Formulating for the Epidermal Barrier: The Science of Body Cleansing

Your skin is not a surface. It is a living, breathing organ—the largest organ in your body—and it is under constant assault. UV radiation. Environmental pollutants. Temperature extremes. Mechanical abrasion. Pathogenic bacteria. And, perhaps most insidiously, your daily cleanser.

When you wash your body, you are not simply removing dirt. You are performing a controlled disruption of the epidermal barrier, the outermost protective layer that keeps your body's water inside and the outside world's pathogens outside. The formulator's challenge is to cleanse effectively—removing sweat, sebum, environmental grime, and microbial overgrowth—without destroying the very structure that keeps your skin intact.

This is not a trivial problem. Traditional soap, with its alkaline pH and aggressive lipid-stripping action, has been damaging the skin barrier for thousands of years. Modern syndets offer a better path, but only if the formulator understands the architecture of the barrier, the mechanisms of surfactant damage, and the delicate ecosystem of microbes that call your skin home.

This is the science of formulating for the epidermal barrier: brick-and-mortar structure, transepidermal water loss, and the acid mantle that holds it all together.

The Brick and Mortar Structure

The stratum corneum is the outermost layer of the epidermis, composed of 10-20 layers of dead, flattened cells called corneocytes. These cells are the remnants of keratinocytes that migrated upward from the deeper layers of the epidermis, gradually losing their nuclei, organelles, and metabolic machinery as they filled with keratin—a tough, fibrous structural protein. By the time they reach the surface, they are no longer alive. They are bricks.

But bricks alone do not make a wall. The structural integrity of the stratum corneum depends not on the corneocytes themselves, but on the lipid matrix that binds them together. This matrix, often called the "mortar," is composed of three primary lipid classes: ceramides, cholesterol, and free fatty acids, which exist in an approximately 1:1:1 molar ratio (Ananthapadmanabhan et al., 2013).

The Mortar: Ceramides, Cholesterol, and Free Fatty Acids

The lipid mortar is not a random assortment of fats. It is a precisely organized, lamellar (layered) structure in which the lipid molecules are arranged in alternating hydrophobic and hydrophilic sheets. This organization creates a tortuous, hydrophobic pathway that water must navigate to escape from the body—effectively slowing the rate of transepidermal water loss (TEWL) and preventing the entry of irritants and pathogens from the environment.

Ceramides are the most abundant lipids in the stratum corneum, making up approximately 50% of the lipid content by weight (Recent Advances on Topical Application of Ceramides, MDPI, 2017). They are composed of a sphingoid base (such as sphingosine) linked to a long-chain fatty acid. There are at least 12 distinct ceramide subtypes in human skin, each with slightly different chain lengths and hydroxylation patterns, and all of them contribute to the structural integrity of the lipid bilayers.

Cholesterol makes up roughly 25% of the stratum corneum lipids. It fills the gaps between ceramides and free fatty acids, increasing membrane fluidity and preventing the lipid layers from becoming too rigid or crystalline. Cholesterol also plays a critical role in barrier repair: when the stratum corneum is damaged, cholesterol synthesis increases to help restore the lipid matrix.

Free fatty acids (FFAs) make up the remaining 25% and include palmitic acid (C16:0), stearic acid (C18:0), oleic acid (C18:1), and linoleic acid (C18:2). These acids help regulate the fluidity and permeability of the lipid bilayers and contribute to the acidic pH of the skin surface—a topic we will explore in depth shortly.

When the 1:1:1 ratio of ceramides, cholesterol, and free fatty acids is disrupted—either through excessive cleansing, UV damage, or intrinsic aging—the barrier becomes compromised. Water escapes more easily. Irritants penetrate more deeply. The skin becomes dry, tight, itchy, and inflamed (Recent Advances on Topical Application of Ceramides, MDPI, 2017).

What Happens When the Mortar Dissolves

Surfactants, by their very nature, are designed to interact with lipids. The hydrophobic tail of a surfactant molecule burrows into lipid membranes, disrupting their structure and extracting individual lipid molecules into micelles. This is exactly what makes surfactants effective at removing sebum and oils from the skin surface—but it is also what makes them potentially destructive to the stratum corneum.

When you wash with a harsh surfactant—particularly small-molecule sulfates like SLS—the surfactant does not discriminate between surface sebum and the structural lipids of the lipid matrix. It extracts ceramides, cholesterol, and free fatty acids from the intercellular spaces, leaving behind a porous, leaky barrier (Ananthapadmanabhan et al., 2013). The corneocytes remain, but without the mortar to hold them together, the barrier cannot function.

