Atopic eczema or dermatitis (AD) often starts in infancy and the good news is that for most children it spontaneously resolves by the age of seven. However, AD doesn’t like to conform and so for some, AD remains until puberty, may return in later adulthood and for the very unlucky stays with them throughout their lives.
Unfortunately for some children, the early onset of AD also signals the start of the ‘atopic march’, with the appearance of hay fever and even asthma, either in tandem with the AD or in some cases instead of (1).
In addition, whilst more boys are diagnosed with allergies in childhood, in adulthood women are significantly more likely to be diagnosed with a food allergy and the menopause has been identified as a time when AD flares can either increase or disappear. (17,18).
So why do some people get AD?
Helping clients with AD is my vocation, as I have suffered from this condition since I was 6 months old. I am so interested in this topic that I have just completed a Master of Science with a dissertation entitled: ‘Examine how nutrition can be used as a complementary tool for the support of eczema/chronic atopic dermatitis (AD)' and I will share some of what I learnt below:
Multiple causes have been identified including skin barrier disruption, mutations in the filaggrin gene, gut microbiome (gut bacteria) imbalance, as well as immunological (allergy/intolerances) and environmental triggers, yet there is still no definition of what causes AD. This lack of definitive cause leads to dermatologists and allergy specialists telling their patients that eczema is uncurable and that it can only be modulated by use of corticosteroids and other topical creams and emollients (2,3).
There are, however, several areas of research that might shed more light.
You may have heard of leaky gut, but it could be that AD sufferers have leaky skin which may be caused by the mutation of a skin protein gene called filaggrin (FLG). Basically, FLG is used to seal the skin barrier and acts to both stop water loss and potential pathogens crossing into the bloodstream. What this means in practice is that whilst the water loss creates the dry, flaky and itchy skin so well-known to eczema sufferers, the ‘leaky skin’ could also be allowing environmental and even food allergens to cross, triggering an immune reaction and inflammation. Up to 48% of AD sufferers have been found to carry this mutated FLG gene (FLG-null-allele) which makes it a very exciting area of research. (4–6).
The FLG research has also been linked to another area of AD research, the ‘dual allergen exposure hypotheses’ (12) relating to inappropriate immune response. This area of research suggests that the FLG affected ‘leaky skin’ exposes the AD sufferer to food antigens via touch. The food particle enters the bloodstream via the skin and is quickly identified as a foreigner by the person’s immune system. This causes the body to go into high alert, triggering inflammation and labelling that food antigen as a future threat. A vicious cycle then ensues with the inflammation causing further damage to the skin barrier and leading to even more risk of exposure to food and environmental antigens.
Recent studies have found that this type of food antigen exposure can lead to subsequent ingested food sensitivities and intolerances and provides a potential explanation as to why so many AD sufferers know that they react to certain foods, despite negative allergy testing. (13).
Studies have shown that child AD sufferers are at higher risk of IgE mediated food allergies but also non-IgE Mediated (delayed) allergies (14). Diagnoses are made via either a blood draw to test for specific IgE antibodies or via Skin Prick Test (15). Other possible tests include the Atopy Patch Test, IgG testing and the Elimination Diet. In children caution must be applied to the Elimination Diet as it is thought that continuous consumption of a trigger food will result in it being better tolerated and that the removal of this food from the diet for a period may result in an increased risk of severe allergy or even anaphylaxis (16).
The gut microbiome has become a key research focus within the last decade, both in terms of health generally but also specifically in relation to AD. Intestinal hyperpermeability (leaky gut) and gut microbiome (bacteria) imbalance are linked to worsened immunity, higher rates of inflammation and risk of allergies and intolerances. AD patients have been identified as being at higher risk of both these (10,11).
Recently research has started to focus on the skin microbiome (bacterial population). This research has identified that individuals with atopic eczema suffer from skin microbiome dysbiosis (imbalance) with a skew to an overgrown population of staphylococcus epidermidis and staphylococcus aureus (7,8). My clinical experience has often found individual clients who demonstrate a link between both skin and gut dysbiosis (9) and this is an area I am passionate about.
Nutritional Strategies
As mentioned in the introduction, AD doesn’t like to conform. Whilst there are some common recommendations to all AD sufferers, no two nutrition recommendations are alike, just like no two people’s skin or gut microbiomes are alike. What may work for one, will not work for another.
Supporting clients with this condition involves the combining of many pieces of information with practitioner knowledge. Seeking out the individualised manner of eating that allows that person to eat the most varied diet possible, whilst being aware of those foods and environmental triggers that may cause a flare.
The main objective is to provide the empowerment that allows for each client to have a sense of control, whilst having the knowledge to face new challenges, in line with AD’s non-conformist tendencies.
Below are some of the key nutrients that research has found to be supportive for AD sufferers:
Pre and Probiotics. The World Allergy Organisation guidelines (7) promotes the use of probiotics for women during pregnancy and breastfeeding.
Vitamin D3. Multiple studies have identified that AD sufferers were more likely to be vitamin D deficient than the normal population and vitamin D deficiency has been linked to increased inflammation and thus AD severity (20)
Omega 3 Fatty Acids. Some studies have found that whilst maternal, pre-pregnancy supplementation of omega-3 fatty acids commonly marketed as fish oils, had no impact on preventing atopic dermatitis onset, regular oily fish intake or omega 3 supplementation in children and adults can reduce flare onset and severity of flare occurrence (16,22,23)
Whilst a deficiency in zinc status has been long thought to be linked to AD, studies using supplementation did not show any benefits (25,26).
Article written by Jessica Fonteneau, MSc, DipIoN, mBANT, mAFNBE, CNHC Reg
www.jessicafonteneaunutrition.com
References
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