The Baumann Skin Typing System 117 Leslie S. Baumann Contents Introduction ........................................ 1579 Skin Hydration: The Oily (O) To Dry (D) Continuum ......................................... 1582 Stratum Corneum (SC) ............................. 1582 Natural Moisturizing Factor (NMF) ................ 1583 Aquaporin-3 ........................................ 1583 Sebum ............................................... 1584 Differences in Skin Care for Oily and Dry Skin . . . 1585 Oily Skin Care ...................................... 1585 Dry Skin Care ....................................... 1585 Occlusives .......................................... 1585 Humectants ......................................... 1586 Collagen and Polypeptide Ingredients ............. 1588 Skin Sensitivity: The Sensitive (S) to Resistant (R) Continuum ......................... 1588 Acne Type .......................................... 1588 Rosacea Type ....................................... 1589 Stinging Type ....................................... 1589 Allergic Type ....................................... 1590 Treatment Approaches for Sensitive Skin .......... 1590 Skin Pigmentation: The Pigmented (P) to Nonpigmented (N) Continuum ................ 1590 Skin Aging: The Wrinkled (W) to Tight (T) Continuum ......................................... 1591 Skin Care Regimens Based on Baumann Skin Type ............................... 1593 Summary ........................................... 1593 References .......................................... 1594 Abstract The biology of various skin phenotypes, such as oily, dry, acne-prone, rosacea-prone, dyschromia, and photoaged, affects the interac- tion and efficacy of cosmeceutical ingredients. This chapter will review how cosmeceuticals influence basic skin biology and how they inter- act with each other in various patient pheno- types, as characterized by the Baumann Skin Typing System (BSTS). Developed in 2004, the BSTS, derived from a scientifically validated questionnaire, offers specific guidance for phy- sicians and patients/consumers in identifying the most suitable ingredients and skin products as it takes into account multiple concurrent cutaneous characteristics and gathers historical data. The reader will be provided with knowl- edge of the basic science of different skin issues and will obtain a scientific perspective on how to design skin care regimens, combine cosmeceuticals with prescription medications, educate staff and patients on their proper use, and ethically prescribe skin care products using this standardized methodology. Introduction As of 2011, the cosmeceutical industry was con- sidered to be a $6.5 billion business [1], and global sales of topical cosmeceuticals surpassed $33 billion in 2012, with projected sales exceed- ing $42 billion by 2017 [2]. The promise of L.S. Baumann (*) Baumann Cosmetic and Research Institute, Miami, FL, USA e-mail: [email protected]; [email protected]# Springer-Verlag Berlin Heidelberg 2017 M.A. Farage et al. (eds.), Textbook of Aging Skin, DOI 10.1007/978-3-662-47398-6_88 1579
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The Baumann Skin Typing System 117Leslie S. Baumann
AbstractThe biology of various skin phenotypes, suchas oily, dry, acne-prone, rosacea-prone,dyschromia, and photoaged, affects the interac-tion and efficacy of cosmeceutical ingredients.This chapter will review how cosmeceuticalsinfluence basic skin biology and how they inter-act with each other in various patient pheno-types, as characterized by the Baumann SkinTyping System (BSTS). Developed in 2004, theBSTS, derived from a scientifically validatedquestionnaire, offers specific guidance for phy-sicians and patients/consumers in identifyingthe most suitable ingredients and skin productsas it takes into account multiple concurrentcutaneous characteristics and gathers historicaldata. The reader will be provided with knowl-edge of the basic science of different skin issuesand will obtain a scientific perspective on howto design skin care regimens, combinecosmeceuticals with prescription medications,educate staff and patients on their proper use,and ethically prescribe skin care products usingthis standardized methodology.
Introduction
As of 2011, the cosmeceutical industry was con-sidered to be a $6.5 billion business [1], andglobal sales of topical cosmeceuticals surpassed$33 billion in 2012, with projected sales exceed-ing $42 billion by 2017 [2]. The promise of
# Springer-Verlag Berlin Heidelberg 2017M.A. Farage et al. (eds.), Textbook of Aging Skin,DOI 10.1007/978-3-662-47398-6_88
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financial success has resulted in the discovery ofmany new cosmeceutical technologies and signif-icant advances in understanding skin science andthe effects on skin by topically applied substances.The emergence of many new ingredients and top-ical formulations has manifested in an abundanceof products on the market, exaggerated marketingclaims, and confusion on the part of consumers,aestheticians, and physicians. The major currentchallenge is to sift through the copious technolo-gies and formulations and match cosmeceuticaltechnologies to the appropriate type of skin. Asnew genetic data lead to advances in skin caretechnologies, the importance of the genotype aswell as the phenotype cannot be overstated. Aningredient is only efficacious when it is placed onthe correct skin phenotype. Combining ingredi-ents affects their chemical structure, efficacy, andpenetration; therefore, the order in which productsare placed on the skin is important. The phenotypeof the skin will also affect how ingredients pene-trate into the skin and react with each other. Inorder to maximize outcomes with cosmeceuticals,there are many steps that should be taken to prop-erly match a skin care regimen with the properskin phenotype (Table 1).
The Baumann Skin Typing System (BSTS)was developed in 2004 and classifies skinaccording to four dichotomous parameters: dry
or oily, sensitive or resistant, pigmented ornonpigmented, and wrinkled or unwrinkled.Simultaneously assessing the skin based on thesefour non-mutually exclusive parameters yields16 potential and distinct skin phenotypes(Table 2). The Baumann Skin Type® designationsfor each phenotype are derived from a scientifi-cally validated questionnaire known as theBaumann Skin Type Indicator (BSTI). TheBaumann Skin Type can change after significantalterations in lifestyle habits, hormones, medicalcondition, and environment and therefore shouldbe retaken annually or when the current skin careregimen seems insufficient [3, 4].
The BSTS, by nature, offers specific guidancefor physicians and patients/consumers in identify-ing the most suitable ingredients and skin prod-ucts as it takes into account multiple concurrentcutaneous characteristics and gathers historicaldata. The questionnaire probes how the skin reactsin various situations, allowing the collection ofhistorical data and the current skin condition.
