Acne vulgaris is a skin disorder occurring in all age groups, but most frequently seen in adolescents and young adults. Most teens in Western countries experience some degree of acne, which generally resolves as androgen levels decline. Some cases, however, persist into adulthood or have their onset in adulthood.
Acne is an inflammatory condition of the hair follicle-sebaceous gland complex (the pilosebaceous unit). Follicular hyperkeratinization, increased sebum production, overgrowth of Cutibacterium acnes (C. acnes, formerly Propionibacterium acnes) bacteria, and subsequent inflammation lead to its clinical manifestations. Plugs found in acne follicles are composed of keratin from surrounding keratinocytes and lipids secreted from sebaceous glands under the influence of androgenic hormones. The lipid-rich sebum serves as a medium for proliferation of C. acnes.
Acne may appear as closed comedones (“whiteheads”) or, when excessive distention forces open the follicular orifice, open comedones (“blackheads”). Oxidation of the lipid and melanin causes the darkened appearance of open comedones.
Acne most commonly affects areas of the body with the greatest number of sebaceous glands. These include the face, upper back, neck, chest, and upper arms. Mild acne is not inflammatory and involves only a small number of open or closed comedones. Moderate-to-severe acne involves inflammation of the dermis surrounding the pilosebaceous unit. This inflammation is due to follicular rupture, spilling of free fatty acids (resulting from the hydrolysis of triglycerides by C acnes), and the release of lysosomal enzymes from neutrophils attracted by chemotactic factors released by C acnes. This process results in the formation of pustules, papules, or nodules that cover a large area of skin. Scarring and hyperpigmentation can also occur, which is more common in patients with darker complexions.
Cosmetics (acne cosmetica). Skin and hair products that contain oils or dyes can cause acne lesions. Water-based cosmetics are less comedogenic.
Repetitive skin trauma (acne mechanica). Rubbing (even with cleansing agents), scrubbing, or occlusive clothing (e.g., bra straps, helmets, turtlenecks) can promote inflammatory reactions in the lesions.
Environmental exposures. Humidity and sweating can exacerbate acne. Exposure to certain chemicals (e.g., dioxin and other halogenated hydrocarbons) that are found in herbicides and other industrial products can cause severe inflammatory acne-type reactions (chloracne) and scarring.
Drugs (acne medicamentosa). Certain drugs are likely to cause acne, including corticosteroids, phenytoin, isoniazid, disulfiram, lithium, progesterone-only contraceptives, and B vitamins.
Diet. Skim milk intake and high-glycemic-load diets have been linked to acne (see Nutritional Considerations below).
Genetics. Genetics may play a role in more severe forms of acne, especially in persistent and late-onset cases. The role of genes in mild adolescent acne is uncertain.
Stress. Stress is believed to be associated with acne exacerbations, but further study is required to establish this connection.
Hormones. Endocrine disorders marked by excess androgens or insulin resistance, such as congenital adrenal hyperplasia and polycystic ovarian syndrome, may trigger the development of acne vulgaris.
Acne vulgaris is a clinical diagnosis. History and dermatologic examination are necessary to characterize the distribution and types of acne lesions, and to evaluate underlying medical disorders.
Fever and arthralgia in a patient with severe inflammatory acne suggest acne fulminans, a serious disease that requires immediate treatment with systemic corticosteroids and isotretinoin (see below).
Women with oligomenorrhea, hirsutism, male- or female-pattern alopecia, infertility, acanthosis nigricans, and truncal obesity should be evaluated for hyperandrogenism, which may be caused by polycystic ovarian syndrome or an androgen-secreting tumor.
Treatment should address both the physical and psychological effects of acne and should be guided by the severity and type of lesions. Light and laser therapies may be used but the role of these modalities is not clearly defined at this time.
Several topical therapies are used to treat noninflammatory acne.
Retinoids (e.g., retinol, tretinoin, adapalene, tazarotene) decrease follicle hyperkeratinization and are commonly recommended as part of the treatment for any degree of acne. Retinoids also accelerate the resolution of hyperpigmentation caused by acne induced inflammation. They are available in various preparations, including creams, gels and microgels (which are less irritating), solutions, and pads. Skin irritation and photosensitivity may occur. This class of medications should not be used during pregnancy, especially tazarotene.
As of July 2016, the FDA approved adapalene as an over-the-counter medication for individuals 12 and older.
