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Table of Contents
Vol. 25, No. 5, 2012
Issue release date: August 2012
Section title: Review
Skin Pharmacol Physiol 2012;25:227–235
(DOI:10.1159/000338978)

Oily Skin: An Overview

Sakuma T.H. · Maibach H.I.
University of California, San Francisco, Calif., USA
email Corresponding Author

Abstract

Oily skin (seborrhea) is a common cosmetic problem that occurs when oversized sebaceous glands produce excessive amounts of sebum giving the appearance of shiny and greasy skin. This paper overviews the main concepts of sebaceous gland anatomy and physiology, including the biosynthesis, storage and release of sebum, as well as its relationship to skin hydration and water barrier function. We also address how skin oiliness may vary according to diet, age, gender, ethnicity and hot humid climates. The deeper understanding of this skin type provides the opportunity to better guide patients regarding skin care and also assist in the development of sebosuppressive agents.

© 2012 S. Karger AG, Basel


  

Key Words

  • Oily skin
  • Sebum
  • Sebaceous gland
  • Skin care

 Introduction

Oily skin (seborrhea) is common, affecting men as well as women and typically starting just before puberty. Oily skin looks shiny and greasy, and is frequently accompanied by large pores. It contributes to the development of acne and may be a cosmetic problem. It can negatively affect the patients’ self-image and have detrimental psychosocial effects. Many individuals feel embarrassed and annoyed with the appearance of their oily skin, and the unpleasant feeling of uncleanness is also a source of complaint [1,2,3].

The relevance of a seemingly trivial matter becomes evident when we realize its constant frequency in women’s magazines or beauty websites and, most impressively, numerous products marketed by the cosmetics industry intended for this skin type. However, together with its popularity come speculation, controversy and myths. It is common to read inaccurate information conveyed by the media. In this manner, this overview attempts to fill the information gap of this common cosmetic problem, bridging scientific data to clinical practice.

 

 Skin Surface Oil Source

The sebaceous gland, through its holocrine activity, excretes a complex mixture of lipids called sebum onto the skin surface. Other lipid sources are the epidermal keratinocytes, which, during their final stages of differentiation, extrude lamellar granules into intercellular spaces of the stratum corneum. They consist of lipid packages that fill these intercellular spaces like mortar or cement, ensuring the skin permeability barrier [4,5,6].

The relative contribution of lipid from each source depends upon the number of sebaceous glands present at the site sampled [7,8], with as many as 900 glands/cm2 on the face to less than 50 on the forearm [7]. On sebaceous gland-rich areas, such as the face, lipids produced by the epidermal cells represent an insignificant fraction of the total extractable surface lipid. In adults, the amount of surface lipid on the forehead, for example, normally varies between 150 and 300 µg of lipid/cm2, of which the epidermal contribution is only 5–10 µg or 3–6% [9,10]. However, when sebaceous gland development is minimal, as in the prepubertal child, or absent, as in the palms and soles, epidermal lipids constitute the major surface lipid [5].

Sebum forms an amorphous sheet of variable thickness on the skin. It can be <0.5 µm or even negligible in sebum-poor areas, or >4 µm in some areas of the sebum-rich face [11].

With the knowledge that the face is rich in sebaceous glands and that the epidermal lipids are probably delivered to the surface at a constant rate as epidermal cells mature [5], we conclude that a global overvolume of sebaceous glands is the cause of oily skin. Areas commonly affected include those that have a higher sebaceous gland density, such as the face, ears, scalp and the upper trunk [8].

 

 Skin Surface Oil Composition

The average composition of human sebum in adults consists of 57.5% triglycerides and their hydrolysis products, 26.0% wax esters, 12.0% squalene, 3.0% cholesterol esters and 1.5% cholesterol [9]. Among these, squalene and wax esters are unique to human sebum and not found anywhere else in the body nor among the epidermal surface lipids [5,12,13,14,15].

By comparison, the human epidermal (stratum corneum) lipid is comprised of 50% ceramides, 25% cholesterol, 15% of free fatty acids [16] as well as smaller amounts of cholesterol esters and cholesterol sulfate [17]. In contrast to the free-flowing oils of the sebaceous gland, the epidermal lipids are in a solid state at room temperature.

 

 Sebaceous Gland Anatomy

The sebaceous gland is located in the reticular dermis, where it is usually found in association with hair follicles, forming the pilosebaceous unit [8,14]. The lanugo pilosebaceous units of the face can be of two types: the most common is superficial, tiny and its ostia and minute hairs are invisible to the naked eye. Its sebaceous glands are disproportionately large, as are all lanugo follicles. The less numerous type have multilobular sebaceous glands of extravagant size and depth, greater in volume than the much smaller glands of the superficial, tiny follicles. It empties to the skin surface through a wide duct, which is in fact the follicle, and is joined by a tiny hair of insignificant proportions. Their ostia are easily visible as the pores of adult facial skin and the gaping orifices are highly prominent in many oily patients, especially on the cheeks. This type of sebaceous follicles is practically limited to the face, scalp and upper trunk. The tiny superficial hair follicles outnumber these huger sebaceous follicles by a ratio of about 3:1, being evenly dispersed among them. The hairs associated with the huge sebaceous follicles are larger than those of the superficial hair follicles and are the ones generally seen with the naked eye [18]. This type of sebaceous follicles contributes by far to the greatest quantity of facial sebum. The oily appearance commonly found on the ‘T’ zone (forehead, nose and chin) reflects the dominance of these sebaceous follicles. Pagnoni et al. [19] found that sebum output and density of follicles followed a centrolateral decreasing gradient, and Lopez et al. [20] showed that such a ‘T’-like distribution could indeed be clearly observed even in the women presenting the lowest mean value of sebum casual level1. We conclude that all skins are of a ‘combination’ type, with increased sebum values on the ‘T’ zone compared to the rest of the face, regardless if the skin is oily or not.

 

 Biosynthesis, Storage and Release of Human Sebum

The quantity of lipids delivered in a given time per unit area is proportionate to the total glandular volume (size and number of glands), a function of the total number of sebaceous cells generated. Miescher and Schonberg [22] performed planimetric measurements of glandular size (actually surface area) in biopsy specimens and showed that the ratio between lipid delivery and glandular size was constant; that is, the larger the glands, the more sebum produced in a given time [18].

