Skin pH and eczema
pH is critical for many biological processes. Many chemical and enzymatic reactions have strong pH dependence. It is, therefore, no surprise that pH is highly regulated in living organisms, and within each organism, different organs, tissues, or even cells maintain very specific and often very narrow pH ranges. Skin surface pH ranges between 4 and 6, while the pH of the living epidermis is about 7.4.1,2 The 2-3 pH unit difference between the living epidermis and the skin surface corresponds to 100-1000 times difference in proton concentration gradient over a short distance of 15-20 um. This acidic skin surface pH and the pH gradient have been shown to have importance for many processes involved in the synthesis and maintenance of the skin barrier.3–6 Two enzymes, acidic sphingomyelinase, and β-glucocerebrosidase, that are involved in ceramide formation have pH optima of ~5.7,8 The acidic pH is also involved in the regulation of stratum corneum desquamation and regulates the activity of the proteolytic enzymes, serine proteases kallikreins. Low acidic pH keeps kallikreins (protease family) in check and elevated pH results in rapid degradation of corenodesmosomes and consequently in compromised SC integrity.9 Since the skin surface pH and the barrier homeostasis are codependent, it is not surprising that disrupted skin surface pH is observed in several skin disorders, such as atopic dermatitis,10 irritant contact dermatitis,11 diaper dermatitis,12 or Ichthyosis Vulgaris.3
What is the optimal skin surface pH?
The fact that the skin surface pH slightly varies with age, body location, ethnicity, or even circadian rhythms, makes it difficult to determine one optimal pH value.13 Most of the numbers given as the natural skin surface pH come from the pH averages of the distributions measured in the different studies. Given that most of the environmental factors affecting skin surface, tend to increase skin surface pH, one could expect that reported averages may be skewed toward the higher values. Lambers et al. measured skin surface on the volar forearm of 330 volunteers before and after 24 hours period without contact with water or any cosmetic products. The initial average pH value for the entire group was 5.13 and after 24 hours 4.93 with the accompanying standard deviation decrease from 0.56 to 0.45. They observed that the subjects with the initial pH 5 or higher (n=185) tended to drop pH, the subjects with the initial pH between 4.5 and 5 (average 4.74) tended to stay in this range, and subjects with the initial pH 4.5 or lower tended to increase pH after the 24 hours period. Based on this observation, they concluded that the natural skin surface pH could be around 4.7.14
Skin pH is elevated in eczema
Atopic dermatitis (AD) or atopic eczema is the most common and most studies dermatitis. AD is a chronic inflammatory disorder characterized by a red and itchy rash. It often develops in children but it can start at any age.15 It is a chronic condition with periodic flareups. The pathophysiology of AD is complex, involving barrier dysfunction, alteration in cell-mediated immune response, IgE mediated hypersensitivity, and environmental factors.15 Skin barrier dysfunction is considered to be the first step in the development of the atopic dermatitis symptoms.16–18 A number of studies showed that skin surface pH is elevated (between 0.1 and 0.9 pH unit) in patients affected by atopic dermatitis and the increase correlates with the severity of the symptoms. The elevated pH observed in AD patients increased in the following order: healthy skin, uninvolved skin in patients with lesions, uninvolved skin in patients with an active lesion, pre-lesional skin, and lesional skin.10,19–22 It is important to note that the increased skin surface pH in atopic dermatitis can contribute to the further progression of the pathology of AD. Disruption of this vicious cycle is, therefore, critical to stopping the progression of the atopic march. Acidification of the skin surface has been suggested as a potential therapeutic approach in AD.
