Tag Archives: atopic dermatitis

NeoGenesis’ New Topical Probiotic Products, MB-2 and MB-3, Feature 5 Strains of Live, Colonizing Symbiotic Bacteria

Based on many recent scientific studies of using live, symbiotic bacteria in a topical application, NeoGenesis has launched a new probiotic, topical skin care product (MB-2) and will be launching MB-3 soon. I briefly explain some of the science for using topical probiotic products in this post.

I’ve been publishing about (Maguire and Maguire, 2017) and developing topical probiotic products (MB-1 was launched in 2015) for well over a decade. The data for topical symbiotic bacteria colonizing and benefiting the skin are rapidly accumulating. For example, topically applied Lactobacilli have been found to temporarily colonize the skin and to directly compete with skin pathogens through adhesion inhibition, production of antimicrobial metabolites, and by influencing pathogen metabolism. The competitive anti-pathogenic action of Lactobacilli has been described mechanistically for common skin pathogens, such as Staphylococcus aureus, Cutibacterium acnes, and Candida albicans (DeLanghe et al, 2021). Recently, studies of live Lactobacillus crispatus (LBC) demonstrated benefit to the skin when compared to inactivated LBC biomass, stimulating collagen in vitro. Moreover, the live LBC was stable in formulations not containing antimicrobial preservatives and was found to improve dermis density and wrinkle appearance in vivo.

Microbes and human cells have co-evolved for billions of years, through which they have been exposed to many types of molecules produced by each other and acting in bidirectional signaling pathways (Wu et al, 2025). For example, Lactobacilli have an immunomodulatory capacity associated with a reduction in excessive skin inflammation (Delanghe et al, 2021). Their influence on the immune system is mediated by bacterial metabolites and cell wall-associated or excreted microbe-associated molecular patterns (MAMPs). Lactobacilli acting as immune modulators associated with a reduction in excessive skin inflammation exert their influence on the immune system by secreting many bacterial metabolites, a type of postbiotic (this is a term I introduced in 2019; Maguire and Maguire, 2019), along with the cell wall-associated MAMPs that are not released but integrated into the cell of the bacterium. In addition, Lactobacilli can also enhance the skin barrier function, which is often disrupted as a result of infection, trauma, or in inflammatory skin diseases such as eczema and psoriasis. Lebeer et al (2022) found that the Lactobacillis species L. crispatus, L. iners, L. gasseri, and L. jensenii, all still belonging to the genus Lactobacillus strictu sensu, have a broader human adaptation to stratified epithelium than merely the human vaginal epithelial cells, based on their association with healthy skin. In other words, Lactobacilli colonize the skin just as they do in other epithelial tissues. However, these colonies of bacteria on the skin can be disrupted by a number of extrinsic and intrinsic factors, such as harsh chemicals and aging. For example, aged skin contains significantly fewer L. crispatus (a beneficial symbiont) than young skin. Let’s now breiefly look at how symbiotic bacteria benefit the skin through quorum sensing and the release of post-biotic molecules, including molecules that will inhibit pathogenic bacteria such as certain strains of Staphlacoccus aureus.

Quorum Sensing and Post-Biotic Release

Mechanisms of quorum sensing is different for gram-positive versus gram-negative bacteria. Regardless, quorum sensing molecules (AIP or QS molecules) can work within species or on other species to control growth. This is an important means by which symbiotic bacteria, such as B. subtilis, can inhibit pathogenic bacteria such as S. aureus.

As bacteria grow, they secrete and sense signaling molecule in the surrounding environment. By detecting variations in the concentration of these signal molecules, bacteria can modulate the expression of related genes, thereby regulating associated behaviors. Consequently, interfering in bacterial QS signaling to either promote or inhibit the development of lactic acid bacteria (LAB) biofilms holds substantial significance in terms of enhancing skin immunity, promoting skin health.

Quorum sensing allows bacteria to communicate and coordinate collective behaviors by sensing population density through chemical signals, or autoinducers. While primarily species-specific, interspecies communication also occurs when different bacteria produce or detect shared autoinducers like autoinducer-2 (AI-2), a “universal” signal molecule used by many species. This interspecies communication can lead to either cooperation or competition, influencing functions such as biofilm formation, virulence, and resistance against other microbes.