Acid preparations (e.g., salicylic acid, azelaic acid, glycolic acid, and lactic acid) also decrease follicle hyperkeratinization. Salicylic acid is the most commonly used acid and is available over the counter. Azelaic acid may be effective for acne induced hyperpigmentation.
Benzoyl peroxide is an effective topical treatment that has antibacterial and comedolytic properties. In patients with inflammatory lesions, it may be used in combination with a topical antibiotic, such as clindamycin, or a topical retinoid.
Topical tea tree oil exhibits antimicrobial and anti-inflammatory properties. There is evidence of a reduction in acne lesions with consistent application.
Extraction of comedones may also be performed by a trained clinician.
Inflammatory acne is often treated with multiple topical therapies, which are more effective than either agent alone.4 Benzoyl peroxide, topical antibiotics (e.g., erythromycin, dapsone, clindamycin), retinoids, and acids are commonly used.
Oral antibiotics (tetracyclines or macrolides) are indicated for moderate inflammatory pustular acne. Treatment should be as brief as possible. An optimal goal is 3-4 months, or when there is no response or further improvement in lesions.
In females with clinical or laboratory evidence of hyperandrogenism, the oral antiandrogen spironolactone can be utilized. Additionally, many females may benefit from specific formulations of hormonal contraceptives.
Severe acne can be treated with intensive topical and oral treatment.
Oral antibiotics are indicated for an extended period of time, but bacterial resistance may occur with prolonged therapy.
Isotretinoin is usually reserved for the most severe cases of nodulocystic acne, or acne that is refractory to combination treatment. It is extremely effective, but is expensive and has many potential adverse effects, including teratogenicity. Close follow-up is necessary for laboratory work, including pregnancy tests, liver function tests, lipid panels, and complete blood counts. Treatment usually lasts 20 weeks and may result in permanent remission.
Systemic corticosteroids should be added if the acne worsens with initiation of isotretinoin. Intralesional steroid injection is also very effective for larger inflammatory lesions.
Many patients benefit from some level of maintenance therapy after their initial treatment phase, as acne lesions typically recur over time. The best maintenance therapy is still being evaluated, but topical retinoids have the best evidence and benefit-to-risk ratio at this time.
Several nutritional factors have been shown to be associated with the risk of acne:
Excess body weight. Acne is more common in overweight individuals, due in part to insulin resistance.
Western diets. Indigenous populations that eat largely plant-based diets composed mainly of unprocessed or minimally processed foods high in carbohydrate and fiber (e.g., tubers, fruit, vegetables, peanuts, corn, and rice), and emphasizing unsaturated rather than saturated fats, are largely free of acne. In contrast, acne is common in countries following Westernized diets.,, As immigrants to Western countries become acculturated to a Western diet, their previously low incidence of acne rises to the levels found in Western societies.
Dairy products. The Nurses’ Health Study II, including more than 47,000 participants, showed that those who reported having consumed the most whole milk during adolescence were about 12% more likely to have had severe acne. Those who had consumed the most skim milk were 44% more likely to have had severe acne. That is, skim milk appeared to present greater risk than full-fat milk.
Because that study relied on participants’ memories of their diets as adolescents, the same researchers conducted a prospective study, including 4,273 boys and 6,094 girls, aged 9 to 15 years, followed over a 3-year period. Study results mirrored the earlier findings. Milk consumption was associated with acne, and skim milk was implicated at least as much as whole milk., Skim is much lower in fat, but higher in both protein and lactose.
Glycemic load. Clinical trials have suggested that foods with a high glycemic index may contribute to acne, and low-glycemic-index foods may be helpful in treatment.,, Low-glycemic-index foods include most fruits, green vegetables, some grains (e.g., oats and barley), pasta, sweet potatoes, nuts, and beans and other legumes. Examples of high-glycemic-index foods include sugar, wheat breads, white potatoes, and many cold cereals. Individually these foods are not necessarily problematic; rather, the problem likely results from the overall glycemic load of the diet, which may act by causing abnormalities in lipids and insulin, described below.
Inadequate zinc. Low serum zinc levels are associated with greater severity of acne lesions. Zinc supplements have been used to effectively treat inflammatory acne and are reportedly more effective for severe than mild-to-moderate acne, although gastrointestinal distress occurs more often with high doses.
The biological mechanisms linking Western diets, particularly dairy products, to acne appear to relate to hormonal effects. The effects of a surge in hormones (androgens) during puberty apparently combine with the ability of a Western diet to raise levels of IGF-1 and insulin, thereby making androgens and androgen precursors more available.