The fully developed adult sebaceous gland contains sebocytes at different stages of differentiation. Its peripheral zone is composed of mitotically active sebocytes, which differentiate towards the center of the gland. During this process, they lose their mitotic activity, increase their size and accumulate lipid droplets. Then, the terminally differentiated sebocytes disintegrate and release their content to the skin surface via holocrine secretion. This continuous differentiation activity is under the control of paracrine, endocrine and neural mediators acting on a wide array of receptors expressed by sebocytes [12,14].

Until 1947, researchers stated that the sebum accumulated on the skin surface was the chief force regulating the gland’s excretory activity. Surface loss would accelerate sebum production, and skin surface saturation would lead the gland to shut down. However, Kligman and Shelley [18] performed experiments that dismissed this concept, termed by them as the ‘positive feedback theory’. Instead, they proposed that the sebaceous gland functions continuously, without regard to what is on the surface [18]. They demonstrated that the remarkable ability of sebum to spread over the skin surface could lead to the false impression that the sebaceous glands were in ‘sleep mode’. After preventing sebum from flowing away or being wiped off during the lipid’s collection, they obtained an average of 3.13 mg of sebum per 10 cm2 on the volunteer’s forehead, compared to the amount of 1.4 mg per 10 cm2 when such precaution was not taken. Hence, the reason why the values of sebum collected from the skin are relatively constant is related to the fact that after a few hours, the skin surface of the studied site (e.g. the forehead) becomes saturated, and the excess spreads over to surrounding areas of the face.

The ‘positive feedback’ theory was questioned after the explanation of a curious phenomenon that led many workers to support it. Literature data demonstrate that the more frequently sebum is collected from a given area, the larger the sum that will be obtained in equivalent time periods; for example, the sum of the quantities of lipids collected at several short intervals greatly exceeds the amount collected at a single removal at the end of the same length of time.

Kligman and Shelley [18] ascribed this phenomenon to the follicular reservoir (the duct which connects the sebaceous gland located in the dermis to the skin surface), whose importance was later demonstrated by Downing et al. [23]. They measured sebum secretion in human skin over a period of 24 h and observed that it declines over a period of 12 h and then remains constant for the remaining 12 h. It was inferred that the final, sustainable rate represents the true rate at which sebum is secreted by the sebaceous glands, and that the additional sebum collected at earlier intervals was obtained from an accumulation in the stratum corneum or in the follicular canals. In this manner, Millns and Maibach [24] stated that the sebum measured on the skin surface should be seen as the end product of what they called a ‘multifunctional sebaceous apparatus’, which involves not only sebum production but also sebum storage (a volume function) and surface delivery (a rate function).

With this three-component model in mind, it is easier to elucidate the ‘positive feedback’ misunderstanding. The lipid which rapidly reappears on the skin surface soon after defatting of a sebaceous-rich area, such as the face, is actually derived from preformed sebum stored in the follicular reservoir. This preformed sebum would flow out of the follicular reservoir into the meshy spaces of the stratum corneum, through a capillarity mechanism, refilling the space previously occupied by the removed sebum.

The rate of replenishment is proportional to the size, number of glands and the amount of preformed sebum that can be stored in the follicular reservoir. On the forehead, total replacement of the removed sebum is expected after 3 h (if sebum run off is prevented), and sometimes even after 2 h in oily skin volunteers [18]. After defatting the skin by wiping the skin several times with an ether-soaked cloth, Butcher and Parnell [25] observed clear follicular droplets of sebum under the stereoscopic microscope (×12) within 15 min. These became visible to the naked eye in 40 min, giving the skin a star-spangled appearance under bright light.

Kligman and Shelley [18] also demonstrated that it is probably impossible to exhaust the forehead follicular reservoirs completely. After applying absorbent cigarette papers to the forehead of 2 volunteers every 10 min for 6 h, large oil globules could still be expressed by hemostat compression. Also, neither ether nor absorptive papers significantly removed oil from the follicular reservoir. The authors stated that there is no physiological way to empty it [18].

Based on these data and contrary to what many think, overwashing the skin does not cause sebum overproduction, but just leads preformed sebum to flow up through a capillarity mechanism.

 

 Skin Oiliness Assessment

Sebum present at the skin surface can be objectively measured non-invasively using one of several methods based on absorbent paper pads, photometric assessment (e.g. Sebumeter® SM810; CK electronic), bentonite clay and lipid-sensitive tapes (e.g. Sebutape®; CuDerm Corp.). Since many environmental and biological factors influence the data, rigorous methodological designs are mandatory. The Sebumeter SM810 and Sebutape are widely used. The Sebumeter affords direct photometric reading of the lipid collected on a probe of opaque plastic strip after a 30-second skin contact. Increases in transparency are directly proportional to the sebum present. The digital read-out displayed as micrograms per square centimeter provides estimated total amount of lipids present on the skin at one time point. The Sebutape is a white porous tape that traps oil and becomes translucent. After removal from the skin, it is laced in a black background. A pattern of dots of variable sizes and density develops, proportional to the amount of sebum delivered. This pattern is matched to a grading scale to generate a numerical report (details provided in [22,26]).

Arbuckle and colleagues [1,2] developed and validated the content of two questionnaires focusing on the patients’ self-assessment of skin oiliness. The first one, the ‘Oily Skin Self-Assessment Scale’ (OSSAS), measures facial oily skin severity and consists of three questionnaires that assess subjects’ oily facial skin through visual perception of oily skin, tactile perception of oily skin and sensation of oily skin questions. The second one, the ‘Oily Skin Impact Scale’ (OSIS), assesses the emotional impact of oily skin using two questionnaires. One evaluates the subjects’ annoyance and the other their self-image/self-concept. OSSAS scales have low correlations with the Sebumeter data [2]. As the validity of the Sebumeter has not been demonstrated, it is difficult to interpret this result. Note that the reliability of self-assessment questionnaires might be affected by numerous environmental (e.g. humidity, season of the year) and biological conditions (e.g. hormonal fluctuations), and, most importantly, it depends on the individuals’ subjective perception of skin oiliness. Self-perception of physical appearance may not always correspond with the biophysical measurements.

Another validated questionnaire is the Oily Skin Self-Image Questionnaire (OSSIQ), developed with 18-item questions to assess perception as well as behavioral and emotional consequences associated with oily skin. In contrast to previous studies, OSSIQ scores accorded with objective sebum level measurements [3].