Each of the distinct Baumann Skin Types dis-play characteristics that determine which ingredi-ents are beneficial and which are deleterious. Forexample, a person with dry, sensitive, pigmented,wrinkle-prone skin (DSPW) would require signif-icantly different skin care products than a personwith oily, resistant, nonpigmented, “tight” (notwrinkle-prone) skin (ORNT). Oily-resistant skintypes have a strong skin barrier with an extra layerof sebum to prevent penetration of ingredients;therefore, individuals with this skin type requirean increased concentration of active ingredients orpenetration enhancers to demonstrate efficacy.Dry, sensitive skin types, on the other hand, havean impaired barrier that allows increased penetra-tion of ingredients; these individuals are moreprone to inflammation. In the DSPW type, theskin-lightening ingredients and antiaging ingredi-ents that are required should not be ones that willincite inflammation. Lower concentrations can beused because of the defect in the skin barrier.Morethan 300,000 people worldwide have taken theBSTI, and it is used by multiple dermatologistsaround the world to diagnose patient skin pheno-type. It has been shown to be valid for all ethnic-ities, ages, and genders. The most recent version
Table 1 How tomaximize outcomes from cosmeceuticals
1. Know ingredient science
2. Understand cosmeceutical formulation
3. Understand manufacturing and packaging
4. Understand ingredient interactions
5. Choose the best products from each brand
6. Combine products from various brands to form setregimens
7. Diagnose the patient’s Baumann Skin Type® using thevalidated BSTI (5)
8. Match the regimen to the correct skin type
9. Test the regimens on each individual skin type
10. Take baseline photographs and standardizedmeasurements
11. Educate your patients (clients) to increase compliance
12. Schedule regular follow-up visits to adjust theregimen
13. Ensure proper use of the correct products
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of the BSTI questionnaire is only accessibleonline to physicians who have met various criteriaand completed a training program to ensure theproper use of ingredients [5]. The BSTI is instru-mental in diagnosing skin type and helping thedoctor or designee prescribe the propercosmeceuticals, over-the-counter and prescriptionmedications, and procedures that are most appro-priate for the patient’s Baumann Skin Type®. Thenon-identifying data culled from the BSTI has thepotential to broaden our knowledge of skin types,their prevalence around the world, and how toimprove patient outcomes. It also allows standard-ization in study subject recruitment so that onlycertain skin phenotypes are included in researchstudies. The BSTI and its use are beyond thescope of this chapter; however, information on
how to apply to be chosen to use this system canbe found at STSFranchise.com. The program isdesigned to be used under the guidance of a phy-sician and incorporates prescription and nonpre-scription products and in-office therapies.
The four parameters on which the BSTI isbased will guide the discussion in this chapter.Emphasis will be placed on defining the charac-teristics of these dichotomies and focusing onpertinent basic science. Various aspects of the16 skin phenotype variations will be describedin the process. Cutaneous aging is explained inthe context of the wrinkled (W) to tight(T) continuum. Approaches to skin care or treat-ment options that follow from the BSTS will alsobe cited, with noninvasive, mostly topical thera-pies addressed.
Table 2 The BSTS skin type paradigm. Each of the Baumann Skin Types® is assigned a color and a number
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Skin Hydration: The Oily (O) To Dry (D)Continuum
Oily skin is caused by the excess production ofsebum; dry skin, also known as xerosis, is associ-ated with a complex, multifactorial etiologyincluding an impaired barrier. Individuals withoily skin often are unable to find a sunscreen thatthey can tolerate due to greasiness, while peoplewith dry skin types are more easily irritated byretinoids and acne medications. The most impor-tant factors that regulate the degree of dryness/oiliness are stratum corneum lipids, sebum, natu-ral moisturizing factor, and aquaporin, a discus-sion of which follows [6].
Stratum Corneum (SC)
The role of the stratum corneum (SC), particularlyits ability to maintain skin hydration, is the mostsignificant factor in preventing or setting the stagefor xerosis. The SC is composed of keratinocytessurrounded by a coating of ceramides, cholesterol,and fatty acids, among other constituents. Theseprimary components of the SC, when present inthe appropriate amount and balance, assist inprotecting the skin and keeping it watertight.The stimulation of lipid synthesis andkeratinocyte proliferation by multiple factors,including diet, medications, hormones, andimmunomodulators such as cytokines, contributesto maintaining SC equilibrium [7].
When ceramides, cholesterol, and fatty acidsare imbalanced, the SC endures a cascade of inter-related events, resulting in a reduced capacity tomaintain water and increased susceptibility toexogenous elements, thereby elevating suscepti-bility to skin surface sensitivity and xerosis. Suchan impairment in the SC is measurable as anincrease in transepidermal water loss (TEWL).When the skin becomes dehydrated, the desqua-mation of corneocytes is adversely affectedbecause the enzymes necessary for desmosomemetabolism require water [8]. The abnormal orcompromised desquamation leads to a visible col-lection of keratinocytes manifesting in skin
surface irregularities that result in skin that feelsrough and loses radiance because it poorly reflectslight [9]. This is a common complaint of patientsthat say that their skin “looks old” or “is no longerglowing.”Many skin care companies take advan-tage of this imbalance by offering demonstrationsof their products that exfoliate, resulting in aninstant glow to the skin that often prompts thecustomer to purchase the product. However,these exfoliating products are treating the symp-tom of roughness but not the underlying cause,which is dehydration.
Not all moisturizers that contain ceramides,cholesterol, and fatty acids are effective atrepairing the skin barrier because the ceramidesand fatty acids must mimic the naturally occurringthree-dimensional structure of the multilamellarbilayer of lipids known as the skin barrier.For example, a moisturizer that contains increasedfatty acid levels and decreased ceramide levelscauses a perturbation in the lipid bilayer of theSC, which is also linked to xerosis [10]. For thisreason, moisturizers designed to repair the skinbarrier must contain the proper ratio of fattyacids, ceramides, and cholesterol. In addition, thetype of fatty acid is important. Oleic acid, becauseof the structure of its fatty acid chains, causes tinyholes in the skin barrier, while other fatty acidssuch as stearic acid are able to pack in closertogether, thereby strengthening the skin barrier[11]. There are synthetic “multilamellar emul-sions” such as MLE technology (myristoyl/palmitoyl oxostearamide/arachamide MEA) thatutilize fatty acids and ceramides that mimic thesame three-dimensional structure as the nativebilayer membrane [12].
The skin’s protective lipid bilayer needs con-stant replenishment in those whose underlyingmechanisms are insufficient to produce adequateamounts of ceramides, fatty acids, and cholesterolbecause this lipid bilayer is susceptible to delete-rious effects induced by exogenous factors such asultraviolet (UV) radiation, detergents, acetone,chlorine, and prolonged water exposure. Changesin temperature, humidity, and pH affect cohesionand desquamation of corneocytes from the SC byactivating numerous extracellular proteases [13],
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which in turn can impact the skin’s protectivelayer by thinning or thickening the SC.
Improving skin hydration by strengthening theskin barrier in dry skin types begins with the selec-tion of a nonfoaming cleanser. Foaming cleansersshould be avoided because they often have deter-gents (surfactants) that surround and remove thelipids from the SC. A barrier repair moisturizershould be used twice a day and should contain a1:1:1 ratio of ceramides, fatty acids, and choles-terol. The optimal fatty acids are linoleic, palmitic,and stearic acids, which have been shown to repairthe skin barrier within 2 h when applied exoge-nously [14]. These fatty acids are found in largeamounts in some natural ingredients such asalmond oil, argan oil, shea butter, sunflower oil,safflower oil, grape seed extract, and macadamiaoil, as well as in synthetic ingredients such asglyceryl stearate and myristoyl/palmitoyloxostearamide/arachamide MEA.