The result is a phenomenon familiar to anyone who has ever washed with harsh soap: that tight, dry, uncomfortable feeling that sets in within minutes of toweling off. It is not merely "dryness" in the colloquial sense. It is barrier disruption, and the tightness you feel is your skin desperately trying to retain what little moisture it has left.

Transepidermal Water Loss (TEWL): Measuring Barrier Damage

The most widely used clinical metric for assessing skin barrier integrity is transepidermal water loss (TEWL), defined as the rate at which water evaporates from the skin surface into the surrounding air, measured in grams per square meter per hour (g m⁻² h⁻¹) (Kubota et al., 2021).

In healthy, intact skin, TEWL is typically in the range of 4-8 g m⁻² h⁻¹. This low rate of water loss reflects the effectiveness of the lipid matrix in slowing the diffusion of water molecules through the stratum corneum. But when the barrier is disrupted—whether by surfactants, UV exposure, mechanical abrasion, or disease—TEWL increases dramatically.

How Surfactants Increase TEWL

Surfactants increase TEWL through two primary mechanisms: lipid extraction and protein denaturation.

Lipid extraction is the more straightforward mechanism. As discussed earlier, surfactants dissolve and remove the ceramides, cholesterol, and free fatty acids from the intercellular lipid matrix, leaving behind gaps and increasing the permeability of the barrier. Studies have shown that even a single wash with SLS can significantly reduce the total lipid content of the stratum corneum, with the effects persisting for hours after rinsing (Ananthapadmanabhan et al., 2013).

Protein denaturation is more subtle but equally damaging. Surfactants—especially anionic surfactants with small molecular size—adsorb to the surface of corneocytes and denature the keratin proteins within them. This denaturation causes the corneocytes to swell, exposing new water-binding sites and leading to an initial hyper-hydration of the stratum corneum (Kubota et al., 2021). While this might sound beneficial, it is not. The swelling disrupts the tight packing of the corneocytes and increases the spacing between cells, which in turn increases the permeability of the barrier to water loss.

Over time, this combination of lipid extraction and protein swelling leads to a cascade of barrier dysfunction: increased TEWL, reduced hydration, impaired desquamation (the shedding of dead skin cells), and activation of inflammatory pathways. The skin becomes dry, rough, flaky, and prone to irritation.

In controlled studies, exposure to SLS has been shown to increase TEWL from a baseline of approximately 5 g m⁻² h⁻¹ to over 40 g m⁻² h⁻¹—an eight-fold increase (Ananthapadmanabhan et al., 2004). This is not a minor cosmetic inconvenience. It is measurable, clinically significant barrier damage.

The Tight, Dry, Itchy Feeling Explained

The sensation of tightness after washing with harsh soap is a direct consequence of increased TEWL. As water evaporates from the stratum corneum faster than it can be replenished from the deeper layers of the epidermis, the corneocytes shrink and contract. This physical contraction of the skin is what you perceive as tightness.

The dryness that follows is the result of prolonged water loss. Without an intact lipid matrix to slow evaporation, the stratum corneum becomes dehydrated, losing its flexibility and becoming brittle. This is why skin "cracks" in cold, dry weather after washing with harsh cleansers—the combination of low environmental humidity and compromised barrier function creates a perfect storm of dehydration.

The itching, finally, is an inflammatory response. When the barrier is disrupted, the immune system detects the breach and releases inflammatory mediators—cytokines, histamines, and prostaglandins—that trigger the sensation of itch. Scratching provides temporary relief but further damages the barrier, perpetuating a vicious cycle of inflammation and disruption.

Sebum: Friend or Foe?

Sebum is the oily secretion produced by the sebaceous glands, which are attached to hair follicles throughout the body (though they are most concentrated on the face, scalp, and upper back). Sebum is composed primarily of triglycerides, wax esters, squalene, and free fatty acids—a complex mixture of lipids that serves several critical functions.

Sebum's Protective Role

At baseline levels, sebum is protective. It forms a thin, hydrophobic film on the surface of the skin that helps to: - Reduce TEWL by adding an additional lipid layer on top of the stratum corneum - Lubricate the skin, preventing friction and mechanical damage - Deliver antioxidants (such as squalene and vitamin E) to the skin surface - Support the acid mantle by contributing free fatty acids that lower surface pH

In this sense, sebum is not something to be eliminated—it is part of the skin's natural defense system.

