Atopic dermatitis (AD), an inflammatory skin condition is a form of eczema. Eczema refers to a group of conditions that cause inflamed skin. There are many types of eczema. Atopic dermatitis is the most common type. Recent studies of AD have found that both structural abnormalities of the skin and immune dysregulation play important roles in the pathophysiology of the disease.  Impairment of epidermal barrier function, for example, owing to deficiency in the structural protein filaggrin, can promote inflammation and infiltration of immune cells, such as T cells. And, as we age, immune cells, such as macrophages, become more inflammatory because of a loss of certain calcium pumps within the mitochondria (mCa²+). Specifically, mCa²⁺ uptake capacity in macrophages drops significantly with age. This amplifies Ca²⁺ signaling in the cytosol of the macrophage and promotes NF-κB activation, rendering the macrophages prone to chronic low-grade inflammatory output at baseline and hyper-inflammatory when stimulated. This means if you have interrupted skin barrier, and a trigger penetrates and presents in the skin, older people will likely have an exaggerated, pro-inflammatory macrophage response that elicits an inflammatory cascade. While this phenomenon increases with age, many people with inflammatory skin conditions can experience this too. While macrophages are necessary for normal skin function, the inflammatory types are not. One way to reset macrophage types from an inflammatory state to an anti-inflammatory, pro-repair state is the use of skin derived mesenchymal stem cell secretome (stem cell released molecules). This so-called S²RM technology is available in Neogenesis Recovery. Our studies have found Recovery to work well to quell the inflammation associated with psoriasis and AD.

Therefore, optimal management of AD requires a multifaceted approach to heal and protect the skin barrier and address the complex immunopathogenesis of the disease. Other types of eczema include contact dermatitis, nummular eczema, and dyshidrotic eczema. People often say atopic dermatitis when referring to any one of these conditions. Although eczema involves an immune response, it is not considered an autoimmune condition because eczema is not self-triggered, rather it is induced by environmental factors. However, once chronic inflammation is induced, tissue breakdown from the inflammation can elicit an autoimmune response and become self-sustaining. That is, inflammation induces tissue breakdown that causes sterile inflammation, which then leads to further tissue breakdown. And the cycle continues. At this point, if the environmental trigger is stopped, an autoimmune response may continue from the damage signals emanating from the structural breakdown of the epidermis. This process is called inflammaging. People with AD have a higher prevalence and incidence of autoimmune conditions compared to the general population. BTW, the epidemiological terms, prevalence is about what’s out there, while incidence tells you what’s new.

In 2000, the American Academy of Dermatology (AAD) warned Americans: eczema was on the rise. In the warning, the group of dermatologists said that the rate of atopic dermatitis, a form of eczema, had nearly tripled since 1970. This provides evidence that the disease is a consequence of environment and not hereditary-genetics. At the time, it was estimated that nearly 6 percent of all Americans had the condition that can cause itchy, red, and scaly skin. Today, the National Eczema Foundation estimates that at least 10 percent of Americans have eczema, and that one in ten people will have eczema in their lifetime. I want to stress that this is an inflammatory disease where the skin’s innate and adaptive immune systems have gone awry. Immune cells are abnormally activated and may be found in parts of the skin, the epidermis, where they are not normally resident as happens in a similar disease called psoriasis. Itch (pruritis) is associated with neuroinflammation of the skin’s, part of the neuro‐immuno‐cutaneous (NIC) system. The skin’s microbiome will also be altered, a dysbiosis occurs where Staphylococcus aureus proliferates in overabundance. And remember, as I always stress, inflammation in the skin means inflammation in the body.

Exposure to tailpipe emissions is a big factor in eczema. Diisocyanates from auto exhausts show temporospatial and epidemiological association with AD while also inducing eczematous dysbiosis. As the authors of this study correctly point out, “The prominent AD paradigm is that the disease has a multifactorial pathology, but with frequent reference to genetic predispositions causing defects in barrier and/or inflammatory pathways. However, the stark post-industrialization increase in AD prevalence strongly suggests that environmental factors must play a substantive role.” In other words, eczema is another environmental disease – forget the genetics-hereditary hype.

What to do? Cleanse the skin daily with a gentle cleanser. No harsh alcohol cleanser or those with strong surfactants such as sodium lauryl sulfate (SLS). In this way you’ll remove those environmental toxins, antigens, allergens, and haptens that can trigger the inflammatory response. Use something mild like NeoGenesis Cleanser, or a similar mild cleanser. Be very careful to choose products without harsh chemicals that degrade the barrier and have allergic triggers. BTW, I’ve formulated a new cleanser for eczema and other inflammatory skin conditions that is currently in testing. More about this in future posts. I also have a new topical probiotic (yes, it’s really possible to do this) that I’ve formulated, also in testing. It remediates the dysbiosis associated with eczema. And because barrier function is perturbed in these conditions, using a product to restore the function of the stratum corneum and its barrier function is very important. This helps to prevent those environmental triggers from penetrating into the skin and inducing an immune response. Using a product, such as Neogenesis Barrier Renewal Cream, can help to rebuild the skin’s natural barrier function, preventing those triggers from entering the skin.

I have a trio of products that I’ve formulated for these skin conditions, and I’ll have more to say in the months ahead about how well they are working. The formulas are backed by decades of research, and while early results are promising, it will be interesting to see for what conditions they work best in real world studies. Stay tuned.