Natural Moisturizing Factor (NMF)
Natural moisturizing factor (NMF) is an intracel-lular, hygroscopic substance present only in theSC. Low NMF levels are correlated with xerosisand ichthyosis vulgaris. NMF is produced bylamellar bodies via the breakdown of the proteinfilaggrin (or filament-aggregating protein).Filaggrin is composed of lactic acid, urea, citrate,and sugars and is broken down into free aminoacids, such as arginine, glutamine (glutamic acid),and histidine by a cytosolic protease in the outerlayer of the SC [15]. These water-soluble freeamino acids remain inside the keratinocytes asNMF and play an integral intracellular humectantrole by maintaining water within skin cells. Theprocess of NMF production is elegantly con-trolled by ambient humidity levels. Aspartate pro-tease (cathepsin), the enzyme responsible for therate of filaggrin decomposition, has been shown tobe susceptible to changes in ambient humidity,allowing fluctuations in NMF production [16].After an individual enters a low-humidity envi-ronment, NMF synthesis usually increases overthe course of several days [17]. UV radiation as
well as surfactants (detergents) can suppress thedevelopment of NMF.
As of yet, no products or procedures have beendeveloped that have the capacity to artificiallyinfluence or regulate NMF synthesis because itsintracellular location makes it difficult to replacetopically. The best course of action is to avoidfoaming cleansers (detergents) and UV exposureto preserve native NMF.
Aquaporin-3
Aquaporin (AQP)-3 is member of a subclass ofaquaporins labeled aquaglyceroporins, whichselectively transport water, glycerol, urea, andother small solutes through a water channel pro-tein. AQP-3 exerts an influential role in skinhydration by regulating this water channel [18].AQP-3 is found in the kidney, lungs, and GI tractand in human epidermal keratinocytes [19].The water conduction function in the skin occursalong an osmotic gradient beneath the SC, therebyfacilitating the hydration of skin layers belowthe SC.
In the superficial SC, a high concentration ofsolutes (Na+, K+, and Cl�) and a low concentra-tion of water (13–35 %) [20] generate in thesteady-state gradients of solutes and water fromthe skin surface to the viable epidermalkeratinocytes [21–23]. The molecular mecha-nisms of fluid transport across epidermalkeratinocyte layers and the relationship betweenkeratinocyte fluid transport and SC hydrationhave not been elucidated. It is hypothesized thatAQP-3 enhances transepidermal water move-ment to protect the SC from evaporation fromthe skin surface and/or to spread water gradientsthroughout the epidermal keratinocyte layer[19]. In one study, researchers noted that thewater permeability of human epidermalkeratinocytes was inhibited by mercurials andlow pH, which was consistent with AQP-3involvement [19]. Another study found signifi-cantly lower water and glycerol permeability,and conductance measurements revealed muchlower SC water content in AQP-3 null mice,
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supporting previous evidence that AQP-3 func-tions as a plasma membrane water/glyceroltransporter in the epidermis [24]. Water transportacross AQP-3 was found to be slower in skinthan in other tissues [25].
Despite the fact that some cosmeceutical man-ufacturers boast of aquaporin on their ingredientlists, it is not possible to exogenously insertAQP-3 into the keratinocyte membrane. At thistime, the only way to affect aquaporin functionwith a topical formulation is with extracts thatstimulate AQP-3 function. A solitary example isan extract of the herb Ajuga turkestanica, whichhas been shown to enhance the activity of AQP-3[26]. At the time of publication of this chapter, noother ingredients have been able to mimic thisactivity.
Sebum
Sebum is the oily secretion of the sebaceousglands that contains wax esters, sterol esters, cho-lesterol, di- and triglycerides, and squalene.Sebum imparts an oily protective film on thesurface of the skin but also plays a causal role inthe formation of comedones and acne [27]. Theexact composition of sebum is determined bygenetics, diet, medications, and other poorlyunderstood factors. Sebum, which is an importantsource of the antioxidant vitamin E, confers cuta-neous protection from exogenous factors such asUV light. It also functions as an occlusive mois-turizer on the skin’s surface, impeding TEWL.Subjects with an impairment in the lipid bilayersurrounding the keratinocytes in the SC skin maysuffer less from dehydration and irritant(or allergen)-mediated inflammation when ahigher level of protective sebum is present.When sebum production is below the normalrange, it is thought by some to play a role in thedevelopment of dry skin, especially when it coin-cides with an impaired skin barrier [28]. It isimportant to note that low sebaceous gland activ-ity has not been shown to cause xerosis in theabsence of an impaired skin barrier. In fact, theprotective role that sebum plays in preventing skinxerosis seems to be independent of skin barrier
function because skin with few sebaceous glands,as in prepubertal children, can manifest normalskin barrier function [29]. In addition, barrierfunction or SC lamellar membranes are notimpacted by the pharmacologic involution ofsebaceous glands with supraphysiologic isotreti-noin doses resulting in dry skin [30–32].
Sebum likely exerts its skin-hydrating effectthrough occlusive activity rather than an influenceon barrier function. The protective effect of glan-dular lipids is demonstrated by the meibomianglands, which are modified sebaceous glandslocated in the eyes that have the capacity to staveoff dryness by preventing tear evaporation [33,34]. The separate role of sebum in skin hydrationwas demonstrated in a study that assessed perme-ability barrier homeostasis and SC hydration inasebia J1 mice with sebaceous gland hypoplasia[35]. The asebia mice had consistent levels of thethree primary barrier lipids (ceramides, free ste-rols, and free fatty acids) and normal barrier func-tion but were sebum deficient. The researchersdemonstrated that the asebia J1 mice manifestedreduced SC hydration, implying that while anintact intercellular membrane bilayer system suf-fices for permeability barrier homeostasis, thepresence of sebum is necessary for normal SChydration.
The investigators in the asebia J1 study notedthat the topical application of glycerol restorednormal SC hydration to the sebum-deficient mice.Glycerol is a humectant that helps bind water to theskin’s surface. Sebaceous gland-derived triglycer-ides (TG) are hydrolyzed to glycerol before trans-port to the skin surface in normal skin. In fact, theuse of glycerol has also been demonstrated to beeffective in accelerating SC recovery [36]. For thisreason, sebum has both an occlusive and a humec-tant effect on the skin’s surface and, throughhydrolyzation of its triglycerides to glycerol, hasthe ability to hasten barrier repair.