When Sebum Goes Wrong: Oxidation and Body Acne

The problem arises when sebum accumulates on the skin surface for extended periods, especially in warm, humid environments. Over time, the lipids in sebum undergo oxidation, breaking down into smaller, pro-inflammatory molecules such as squalene peroxide and oxidized fatty acids. These oxidized lipids can penetrate the hair follicle and trigger inflammation, leading to body acne (bacne, chest acne, etc.) (Blaak et al., 2022).

Additionally, excess sebum provides a nutrient source for opportunistic bacteria such as Cutibacterium acnes (formerly Propionibacterium acnes), which metabolize triglycerides into free fatty acids that further irritate the follicle lining and promote acne formation.

The Balance: Remove Excess Without Stripping the Foundation

The formulator's challenge is to design a body cleanser that removes excess, oxidized sebum from the skin surface—preventing acne and microbial overgrowth—without stripping away the structural lipids of the stratum corneum or disrupting the natural sebum film that protects the barrier.

This is where surfactant selection becomes critical. Harsh, small-molecule surfactants like SLS do not distinguish between surface sebum and intercellular lipids—they extract both indiscriminately, leaving the skin stripped and vulnerable. Large-molecule surfactants like SCI, by contrast, remain on the surface, removing oxidized sebum and environmental dirt without penetrating the stratum corneum to disrupt the lipid matrix beneath.

This is not about "gentleness" as a marketing buzzword. It is about selectivity—choosing a cleanser that targets what needs to be removed while preserving what needs to stay.

The Acid Mantle and pH

The term acid mantle was coined in 1928 by dermatologists Marchionini and Haüser to describe the slightly acidic surface pH of human skin (The Origin, Intricate Nature, and Role of the Skin Surface pH, MDPI, 2025). For nearly a century, dermatologists and cosmetic chemists have recognized that this acidic pH is not incidental—it is essential for barrier integrity, immune defense, and microbial balance.

The Skin's Natural pH: 4.5 - 5.5

Healthy human skin maintains a surface pH between 4.5 and 5.5, with slight variations depending on body site, age, sex, and environmental conditions (The Evaluating Skin Acid–Base Balance After Application of Cold-Processed and Hot-Processed Natural Soaps, MDPI, 2024). This acidity is generated primarily by the free fatty acids in the stratum corneum and sebum, as well as by acidic metabolites produced by the skin microbiome.

The acidic pH serves several critical functions: 1. Maintains lipid lamellar structure: The organization of the lipid bilayers in the stratum corneum is pH-dependent. At acidic pH, the lipids are tightly packed and well-ordered, creating an effective barrier. At neutral or alkaline pH, the lipid structure becomes disordered and permeable (The Origin, Intricate Nature, and Role of the Skin Surface pH, MDPI, 2025).

1. Activates barrier repair enzymes: Enzymes involved in ceramide synthesis and lipid processing (such as beta-glucocerebrosidase and acidic sphingomyelinase) function optimally at acidic pH. When pH rises, these enzymes are less active, and barrier repair is impaired.

2. Inhibits pathogenic bacteria: Most pathogenic bacteria, including Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa, prefer neutral to slightly alkaline environments and are inhibited by acidic pH (The Skin Microbiome and Bioactive Compounds, MDPI, 2025).

3. Supports commensal microbiota: The beneficial bacteria that colonize healthy skin—such as Staphylococcus epidermidis and Cutibacterium acnes (in balanced amounts)—are acidophilic, meaning they thrive at acidic pH and are outcompeted by pathogens when pH rises.

The Microbiome Connection

Your skin is home to trillions of microorganisms—bacteria, fungi, viruses, and mites—collectively referred to as the skin microbiome. Far from being passive hitchhikers, these microbes play active roles in barrier defense, immune regulation, and even wound healing.

The composition of the skin microbiome is highly pH-dependent. At the skin's natural pH of 4.5 - 5.5, beneficial bacteria such as Staphylococcus epidermidis dominate. S. epidermidis produces antimicrobial peptides that inhibit pathogenic bacteria, modulates the host immune response to reduce inflammation, and even synthesizes ceramides that contribute to barrier integrity (The Skin Microbiome and Bioactive Compounds, MDPI, 2025).