 

 Sebaceous Gland Function Regulation

The sebaceous gland is an androgen target organ, stimulated to produce sebum at puberty and beyond by androgens [27]. Akamatsu et al. [28] demonstrated that testosterone and 5-alpha-dihydrotestosterone (5α-DHT) stimulated the proliferation of facial cultured human sebocytes in a significant dose-dependent manner. Also, according to their experiments, the effect of testosterone and 5α-DHT on the proliferation of cultured human sebocytes may depend on the localization of the sebaceous glands at different skin regions. Androgens are more effective in increasing the proliferation of facial than non-facial sebocytes [27,28].

It has been proposed that, besides abnormal circulating androgen levels, sebum production can be increased by overproduction of androgens in the pilosebaceous units due to enhanced expression and activity of androgenic enzymes or/and by overexpression or hyperresponsiveness of androgen receptors [29].

Conversion of testosterone to 5α-DHT (an intracellular metabolite of testosterone and the most active androgen in upregulating sebum production) is induced by the enzyme 5α-reductase. 5α-reductase type 1 activity is significantly higher in sebaceous glands compared to other skin compartments. Furthermore, facial sebaceous glands exhibit higher 5α-reductase type 1 activity than sebaceous glands from non-acne-prone areas.

Using the human sebocyte culture model, thyroid-stimulating hormone, hydrocortisone and, especially, insulin significantly stimulated proliferation of human sebocytes maintained in a serum-free medium in a dose-dependent manner. These results indicate that not only androgens but also other hormones may modulate sebocyte activity, leading to a complex regulation of the sebaceous gland [27].

 

 Sebum Secretion: Role of Diet

Diet may be an important source of substrate for sebum synthesis. It is synthesized de novo in the gland from several sources (e.g. glucose, acetate and fatty acids); however, some dietary lipids (especially fatty acids) can also pass unchanged from the circulation to the sebaceous cells. It is presumed that undifferentiated cells of the sebaceous gland acquire the dietary lipids whilst in the basal layer exposed to the circulation [15].

Fulton et al. [30] measured the effect of excessive chocolate ingestion on 5 healthy adult male volunteers. All volunteers ingested two chocolate bars daily for 1 month. Although the authors concluded that chocolate and fat did not alter sebum composition and output, at the end of the study, an increase in collected sebum was observed in 3 of the 5 volunteers [30]. Pochi et al. [31] investigated the response of the sebaceous gland to total caloric deprivation in 18 obese patients undergoing fasts for periods of 4–8 weeks. Sebum release reduced in an average of 40% [31]. These data may indicate that the composition and quantity of food could, when changed significantly, produce measurable variation in the sebaceous gland product [32].

Diets rich in carbohydrates with a high glycemic index are associated with hyperglycemia, reactive hyperinsulinemia and increased formation of insulin-like growth factor-1 (IGF-1). Except for cheese, milk and all dairy products also have potent insulinotropic properties, far exceeding those expected from their low glycemic indexes [33]. Insulin and IGF-1 levels also peak during late puberty and gradually decline until the third decade [34]. Insulin and IGF-1 stimulate sebaceous gland lipogenesis in vitro by increasing the expression of a transcription factor (SREBP-1) that regulates numerous genes involved in lipid biosynthesis [35]. IGF-1 also mediates the induction of androgen production and stimulation of peripheral androgen metabolism. Its signaling alleviates androgen receptor repression by the repressive protein Foxo1, resulting in androgen receptor gain-of-function. Thus, IGF-1 has direct influence on the intracrine androgen regulation of the skin and potentiates androgen signaling by the induction of 5α-reductase activity and activation of the androgen receptor [34].

Vora et al. [36] compared facial sebum levels with serum IGF-1 levels in 16 patients (mean age 19.5 ± 2 years) with acne. They found a positive correlation between the mean facial sebum excretion (µg cm–2) and serum IGF-1 [36]. Smith et al. [34] compared the endocrine effects of an experimental low glycemic-load diet with a conventional high glycemic-load diet on 43 patients with acne. After 12 weeks, the low glycemic-load diet group showed a significant improvement in insulin sensitivity and a reduction in testosterone bioavailability and DHEAS concentrations [34].

Smith et al. [15] found that volunteers on a low glycemic-load diet demonstrated an increase in the saturated fatty acid/monounsaturated fatty acid ratio compared to a decrease in the control group. However, they did not detect an effect of the dietary intervention on sebum output [15]. Recent evidence suggests that only monounsaturated fatty acids induce hyperkeratinization and epidermal hyperplasia similar to that seen in comedo formation, whereas saturated fatty acids have little effect [37]. Further studies are required to better clarify the underlying role of diet in sebaceous gland physiology.

 

 Genetic Influence

A twin study investigating sebum secretion in 20 pairs of adolescent acne twins found that, differently from dizygotic twins, the sebum secretion rate was homogeneous between monozygotic twins [38]. Several genes regulate sebaceous gland function. Overexpression of the ageing-associated gene Smad7 in adult transgenic mice has been correlated with hyperplasia of the sebaceous gland, and c-myc overexpression has been shown to be associated with enhanced sebaceous lipid synthesis and to have a drastic decrease with age. Parathyroid hormone-related protein knock-out mice presented hypoplastic sebaceous glands, whereas parathyroid hormone-related protein overexpression led to sebaceous gland hyperplasia [39].

 

 Age, Gender, Ethnic and Seasonal Variation

Differences in sebum secretion at various times of life have been associated with concomitant changes in endogenous androgen production. Sebaceous glands are well developed in neonates, but their size decreases dramatically a few weeks after birth, starts to rise again with the adrenarche and reaches its maximum in young adults. While the number of sebaceous glands remains the same during life, sebum secretion rates are highest in the 15–35-year-olds and decline continuously throughout the adult age range [40]. At any age range, the mean sebum values in men exceed those of women. Although surface lipid levels fall with age, paradoxically, the sebaceous glands become larger, rather than smaller, as a result of decreased cellular turnover [5,39,41,42,43]. This could explain the larger pores observed on the elderly face.

Black subjects have larger sebaceous glands which contribute to the increased sebum secretion. Hillebrand et al. [44] reported that African-Americans showed significantly more sebum excretion than East Asians. African-Americans also had a greater pore count fraction, but the number of pores increased with age in all races [45]. Kligman and Shelley’s [18 ] comparative racial study also confirmed these observations. Blacks presented higher sebum casual levels compared to Whites [18]. However, the results of Pochi and Strauss [46] and Grimes et al. [47] showed no consistent difference in sebaceous gland activity between black and white skin.

