymic stromal lymphopoetin, an inflammatory cytokine secreted by barrier defective skin. High urinary phthalate levels were found in children with eczema, and maternal exposure to phthalates during pregnancy also increases the risk of disease development (Braun and Sathyanarayana, 2013). Hence, environmental toxicity and plastic exposure may be a big problem for many individuals.
Potential solutions supported by research
Research implementing dietary approaches for improving eczema has produced positive results in many cases:
A two-week “low histamine diet”, excluding high histamine containing foods such as fish, cheese, and fermented products, significantly reduced symptoms in a subgroup with low serum diamine oxidase activity (Maintz et al., 2006). However, this was only effective for people with an established issue with diamine oxidase, so it would probably not be applicable for everyone.
In addition, exclusion of other dietary allergens (mainly eggs, dairy, and wheat) has also produced positive results in the majority of research. The following table provides a brief summary of the evidence base:
Vitamin E supplementation
Daily doses of 400 IU for eight months was beneficial in 50% of subjects, along with reduction of IgE antibodies and almost complete remission in 15% (Tsoureli-Nikita et al., 2002).
Another four month trial administering the same dosage reported symptomatic improvement in 70 individuals for the entirety of the four month study along with no adverse reactions (Faghihi et al., 2015). However, discontinuation led to a recurrence rate similar to the placebo group after three months, which suggests that long-term intervention may be required in this context.
Additionally, one trial tested the efficacy of supplementation with vitamin E, vitamin D, and a combination of both (Javanbakht et al., 2010). The groups treated with individual vitamins both showed a 35% symptomatic improvement. However, the combination of both provided an overall 65% improvement in all measures, suggesting that supplementation with the combination may be more effective.
Supplementation for one month achieved 80% reduction in symptoms compared to 17% for placebo (Sidbury et al., 2008).
Similar results were reported in a larger study involving 107 subjects (Camargo et al., 2014), whilst another randomised control trial also demonstrated improvements in the majority of subjects (Salehi and Amestajani, 2012).
One earlier meta-analysis reported no significant changes (Boyle et al., 2008), whereas a later one found minor benefits in moderate-severe cases (Michail et al., 2008). Moreover, recent larger meta-analyses concluded that probiotics significant improved symptoms in both children and adults (Kim et al., 2014).
In animal research, quercetin was shown to inhibit Th2-related cytokine expression, relieve lesions, and reduce serum IgE and angiogenesis (Jung et al., 2010).
In-vitro data found quercetin to be more effective than cromolyn, a common pharmaceutical treatment for eczema, at inhibiting histamine, prostaglandin D2, and other pro-inflammatory cytokines (Weng et al., 2012).
A recent human clinical trial in 52 patients involving 2g quercetin daily attenuated symptoms and decreased inflammation (Mehrbani et al., 2015).
Topical coconut oil application was shown to be effective at decreasing S.aureus skin colonisation (Verallo-Rowel et al., 2008), and improving skin capacitance, severity values, pruritis, and transepidermal water loss (Evangelista et al., 2014).
Application of aloe vera gel may also reduce Th2-induced inflammatory responses in chronic eczema (Finberg, Muntingh and van Rensburg, 2015).
Matricaria flower extract demonstrated similar anti-inflammatory activity to that of 0.25% hydrocortisone in eczematous lesions (Shadi and Talal, 2015). Additionally, matricaria flower cream was superior in reducing itching, redness, and desquamation (Shadi and Talal, 2015).
Basic protocol for supporting eczema
People are individual, and so black-and-white fixed approaches cannot be applied to every different person. For example, whilst one factor may be causing symptoms in one person, it may be something entirely different in another person. This highlights the fact that biochemical individuality is key, and why testing can be useful in identifying each individual's requirements.
Approaching a condition like eczema from a functional medicine perspective involves investigation (via testing) and personal experimentation to see what actually works. However, rough overview of how I might approach this condition follows: I would focus on removing common potential allergens, reducing inflammation, and supporting immune system regulation.