For example, colonization of the skin by Staphylococcus aureus is associated with exacerbation of atopic dermatitis (AD). Proteases and phenol-soluble modulin α (PSMα) secreted by S. aureus leads to endogenous epidermal proteolysis and skin barrier damage that promotes inflammation (Williams et al, 2019). Other species of bacteria residing on normal skin can produce autoinducing peptides that inhibit the S. aureus agr system, in turn decreasing PSMα expression. A number of bacteria types, such as Bacillus subtilis (it secretes lactic acid), can quorum sense (Spacacan et al, 2020) and react to the S. aureus overcolonization by inhibiting the S. aureus through disruption of their QS system (Leistikow et al, 2024).

Quorum-sensing systems in the skin can be divided into two paradigmatic classes: LuxI/LuxR–type quorum-sensing systems in Gram-negative bacteria and oligopeptide/two-component–type quorum-sensing circuits in Gram-positive bacteria. All of this is very complicated, relaizing that bacteria have elaborate chemical signaling systems that enable them to communicate within and between species is only recently been explored and the field is emerging quickly. Based on our current knowledge, I’ve developed two new products, MB-2 and MB-3, using symbiotic, live bacteria known to perform QS or interfere with QS in other bacteria strains and promote skin benefits, including reduced inflammation and barrier function rebuild.

Interspecies Quorum Sensing Fosters Both Competition and Collaboration

To be clear, quorum sensing between different bacterial species occurs as well. For example, some species cannot produce their own autoinducers, but have receptors for the autoinducer molecules of other species, allowing them to sense and respond to others in their environment. Like human behavior, bacteria behavior operates on a continuum of individualism and collectivism. This quality can breed conflict, but also collaboration and interspecies quorum sensing can take both forms. In other words, the good guys, the symbiotic bacteria, can work together through quorum sensing among themselves (intraspecies quorum sensing) to inhibit the bad guys, the pathogenic bacteria, through interspecies quorum sensing. The good guys can be fighting some bacterial species, such as S. aureus, that use quorum sensing to enhance each other’s virulence.

Let’s now look at the five symbiotic bacteria that are contained in MB-2 and MB-3

Lactobacillus plantarum

Lactobacillus plantarum treatment reduced wound bacterial load, neutrophils, apoptotic and necrotic cells, modified IL-8 production and induced wound healing (Peral et al, 2010). When topically applied to a disease skin model for acne, L. plantarum induced a significant reduction in viability of virulent bacteria phylotypes, lipid production, and modulated inflammatory markers (Podrini et al, 2023).  Further, L. plantarum whole cultures promote tissue repair, and this bacterium may also improve the healing of diabetic wounds in rats through the regulation of inflammatory cytokines (Ishi et al, 2023). In a study of 23 subjects, topical L. plantarum in a cream formulation was found to benefit skin aging properties, including TEWL, barrier function, and wrinkles (Elvebakken et al, 2023).

 Lactobacillus crispatus

An oily suspension containing Lactobacillus crispatus and Lacticaseibacillus paracasei was found to benefit Seborrheic dermatitis (Truglio et al, 2024). In a study of 29 women with topical application of L. crispatus, the density of the sub-epidermal zone significantly increased vs baseline by 11% and of the dermis by 6% (+5% vs placebo). As I mentioned in the introduction,, studies of live Lactobacillus crispatus (LBC) demonstrated benefit to the skin when compared to inactivated LBC biomass, stimulating collagen in vitro. Moreover, the live LBC was stable in formulations not containing antimicrobial preservatives and was found to improve dermis density and wrinkle appearance in vivo.

Bacillus subtilis

Topical application of live Bacillus subtilis has been found to reduce the number of pathogenic bacteria in skin, including S. aureus (Moskovicz et al, 2021; Piewngam et al, 2023). Topical application also helps to reduce acne breakouts (Ma’or et al, 2023). B. subtilis is being developed for drug delivery for a number of reasons (Montgomery et al, 2024). It may have advantages over other candidate bacteria as a platform for drug delivery to the skin because of its safety profile and genetic tractability. It is found in the skin microflora and is metabolically active on the skin. It is nonpathogenic and has natural antimicrobial properties against pathogenic staphylococci and fungi. B. subtilis has generally regarded as safe status from the FDA, and multiple B. subtilis probiotic products as well as a genetically modified strain of B. subtilis are currently commercially available. Further, an important characteristic of B. subtilis is that it is commonly used in biotechnology for the production of proteins, vitamins, and antibiotics because of its efficient protein secretion system, and ease of cultivation, factors that mean it can work well when topically applied to the skin as a probiotic.