Experiments of Cunliffe et al. [48] demonstrated that the sebum excretion rate varies directly with temperature, so that an increase in temperature of 1°C produces an increase in the sebum excretion rate in the order of 10%. This result might reflect a change in the rate of delivery of sebum to the skin surface due to alterations in sebum viscosity, or an increase in the rate of absorption by the collecting papers. The possibility of sebum production increase was dismissed as the changes occurred within 90 min and the sebaceous gland turnover rate approximates 7 days [48,49,50]. Youn et al. [51] measured facial sebum secretion seasonally for 1 year and found summer to be the highest sebum-secreting season.

Kligman and Shelley [18], while comparing lipoid deliveries in atropinized and non-atropinized sites of sweating subjects, made an observation of clinical significance. Although visible oil droplets formed in the dry atropinized sites, the skin showed no evidence of being greasy or oily. In the symmetrical sweating site, oiliness was prominent. According to them, the clinical impression of oiliness would not be a reliable index of surface lipids (this could explain the differences observed between the Sebumeter measurements and the subjective questionnaire results obtained by Arbuckle et al. [1]). The presence of sweat would impart the clinical appearance of oiliness. According to the authors, how oily a subject will appear at any one time will be influenced by the chance of his/her having recently sweated or having been in an environment of high humidity. It is easy to understand why oiliness is less prominent in winter and, conversely, so marked in hot humid climates. Possibly, it is the emulsification of sweat with oil that is responsible for the oily appearance.

Kligman and Shelley [18 ] also graded 12 white males in terms of clinical greasiness and determined their casual levels. In general, the casual levels were not higher in those whom they estimated to be greasier. In fact, the two highest levels in the group were in subjects judged to be non-greasy. They concluded that marked and persistent greasiness truly reflects increased quantities of surface lipids, but sudden or intermittent greasiness is more likely due to sweating. Warming or cooling the skin changes the flow to the surface by making the preformed sebum either more or less viscous. Therefore, after defatting the skin, the flow to the surface can be expected to be strongly temperature dependent. Furthermore, the wicking power of the emptied capillary reservoir will be greater when the liquid is less viscous. The increased greasiness of the face in the summer or in tropical climates may simply be an expression of increased eccrine sweating or a decreased sebum viscosity [18]. Correlations between sebum secretion and diet, genetic influence, age, gender as well as ethnic and seasonal variations are summarized in table 1.

TAB01
Table 1. Correlations between sebum secretion and diet, genetic influence, age, gender as well as ethnic and seasonal variation

 

 Sebum: Protective Effects

The functions attributed to sebum in humans include the delivery of fat-soluble antioxidants to the skin surface and antimicrobial activity [12]. Sebum mantles the epidermis, representing the ultimate barrier of the body against exogenous oxidative insults. It is believed to deliver antioxidants to the surface in the form of vitamin E (α-tocopherol) and CoQ10 [52].

Squalene is the first human skin surface lipid targeted by oxidative stresses such as sun light and, as a consequence, is depleted where a toxic photo-oxidation product (squalene monohydroperoxide isomers) is produced [53]. Passi et al. [54] demonstrated that exposure of sebum to UV irradiation (4 MED) depleted 84.2% of vitamin E, 70% of CoQ10 and only 13% of squalene, while 10-MED UV exposure produced a 26% loss of squalene. The same UV dose when applied in the absence of vitamin E and CoQ10 produced a 90% decrease in squalene [54]. This antioxidant function of sebum is important as the buildup of reactive oxygen species on the skin surface can cause a breakdown of the skin barrier and signs of aging [8].

Sebocytes are part of the innate immune system. By sonicating total sebum into bacterial culture medium, Wille and Kydonieus [55] observed that the Gram-positive bacteria tested (Staphylococcus aureus, Streptococcus salivarius) were exceedingly susceptible to sebum, with a significant (>4 orders of magnitude) decrease in the number of viable cells. However, most Gram-negative bacteria tested (Escherichia coli, Pseudomonas aeruginosa and Echinococcus faecalis) were unaffected. Fractionation of the human sebum lipids showed that the C16:1Δ6 isomer of palmitoleic acid (cPA) was the most active anti-bactericidal fatty acid component and the most active fraction in blocking the adherence of a pathogenic strain of Candida albicans to the porcine stratum corneum [55].

 

 Sebum: Undesirable Effects

Besides surface oiliness, excess sebum blocks pores, provides nourishment to bacteria that live upon the skin (Propionibacterium acnes) and contributes to acne flare-ups. Along with increased sebum secretion rate, quantitative modifications of sebum are also likely to occur in acne [12].

Sebum participates in the induction of comedo formation, which represents the retention of hyperproliferating ductal corneocytes in the pilosebaceous duct [56]. Upon oxidative challenge (e.g. UV radiation), squalene is readily oxidized to squalene peroxide, which is comedogenic. Comedones have been triggered by exposing rabbit ears to irradiated squalene. A positive correlation exists between the degree of squalene peroxidation and the size of the comedones elicited. In addition, marked hyperplasia and hyperkeratosis of the epithelium in the follicular infundibulum and marked proliferation of sebaceous glands were observed.

In vitro data showed that squalene peroxide beyond the induction of HaCaT keratinocytes proliferation led also to the upregulation and release of inflammatory mediators, which indicate a pro-inflammatory activity of by-products of squalene oxidation. The strategy that skin adopts to limit the potentially harmful effects of peroxidated squalene relies on the vitamin E supply to the skin surface, mentioned previously [12].

 

 Sebum and Water Barrier Function

The stratum corneum is an efficient biological barrier membrane, protecting the underlying living tissue from water loss, etc. Despite being on the skin surface, sebum does not seem to influence this function. Fluhr et al. [57] studied asebia J1 mice, which display profound sebaceous gland hypoplasia, and found transepidermal water loss levels comparable to those of control animals, and the ability to acutely restore permeability barrier function to normal after acute disruption was unchanged [58].

 

 Sebum and Hydration

Note that skin oiliness is a property of the sebaceous glands and that skin moisture is largely a property of the stratum corneum. Low sebum secretion and high water content are considered main features of fair skin. The latter is dependent upon the rates of water movement into and out of this tissue (barrier function), as well as upon the ability of the stratum corneum to retain water [59,60]. Hydrated skin is soft and smooth, and reflects the optimum water content in the superficial stratum corneum. It results from the complex and perfect interaction of water-holding substances, (i.e. amino acids produced by proteolysis of filaggrin that occurs during their slow upward movement in the stratum corneum), lactate and potassium derived from sweat as well as intercellular lipids, specially their major component ceramides that play a crucial role in providing barrier function to the stratum corneum [59]. In conjunction with cholesterol, free fatty acids and cholesterol sulfate, they form arrays of hydrophobic chains, constructing lipid bilayers with closely packed interiors which dramatically reduce their permeability to water and solutes. Commonly used tools to assess skin hydration are the Corneometer® (CK electronic), the Skin Surface Hygrometer (Skicon-200) and the DermaPhase meter (Nova DPM 9003), which measure capacitance, conductance and impedance-based capacitance, respectively [61].