Dietary exclusion of gluten-containing grains and cow’s dairy products for at least four weeks: Anti-gliadin IgG antibodies, as were found in eczema patients, commonly present alongside cow’s dairy-related anti-casein IgG antibodies (Vojdani and Kharrazian, 2013). Since IgG-mediated food sensitivities may contribute to intestinal leaky gut and immune hyper-reactivity, gluten and dairy consumption in sensitive individuals could theoretically contribute to eczema. Hence, temporary dietary exclusion may be merited.
Probiotic supplementation: Research on probiotics has gone through a rapid global expansion in recent years (Sanders, Shane and Merenstein, 2016), and supporting evidence for their use in eczema has grown with more recent publications. Probiotic-rich foods such as coconut kefir, kombucha, sauerkraut and kimchi should experimented with taken daily. However, symptoms should be monitored closely because some probiotic strains like Lactobacillus casei are histamine-producing (Thomas et al., 2012), and may therefore be problematic in individuals with poor histamine metabolism. If probiotics were not tolerated, they could be replaced with specific strains like Lactobacillus Plantarum which are capable of histamine degradation.
Optimise vitamin D status through dietary intake and sunlight exposure: Rich dietary sources including oily fish, pasture-raised eggs, and offal (Schmid and Walther, 2013) should be consumed liberally. These foods are also rich in zinc, which may improve eczema symptoms in those individuals who are insufficient. Skin sunlight exposure is the most efficient method of improving vitamin D status (Wacker and Holick, 2013), and at least fifteen minutes is required to maintain optimal levels (Hartley et al., 2015). However, since the UK latitude does not permit vitamin D synthesis throughout autumn and winter (Webb et al., 2018), supplementation at with at least 1600IU cholecalciferol may be advised depending on individual test results.
Optimise vitamin E status: Supplementation with 400IU/day may be suitable, along with increased dietary intake through consuming foods such as spinach, beets, avocado, and raw peppers. These ingredients could be incorporated into salads that can be eaten daily.
Quercetin supplementation: Two grams daily might be trialled for a 4 week period.
Finally, reducing exposure to heavy metals and synthetic cosmetics, personal care products, and other chemical sources is advised. Adherence to a diet of exclusively organic whole foods may minimise consumption preservatives and metal-containing pesticides. Avoiding consumption of large mercury-contaminated fish such as tuna and swordfish may also reduce metal burden (Myers, 2007). Instead, smaller fish like sardines and kippers are viable alternatives. Replacing plastic water bottles, utensils, and food storage with glass alternatives, filtering household water, and avoiding vacuum-packed foods may reduce phthalate exposure. I would also recommend replacement of shampoos and soaps with sodium lauryl sulfate-free, non-synthetic brands. Furthermore, washing the affected skin areas with soap should be minimised to support pH normalisation of the skin (Panther, 2015).
Barcik, W., Pugin, B., Westermann, P., Perez, N., Ferstl, R., Wawrzyniak, M., Smolinska, S., Jutel, M., Hessel, E., Michalovich, D., Akdis, C., Frei, R. and O'Mahony, L. (2016). Histamine-secreting microbes are increased in the gut of adult asthma patients. Journal of Allergy and Clinical Immunology, [online] 138(5), pp.1491-1494.e7. Available at: https://www.jacionline.org/article/S0091-6749(16)30709-6/fulltext#appsec1.4 [Accessed 1 Jun. 2018].
Boyle, R., Bath-Hextall, F., Leonardi-Bee, J., Murrell, D. and Tang, M. (2008). Probiotics for treating eczema. Cochrane Database of Systematic Reviews. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/18843705/ [Accessed 1 Jun. 2018].
Braun, J. and Sathyanarayana, S. (2013). Phthalate exposure and childrenʼs health. Current Opinion in Pediatrics, [online] 25(2), pp.247-254. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23429708 [Accessed 1 Jun. 2018].
Camargo, C., Ganmaa, D., Sidbury, R., Erdenedelger, K., Radnaakhand, N. and Khandsuren, B. (2014). Randomized trial of vitamin D supplementation for winter-related atopic dermatitis in children. Journal of Allergy and Clinical Immunology, [online] 134(4), pp.831-835.e1. Available at: https://www.ncbi.nlm.nih.gov/pubmed/25282565 [Accessed 1 Jun. 2018].
di Nardo, A., Sugino, K., Wertz, P., Ademola, J. and Maibach, H. (1996). Sodium lauryl sulfate (SLS) induced irritant contact dermatitis: a correlation study between ceramides and in vivo parameters of irritation. Contact Dermatitis, [online] 35(2), pp.86-91. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8917825 [Accessed 2 Jun. 2018].