But when skin pH rises—as it does after washing with alkaline soap (pH 9-11)—the microbial balance shifts. S. epidermidis is suppressed, while opportunistic pathogens like Staphylococcus aureus proliferate. S. aureus is a major contributor to atopic dermatitis, eczema, and skin infections, and its overgrowth is strongly associated with elevated skin pH (The Evaluating Skin Acid–Base Balance After Application of Cold-Processed and Hot-Processed Natural Soaps, MDPI, 2024).

Similarly, elevated pH favors the pathogenic yeast Candida albicans, which can transform from its benign commensal form into a virulent, invasive form when the acid mantle is disrupted.

Alkaline Soap and Microbiome Disruption

Traditional soap, with its pH of 9-11, is catastrophic for the acid mantle. Even a single wash with soap elevates skin pH to 8-10 for a period of 1-2 hours before the skin's natural buffering systems can restore acidity (The Evaluating Skin Acid–Base Balance After Application of Cold-Processed and Hot-Processed Natural Soaps, MDPI, 2024). During this window, the skin is vulnerable: barrier enzymes are inactive, pathogenic bacteria proliferate, and the lipid structure is disordered.

With repeated washing—as most people do daily—the skin never fully recovers. The acid mantle is chronically disrupted, the microbiome is chronically imbalanced, and the barrier is chronically compromised. This is why people who use traditional soap often experience dry, itchy, inflamed skin, despite moisturizing diligently. The problem is not a lack of moisturizer—it is the cleanser.

Syndets formulated at a pH of 4.5 - 5.5, by contrast, preserve the acid mantle. They do not elevate skin pH. They do not disrupt the microbiome. They cleanse the surface while leaving the underlying barrier and microbial ecosystem intact.

This is not a luxury. It is a necessity for long-term skin health.

Surfactant Selection for Body Skin

Given what we now understand about the brick-and-mortar structure of the stratum corneum, the mechanisms of TEWL, and the critical importance of the acid mantle, the criteria for choosing surfactants for body cleansers become clear.

We need surfactants that: 1. Do not penetrate the stratum corneum (large molecular size) 2. Do not extract structural lipids (selectivity for surface sebum over intercellular lipids) 3. Do not denature proteins (low charge density, synergistic co-surfactant use) 4. Can be formulated at pH 4.5 - 5.5 (syndets, not soap)

Why SCI is Ideal for Body Bars

Sodium Cocoyl Isethionate (SCI) meets all of these criteria. As we established in Part 1 of this series, SCI micelles have a radius of approximately 33.5 Å, which is larger than the aqueous pores of the stratum corneum (29 ± 5 Å). This means SCI cannot penetrate the barrier—it remains on the surface, where it gently lifts away surface sebum, sweat, and environmental dirt (Ananthapadmanabhan et al., 2004).

SCI is also selective for sebum over structural lipids. Research has shown that cleansing with SCI preserves the free fatty acid content of the stratum corneum significantly better than cleansing with SLS, resulting in lower TEWL and faster barrier recovery (Ananthapadmanabhan et al., 2013). This selectivity is attributed to SCI's inability to penetrate deeply into the lipid bilayers, where the structural ceramides and cholesterol reside.

Finally, SCI produces a rich, creamy lather and can be formulated into solid bars that are stable, cost-effective, and consumer-friendly. For body cleansing, it is the gold standard.

The Role of CAPB in Mixed Micelles

While SCI is mild on its own, its mildness can be further enhanced by combining it with Cocamidopropyl Betaine (CAPB), an amphoteric surfactant. As discussed in Part 1, CAPB forms mixed micelles with anionic surfactants like SCI, creating larger, less charged aggregates that are even less likely to denature proteins or disrupt the barrier (Wolf et al., 2001).

The optimal ratio of SCI to CAPB for body cleansers is approximately 2:1 by weight of active surfactant. At this ratio, the formulation exhibits: - Enhanced foam stability and creaminess - Reduced TEWL compared to SCI alone - Improved sensory feel (less squeaky, more moisturizing) - Lower irritation potential for sensitive skin

For most body bar formulations, this combination of SCI + CAPB provides an ideal balance of efficacy and mildness.

When to Add Decyl Glucoside

For individuals with extremely sensitive skin, eczema, or atopic dermatitis, even SCI + CAPB may be too aggressive. In these cases, formulators can incorporate Decyl Glucoside—a non-ionic, sugar-derived surfactant that is among the mildest cleansers available (CIR, n.d.).