Harsh cleaners or overwashing the skin to remove excess sebum might remove these lipids from the stratum corneum surface, resulting in excessive skin drying. Another essential factor to guarantee minimally permeable water barrier is the physical state of the lipid chains in the non-polar regions of the bilayers. Due to their high melting point, at physiological temperature they are mainly in a solid crystalline or gel state, enabling low lateral diffusional properties. Contrary to the permeability barrier results, Fluhr et al. [57] found that the water-holding capacity of the stratum corneum was reduced in asebia J1 mice. This appeared to be due to a decrease in glycerol, a well-known humectant and a potential catabolic product of sebaceous gland-derived triglycerides.

We conclude that the intuitive belief that a low sebum secretion rate is the main cause of dry skin is not accurate, although sebum seems to play a minor role in skin hydration. It is also inappropriate to use the term dry skin as the opposite of oily skin. If dry skin represented the opposite of greasy skin, one should expect little sebum in xerotic conditions. In many types of xerosis, however, sebum excretion remains in the physiological range [8]. The skin should be better referred as oily or non-oily when referring to the sebum content or, when regarding water content, dry or non-dry.

 

 Conclusions

Oily skin is a common cosmetic problem that occurs when oversized sebaceous glands produce excessive amounts of sebum, giving the appearance of shiny and greasy skin. These glands are under androgen control of and appear influenced by increased IGF-1 generation by high glycemic-index diets. Age, gender, ethnicity and hot humid climates may also play a role in skin oiliness variations. With this overview, we shed some scientific light to some common daily questions and misconceptions, such as why overwashing the skin does not cause sebum overproduction but may cause dryness, why all skin are of a ‘combination’ type and why dry skin is not the opposite of oily skin. The deeper understanding of this type of skin provides the opportunity to better guide patients regarding skin care and also assist in the development of sebosuppressive agents.

 

 Disclosure Statement

The authors have no conflicts to declare.


  

Footnotes

Footnote 1
The sebum casual level (CL) is defined as the amount of lipids present at equilibrium when the skin surface remains untouched for several hours [21].

e 1
The sebum casual level (CL) is defined as the amount of lipids present at equilibrium when the skin surface remains untouched for several hours [21].


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  14. Tóth BI, Oláh A, Szöllosi AG, Czifra G, Bíró T: ‘Sebocytes’ makeup’: novel mechanisms and concepts in the physiology of the human sebaceous glands. Pflugers Arch 2011;461:593–606.
  15. Smith RN, Braue A, Varigos GA, Mann NJ: The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. J Dermatol Sci 2008;50:41–52.
  16. Feingold KR: Thematic review series: skin lipids. The role of epidermal lipids in cutaneous permeability barrier homeostasis. J Lipid Res 2007;48:2531–2546.
  17. Proksch E, Holleran WM, Menon GK, Elias PM, Feingold KR: Barrier function regulates epidermal lipid and DNA synthesis. Br J Dermatol 1993;128:473–482.
  18. Kligman AM, Shelley WB: An investigation of the biology of the human sebaceous gland. J Invest Dermatol 1958;30:99–125.
  19. Pagnoni A, Kligman AM, el Gammal S, Stoudemayer T: Determination of density of follicles on various regions of the face by cyanoacrylate biopsy: correlation with sebum output. Br J Dermatol 1994;131:862–865.
  20. Lopez S, Le Fur I, Morizot F, Heuvin G, Guinot C, Tschachler E: Transepidermal water loss, temperature and sebum levels on women’s facial skin follow characteristic patterns. Skin Res Technol 2000;6:31–36.
  21. Piérard GE, Piérard-Franchimont C, Marks R, Paye M, Rogiers V: EEMCO guidance for the in vivo assessment of skin greasiness. The EEMCO Group. Skin Pharmacol Appl Skin Physiol 2000;13:372–389.
  22. Miescher G, Schonberg A: Untersuchungen über die Funktion der Talgdrüsen. Bull Schweiz Akad Med Wiss 1944;1:101.
  23. Downing DT, Stranieri AM, Strauss JS: The effect of accumulated lipids on measurements of sebum secretion in human skin. J Invest Dermatol 1982;79:226–228.
  24. Millns JL, Maibach HI: Mechanisms of sebum production and delivery in man. Arch Dermatol Res 1982;272:351–362.
  25. Butcher EO, Parnell JP: The distribution and factors influencing the amount of sebum on the skin of the forehead. J Invest Dermatol 1948;10:31–38.
  26. Piérard-Franchimont C, Quatresooz P, Piérard GE: Sebum production; in Farage MA, Miller KW, Maibach HI (eds): Textbook of Aging Skin. Berlin/Heidelberg, Springer, 2009, pp 343–352.
  27. Zouboulis CC, Xia L, Akamatsu H, Seltmann H, Fritsch M, Hornemann S, Rühl R, Chen W, Nau H, Orfanos CE: The human sebocyte culture model provides new insights into development and management of seborrhoea and acne. Dermatology 1998;196:21–31.
  28. Akamatsu H, Zouboulis CC, Orfanos CE: Control of human sebocyte proliferation in vitro by testosterone and 5-alpha-dihydrotestosterone is dependent on the localization of the sebaceous glands. J Invest Dermatol 1992;99:509–511.
  29. Chen WC, Zouboulis CC: Hormones and the pilosebaceous unit. Dermatoendocrinol 2009;1:81–86.
  30. Fulton JE Jr, Plewig G, Kligman AM: Effect of chocolate on acne vulgaris. JAMA 1969;210:2071–2074.