Dokmeci, E. and Herrick, C. (2008). The Immune System and Atopic Dermatitis. Seminars in Cutaneous Medicine and Surgery, [online] 27(2), pp.138-143. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18620135 [Accessed 2 Jun. 2018].
Evangelista, M., Abad-Casintahan, F. and Lopez-Villafuerte, L. (2013). The effect of topical virgin coconut oil on SCORAD index, transepidermal water loss, and skin capacitance in mild to moderate pediatric atopic dermatitis: a randomized, double-blind, clinical trial. International Journal of Dermatology, [online] 53(1), pp.100-108. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24320105 [Accessed 1 Jun. 2018].
Faghihi, G., Jaffary, F., Mokhtarian, A. and Hosseini, S. (2015). Effects of oral vitamin E on treatment of atopic dermatitis: A randomized controlled trial. Journal of Research in Medical Sciences, [online] 20(11), p.1053. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4755091/ [Accessed 1 Jun. 2018].
Finberg, M., Muntingh, G. and van Rensburg, C. (2015). A comparison of the leaf gel extracts of Aloe ferox and Aloe vera in the topical treatment of atopic dermatitis in Balb/c mice. Inflammopharmacology, [online] 23(6), pp.337-341. Available at: https://www.researchgate.net/publication/266939234_A_comparative_study_for_the_topical_treatment_of_atopic_dermatitis_with_Aloe_ferox_and_Aloe_vera_in_Balbc_mice [Accessed 1 Jun. 2018].
Finn, R., Harvey, M., Johnson, P., Verbov, J. and Barnes, R. (1985). Serum IgG antibodies to gliadin and other dietary antigens in adults with atopic eczema. Clinical and Experimental Dermatology, 10(3), pp.222-228.
Hartley, M., Hoare, S., Lithander, F., Neale, R. and Lucas, R. (2015). Comparing the effects of sun exposure and vitamin D supplementation on vitamin D insufficiency, and immune and cardio-metabolic function: the Sun Exposure and Vitamin D Supplementation (SEDS) Study. BMC Public Health, [online] 15(1). Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391331/ [Accessed 31 May 2018].
Hon, K., Wang, S., Hung, E., Lam, H., Lui, H., Chow, C., Ching, G., Fok, T., Ng, P. and Leung, T. (2010). Serum levels of heavy metals in childhood eczema and skin diseases: Friends or foes. Pediatric Allergy and Immunology, [online] 21(5), pp.831-836. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20337961 [Accessed 1 Jun. 2018].
Ionescu, G. and Kiehl, R. (1988). Monoamine and diamine oxidase activities in atopic eczema. Allergy, [online] 43(4), pp.318-319. Available at: https://www.ncbi.nlm.nih.gov/pubmed/3133954 [Accessed 1 Jun. 2018].
James, J. (2016). Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms. The Journal of Immunology, [online] 198(3), pp.1164-1171. Available at: http://www.jimmunol.org/content/198/3/1164 [Accessed 1 Jun. 2018].
Javanbakht, M., Keshavarz, S., Djalali, M., Siassi, F., Eshraghian, M., Firooz, A., Seirafi, H., Ehsani, A., Chamari, M. and Mirshafiey, A. (2010). Randomized controlled trial using vitamins E and D supplementation in atopic dermatitis. Journal of Dermatological Treatment, [online] 22(3), pp.144-150. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20653487 [Accessed 1 Jun. 2018].
Jones, G. (2014). Interpreting Vitamin D Assay Results: Proceed with Caution. Clinical Journal of the American Society of Nephrology, [online] 10(2), pp.331-334. Available at: http://cjasn.asnjournals.org/content/10/2/331.full [Accessed 1 Jun. 2018].