Bacillus coagulans

LactoSporin, a metabolite of Bacillus coagulens, cream topically applied for 10 weeks resulted in a significant reduction in visibility of wrinkles around crow’s feet, nasolabial folds, frown lines, and facial fine lines compared to baseline and placebo by dermatological and Antera imaging assessments (Majeed et al, 2023). . Optimal conditions for growth include a temperature range of 30–50°C and a pH level of 5.5–6.5, matching the surface of the skin. This bacterium exhibits weak adhesion to epithelial cells, which prevents long-term colonization, but allows temporary colonization and yielding positive effects.

Lactoccus lactis

Various strains of L. lactis have recently been reported to induce anti-inflammatory activity in vitro (Luerce et al, 2014). Administration of L. lactis LB 1022 improved clinical AD symptoms, decreased serum IgE and suppressed the Th2 cytokines secretion, such as IL4, IL-13, and TSLP in blood, which are factors found to be elevated by AD. Similarily, oral L. lactis LB 1022 may have a protective effect against AD by reducing high IgE serum levels and Th2-related responses that arise from an imbalance in the gut microbiota. Topical application of L. lactis is likely to have similar effects on AD, but given the likely lower colonization levels when topically applied, requires more frequent dosing to achieve similar positive results. It is also possible that L. lactis ferments glycans on the surface of the skin, thus producing beneficial lactic acid that may then be fermented into beneficial short chain fatty acids which then regulate the immune system and reduce inflammation.

Summary

As you can read here in the studies I’ve mentioned, there is much accumulating evidence for the benefits of the 5 types of symbiotic bacteria that I’ve chosen to include in our NeoGenesis MB-2 and MB-3 products. Working with a number of dermatologists in the USA, we’ve had remarkable postive results in compromised, inflammatory skin conditions where MB-2 (bacteria in an occlusive base) serves those conditions with interupted barrier function, such as atopic dermatitis and MB-3 (in a non-occlusive oil base) serves those conditions with a more intact barrier and oily and pustule-prone skin.

Epithelial Barrier Dysfunction in Noncommunicable and Communicable Diseases

The modern world’s dramatic increase in the number and types of chemicals in which man is exposed, a major part of of someone’s exposome, responsible for about 90% of diseases (not genetics), is causing a dramatic rise in noncommunicable and communicable diseases. Over 350 000 chemicals and mixtures of chemicals have been registered for production and use, up to three times as many as previously estimated, and an underestimate of the true number of chemical types that have been produced and commercialized. As the skin and other epithelial tissues are compromised and exposed to communicable diseases, skin and epithelial transmitted diseases are on the rise. For example, the shingles virus can enter through the skin or the epithelial tissue in our respiratory tract, and having shingles can even lead to increased risk of dementia (2nd Ref). Further, a compromised skin epithelial barrier caused by environmental factors such as mechanical trauma, exposure to exogenous proteases in microorganisms and our food, detergents, and air pollution can activate the innate and adaptive immune systems, inducing keratinocytes to release pro-inflammatory cytokines and chemokines and enhancing the antigen presentation by intradermal Langerhans cells (LCs) and dermal DCs and activating T-cells. In turn, for example, activation of T2 type T-cells leads to IL-4, IL-5, and IL-13 secretion, provoking skin barrier alteration, immune cell infiltration into skin, and itch as observed in atopic dermatitis. 

The first essential step to skin immunity is the epithelial barrier, as infection and resulting inflammation are impossible without first breaching it. Epithelia, coated with a sugary glycocalyx, not only comprise our skin but also the mucosal membranes that line our organs. Their ability to secrete squalene, mucus, lipids, and antimicrobials help protect against pathogen invasion. Additionally, epithelia can prevent inflammation by physically shoving out cells infested with toxins, allergens, antigens, pathogens, or other damage by seamlessly extruding them. This is a strategy employed by not only epithelia, but also our hair does the same as it sheds. Given that chronic inflammation could stem from a defective epithelial barrier, the current approach of treating only the inflammation will only partially mitigate symptoms of a more central problem, ongoing wound healing and disrupted barrier.

Scientists now understand that in patients with allergic disease, regardless of tissue location, the homeostatic balance of the epithelial tissue barrier is skewed toward loss of differentiation, reduced junctional integrity, and impaired innate defense and a hyperactive adaptive (trained immunity) immune system. Importantly, epithelial dysfunction characterized by these traits appears to pre-date a predisposition to immunological responses against a range of antigens or allergens, and development of allergic disease.