    External Resources

  31. Pochi PE, Downing DT, Strauss JS: Sebaceous gland response in man to prolonged total caloric deprivation. J Invest Dermatol 1970;55:303–309.
  32. Michaëlsson G: Diet and acne. Nutr Rev 1981;39:104–106.
  33. Melnik BC, Schmitz G: Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol 2009;18:833–841.
  34. Smith RN, Mann NJ, Braue A, Mäkeläinen H, Varigos GA: The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: a randomized, investigator-masked, controlled trial. J Am Acad Dermatol 2007;57:247–256.
  35. Smith TM, Gilliland K, Clawson GA, Thiboutot D: IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway. J Invest Dermatol 2008;128:1286–1293.
  36. Vora S, Ovhal A, Jerajani H, Nair N, Chakrabortty A: Correlation of facial sebum to serum insulin-like growth factor-1 in patients with acne. Br J Dermatol 2008;159:990–991.
  37. Katsuta Y, Iida T, Inomata S, Denda M: Unsaturated fatty acids induce calcium influx into keratinocytes and cause abnormal differentiation of epidermis. J Invest Dermatol 2005;124:1008–1013.
  38. Walton S, Wyatt EH, Cunliffe WJ: Genetic control of sebum excretion and acne – a twin study. Br J Dermatol 1988;118:393–396.
  39. Zouboulis CC, Boschnakow A: Chronological ageing and photoageing of the human sebaceous gland. Clin Exp Dermatol 2001;26:600–607.
  40. Jacobsen E, Billings JK, Frantz RA, Kinney CK, Stewart ME, Downing DT: Age-related changes in sebaceous wax ester secretion rates in men and women. J Invest Dermatol 1985;85:483–485.
  41. Plewig G, Kligman AM: Proliferative activity of the sebaceous glands of the aged. J Invest Dermatol 1978;70:314–317.
  42. Pochi PE, Strauss JS, Downing DT: Age-related changes in sebaceous gland activity. J Invest Dermatol 1979;73:108–111.
  43. Zouboulis CC: Acne and sebaceous gland function. Clin Dermatol 2004;22:360–366.
  44. Hillebrand GG, Miyamoto K, Schnell B, Ichihashi M, Shinkura R, Akiba S: Quantitative evaluation of skin condition in an epidemiological survey of females living in northern versus southern Japan. J Dermatol Sci 2001;27(suppl 1):S42–S52.
  45. Rawlings AV: Ethnic skin types: are there differences in skin structure and function? Int J Cosmet Sci 2006;28:79–93.
  46. Pochi PE, Strauss JS: Sebaceous gland activity in black skin. Dermatol Clin 1988;6:349–351.
  47. Grimes P, Edison BL, Green BA, Wildnauer RH: Evaluation of inherent differences between African American and white skin surface properties using subjective and objective measures. Cutis 2004;73:392–396.
  48. Cunliffe WJ, Burton JL, Shuster S: The effect of local temperature variations on the sebum excretion rate. Br J Dermatol 1970;83:650–654.
  49. Williams M, Cunliffe WJ, Williamson B, Forster RA, Cotterill JA, Edwards JC: The effect of local temperature changes on sebum excretion rate and forehead surface lipid composition. Br J Dermatol 1973;88:257–262.
  50. Downing DT, Strauss JS: On the mechanism of sebaceous secretion. Arch Dermatol Res 1982;272:343–349.
  51. Youn SW, Na JI, Choi SY, Huh CH, Park KC: Regional and seasonal variations in facial sebum secretions: a proposal for the definition of combination skin type. Skin Res Technol 2005;11:189–195.

    External Resources

  52. Thiele JJ, Weber SU, Packer L: Sebaceous gland secretion is a major physiologic route of vitamin E delivery to skin. J Invest Dermatol 1999;113:1006–1010.
  53. Ekanayake Mudiyanselage S, Hamburger M, Elsner P, Thiele JJ: Ultraviolet a induces generation of squalene monohydroperoxide isomers in human sebum and skin surface lipids in vitro and in vivo. J Invest Dermatol 2003;120:915–922.
  54. Passi S, De Pità O, Puddu P, Littarru GP: Lipophilic antioxidants in human sebum and aging. Free Radic Res 2002;36:471–477.
  55. Wille JJ, Kydonieus A: Palmitoleic acid isomer (C16:1delta6) in human skin sebum is effective against gram-positive bacteria. Skin Pharmacol Appl Skin Physiol 2003;16:176–187.
  56. Cunliffe WJ, Holland DB, Jeremy A: Comedone formation: etiology, clinical presentation, and treatment. Clin Dermatol 2004;22:367–374.

    External Resources

  57. Fluhr JW, Mao-Qiang M, Brown BE, Wertz PW, Crumrine D, Sundberg JP, Feingold KR, Elias PM: Glycerol regulates stratum corneum hydration in sebaceous gland deficient (asebia) mice: J Invest Dermatol 2003;120:728–737.
  58. Menon GK, Kligman AM: Barrier functions of human skin: a holistic view. Skin Pharmacol Physiol 2009;22:178–189.
  59. Choi EH, Man MQ, Wang F, Zhang X, Brown BE, Feingold KR, Elias PM: Is endogenous glycerol a determinant of stratum corneum hydration in humans? J Invest Dermatol 2005;125:288–293.
  60. Wiedersberg S, Leopold CS, Guy RH: Effects of various vehicles on skin hydration in vivo. Skin Pharmacol Physiol 2009;22:128–130.
  61. Lee CM, Maibach HI: Bioengineering analysis of water hydration; in Maibach HI (ed): A Dermatological View from Physiology to Therapy. Alluredbooks, 2011.

  

Author Contacts

Thais H. Sakuma
252 Swain Way
Palo Alto, CA 94304 (USA)
Tel. +1 650 919 4842
E-Mail thais.sakuma@gmail.com

  

Article Information

This paper is dedicated to the memory of Prof. Albert M. Kligman and Prof. Walter B. Shelley.

Received: July 18, 2011
Accepted after revision: April 20, 2012
Published online: June 20, 2012
Number of Print Pages : 9
Number of Figures : 0, Number of Tables : 1, Number of References : 61

  

Publication Details

Skin Pharmacology and Physiology (Journal of Pharmacological and Biophysical Research)

Vol. 25, No. 5, Year 2012 (Cover Date: August 2012)

Journal Editor: Lademann J. (Berlin)
ISSN: 1660-5527 (Print), eISSN: 1660-5535 (Online)

For additional information: http://www.karger.com/SPP


Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

Abstract

Oily skin (seborrhea) is a common cosmetic problem that occurs when oversized sebaceous glands produce excessive amounts of sebum giving the appearance of shiny and greasy skin. This paper overviews the main concepts of sebaceous gland anatomy and physiology, including the biosynthesis, storage and release of sebum, as well as its relationship to skin hydration and water barrier function. We also address how skin oiliness may vary according to diet, age, gender, ethnicity and hot humid climates. The deeper understanding of this skin type provides the opportunity to better guide patients regarding skin care and also assist in the development of sebosuppressive agents.

