You don't just 'get' eczema and it's not contagious. It's a multifactorial inflammatory skin disease that's highly heritable. Genetic predisposition, epidermal barrier disruption and dysregulation of the immune system are the critical components leading to the progression of eczema (atopic dermatitis).
The filaggrin (FLG)gene codes for the structural protein filaggrin and mutations in FLG, particularly homozygous mutations, are associated with an increased risk for severe eczema. Deficiency in filaggrin protein results in structural impairment of the stratum corneum (the outer layer of the skin) with loss of water and lipid damage. This damage to the skin barrier allows pathogens and allergens entry into the skin. Other genes such as SPINK5, INTERLEUKIN genes, and VDR genes are also worth noting and polymorphisms within these genes may also contribute to increased risk for disease progression and severity. I would also test for HLA gluten intolerance as well as NCGS (non-celiac gluten sensitivity) .
Did you know that the skin microbiome is incredibly diverse? There are over 1000 different bacterial species, about 80 varieties of fungal species, multiple viruses and a highly active SALT (skin-associated lymphoid tissue) just as there is a GALT (gut-associated lymphoid tissue)?
Just like the gut microbiome, skin dysbiosis may also occur. With water loss and barrier disruption, the skin microbiome may become dysfunctional. There is usually a concomitant decreased expression of AMP (antimicrobial peptides) and predisposition to Staphylococcus aureus infection.
S. aureus and/or numerous allergens, microbes, pathogens enter the cells and the immune system kicks into action.
The antigens are presented by the dendritic cells to the naive T cells. The naive T cells differentiate into a Th2 response which is the main response in the acute phase phase response.
The keratinocytes ( skin cells which produce keratin) trigger the release of pro inflammatory cytokines (IL0B1, IL-25,IL-33,TSLP) which activate dendritic and Langerhans cells.
Activated dendritic cells stimulate Th2 to produce IL-4, IL-5, IL-13, IL-31, IL-33 which then further decrease barrier function, filaggrin expression and keratinocyte differentiation as well as increased itch.
The next phase that incorporates the adaptive immune system and chronic eczema is characterised by a Th1, Th17 and Th22 response which results in further thickening and abnormal keratinocyte proliferation. This unresolved immune dysfunction perpetuates and this dry, itchy, cracked skin skin condition is extremely difficult to cope with on many levels.
There are 5 things on the list to tackle;
REMOVING the triggers requires an intense process of identifying triggers. Testing for food and inhalant allergens (IgE)as well as food sensitivities (IgG), stool testing and an elimination diet to the remove the usual suspects are the starting points.
Stress is a huge trigger for many. Lifestyle and exercise have to be personalised. DNA Health profile will identify biological pathways that may need support as well as indicate food intolerances, vitamin and mineral requirements.
REPLACE. A Stool test or Organic Acid test are ideal instruments for determining a need for digestive enzymes or identifying pathogens. Candida overgrowth is common in eczema, as is S. aureus. The gut microbiome will undoubtably reveal gut dysbiosis in most clients. The skin and gut microbiome are shared, but different.
REINOLCULATE. Once the client is able to absorb and digest nutrients and the triggers have been removed, we can start to reinoculate with probiotics from food and supplements.
REPAIR. Stress has to be addressed and reviewed. Gut healing foods and nutrients such as L-Glutamine and collagen can be introduced. Detoxification pathways will most likely need some support and buffering with nutrition and supplementation.
Skin care is always addressed and discussed with the skin specialist.
REBALANCE. HPA (hypothalamic-pituitary-adrenal) axis. Optimal hormonal balance and lifestyle balance are essential throughout the client's journey.
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