Decyl Glucoside does not produce as much foam as SCI, and it is less effective at removing heavy sebum or oils. But for individuals whose barrier is already compromised, the priority is not aggressive cleansing—it is barrier preservation. A body bar formulated with SCI + CAPB + Decyl Glucoside can provide the gentlest possible cleanse while still maintaining acceptable lather and sensory properties.

What to Avoid (and Why)

For body cleansers, formulators should avoid: - SLS and SLES: Too small, too aggressive, too damaging to the lipid matrix - SCS (Sodium Coco Sulfate): Contains ~50% SLS, still irritating despite being "natural" - Traditional soap: Alkaline pH (9-11), disrupts acid mantle and microbiome, forms soap scum in hard water - High concentrations of any single surfactant: Even mild surfactants can be irritating at concentrations above 20-25%; synergistic blends allow for lower total surfactant content

Formulating the Complete Body Bar

A well-formulated body syndet bar is more than just a blend of surfactants. It requires careful attention to pH, structural integrity, and sensory properties.

Surfactant Blend Ratios

A typical body bar formulation might include: - 35-45% SCI (primary cleanser, capped to prevent irritation) - 20-30% CAPB (co-surfactant for mildness and foam) - 0-10% Decyl Glucoside (optional, for extra mildness) - 10-20% fatty alcohols or acids (cetyl alcohol, stearic acid) for structural integrity and texture - 2-5% superfatting oils (optional; see below)

pH Adjustment and Testing

Because syndets can be formulated at any pH, the formulator must actively adjust the pH to the target range of 4.5 - 5.5. This is typically achieved by adding small amounts of citric acid or lactic acid to the formulation during the manufacturing process.

To test the pH of a solid bar, dissolve a small amount (1-2 grams) in distilled water (50 mL) and measure the pH of the resulting solution with a calibrated pH meter. The in-use pH will be similar, though it may vary slightly depending on the hardness and mineral content of the user's water.

Superfatting for Body Bars: Yes or No?

Superfatting refers to the practice of adding unreacted oils to a cleanser formulation, such that a small amount of oil remains on the skin after rinsing. In traditional soap, superfatting is achieved by using excess fat relative to the lye, leaving 5-10% of the fats unsaponified.

In syndets, superfatting is less common for body bars because the surfactants are already mild and non-stripping. Adding oils to a syndet bar can make the bar feel greasy or leave a residue on the skin, which many consumers dislike.

However, for individuals with very dry skin or eczema, a lightly superfatted body bar (2-5% oils) can provide additional barrier support without feeling heavy. Suitable oils for body bar superfatting include: - Jojoba oil (liquid wax ester, absorbs quickly) - Babassu oil (similar to coconut oil but lighter) - Shea butter (rich in ceramide precursors)

The key is moderation—too much oil will interfere with lather and rinsing.

Testing Barrier Impact

The gold standard for evaluating the mildness of a body cleanser is TEWL measurement. Ideally, a new formulation should be tested in a controlled patch study where volunteers wash a defined area of skin with the test product, and TEWL is measured before and after washing, as well as at intervals up to 24 hours later.

A truly mild body bar should cause minimal increase in TEWL (less than 10-15% above baseline) and should allow the barrier to recover fully within 4-6 hours.

For formulators without access to clinical testing equipment, user feedback on tightness, dryness, and irritation can serve as a proxy. If users consistently report that their skin feels tight or dry after using the bar, the formulation likely needs adjustment—either by increasing the proportion of CAPB, lowering the total surfactant concentration, or adding a small amount of superfatting oil.

The Potionologie Approach

At Potionologie, our body bar philosophy is simple: cleanse effectively, preserve the barrier.

We formulate our body syndet bars with SCI as the primary surfactant, buffered with CAPB at a 2:1 ratio to create mild, stable, protein-sparing mixed micelles. We adjust the pH to 4.5 - 5.5 using citric acid, ensuring that the acid mantle is preserved and the skin microbiome remains balanced. We avoid SLS, SLES, SCS, and traditional soap entirely—not because they are "toxic," but because they are incompatible with the long-term health of the epidermal barrier.

We do not routinely superfat our body bars, because we have found that the mildness of the SCI + CAPB blend makes superfatting unnecessary for most users. However, for customers with eczema or clinically dry skin, we offer a sensitive skin variant that includes 3% jojoba oil, providing additional lipid support without compromising lather or rinsability.

We test every formulation in hard water, because we know that many of our customers live in regions with high mineral content, and we refuse to create products that leave soap scum or waxy buildup on the skin.