Jung, M., Hur, D., Song, S., Park, Y., Kim, T., Bang, S., Kim, S., Song, H., Park, H. and Cho, D. (2010). Tannic Acid and Quercetin Display a Therapeutic Effect in Atopic Dermatitis via Suppression of Angiogenesis and TARC Expression in Nc/Nga Mice. Journal of Investigative Dermatology, [online] 130(5), pp.1459-1463. Available at: http://www.jimmunol.org/content/184/1_Supplement/97.7 [Accessed 1 Jun. 2018].
Karabacak, E., Aydin, E., Kutlu, A., Ozcan, O., Muftuoglu, T., Gunes, A., Dogan, B. and Ozturk, S. (2016). Erythrocyte zinc level in patients with atopic dermatitis and its relation to SCORAD index. Advances in Dermatology and Allergology, [online] 5, pp.349-352. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110625/ [Accessed 1 Jun. 2018].
Kim, J., Yoo, S., Jeong, M., Ko, J. and Ro, Y. (2014). Hair Zinc Levels and the Efficacy of Oral Zinc Supplementation in Patients with Atopic Dermatitis. Acta Dermato Venereologica, [online] 94(5), pp.558-562. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24473704 [Accessed 1 Jun. 2018].
Kim, S., Ah, Y., Yu, Y., Choi, K., Shin, W. and Lee, J. (2014). Effects of probiotics for the treatment of atopic dermatitis: a meta-analysis of randomized controlled trials. Annals of Allergy, Asthma & Immunology, [online] 113(2), pp.217-226. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24954372 [Accessed 1 Jun. 2018].
Langdon, A. (2016). The effects of antibiotics on the microbiome throughout development and alternative approaches for therapeutic modulation. Genome Medicine, [online] 8(1). Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831151/ [Accessed 2 Jun. 2018].
Levy, M., Kolodziejczyk, A., Thaiss, C. and Elinav, E. (2017). Dysbiosis and the immune system. Nature Reviews Immunology, [online] 17(4), pp.219-232. Available at: https://www.weizmann.ac.il/immunology/elinav/sites/immunology.elinav/files/2017_elinav_nri.pdf [Accessed 1 Jun. 2018].
Maintz, L., Benfadal, S., Allam, J., Hagemann, T., Fimmers, R. and Novak, N. (2006). Evidence for a reduced histamine degradation capacity in a subgroup of patients with atopic eczema. Journal of Allergy and Clinical Immunology, [online] 117(5), pp.1106-1112. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16675339 [Accessed 1 Jun. 2018].
Maintz, L. and Novak, N. (2007). Histamine and histamine intolerance. The American Journal of Clinical Nutrition, 85(5), pp.1185-1196.
Mehrbani, M., Choopani, R., Fekri, A., Mehrabani, M., Mosaddegh, M. and Mehrabani, M. (2015). The efficacy of whey associated with dodder seed extract on moderate-to-severe atopic dermatitis in adults: A randomized, double-blind, placebo-controlled clinical trial. Journal of Ethnopharmacology, [online] 172, pp.325-332. Available at: https://www.ncbi.nlm.nih.gov/pubmed/26151244 [Accessed 1 Jun. 2018].
Michail, S., Stolfi, A., Johnson, T. and Onady, G. (2008). Efficacy of probiotics in the treatment of pediatric atopic dermatitis: a meta-analysis of randomized controlled trials. Annals of Allergy, Asthma & Immunology, [online] 101(5), pp.508-516. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19055205/ [Accessed 1 Jun. 2018].
Mihály, J., Gamlieli, A., Worm, M. and Rühl, R. (2011). Decreased retinoid concentration and retinoid signalling pathways in human atopic dermatitis. Experimental Dermatology, [online] 20(4), pp.326-330. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21410762 [Accessed 1 Jun. 2018].
Myers, G. (2007). Nutrient and Methyl Mercury Exposure from Consuming Fish. The Journal of Nutrition, [online] 137(12), pp.2805-2808. Available at: https://academic.oup.com/jn/article/137/12/2805/4750751 [Accessed 2 Jun. 2018].