Many factors contribute to sebum productionrates. The age-related trajectory of sebum produc-tion levels is well understood. During childhood,sebum levels are usually low, then rise in themiddle-to-late teens, and remain relatively stablefor decades until declining in the 7th and 8thdecades as endogenous androgen production falls
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[37]. Sebum production is also affected by diet andstress, but the influence of these is not well under-stood. Androgenic hormones are well known toincrease sebaceous gland activity. Genetic predis-position to sebum production was demonstrated ina fascinating study of 20 pairs each of identical andnonidentical like-sex twins. Almost equivalentsebum excretion rates were observed in the identi-cal twins, but there were significant variations insebum production among the nonidentical twins,demonstrating the strong genetic influence onsebum secretion rates [38].
Differences in Skin Care for Oilyand Dry Skin
An intact SC and skin barrier, normal levels ofNMF and hyaluronic acid (HA), normal AQP-3activity, and balanced sebum secretion togethercharacterize an ideal cutaneous state. The goal ofa properly designed skin care regimen is toachieve this idealized state by removing excesssebum in oily skin types and repairing the skinbarrier in dry skin types.
Oily Skin Care
Treatment of individuals with oily skin should beaimed at decreasing surface sebum levels withsurfactant-containing foaming cleansers becausethere are no topical ingredients that have convinc-ingly demonstrated the ability to decrease sebumproduction, despite manufacturer claims to thecontrary. Oral retinoids, oral spironolactone, andoral contraceptives have been well established aseffective in reducing sebaceous gland activity, buttopical retinoids and topical antiandrogens havenot yet been demonstrated to exhibit this capacity.Oily skin types should avoid lipid-laden moistur-izers such as heavy creams and oils. Gels, serums,and light lotions are a better choice for oily skintypes. Oily types often omit sunscreen because ofthe greasiness associated with chemical sunscreeningredients and dimethicone, which is often foundin SPF preparations. Choosing an SPF that doesnot have oily components will increase sunscreencompliance in oily types. Omitting a moisturizer
in the morning and using a sunscreen instead isone way to increase sunscreen compliance in oilyskin types. Oily skin types must cleanse the facecompletely at night to remove make up, sun-screen, dimethicone, dirt, and other debris thatcan contribute to comedone formation.
Dry Skin Care
An impaired skin barrier and diminished NMFcharacterize xerotic skin. Skin care should aim topreserve and replace skin lipids. Harsh foamingdetergents (present in hand, body, and facialcleansers) strip lipids and NMF from the skinand should be avoided by all patients with dryskin. Individuals with dry skin should also beadvised to abstain from protracted bathing, espe-cially in hot or chlorinated water. People withextremely dry skin use humidifiers inlow-humidity environments and apply moistur-izers two to three times daily and after bathing.Moisturizers should include barrier repair ingre-dients in a 1:1:1 ratio of ceramides, fatty acids,and cholesterol. In addition, occlusive and humec-tant ingredients can be added to boost skin hydra-tion. Dry skin is very prevalent, especially in thewinter as evidenced by the fact that of all the OTCtopical skin care product types, moisturizers arethe third most frequently recommended [39]. It isimportant to remember that sebaceous glands areonly found on the face, back, and chest. There-fore, some patients who demonstrate oily facialskin that is masking an impaired skin barrier willexhibit dry skin on the limbs and body.
Moisturizers are typically packaged as water-in-oil emulsions or oil-in-water emulsions or as anoil. A brief discussion follows of the differencesamong moisturizer types, which is important to apractitioner’s knowledge base in terms of offeringappropriate product selection recommendations topatients.
Occlusives
Occlusive agents are lipid-filled compounds thatmimic the effects of sebum and are incorporated
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into skin care formulations in order to coat the SCand prevent TEWL. In addition to inhibitingTEWL, occlusives exhibit emollient propertiesand are therefore appropriate products for smooth-ing the roughness associated with dry skin.
Petrolatum and mineral oil were once thoughtto be the most effective occlusive ingredients.Used as a skin care product since 1872, petrola-tum was considered one of the best moisturizersand is still the gold standard by which other occlu-sive agents are measured [40]. For example, pet-rolatum displays a resistance to water vapor lossthat is 170 times that of olive oil [41]. Manyconsumers deem petrolatum to be cosmeticallyunacceptable because of its greasy texture, andprefer a more “environmentally friendly” option,but efficacy of moisturizers is still often comparedto that of petrolatum. Other frequently used occlu-sive ingredients include paraffin, squalene, sili-cone derivatives (dimethicone, cyclomethicone),almond oil, argan oil, soybean oil, grape seed oil,macadamia nut oil, propylene glycol, lanolin, lec-ithin, stearyl stearate, and beeswax [42, 43].
Lanolin, which is derived from the sebaceoussecretions of sheep, warrants special mention. Itcontains the important SC lipid cholesterol andcan coexist with SC lipids as solids and liquids atphysiologic temperatures. However, lanolin hasbeen identified as an allergen [44] and is derivedfrom animals, which has greatly lessened its pop-ularity. Functioning as both a humectant and anocclusive agent, propylene glycol (PG) is an odor-less liquid that also exhibits antimicrobial andkeratolytic activity. In addition, PG has been dem-onstrated to contribute to the cellular penetrationof some drugs, such as minoxidil and steroids.Although believed to be a weak sensitizer, PGmay provoke or factor into contact dermatitis byfacilitating allergen penetration into theepidermis [45].
Occlusive ingredients are a temporary solutionfor smoothing skin and helping prevent TEWL,but they are not a replacement for barrier repairingredients, and they do not confer long-lastingbenefits. Once an occlusive product is removedfrom the skin, TEWL returns to its previous level.The reduction of TEWL by more than 40 %,which can result from overuse of occlusive agents,
poses a risk of maceration with increased bacterialevels; therefore, occlusive agents are typicallyused in combination with humectant ingredientsto decrease the amount of occlusion needed torestore hydration [46].
Humectants
Humectants are hygroscopic, water-soluble sub-stances that strongly bind water. In conditionswith at least 80 % humidity, humectants appliedto the skin exhibit the capacity to attract waterfrom the external environment to the skin sur-face. In low-humidity conditions, however,humectants applied to the skin can absorb waterfrom the deeper epidermis and dermis, thus con-tributing to TEWL and exacerbating xerosis[47]. Combining humectants with occlusiveproducts decreases TEWL and skin dehydrationin a low-humidity environment. Cosmetic mois-turizers are often formulated with humectants inorder to prevent product evaporation and thick-ening, thus extending the product’s shelf-life. Bydrawing water into the skin, humectants engen-der a minor swelling of the SC, leaving a percep-tion of smoother skin with fewer wrinkles, butthese effects are temporary. Some humectantsimpart other benefits such as emollient and bac-teriostatic properties [48]. Glycerin and glycerolare considered the most effective humectantingredients found in skin care products. Alphahydroxy acids, carboxylic acid, gelatin, honeyand other sugars, panthenol, propylene glycol,sodium hyaluronate, sodium and ammonium lac-tate, sodium pyrrolidine carboxylic acid, sorbi-tol, and urea are among other substances thatfunction as active humectant ingredients [43].Moisturizers typically incorporate occlusive aswell as humectant ingredients, but the benefitsof these are short lived. Some barrier repair mois-turizers incorporate occlusives and humectantsso that the preparation will have both long-termand short-term benefits.