This is not about "natural" or "clean" beauty. It is about formulating with the biology of the skin in mind. It is about understanding that the stratum corneum is not an inert surface to be scrubbed, but a living, dynamic barrier that must be protected if you want healthy, resilient skin.

Conclusion

The skin is not a dishcloth. It is not a plate. It is a complex, multilayered organ with its own chemistry, its own microbial ecosystem, and its own delicate balance of lipids, proteins, and water. When you formulate a body cleanser, you are not just designing something that makes bubbles—you are designing something that interacts with the brick-and-mortar architecture of the stratum corneum, that affects the rate of transepidermal water loss, and that shifts the pH and microbial composition of the acid mantle.

The formulator's responsibility is to cleanse without destroying. To remove sebum without stripping ceramides. To create lather without denaturing proteins. To wash away the dirt of the day without washing away the barrier that keeps your skin intact.

This is why we choose large-molecule surfactants. This is why we formulate at pH 4.5 - 5.5. This is why we avoid traditional soap. Not because it is trendy or marketable, but because the science is unambiguous: the barrier matters, and the choices we make as formulators determine whether that barrier thrives or fails.

In Part 3 of this series, we will turn our attention to hair and scalp, where the challenges are even more complex: a living scalp that requires the same barrier protection as body skin, and a dead hair shaft whose cuticle structure and lipid coating demand their own set of formulation strategies.

For now, it is enough to understand that the body is not one-size-fits-all. The surfactants we choose, the pH we target, and the synergistic blends we design all determine whether our cleansers protect the barrier—or destroy it.

Choose wisely.

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References

Ananthapadmanabhan, K.P., Moore, D.J., Subramanyan, K., Misra, M., & Meyer, F. (2004). Cleansing without compromise: The impact of cleansers on the skin barrier and the technology of mild cleansing. Dermatologic Therapy, 17(Suppl. 1), 16-25. https://doi.org/10.1111/j.1396-0296.2004.04s1002.x

Ananthapadmanabhan, K.P., Lips, A., Vincent, C., Meyer, F., Caso, S., Johnson, A., Subramanyan, K., Vethamuthu, M., Rattinger, G., & Schafer, F. (2013). Stratum corneum fatty acids: Their critical role in preserving barrier integrity during cleansing. International Journal of Cosmetic Science, 35(4), 337-345. https://doi.org/10.1111/ics.12042

Blaak, J., Staib, P., Kendall, A.C., Nicolaou, A., & Gijsbers, J.W. (2022). The impact of daily facial cleansing on the lipid barrier in individuals with a sensitive skin. Skin Research and Technology, 28(2), 243-251. https://doi.org/10.1111/srt.13124

Cosmetic Ingredient Review (CIR) Expert Panel. (n.d.). Safety Assessment of Alkyl Glucosides as Used in Cosmetics. Retrieved from https://www.cir-safety.org/

Kubota, K., Okuda, M., Noro, Y., Sekimoto, M., Kojima, H., & Kusakari, Y. (2021). The involvement of protein denaturing activity in the effect of surfactants on skin barrier function. Skin Research and Technology, 27(4), 542-548. https://doi.org/10.1111/srt.12939

MDPI. (2017). Recent Advances on Topical Application of Ceramides to Restore Barrier Function of Skin. Cosmetics, 6(3), 52. https://doi.org/10.3390/cosmetics6030052

MDPI. (2024). The Evaluating Skin Acid–Base Balance After Application of Cold-Processed and Hot-Processed Natural Soaps: A Double-Blind pH Monitoring Study. Cosmetics, 12(3), 120. https://doi.org/10.3390/cosmetics12030120

MDPI. (2025). The Origin, Intricate Nature, and Role of the Skin Surface pH (pHSS) in Barrier Integrity, Eczema, and Psoriasis. Cosmetics, 12(1), 24. https://doi.org/10.3390/cosmetics12010024

MDPI. (2025). The Skin Microbiome and Bioactive Compounds: Mechanisms of Modulation, Dysbiosis, and Dermatological Implications. Molecules, 30(22), 4363. https://doi.org/10.3390/molecules30224363

Wolf, R., Wolf, D., Tüzün, B., & Tüzün, Y. (2001). Soaps, shampoos, and detergents. Clinics in Dermatology, 19(4), 393-397. https://doi.org/10.1016/s0738-081x(01)00188-2