© 2012 S. Karger AG, Basel


  

Author Contacts

Thais H. Sakuma
252 Swain Way
Palo Alto, CA 94304 (USA)
Tel. +1 650 919 4842
E-Mail thais.sakuma@gmail.com

  

Article Information

This paper is dedicated to the memory of Prof. Albert M. Kligman and Prof. Walter B. Shelley.

Received: July 18, 2011
Accepted after revision: April 20, 2012
Published online: June 20, 2012
Number of Print Pages : 9
Number of Figures : 0, Number of Tables : 1, Number of References : 61

  

Publication Details

Skin Pharmacology and Physiology (Journal of Pharmacological and Biophysical Research)

Vol. 25, No. 5, Year 2012 (Cover Date: August 2012)

Journal Editor: Lademann J. (Berlin)
ISSN: 1660-5527 (Print), eISSN: 1660-5535 (Online)

For additional information: http://www.karger.com/SPP


Article / Publication Details

First-Page Preview
Abstract of Review

Received: 7/18/2011
Accepted: 4/20/2012
Published online: 6/20/2012
Issue release date: August 2012

Number of Print Pages: 9
Number of Figures: 0
Number of Tables: 1

ISSN: 1660-5527 (Print)
eISSN: 1660-5535 (Online)

For additional information: http://www.karger.com/SPP


Copyright / Drug Dosage

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

References

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    External Resources

  2. Arbuckle R, Clark M, Harness J, Bonner N, Scott J, Draelos Z, Rizer R, Yeh Y, Copley-Merriman K: Item reduction and psychometric validation of the Oily Skin Self Assessment Scale (OSSAS) and the Oily Skin Impact Scale (OSIS). Value Health 2009;5:828–837.

    External Resources

  3. Segot-Chicq E, Compan-Zaouati D, Wolkenstein P, Consoli S, Rodary C, Delvigne V, Guillou V, Poli F: Development and validation of a questionnaire to evaluate how a cosmetic product for oily skin is able to improve well-being in women. J Eur Acad Dermatol Venereol 2007;21:1181–1186.
  4. Downing DT, Stewart ME, Wertz PW, Colton SW 6th, Strauss JS: Skin lipids. Comp Biochem Physiol B 1983;76:673–678.
  5. Strauss JS, Pochi PE, Downing DT: Skin lipids and acne. Annu Rev Med 1975;26:27–32.
  6. Michaels AS, Chandrasekaran SK, Shaw JE: Drug permeation through human skin: theory and in vitro experimental measurement. Am Inst Chem Eng J 1975;21:985–996.
  7. Nicolaides N: Skin lipids: their biochemical uniqueness. Science 1974;186:19–26.
  8. Smith KR, Thiboutot DM: Thematic review series: skin lipids. Sebaceous gland lipids: friend or foe? J Lipid Res 2008;49:271–281.
  9. Greene RS, Downing DT, Pochi PE, Strauss JS: Anatomical variation in the amount and composition of human skin surface lipid. J Invest Dermatol 1970;54:240–247.
  10. Man MQ, Xin SJ, Song SP, Cho SY, Zhang XJ, Tu CX, Feingold KR, Elias PM: Variation of skin surface pH, sebum content and stratum corneum hydration with age and gender in a large Chinese population. Skin Pharmacol Physiol 2009;22:190–199.
  11. Sheu HM, Chao SC, Wong TW, Yu-Yun Lee J, Tsai JC: Human skin surface lipid film: an ultrastructural study and interaction with corneocytes and intercellular lipid lamellae of the stratum corneum. Br J Dermatol 1999;140:385–391.
  12. Picardo M, Ottaviani M, Camera E, Mastrofrancesco A: Sebaceous gland lipids. Dermatoendocrinol 2009;1:68–71.
  13. Pappas A: Epidermal surface lipids. Dermatoendocrinol 2009;1:72–76.
  14. Tóth BI, Oláh A, Szöllosi AG, Czifra G, Bíró T: ‘Sebocytes’ makeup’: novel mechanisms and concepts in the physiology of the human sebaceous glands. Pflugers Arch 2011;461:593–606.
  15. Smith RN, Braue A, Varigos GA, Mann NJ: The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. J Dermatol Sci 2008;50:41–52.
  16. Feingold KR: Thematic review series: skin lipids. The role of epidermal lipids in cutaneous permeability barrier homeostasis. J Lipid Res 2007;48:2531–2546.
  17. Proksch E, Holleran WM, Menon GK, Elias PM, Feingold KR: Barrier function regulates epidermal lipid and DNA synthesis. Br J Dermatol 1993;128:473–482.
  18. Kligman AM, Shelley WB: An investigation of the biology of the human sebaceous gland. J Invest Dermatol 1958;30:99–125.
  19. Pagnoni A, Kligman AM, el Gammal S, Stoudemayer T: Determination of density of follicles on various regions of the face by cyanoacrylate biopsy: correlation with sebum output. Br J Dermatol 1994;131:862–865.
  20. Lopez S, Le Fur I, Morizot F, Heuvin G, Guinot C, Tschachler E: Transepidermal water loss, temperature and sebum levels on women’s facial skin follow characteristic patterns. Skin Res Technol 2000;6:31–36.
  21. Piérard GE, Piérard-Franchimont C, Marks R, Paye M, Rogiers V: EEMCO guidance for the in vivo assessment of skin greasiness. The EEMCO Group. Skin Pharmacol Appl Skin Physiol 2000;13:372–389.
  22. Miescher G, Schonberg A: Untersuchungen über die Funktion der Talgdrüsen. Bull Schweiz Akad Med Wiss 1944;1:101.
  23. Downing DT, Stranieri AM, Strauss JS: The effect of accumulated lipids on measurements of sebum secretion in human skin. J Invest Dermatol 1982;79:226–228.
  24. Millns JL, Maibach HI: Mechanisms of sebum production and delivery in man. Arch Dermatol Res 1982;272:351–362.
  25. Butcher EO, Parnell JP: The distribution and factors influencing the amount of sebum on the skin of the forehead. J Invest Dermatol 1948;10:31–38.
  26. Piérard-Franchimont C, Quatresooz P, Piérard GE: Sebum production; in Farage MA, Miller KW, Maibach HI (eds): Textbook of Aging Skin. Berlin/Heidelberg, Springer, 2009, pp 343–352.
  27. Zouboulis CC, Xia L, Akamatsu H, Seltmann H, Fritsch M, Hornemann S, Rühl R, Chen W, Nau H, Orfanos CE: The human sebocyte culture model provides new insights into development and management of seborrhoea and acne. Dermatology 1998;196:21–31.
  28. Akamatsu H, Zouboulis CC, Orfanos CE: Control of human sebocyte proliferation in vitro by testosterone and 5-alpha-dihydrotestosterone is dependent on the localization of the sebaceous glands. J Invest Dermatol 1992;99:509–511.
  29. Chen WC, Zouboulis CC: Hormones and the pilosebaceous unit. Dermatoendocrinol 2009;1:81–86.
  30. Fulton JE Jr, Plewig G, Kligman AM: Effect of chocolate on acne vulgaris. JAMA 1969;210:2071–2074.