From the disease perspective, trained immunity is beneficial, as it improves the host’s defense against subsequent infection from pathogens. However, it can also be detrimental and result in overly active immune responses or chronic inflammation.  Even the innate immune system has some memory, given evidence that components in House Dust Mite extract activate and likely train macrophages to produce high amounts of CCL17, IL-6, and cysteinyl leukotrienes following re-exposure to HDM through the TNF-α and PGE2 pathways. Thus, an activated immune system, one that has memory and is primed to react, can lead to sensitivities that may be triggered by an overabundance of chemicals in the environment, and those sensitivities heightened by a disrupted barrier.

Evidence that epithelial barrier dysfunction explains the growing prevalence and exacerbations of inflammatory diseases such as eczema has grown through many studies performed world-wide. Diseases encompassed by the epithelial barrier theory share common features such as an increased prevalence after the 1960s that cannot be accounted soley by the emergence of improved diagnostic methods. They are indeed increasing in prevalence, i.e. the number of afflictions per 1,000 people.

Eepithelial barrier dysfunction enables the microbiome’s translocation from the skin’s surface to interepithelial and deeper subepithelial areas, doing in combination with allergens, toxins, pathogens, and pollutants. Thereafter, microbial dysbiosis and possible infection, characterized by colonization of opportunistic pathogenic bacteria and loss of the number and biodiversity of commensal bacteria results. Local inflammation, impaired tissue regeneration, and remodeling characterize the skin that suffers from impaired barrier. For example, commensal bacteria on the skin’s surface are important for epidermal lipid synthesis and improve barrier function. The skin’s microbiome is therefore critical to maintaining epidermal barrier function. The infiltration of inflammatory cells and inflammatory cytokines to affected tissues is part of the immune system’s response to erradicate invading bacteria, allergens, toxins, and pollutants away from the deep tissues. As Peter Elias, M.D. has written, “AD [atopic dermatitis] can be considered a disease of primary barrier failure, characterized by both a defective permeability (Proksch et al., 2006, and references therein) and antimicrobial function.” Further, inflammatory cells and inflammatory cytokines that migrate from the skin to other organs may play roles in the exacerbation of various inflammatory diseases in other organs. Thus, inflammation iniated in the skin may contribute to chronic inflammatory diseases in other tissues.

What Dr. Elias has been saying is that the permeability-barrier abnormality in AD is not merely an epiphenomenon but rather the “driver” of disease activity, an “outside–inside view of disease pathogenesis” (Elias and Feingold, 2001). The evidence for this is: (1) the extent of the permeability-barrier abnormality parallels severity of disease phenotype in AD, (2) both clinically uninvolved skin sites and skin cleared of inflammation for as long as 5 years continue to display significant barrier abnormalities, (3) topical artificial barrier therapy comprises effective ancillary therapy, and (4) specific replacement therapy, which targets the prominent lipid abnormalities that account for the barrier abnormality in AD, not only corrects the permeability-barrier abnormality but also comprises effective anti-inflammatory therapy for AD (Figure 1; Chamlin et al., 2002). Thus, inflammation in AD may begin with insults from without, i.e. the exposome.

That barrier insult can then activate epithelial cells in the skin, keratinocyes, which are non-professional immune cells, but do possess MHC-II molecules, that present antigens to professional immune cells, such as T-cells. Thus, with disrupted barriier, the keratinocytes can recognize antigens and present them to the immune system, leading to inflammation. More and more, scientists are discovering how epithelial cells are part of the immune system, regardless in which organ they exist. Key here is to protect barrier function in all of our epithelial tissues, including the skin.

So if inflammatory diseases such as eczema and psoriasis are environmentally triggered and lead to barrier dysfunction and resultant inflammation, what can we do?

First, calm the inflammation. It’s destructive and further degrades the epidermal barrier. S2RM technology (in NeoGenesis Recovery) is great for reducing inflammation, doing so in both the innate and adaptive immune systems.

Second, use a topical product that provides the 3 lipids and natural moisturizing factors that are needed to rebuild normal stratum corneum and barrier function. One product to use is NeoGenesis Barrier Renewal Cream (BRC).

Third, use a product that provides instantaneous barrier function and commensal bacteria. The instantaneous barrier allows the BRC to rebuld the natural barrier function over time, and the commensal bacteria help to rebuild the barrier through activation of lipid synthesis by skin cells. The commensal bacteria in Neogenesis MB-2 also help to reduce the Staphylococcus aureus infection often assicated with disrupted barrier function.

So remember, these inflammatory skin conditions are triggered by the environment. Therefore, their treatment and prevention means that if you change your environment, you can prevent or treat these diseases. Part of changing your environment is the careful choice of topical products to reduce inflammation and renormalize the structure and function of your skin.