Overgaard, L., Main, K., Frederiksen, H., Stender, S., Szecsi, P., Williams, H. and Thyssen, J. (2017). Children with atopic dermatitis and frequent emollient use have increased urinary levels of low-molecular-weight phthalate metabolites and parabens. Allergy, [online] 72(11), pp.1768-1777. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/all.13157 [Accessed 1 Jun. 2018].
Pacheco-Gonzalez, R., Garcia-Marcos, P. and Garcia-Marcos, L. (2015). Vitamin D and Atopic Dermatitis. Mini-Reviews in Medicinal Chemistry, [online] 15(11), pp.927-934. Available at: http://www.eurekaselect.com/131442/article [Accessed 1 Jun. 2018].
Panther, D. (2015). The Importance of Acidification in Atopic Eczema: An Underexplored Avenue for Treatment. Journal of Clinical Medicine, [online] 4(5), pp.970-978. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470210/ [Accessed 2 Jun. 2018].
Pinzer, T., Tietz, E., Waldmann, E., Schink, M., Neurath, M. and Zopf, Y. (2017). Circadian profiling reveals higher histamine plasma levels and lower diamine oxidase serum activities in 24% of patients with suspected histamine intolerance compared to food allergy and controls. Allergy, [online] 73(4), pp.949-957. Available at: https://onlinelibrary.wiley.com/doi/full/10.1111/all.13361 [Accessed 1 Jun. 2018].
Salehi, B. and Amestajani, M. (2012). Vitamin D supplementation in the treatment of atopic dermatitis: a clinical trial study. Journal of Drugs & Dermatology. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/22395583/ [Accessed 1 Jun. 2018].
Sanders, M., Shane, A. and Merenstein, D. (2016). Advancing probiotic research in humans in the United States: Challenges and strategies. Gut Microbes, [online] 7(2), pp.97-100. Available at: https://www.tandfonline.com/doi/full/10.1080/19490976.2016.1138198 [Accessed 1 Jun. 2018].
Schmid, A. and Walther, B. (2013). Natural Vitamin D Content in Animal Products. Advances in Nutrition, [online] 4(4), pp.453-462. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941824/ [Accessed 31 May 2018].
Shadi, T. and Talal, A. (2015). A review of four common medicinal plants used to treat eczema. Journal of Medicinal Plants Research, [online] 9(24), pp.702-711. Available at: https://www.researchgate.net/publication/289675826_A_review_of_four_common_medicinal_plants_used_to_treat_eczema [Accessed 1 Jun. 2018].
Sheen, Y., Jee, H., Kim, D., Ha, E., Jeong, I., Lee, S., Baek, H., Lee, S., Lee, K., Lee, K., Jung, Y., Sung, M., Kim, M. and Han, M. (2018). Serum zonulin is associated with presence and severity of atopic dermatitis in children, independent of total IgE and eosinophil. Clinical & Experimental Allergy. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/29682826 [Accessed 1 Jun. 2018].
Sidbury, R., Sullivan, A., Thadhani, R. and Camargo, C. (2008). Randomized controlled trial of vitamin D supplementation for winter-related atopic dermatitis in Boston: a pilot study. British Journal of Dermatology, [online] 159(1), pp.245-247. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18489598 [Accessed 1 Jun. 2018].
Thomas, C., Hong, T., van Pijkeren, J., Hemarajata, P. and Trinh, D. (2012). Histamine Derived from Probiotic Lactobacillus reuteri Suppresses TNF via Modulation of PKA and ERK Signaling. PLoS ONE, [online] 7(2), p.e31951. Available at: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0031951 [Accessed 1 Jun. 2018].
Tsakok, T., McKeever, T., Yeo, L. and Flohr, C. (2013). Does early life exposure to antibiotics increase the risk of eczema? A systematic review. British Journal of Dermatology, [online] 169(5), pp.983-991. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23782060 [Accessed 2 Jun. 2018].
Tsoureli-Nikita, E., Hercogova, J., Lotti, T. and Menchini, G. (2002). Evaluation of dietary intake of vitamin E in the treatment of atopic dermatitis: a study of the clinical course and evaluation of the immunoglobulin E serum levels. International Journal of Dermatology, [online] 41(3), pp.146-150. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12010339 [Accessed 2 Jun. 2018].