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It is well documented that individuals who are prone to acne produce more oil than those who are not. However, not all individuals with oily skin experience acne breakouts. While sebum is a necessary component for the development of acne, high oil levels alone are not sufficient to cause acne. In addition to the quantity of oil produced, there are qualitative differences in oil among people who are acne-prone compared to those who are not.

Sebum Composition

Sebum is primarily comprised of natural fats. Triglycerides and fatty acids make up almost 60 percent of sebum, wax esters account for approximately 25 percent, and squalene comprises the remaining 12 to 15 percent.1 In individuals with acne, there is a well-documented decrease in the concentration of linoleic acid that is accompanied by an increase in the concentration of squalene. This alteration in epidermal lipids plays a pivotal role in the pathogenesis of acne.

Linoleic acid is a building block for the production of certain ceramides in the skin. Low levels of linoleic acid in the sebum of acne-prone patients result in insufficient production of these ceramides, which helps explain the deficiency of ceramides that has been demonstrated in individuals with acne.2 In fact, a relationship between ceramide deficiency and acne severity has been demonstrated. Studies have shown that more severe acne is associated with a greater deficiency of ceramides in the skin.3 Ceramide deficiency contributes to skin barrier dysfunction, which has been directly tied to the follicular hyperkeratinization that drives comedone formation. As keratinocytes stick together within the follicle, it creates a bottleneck that traps sebum within the pores. As sebum levels increase, the pore becomes dilated. Ultimately, this may result in rupture of the wall of the follicle with associated inflammation.4

Squalene is a lipid found uniquely in the sebum of the skin but nowhere else in the body. It is thought to provide protective and emollient effects in the epidermis. Acne-prone patients have been shown to produce higher than normal levels of squalene in their sebum, and squalene is suspected to directly contribute to the development of acne. Squalene is thought to react with environmental stressors in a process known as lipid peroxidation. Here, epidermal lipids like squalene are oxidized, creating reactive, inflammatory compounds. When squalene is exposed to environmental oxidative stressors like pollution and UV light from the sun, it is converted to squalene peroxides that drive the inflammatory cascade characteristic of acne.

Components of Sebum

Ceramides. Ceramide deficiency contributes to skin barrier dysfunction, which has been directly tied to the follicular hyperkeratinization that drives comedone formation.

Squalene. Squalene is thought to directly contribute to the development of acne by reacting with environmental stressors in a process known as lipid peroxidation and producing inflammation.

Vitamin E. Vitamin E is an antioxidant found in sebum; reduced levels of vitamin E correlate with increases in squalene peroxide levels and subsequent inflammation.

The skin has its own natural antioxidant system to neutralize this process, predominantly through Vitamin E in the sebum.5 Acne patients have also been shown to have depleted Vitamin E levels, which correlates with increases in squalene peroxide levels. Studies have shown that topically applied antioxidants are effective in treating acne. One study specifically evaluated the use of topically applied sodium ascorbyl phosphate, a stabilized form of Vitamin C, to treat and prevent acne both in vitro and in vivo.6

Oily versus Acne-prone

The different composition of sebum in patients with acne compared to those without acne is essential to understanding the pathogenesis of acne. This helps explain the differences between oily and acne-prone individuals and can help us better treat patients using therapeutics and cosmetic products that address the specific needs of the skin in acne-prone patients.

1. Picardo M, et al. Sebaceous gland lipids. Dermatoendocrinol. 2009 Mar-Apr; 1(2): 68–71.

2. Ottaviani M, et al. Lipid Mediators in Acne. Mediators Inflamm. 2010; 2010: 858176.

3.Yamamoto A, et al. Impaired water barrier function in acne vulgaris. Arch Dermatol Res. 1995;287(2):214-8.

4. Stewart ME, et a. Dilutional effect of increased sebaceous gland activity on the proportion of linoleic acid in sebaceous wax esters and in epidermal acylceramides. J Invest Dermatol. 1986; 87: 733–736.

5. Packer L, et al. Sebaceous Gland Secretion is a Major Physiologic Route of Vitamin E Delivery to Skin. J Invest Dermatol. 1999; 113 (6): 1006-1010.

6. Klock J et al . Sodium ascorbyl phosphate shows in vitro and in vivo efficacy in the prevention and treatment of acne vulgaris. Int J Cosmet Sci. 2005 Jun;27(3):171-6.

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