Air Pollution and Eczema on the Rise

Air pollution is wreaking havoc on your skin. Simple steps to mitigate the problems associated with pollution include gentle cleansing, topical products to reduce oxidative stress and to restore barrier function.

Whether it’s jet fuel, leaded fuel for non-jet aircraft, auto exhaust, forest fires, wars such as Iraq, Gaza, and the Ukraine, or industrial fumes as causative factors, “the estimated lifetime prevalence of atopic dermatitis has increased 2~3 fold during over the past 30 years, especially in urban areas in industrialized countries, emphasizing the importance of life-style and environment in the pathogenesis of atopic diseases” (Kim, 2015). “Atopic dermatitis (AD) has increased in prevalence to become the most common inflammatory skin condition globally, and geographic variation and migration studies suggest an important role for environmental triggers” (Fadadu et al, 2023).

Air pollution can make people more sensitive to other allergens by eliciting an immune system hyper-response. This can degrade the skin’s barrier function, and now that immune system hyper-alert signaling is more exposed to the outside world and even more sensitive. Essentially, air pollution is opening up the skin by degrading it’s barrier, and making that contact between the skin’s immune system and the environment more robust. Air pollution is a catalyst in a chemical reaction, as scientists at the Max Planck Institute have written, “Fine particulate matter catalyzes oxidative stress.” The key, air pollution is causing oxidative stress in the skin, leading to chronic inflammation, a root cause in many inflammatory skin conditions, including eczema.

The illustration shows the health effects of atmospheric air pollution. The model simulations of Thomas Berkemeier and his team suggest that PM2.5 acts by conversion of a reservoir of reactive oxygen species (such as peroxides) into highly reactive OH radicals. these reactions take place in the epithelial tissue fluid, which is a thin aqueous film in the lungs and skin in which air pollutants dissolve or deposit.

For day-to-day protection from modern man’s air and water pollution and climate change (think increased fires), use air filters for the home and use mineral sunscreens with zinc or titanium, which create a physical barrier that makes it more difficult for airborne pollutants to come into direct contact with the skin. It’s also important to have a good cleansing regime. Wash the pollutants off at night with a gentle cleanser, use a product that reduces the oxidative stress, and then put on a fragrance-free hypoallergenic moisturizer containing free fatty acids, ceramide, and cholesterol that will help the skin barrier heal overnight.

Atopic Dermatitis, Bugs, and Itching

The skin barrier in the epidermis is constantly exposed to microbes and their products. The role of microbes in itch generation was previously unstudied. Deng et al (2023) find that Staphylococcus aureus, a bacterial pathogen associated with itchy skin diseases, directly activates pruriceptor sensory neurons to drive itch.

When the scientists injected MRSA, a type of S. aureus, under the skin of mice, as expected, the mice itched so much that they damaged their skin. But the authors claim to have measured no inflammation associated with the injection. This provides evidence that inflammation is not required for itch to occur.

Instead, research has found that when S. aureus invades the skin, it releases 10 different enzymes, or proteases. One of them, called V8, binds to a protein on nerve cells called proteinase-activated receptor 1, or PAR1. Activation of PAR1 likely starts a chain reaction from the skin neurons, to the spinal cord, and to the brain, which then triggers the urge to itch. In the mouse model used by Deng et al, the itching stopped when researchers used Vorapaxar, a drug that blocks the PAR1 receptor. This may not be the only mechanism by which itching occurs, but this is an important new discovery and gives us much insight into the some of the mechanisms underlying pruritis.

From Deng et al (2023)

As Ogonowska et al (2023) have described, Staphylococcus aureus massively colonizes the skin of patients with atopic dermatitis (AD), and the frequency of detection of multidrug-resistant S. aureus (MRSA) in AD patients is higher than the healthy population, which makes treatment much more difficult. 

There’s hope though, and that hope involves using simple, topically applied symbiotic bacteria that are safe and natural to the skin. One set of bacteria are the nitrifying bacteria (Nitrosomonas, Nitrospira, and Nitrobacter), used in NeoGenesis MB-1. The MB-1 product has been on the market since 2015 and is multifunctional – benefiting a number of skin conditions, including acne. As one mechanism of action, Maguire and McGee (2023) hypothesize the MB-1 acts to destroy pro-inflammatory bacteriophage (viruses) associated with acne through a natural CRISPR mechanism in the probiotic bacteria.