    External Resources

  31. Pochi PE, Downing DT, Strauss JS: Sebaceous gland response in man to prolonged total caloric deprivation. J Invest Dermatol 1970;55:303–309.
  32. Michaëlsson G: Diet and acne. Nutr Rev 1981;39:104–106.
  33. Melnik BC, Schmitz G: Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol 2009;18:833–841.
  34. Smith RN, Mann NJ, Braue A, Mäkeläinen H, Varigos GA: The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: a randomized, investigator-masked, controlled trial. J Am Acad Dermatol 2007;57:247–256.
  35. Smith TM, Gilliland K, Clawson GA, Thiboutot D: IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway. J Invest Dermatol 2008;128:1286–1293.
  36. Vora S, Ovhal A, Jerajani H, Nair N, Chakrabortty A: Correlation of facial sebum to serum insulin-like growth factor-1 in patients with acne. Br J Dermatol 2008;159:990–991.
  37. Katsuta Y, Iida T, Inomata S, Denda M: Unsaturated fatty acids induce calcium influx into keratinocytes and cause abnormal differentiation of epidermis. J Invest Dermatol 2005;124:1008–1013.
  38. Walton S, Wyatt EH, Cunliffe WJ: Genetic control of sebum excretion and acne – a twin study. Br J Dermatol 1988;118:393–396.
  39. Zouboulis CC, Boschnakow A: Chronological ageing and photoageing of the human sebaceous gland. Clin Exp Dermatol 2001;26:600–607.
  40. Jacobsen E, Billings JK, Frantz RA, Kinney CK, Stewart ME, Downing DT: Age-related changes in sebaceous wax ester secretion rates in men and women. J Invest Dermatol 1985;85:483–485.
  41. Plewig G, Kligman AM: Proliferative activity of the sebaceous glands of the aged. J Invest Dermatol 1978;70:314–317.
  42. Pochi PE, Strauss JS, Downing DT: Age-related changes in sebaceous gland activity. J Invest Dermatol 1979;73:108–111.
  43. Zouboulis CC: Acne and sebaceous gland function. Clin Dermatol 2004;22:360–366.
  44. Hillebrand GG, Miyamoto K, Schnell B, Ichihashi M, Shinkura R, Akiba S: Quantitative evaluation of skin condition in an epidemiological survey of females living in northern versus southern Japan. J Dermatol Sci 2001;27(suppl 1):S42–S52.
  45. Rawlings AV: Ethnic skin types: are there differences in skin structure and function? Int J Cosmet Sci 2006;28:79–93.
  46. Pochi PE, Strauss JS: Sebaceous gland activity in black skin. Dermatol Clin 1988;6:349–351.
  47. Grimes P, Edison BL, Green BA, Wildnauer RH: Evaluation of inherent differences between African American and white skin surface properties using subjective and objective measures. Cutis 2004;73:392–396.
  48. Cunliffe WJ, Burton JL, Shuster S: The effect of local temperature variations on the sebum excretion rate. Br J Dermatol 1970;83:650–654.
  49. Williams M, Cunliffe WJ, Williamson B, Forster RA, Cotterill JA, Edwards JC: The effect of local temperature changes on sebum excretion rate and forehead surface lipid composition. Br J Dermatol 1973;88:257–262.
  50. Downing DT, Strauss JS: On the mechanism of sebaceous secretion. Arch Dermatol Res 1982;272:343–349.
  51. Youn SW, Na JI, Choi SY, Huh CH, Park KC: Regional and seasonal variations in facial sebum secretions: a proposal for the definition of combination skin type. Skin Res Technol 2005;11:189–195.

    External Resources

  52. Thiele JJ, Weber SU, Packer L: Sebaceous gland secretion is a major physiologic route of vitamin E delivery to skin. J Invest Dermatol 1999;113:1006–1010.
  53. Ekanayake Mudiyanselage S, Hamburger M, Elsner P, Thiele JJ: Ultraviolet a induces generation of squalene monohydroperoxide isomers in human sebum and skin surface lipids in vitro and in vivo. J Invest Dermatol 2003;120:915–922.
  54. Passi S, De Pità O, Puddu P, Littarru GP: Lipophilic antioxidants in human sebum and aging. Free Radic Res 2002;36:471–477.
  55. Wille JJ, Kydonieus A: Palmitoleic acid isomer (C16:1delta6) in human skin sebum is effective against gram-positive bacteria. Skin Pharmacol Appl Skin Physiol 2003;16:176–187.
  56. Cunliffe WJ, Holland DB, Jeremy A: Comedone formation: etiology, clinical presentation, and treatment. Clin Dermatol 2004;22:367–374.

    External Resources

  57. Fluhr JW, Mao-Qiang M, Brown BE, Wertz PW, Crumrine D, Sundberg JP, Feingold KR, Elias PM: Glycerol regulates stratum corneum hydration in sebaceous gland deficient (asebia) mice: J Invest Dermatol 2003;120:728–737.
  58. Menon GK, Kligman AM: Barrier functions of human skin: a holistic view. Skin Pharmacol Physiol 2009;22:178–189.
  59. Choi EH, Man MQ, Wang F, Zhang X, Brown BE, Feingold KR, Elias PM: Is endogenous glycerol a determinant of stratum corneum hydration in humans? J Invest Dermatol 2005;125:288–293.
  60. Wiedersberg S, Leopold CS, Guy RH: Effects of various vehicles on skin hydration in vivo. Skin Pharmacol Physiol 2009;22:128–130.
  61. Lee CM, Maibach HI: Bioengineering analysis of water hydration; in Maibach HI (ed): A Dermatological View from Physiology to Therapy. Alluredbooks, 2011.