Studies show that keeping skin surface pH below pH 5 has a therapeutic effect on the skin barrier and eczema
Studies in animal models demonstrated that acidification of skin surface by the topical application of low pH formulations can prevent the emergence of atopic dermatitis and prevent atopic march to asthma.23–25
Studies on human subjects have also shown therapeutic effect of skin surface acidification. One study showed that the application of acidic water reduced skin surface pH and decreased levels of resident S. aureus.26 Another study demonstrated that long-term (4 weeks) application of water-in-oil emulsion adjusted to pH 4.0 can result in sustained skin surface pH reduction by ~0.5 pH unit.27 Still, another study showed that low pH formulation of lactic acid (pH 3.7-4) led to a significant decrease in skin surface pH and reduction in transepidermal water loss and consequently improvement in barrier function.28 Hachem et al. demonstrated that acidification of stratum corneum using polyhydroxy acids (lactobionic acid pH 2.8 and gluconolactone pH 3.2) improves permeability barrier homeostasis and improvement in the stratum corneum cohesion and integrity.26 Blaak et al. studied the effect of oil-in-water emulsions at pH 3.5 and 4.0 on aged skin. They demonstrated that the acidic emulsions were able to lower skin surface pH and improve skin barrier function.29 Kilic et al. compared the effect of a 4-week treatment with water-in-oil emulsions with pH 4 and pH 5.8. The pH 4 formulations resulted in a significantly lower skin pH and improved skin hydration as compared to pH 5.8 emulsions in elderly skin. The treatment with pH 4 emulsions also showed the improved structure of lipid lamellae and improved resistance to SDS challenge.30
pH buffering capacity is key to maintaining optimal skin surface pH
pH buffering capacity is the measure of the solution to resist pH change by either absorbing or desorbing H+. The higher the pH buffering capacity the better the solution resist pH change. Currently, most of the cosmetic products on the market don’t specify pH and it is impossible to determine the pH value from the ingredients listed on the product label. Moreover, when considering skincare products, knowing the pH buffering capacity of the product is as important as knowing the pH value of the product. pH alone doesn’t tell how the formulation can withstand pH fluctuation and resist pH change. For example, even if a formulation has pH 5 or lower but very low pH buffering capacity, the formulation may easily change pH when applied on the skin and consequently have very little effect on the skin surface pH. In a 2018 study, Wohlrab and Gebert assessed 58 leave-on products that claim skin barrier protection. They found that only 8 of these 58 products had pH 5 or lower. Out of these 8 products, only 4 had a significant (>0.5 moles) pH buffering capacity 31. Many current formulations don’t have any buffering system and some contain buffers that have a pKa far away from the product’s pH value, making the formulation’s buffer useless in maintaining proper pH.
How our products correct skin surface pH
Soteri products are designed to holistically support skin barrier renewal. In addition to ingredients that support the physical barrier, such as skin mimicking ceramide, cholesterol, and free fatty acid complex, as well as niacinamide and phystosphingosine, they also contain ingredients that support the skin acid mantle over the course of hours. Our patented combination of ingredients (pHrotect™) provide optimal skin surface pH and strong pH buffering capacity. The strong pH buffering capacity is the key to maintain the pH of your skin at the optimal level over the course of hours. This long-lasting pH control provides direct protection against environmental stressors and also stimulates skin barrier repair and renewal.
References
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- Ohman H, Vahlquist A. The pH gradient over the stratum corneum differs in X-linked recessive and autosomal dominant ichthyosis: a clue to the molecular origin of the “acid skin mantle”? J Invest Dermatol. 1998;111(4):674-677. doi:10.1046/j.1523-1747.1998.00356.x
- Proksch E, Jensen J-M, Elias PM. Skin lipids and epidermal differentiation in atopic dermatitis. Clin Dermatol. 2003;21(2):134-144. doi:10.1016/s0738-081x(02)00370-x
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- Adam R. Skin care of the diaper area. Pediatr Dermatol. 2008;25(4):427-433. doi:10.1111/j.1525-1470.2008.00725.x
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- Lowe AJ, Leung DYM, Tang MLK, Su JC, Allen KJ. The skin as a target for prevention of the atopic march. Ann allergy, asthma Immunol Off Publ Am Coll Allergy, Asthma, Immunol. 2018;120(2):145-151. doi:10.1016/j.anai.2017.11.023
- Kim J, Kim BE, Leung DYM. Pathophysiology of atopic dermatitis: Clinical implications. Allergy asthma Proc. 2019;40(2):84-92. doi:10.2500/aap.2019.40.4202
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- Eberlein-König B, Schäfer T, Huss-Marp J, et al. Skin surface pH, stratum corneum hydration, trans-epidermal water loss and skin roughness related to atopic eczema and skin dryness in a population of primary school children. Acta Derm Venereol. 2000;80(3):188-191. doi:10.1080/000155500750042943
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- Danby SG, Cork MJ. pH in Atopic Dermatitis. Curr Probl Dermatol. 2018;54:95-107. doi:10.1159/000489523
- Hatano Y, Man M-Q, Uchida Y, et al. Maintenance of an acidic stratum corneum prevents emergence of murine atopic dermatitis. J Invest Dermatol. 2009;129(7):1824-1835. doi:10.1038/jid.2008.444
- Lee H-J, Yoon NY, Lee NR, Jung M, Kim DH, Choi EH. Topical acidic cream prevents the development of atopic dermatitis- and asthma-like lesions in murine model. Exp Dermatol. 2014;23(10):736-741. doi:10.1111/exd.12525
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- Hachem J-P, Roelandt T, Schürer N, et al. Acute acidification of stratum corneum membrane domains using polyhydroxyl acids improves lipid processing and inhibits degradation of corneodesmosomes. J Invest Dermatol. 2010;130(2):500-510. doi:10.1038/jid.2009.249
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- Blaak J, Wohlfart R, Schürer NY. Treatment of Aged Skin with a pH 4 Skin Care Product Normalizes Increased Skin Surface pH and Improves Barrier Function: Results of a Pilot Study. J Cosmet Dermatological Sci Appl. 2011;01(03):50-58. doi:10.4236/jcdsa.2011.13009
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