These type of nitrifying bacteria in MB-1 have also been found to reduce pruritis and inflammation in humans with atopic dermatitis. Additionally, NeoGenesis is currently testing our second probiotic product that incorporates Bacillus subtilis and Lactobacilli. The bacterium B. subtilis has been found to reduce the S. aureus when topically applied, and Lactobacilli have been found to do the same while reducing the symptoms of AD.

NeoGenesis will have two probiotic products that will be used together in a topical application to renormalize the skin’s microbiome in AD, reduce pruritis, and restore barrier function. Stay tuned.

Reducing Sodium Intake Not Only Reduces Blood Pressure, Skin Inflammation is Reduced

In a recent trial (Gupta et al, 2023), the blood pressure–lowering effect of dietary sodium reduction was comparable with a commonly used first-line antihypertensive medication. Salt in the diet is associated with chronic kidney disease. Sodium also accumulates in the skin, inducing inflammation and eczema, so feel better and look better by cutting the sodium intake that is way too high in most people.

I discuss at length in my book, Thinking and Eating For Two: The Science of Using Systems 1 and 2 Thinking to Nourish Self and Symbionts, how diet is key to all chronic diseases. All of the dietary components work together to largely determine health status – not just one and certainly not just genetic factors. Genetics has little to do with health status for most people. Hereditary factors, such as epigenetic transgenerational inheritance and protein inheritance, may have an important influence, but not genetics. It’s the exposome that counts – i.e. all of the things that you’re exposed to in life – and, all of the things that you’re parents and their parents were exposed to. That’s the transgenerational epigenetic inheritance and protein inheritance aspect of the exposome. Now research at the University of California, San Francisco (UCSF) and UC Berkeley, suggests that high levels of dietary sodium may raise the risk of developing atopic dermatitis.

Many factors can influence health, including that of the skin. I’ll discuss salt here, but other factors such as dairy play a big role too – both for cardiovascular health, and skin health. For example, the induction of antibodies (IgE) by the consumption of dairy can lead to cardiovascular disease and death. And dairy, loaded with antigens such as lactose, whey, and casein (even found in mothers milk because of dairy consumption by mom) can be destructive to the skin, even causing cancer.

As Gupta et al (2023) discovered, dietary sodium reduction significantly lowered blood pressure (BP) in the majority of middle-aged to elderly adults they studied. The decline in BP of those who went from a high- to low-sodium diet was independent of hypertension status and antihypertensive medication use, and was consistent across subgroups. Needless to say, reducing sodium intake did not result in adverse events.

Sodium is an essential mineral and osmolyte for the human body. It is the major cation in the extracellular fluid and as such plays a crucial role in homeostatic processes such as regulation of blood volume, osmolarity, and blood pressure. Therefore, sodium plasma concentration is maintained within a relatively narrow range of around 140 mmol/l. The sodium concentration in the interstitial space (the space in between our cells) can be much higher. We consume just the right amount of sodium when we eat a plant based diet without added sodium. If we eat too much sodium, that excessive salt intake may induce several adverse effects, causing microvascular endothelial inflammation, anatomical remodeling, and functional abnormalities, even in normotensive subjects (those with normal blood pressure). More recent studies have shown that changes in sodium plasma levels not only exert their effects on small resistance arteries, but may also affect the function and structure of large elastic arteries. The issue of salt-sensitivity, which refers to individual susceptibility in terms of BP variations following changes in dietary salt intake, has also been recently debated in its pathophysiological mechanisms and clinical implications.

Excess sodium is also stored in the skin.  In the skin microenvironment, higher sodium concentrations enhance macrophage function, potentially leading to innate immune system-based inflammation. Several studies have provided significant evidence that an elevated sodium concentration has an immunomodulating effect by augmenting proinflammatory and antimicrobial macrophage function as well as T-cell activation. And now we know that sodium has accumulated to high levels in the skin of psoriasis patients (Maifeld et al, 2021). Psoriasis is an inflammatory skin condition, and restricting salt in your diet will help to reduce that inflammation. Same for eczema. Reduce the salt because, for one factor, salt promotes the growth of a bad bacteria called staph aureus which is found in patients who have bad flare ups of eczema. With high salt, the skin is unable to repair itself – it’s in a constant state of inflammation.

Cut the salt and your immune system will operate more normally. It requires time to adjust your taste to the low sodium diet – most of us are addicted to salt. But in time, you lose the addiction, and actually begin to better taste all of the other flavors in your food that were masked by the salt. Bon appetite, Pas de sel!

Eczema on the Rise: What to Do.

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.