GlycerinGlycerin is a potent humectant [49]. Using ultra-structural analyses of skin treated with high-
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glycerin formulations, investigators have demon-strated that this humectant expands the SC byenhancing corneocyte thickness and creatinggreater distance between corneocyte layers [50].In addition, after a 5-year study that compared twohigh-glycerin moisturizers with 16 other popularmoisturizers, including petrolatum preparations,used by 394 patients with severe xerosis,researchers reported that the high-glycerin prod-ucts were the most effective, rapidly restoring dryskin to normal hydration with longer-lastingresults than the other products [9]. Glycerin hasalso been shown to stabilize and hydrate cellmembranes along with the enzymes essential fordesmosome degradation [9]. Glycerin is anothername for glycerol. Glycerol forms the backboneof fatty acids and is therefore released when fattyacids are digested [51].
UreaAlso known as carbamide, urea is an end productof mammalian protein metabolism as well as anNMF constituent. This versatile compoundexhibits humectant and mild antipruritic activity[52]. Urea has been included as an ingredient inseveral hand cream formulations since the 1940s[53]. In addition, it has been successfully used incombination with hydrocortisone, retinoic acid,and other ingredients to facilitate the cutaneouspenetration of these agents [54, 55]. However,despite such findings in the mid-to-late 1980s,skepticism lingered regarding the ability of ureato promote such action. In 2005, the CosmeticIngredient Review (CIR) Expert Panel declaredthat urea does indeed have the capacity toenhance the percutaneous absorption of otherchemicals and, further, that urea is safe for usein cosmetic products [56]. Regarding its humec-tant activity, a 3-week double-blind study com-paring 3–10 % urea cream revealed the studyformulations to be more effective in amelioratingclinical signs of dry skin than the vehicle control.Both creams successfully reduced scaling andenhanced hydration. The 3 % cream caused theskin to appear gold or yellow and had no impacton TEWL, whereas the 10 % cream reducedTEWL, although subjects reported the creamsto be equally effective [57].
Hydroxy AcidsAlpha hydroxy acids (AHAs) are naturally occur-ring organic acids that have been discovered todisplay humectant and exfoliant activity. Glycolicand lactic acids, respectively derived from sugarcane and sour milk, are the AHAs most often usedin moisturizing products and were the first ones tobecome commercially available. Citric, malic, andtartaric acids are among the other AHAs. Topicalpreparations that contain AHAswere demonstratedmore than 40 years ago to confer significant effectson epidermal keratinization [58]. Nearly 20 yearsago, glycolic acid was shown to act as aphotoprotective agent [59]. Salicylic acid, theonly beta hydroxy acid (BHA), is derived fromwillow bark, wintergreen leaves, and sweet birch.BHA functions as a chemical exfoliant and is foundin synthetic form in several topical formulations[60]. At the lowest levels of the SC, corneocytecohesiveness is attacked and eroded by AHAs andBHA, influencing pH in the process, as these ingre-dients break down desmosomes, thus contributingto desquamation [61, 62].
Lactic acid is an AHA as well as a componentof NMF. Lactic acid was first used as part of thedermatologic armamentarium in 1943 for thetreatment of ichthyosis [63]. Since then, in vitroand in vivo experiments have demonstrated thatlactic acid can augment ceramide synthesis bykeratinocytes [53, 64]. This moisturizing AHAingredient has also been shown to combat signsof photoaging. Specifically, 8 % L-lactic acid wasfound to be superior to the vehicle in a double-blind vehicle-controlled study, with statisticallysignificant improvements measured in sallow-ness, skin coarseness, and blotchiness [65].
EmollientsEmollients are substances that fill in the gapsbetween desquamating corneocytes, yielding asmooth skin surface [42]. In addition, emollientformulations improve cohesion, flattening out thecurled edges of individual corneocytes [43]. Asmoother skin surface, in turn, lessens frictionwhile enhancing light refraction. Emollients arecomposed primarily of lipids and oils and mayalso fall into the categories of occlusives orhumectants. Emollients are included in cosmetics
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to hydrate, soften, and smooth the skin. Emollientingredients are divided into classes of com-pounds, including those that exhibit astringent,desiccating, fatting, protective, and protein-rejuvenating activity [49].
Reports of adverse effects linked to moisturiz-ing agents are very rare; reactions are more likelyto be due to other ingredients added to the for-mula. There have been reports of allergic contactdermatitis associated with products that containpreservatives, perfumes, solubilizers, sunscreens,and some other classes of compounds. Specifi-cally, cases of contact dermatitis associated withlanolin, propylene glycol, vitamin E, and KathonCG have been reported [66, 67].
Collagen and Polypeptide Ingredients
It is important for physicians and patients to knowthat the preponderance of collagen “extracts”contained in the host of expensive moisturizerstouted for the capacity to restore collagen lost dueto aging has a molecular weight of15,000–50,000 Da, but only compounds with amolecular weight of 5000 Da or less can actuallypenetrate the SC [46]. In other words, these productscannot deliver on their advertised claims ofreplacing collagen. However, the collagen andother hydrolyzed proteins and polypeptides yield atemporary film on the epidermis that, upon drying,fills in surface depressions and other irregularities.Essentially, the film generated by these productsprovides a subtle stretching out of fine skin wrin-kles. Using a humectant product can further enhancethe fuller or somewhat plumper appearance createdby collagen and polypeptide ingredients. Formula-tions that contain collagen and polypeptide ingredi-ents have little or no effect on TEWL but are usuallylabeled as moisturizers and firming creams.
Skin Sensitivity: The Sensitive (S) toResistant (R) Continuum
Sensitive skin is defined as skin that is susceptibleto inflammation, while resistant skin is not. Indi-viduals with resistant skin rarely experience acne,
rosacea, stinging skin, or contact/irritant dermati-tis. Although resistant skin is as likely to sunburnas other skin types, it has less of a chance ofinflammation due to other causes (such as aller-gens, irritants, and friction) as compared to sensi-tive skin types. In terms of skin care productusage, resistant skin might be considered adouble-edged sword, because individuals withresistant skin can use most skin care productswithout experiencing inflammation or irritation,but products may demonstrate less efficacybecause of less ingredient penetration throughresistant skin. Individuals with resistant skin willachieve better efficacy when hydroxy acids orpenetration-enhancing ingredients are added tothe skin care regimen.
Sensitive skin is an increasingly common com-plaint, whichmay be due in part to the popularity ofbotanical ingredients and fragrances that can incitean allergic response [68]. Sensitive skin can beaccurately categorized into four discrete subtypes:Type 1 (acne type) exhibits the proclivity to developacne; Type 2 (rosacea type) has the propensity toexperience facial redness; Type 3 (stinging type)suffers from episodes of stinging or burning sensa-tions; and Type 4 (allergic type) is prone to allergicand irritant reactions resulting in erythema, pruritus,and skin flaking. Such variations in sensitive skincharacteristics present treatment challenges to theconsumer as products marketed for “sensitive skin”are not specific about which subtype they are for-mulated for and therefore not suitable for all sensi-tive skin subtypes. The four subtypes of sensitiveskin share one salient quality: inflammation. Con-sequently, any sensitive skin treatment programmust focus on reducing and eradicating inflamma-tion and should be undertaken under the care of aphysician who is knowledgeable about the under-lying etiology of the sensitive skin subtypes.Patients may suffer simultaneously from morethan one sensitive subtype, thus requiring morecomplex treatment regimens.
Acne Type
Acne is estimated to affect 40–50 million peoplein the USA annually [69] and is easily the most
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common skin disease [70]. Teenagers and adultwomen are particularly susceptible. The conflu-ence of four primary factors has been implicatedin the pathogenesis of acne including elevatedsebum production, a buildup of incompletely des-quamated keratinocytes inside the hair follicles, thepresence of Propionibacterium acnes bacteria, andinflammation. The characteristic cycle of acne isthe adherence of dead keratinocytes in the hairfollicles due to augmented sebum production, lead-ing to comedones and increased levels of P. acnes,followed by initiation of inflammatory cascades bytoll-like receptors and other cell signaling mecha-nisms. Initiation of the inflammatory responseresults in the development of papules and pustules.The acne cycle from buildup of keratinocytes in thehair follicle to the resulting pustule typically takes8 weeks. For this reason, acne treatment regimensmust include continuous preventative measures inorder to break the acne cycle.
Acne therapy targets the four primary etiologicfactors: decreasing sebum production (with reti-noids or oral contraceptives), unclogging pores(with retinoids or hydroxy acids), stabilizing kera-tinization (with retinoids and hydroxy acids),eliminating bacteria (with benzoyl peroxide, anti-biotics, antimicrobials, blue light, or silver), andreducing inflammation.
Rosacea Type
Approximately 16 million Americans, usuallyadults between 25 and 60 years of age, areaffected by rosacea [71]. Rosacea overlaps withacne because many rosacea sufferers also exhibitpapules and pustules in addition to characteristicfacial redness, flushing, and the formation ofprominent telangiectasias. Although the patho-physiology of rosacea remains to be elucidated,there are many unproven hypotheses about thecause(s). Recent topical vasoconstrictive medi-cations have been used to successfully treat thefacial flushing of rosacea through alpha-agonistactivity; however, these treat the symptomsrather than the underlying cause of rosacea. Inaddition to vasoconstrictive topical medications,rosacea therapy should focus on addition of anti-
inflammatory ingredients to the diet and skin careregimen. Triggers such as spicy and hot foodand/or alcohol should also be avoided. Moistur-izers, serums, and oils used on the face in thesepatients should include anti-inflammatory ingredi-ents such as aloe vera, argan oil, arnica, chamo-mile, colloidal oatmeal, cucumber extract,feverfew, grape seed extract, licochalcone, licoriceextract, niacinamide, salicylic acid, sulfacetamide,sulfur, and zinc [72]. These should be combinedwith oral and topical prescription medications andvascular laser therapies to slow progression of thisbothersome disorder.
Stinging Type
In reaction to various triggers, some people expe-rience a stinging sensation, which is a nonallergicneural sensitivity. The stinging propensity, orpatients characterized as “stingers,” can be iden-tified through various available tests. In particular,the lactic acid stinging test is well regarded andestablished as a method for assessing patients whoreport invisible and subjective cutaneous irrita-tion. The problem is that not all patients sting inresponse to the same substance. For example, onepatient might sting to lactic acid, while anotherstings when in contact with benzoic acid. For thisreason, historical data are more accurate at identi-fying a “stinger” than any physical test. It is worthnoting that the stinging response seen in thesepatients is not necessarily associated witherythema; many patients experience stingingwithout exhibiting redness or other visible skinchanges [73]. However, rosacea patients oftenassociate facial flushing with a sensation of sting-ing or burning, especially when exposed to lacticacid [74]. Patients that are confirmed to have thestinging subtype of sensitive skin should beadvised to avoid topical products containing thefollowing ingredients: AHAs (particularlyglycolic acid), ascorbic acid, benzoic acid,bronopol, cinnamic acid compounds, Dowicil200, formaldehyde, lactic acid, propylene glycol,quaternary ammonium compounds, sodium laurylsulfate, sorbic acid, or urea. When patients desirea form of vitamin C, they can tolerate ascorbyl
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phosphate much better than ascorbic acid becauseascorbic acid is formulated at a low pH, whichleads to stinging in susceptible patients. It is worthnoting that any patient who is beginning a retinoidmay exhibit stinging to almost all ingredientsincluding water during the first few weeks ofretinoid therapy initiation, but this is transientand will resolve once the skin has acclimated tothe retinoid.
Allergic Type
An epidemiologic survey in the UK published in2004 reported that 23 % of women and 13.8 % ofmen displayed adverse reactions to a personal careproduct (e.g., deodorants and perfumes, skin careproducts, hair care products, and nail cosmetics)over the course of 1 year [75]. More recently, in a1999–2006 Brazilian study of 176 patients(154 women and 22 men) who were seen in aprivate office and complained of dermatosesresulting from cosmetics, 45 % had dermatoseslinked to cosmetics, and 14 % had skin lesionsthat were found to be caused by inappropriate useof cosmetics [76]. In addition, several studies havedemonstrated that about 10 % of dermatologicpatients who are patch tested for 20–100 ingredi-ents exhibit allergic sensitivity to at least one ingre-dient common in cosmetic products[75]. Fragrances and preservatives are the mostcommon allergens, and women aged 20–60 yearsold represent the demographic group that experi-ences the majority of these reactions [77]. Individ-uals that are overexposed to skin care products andpatients with an impaired SC, as manifested by dryskin, reportedly have increased susceptibility toallergic reactions [78]. These findings underscoreboth the significance of the allergic subtype as wellas the need for matching skin type and skin careproducts, which the BSTI facilitates.
Treatment Approachesfor Sensitive Skin
The treatment of sensitive skin depends on theunderlying subtype. It is crucial that the type of
sensitive skin be identified and that the patient bereferred to a physician who can offer a prescrip-tion medication combined with the proper skincare regimen to treat the particular type of sensi-tive skin. Those patients that suffer from acne willrequire antimicrobial ingredients and retinoids,while those that suffer from redness will need toavoid causative agents and add prescription rosa-cea medications, anti-inflammatory foods, supple-ments, and skin care products to their dailyregimen. Patients undergoing procedures such assurgery or laser treatments need to discuss pre-and postoperative skin care measures with theirphysicians to avoid complications from their sen-sitive skin. In some cases, silver-containing pil-lowcases and other textiles in combination withskin care products can be used to reducesymptoms.
Skin Pigmentation: The Pigmented (P)to Nonpigmented (N) Continuum
This skin type parameter refers not to skin colorbut to the tendency to develop dyschromia(hyperpigmentation), mainly on the face orchest. Within the BSTS, pigmentary conditionsthat can be ameliorated using topical formulationsor minor dermatologic procedures includeephelides, melasma, post-inflammatory hyperpig-mentation, and solar lentigos. Congenital nevi,seborrheic keratoses, and other skin lesions thatrequire excision or treatment beyond topical skincare are outside the scope of the BSTS system.The mechanisms of pigmentation should beclearly understood in order to prepare physiciansto prevent and treat these anxiety-producing pig-mentary conditions.
The enzymatic breakdown of tyrosine bytyrosinase into dihydroxyphenylalanine (DOPA)and then dopaquinone ultimately results in theproduction of the skin pigment melanin, specifi-cally the two melanin types eumelanin andpheomelanin [79]. Melanin is produced by mela-nocytes utilizing the enzyme tyrosinase and thentransferred via melanosomes to keratinocytes.Melanogenesis can be induced by UV exposureand infrared heat. Melanin production represents
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the cutaneous defense against the insult of UVandinfrared irradiation because when melanocytesaccelerate melanin synthesis and transfer it tokeratinocytes [80], the melanin surrounds andprotects cellular DNA from damage. This is visu-ally noted as skin darkening or tanning [81].
The melanocytes, each of which are typicallyattached to about 30 keratinocytes, load melanininto melanosomes and then transfer the melano-somes into keratinocytes through the PAR-2receptor [82]. PAR-2 is believed to regulate mela-nosome transfer and thus pigmentation, throughinteractions between keratinocytes andmelanocytes [83].
Cutaneous pigmentation can be hindered viathree primary pathways: inhibition of tyrosinase,blocking of the PAR-2 receptor, or exfoliation ofthe melanin-containing keratinocytes. Hydroqui-none, vitamin C, kojic acid, arbutin, mulberryextract, and licorice extract are examples of ingre-dients that inhibit tyrosinase. Soybean trypsininhibitor (STI) and Bowman-Birk inhibitor(BBI), which are proteins contained in naturalsoy, have been found to suppress skin pigmenta-tion development. STI and BBI have also beenshown, in vitro and in vivo, to preventUV-induced pigmentation [84]. Melanosometransfer into keratinocytes is influenced by STIand BBI by dint of their inhibition of the cleavageof PAR-2. The introduction of niacinamide, avitamin B3 derivative, has also been demonstratedto impede the transfer of melanosomes tokeratinocytes [85]. Soy and niacinamide, whichare considered the most effective PAR-2 blockers,are the most commonly used topical agents forinhibiting melanin transfer to keratinocytes. Notall soy is able to block PAR-2, but a completediscussion of soy is beyond the scope of thischapter [86].
In addition to the tyrosinase inhibitors andPAR-2 blockers, exfoliating agents such asAHAs, BHA, and retinoids can sufficiently accel-erate cell turnover to outpace melanin synthesis. Abroad-spectrum sunscreen and sun-protectiveclothing should also be included in any skin careregimen intended to diminish or eliminate thedevelopment of undesired dyschromias. Themost effective way to prevent pigmentary and
other harmful changes to the skin is to practicesun and heat avoidance, within reason. A “P” skintype designation in the BSTS correlates with thepresence of dyschromia and the need for skin-lightening ingredients, while the “N” designationimplies that the skin is even toned.
Skin Aging: The Wrinkled (W) toTight (T) Continuum
Exogenous and endogenous factors play consid-erable roles in the complex, multifactorial processof cutaneous aging. Extrinsic aging, which resultsfrom chronic exposure to various environmentalinsults, particularly UV radiation, is affected bylifestyle choices such as tanning or smoking. Nat-ural intrinsic aging is genetically driven, orcellularly programmed, and is thus inevitableuntil the genes responsible are identified andunderstood. Both pathways ultimately manifestin visible skin alterations, particularly wrinkles,lost elasticity, and skin fragility and thinning.
The BSTI questionnaire identifies “W” orwrinkle-prone individuals based on their habitsand chronological age. Individuals with the fol-lowing habits are more likely to develop wrinklesbecause of the cellular damage that these habitscause: excessive sugar intake, smoking, exposureto pollution, poor nutrition, tanning bed use,increased stress, lack of sleep, and – the biggestculprit – solar exposure. The diverse mechanismsthrough which UV radiation results in damage tothe skin include the development of sunburn cells,as well as pyrimidine and thymine dimers, colla-genase synthesis, loss of elastin, and the promo-tion of an inflammatory response. Aging andphotodamage, in particular, have been associatedwith signaling through the p53 pathway after UV(especially UVB)-induced telomere disruption[87, 88]. Although much remains to be learnedregarding the mechanisms by which UV irradia-tion initiates and promotes deleterious effects, UV(particularly UVA) irradiation is well known asthe cause of photoaging, photocarcinogenesis,and photo-immunosuppression [89]. Insofar asUV irradiation impairs DNA and accelerates telo-mere shortening, this chief cause of extrinsic
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aging can be thought of as exerting an impact onthe natural course of intrinsic aging.
The primary evidence of cutaneous aging is thedevelopment of rhytides (wrinkles), the formationof which is initiated in the lower dermal layers. Itis important to note that few skin care formula-tions can actually penetrate far enough into thedermis or the deeper epidermis to reverse deepwrinkles, despite the multitude of products thattout such a capacity. Preventing loss of collagen,HA, and skin elasticity and at the same timecoercing fibroblasts into increasing collagen andHA production is the primary focus of antiagingskin care [90]. Accordingly, topical products areformulated to prevent the degradation or promotethe synthesis of the three primary skin constitu-ents – collagen, elastin, and HA. Specifically, col-lagen production has been demonstrated to bepromoted by topical preparations of retinoids,vitamin C, and copper peptides, as well as oralvitamin C [91–93]. The synthesis of HA has beenshown in animal models to be stimulated by reti-noids [94, 95], and HA levels are also thought tobe enhanced through glucosamine supplementa-tion [96]. Currently, no products have been shownto be effective, or approved, for spurring elastinsynthesis.
Inflammation reduction is also a significanttarget for wrinkle prevention, because inflamma-tion is known to influence the degradation ofcollagen, elastin, and HA. Antioxidants, whichprotect the skin through several mechanisms, areused in this approach to mitigate ROS activity.This is important because ROS act directly ongrowth factor and cytokine receptors inkeratinocytes, and cutaneous inflammation canbe initiated in these epidermal cells [97]. ROScan also contribute to glycation, a process bywhich a sugar is bound to a protein causing dam-age to the protein.
UV irradiation is the biggest culprit in aging,and it causes its harmful effects by initiating acascade of events that result in downstream signaltransduction by activating mitogen-activated pro-tein (MAP) kinase pathways (extracellular signal-regulated kinase, c-jun N-terminal protein kinase,and p38). These then amass in cell nuclei, forming
c-Fos/c-Jun complexes of transcription factoractivator protein 1, and provoking the matrixmetalloproteinases collagenase, 92 kDagelatinase, and stromelysin to degrade collagenand other cutaneous connective tissue [98, 99].
The direct effects of ROS on cutaneous agingand the overall aging process are less clearlyunderstood. In 2003, Kang et al. demonstratedthat ROS activation of MAP kinase pathwaysinduces collagenase production, thus contributingto collagen degradation [99]. The use of antioxi-dants is believed to block these pathways, thusinhibiting the process of photoaging bypreventing collagenase synthesis and its ensuingdeleterious impact on collagen. Specifically, Kanget al. found that the pretreatment of human skinwith the antioxidants genistein and N-acetyl cys-teine hindered UV induction of the cJun-drivenenzyme collagenase.
The vast array of topical skin care productsinclude antioxidants such as vitamins C and E,coenzyme Q10, argan oil, caffeine, coffeeberry,ferulic acid, feverfew, ginger, grape seed extract,green tea, idebenone, mushrooms, phloretin,polypodium leucotomos, pomegranate,pycnogenol, resveratrol, rosemary, and silymarin[100]. The antioxidant capacity of these com-pounds is well established in the literature; how-ever, their efficacy in topical formulationsdesigned to reverse or diminish the cutaneoussigns of aging is unclear because long-termaging prevention is difficult to prove. Antioxidantuse should be combined with several practicalmeasures including avoiding/limiting solar expo-sure (especially from 10 am to 4 pm), using broad-spectrum sunscreen on a daily basis, avoidingcigarette smoke and pollution, eating a diet highin fruits and vegetables, taking oral antioxidantsupplements and topical antioxidant formulations,regular use of topical retinoids, reduction of sugarin the diet, and averaging 7 h of sleep per night inaddition to stress reduction activities. In the nearfuture, technological innovations in tissue engi-neering and gene therapy may lead to break-throughs in the therapeutic uses of growthfactors, cytokines, and telomerase [101], includ-ing dermatologic applications. At this time, stem
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cells and peptides are not associated with suffi-cient scientific data to support their use in topicalskin care geared to treat wrinkle-prone skin.
Skin Care Regimens Based onBaumann Skin Type
Assessing the four skin type dichotomies together,as discussed above, provides insight into thesimultaneous state or tendencies of an individual’sskin along four different spectra, yielding 16 dif-ferent possible skin type phenotypes (Table 2).Each of the individual Baumann Skin Typesrequires a regimen designed specifically for itsneeds. For example, formulations containingingredients with the capacity to repair the skinbarrier and provide anti-inflammatory activitywould be appropriate selections for a personwith dry, sensitive, nonpigmented, tight skin(DSNT). In addition to barrier repair and anti-inflammatory ingredients, DSNW (dry, sensitive,nonpigmented, wrinkle-prone) skin would requireantiaging ingredients such as ascorbic acid andretinol. However, ascorbic acid and retinol cancause stinging and retinoid dermatitis in the sus-ceptible DSNW skin types; therefore, the order ofdelivery of the agents is essential. In this exam-ple, retinoids should be applied after a moistur-izer that contains both occlusive and barrierrepair ingredients, which will decrease retinolpenetration and minimize side effects. The mois-turizer should also contain anti-inflammatoryingredients. In each skin type, the regimen stepsare adjusted to maximize efficacy and decreaseadverse events. Particular care is taken in choos-ing the order in which products are applied sothat the ingredient interactions are maximized.The actions of ingredients can be greatly alteredby pH, exposure to oxidizing agents, interactionwith other ingredients, and exposure to penetra-tion inhibitors or enhancers. All of these effectsmust be taken into account when choosing thesteps of the skin care regimen.
Environmental conditions, diet, exercise,sleep, and stress can impact skin type by affectingthe barrier, cortisol levels, and inflammatory
cascades. For this reason, it is recommended thatindividuals take a baseline BSTI questionnaireand retake the test when stress, significant lifechanges, or cutaneous symptoms are present. Spe-cifically, stress, pregnancy, menopause, exposureto variable climates or moving to a different cli-mate, and various other significant exogenous orendogenous alterations can manifest in skin typechanges. Essentially, if the skin care regimenstops working, it is time to retake the BSTI ques-tionnaire. With baseline and updated BSTI scores,a physician is better equipped to arrive at a moreholistic, integrated, or informed skin type assess-ment and treatment approach.
Summary
The use of the Baumann Skin Typing System(BSTS), based on the results of the BaumannSkin Type Indicator (BSTI), a self-administeredquestionnaire, allows for the evaluation of skinaccording to four dichotomous spectra – dry oroily, sensitive or resistant, pigmented ornonpigmented, and wrinkled or tight(unwrinkled). The BSTI is only available throughphysicians and is used to develop preset regimensfor patients. By developing the regimens ahead oftime and using a consistent methodology to diag-nose skin type and prescribe skin care, outcomesare improved through staff and patient education.The discussion that arises from the use of theBSTI can also improve the physician–patient rela-tionship, with such communication serving also toeducate the patient about the importance of properskin care. The BSTS is also used in research trialsto select what types of patients are most likely tobenefit from a cosmeceutical ingredient. TheFitzpatrick skin typing system is another skintype classification system that categorizes skinaccording to the skin’s response to ultravioletlight. The Glogau photoaging scale classifiesskin according to the level of skin aging. Patientsself-classify their skin as dry, oily, combination, orsensitive, but there is much disparity about themeaning of each of these. Studies show thatpatients self-classify incorrectly, especially along
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the realms of oily versus dry [102]. Researchersand cosmetic scientists should take the time toproperly categorize the skin type of the subjectsused in cosmeceutical research studies so that theefficacy of ingredients can be properly evaluated.Scientific advances are happening rapidly, andmore advanced ingredients are expected to enterthe market in the next 5 years. These may includeingredients designed to address genetic deficien-cies, the immune system, or organelles such aslysosomes or mitochondria.
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