Androgens are synthesized from cholesterol derived from the bloodstream, and studies have revealed relationships between serum cholesterol concentrations and acne risk. Researchers have also observed worsening of acne with increasing intake of saturated fat (found in dairy products and meat) and trans fatty acids (commonly found in snack foods and fried foods).
The amino acid leucine and other branched-chain amino acids (which are present to a greater degree in animal versus plant protein) increase IGF-1, act as precursors of sebaceous lipids, stimulate keratinocyte proliferation, and promote inflammatory activity of keratinocytes, as well as increasing the availability of androgens and stimulating sebocyte production., Dairy protein also contains steroids and steroid precursors that may stimulate sebum production and induce hyperkeratinization of the pilosebaceous unit.
Diets that represent a high glycemic load may cause hyperinsulinemia when regularly consumed. This results in an increase in IGF-1, a decrease in IGF binding proteins (IGFBPs), and a subsequent increase in keratinocyte proliferation and free androgens. Androgens in turn increase IGF-1, thereby perpetuating a vicious cycle.
See Basic Diet Orders chapter.
Low-fat, high-fiber, nondairy diet may be tried on a prospective basis.
What to Tell the Family
Acne is a common and distressing condition. Some evidence suggests that it may be in some measure preventable by dietary changes. In particular, dairy intake has been associated with the development and worsening of acne in women and could also play a role in men. Likewise, a high-fat diet may be implicated in acne formation. In addition, the use of oil-based cosmetics, excessive scrubbing or rubbing, and occlusive clothing (tight bras, turtlenecks) may worsen the acne lesions. Family members can assist patients with acne by helping them stay on a healthful diet.
- Goulden V, Clark SM, Cunliffe WJ. Post-adolescent acne: a review of clinical features. Br J Dermatol. 1997;136(1):66-70. [PMID:9039297]
- Vora S, Ovhal A, Jerajani H, et al. Correlation of facial sebum to serum insulin-like growth factor-1 in patients with acne. Br J Dermatol. 2008;159(4):990-1. [PMID:18652583]
- Enshaieh S, Jooya A, Siadat AH, et al. The efficacy of 5% topical tea tree oil gel in mild to moderate acne vulgaris: a randomized, double-blind placebo-controlled study. Indian J Dermatol Venereol Leprol. 2007;73(1):22-5. [PMID:17314442]
- Strauss JS, Krowchuk DP, Leyden JJ, et al. Guidelines of care for acne vulgaris management. J Am Acad Dermatol. 2007;56(4):651-63. [PMID:17276540]
- Eady EA, Bojar RA, Jones CE, et al. The effects of acne treatment with a combination of benzoyl peroxide and erythromycin on skin carriage of erythromycin-resistant propionibacteria. Br J Dermatol. 1996;134(1):107-13. [PMID:8745894]
- Purdy S, de Berker D. Acne. BMJ. 2006;333(7575):949-53. [PMID:17082546]
- Melnik BC, John SM, Plewig G. Acne: risk indicator for increased body mass index and insulin resistance. Acta Derm Venereol. 2013;93(6):644-9. [PMID:23975508]
- Melnik B. Dietary intervention in acne: Attenuation of increased mTORC1 signaling promoted by Western diet. Dermatoendocrinol. 2012;4(1):20-32. [PMID:22870349]
- Kucharska A, Szmurło A, Sińska B. Significance of diet in treated and untreated acne vulgaris. Postepy Dermatol Alergol. 2016;33(2):81-6. [PMID:27279815]
- Lynn DD, Umari T, Dunnick CA, et al. The epidemiology of acne vulgaris in late adolescence. Adolesc Health Med Ther. 2016;7:13-25. [PMID:26955297]
- Campbell CE, Strassmann BI. The blemishes of modern society? Acne prevalence in the Dogon of Mali. Evol Med Public Health. 2016;2016(1):325-337. [PMID:27651516]
- Adebamowo CA, Spiegelman D, Danby FW, et al. High school dietary dairy intake and teenage acne. J Am Acad Dermatol. 2005;52(2):207-14. [PMID:15692464]
- Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in adolescent girls. Dermatol Online J. 2006;12(4):1. [PMID:17083856]
- Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in teenaged boys. J Am Acad Dermatol. 2008;58(5):787-93. [PMID:18194824]
- Augustin LS, Kendall CW, Jenkins DJ, et al. Glycemic index, glycemic load and glycemic response: An International Scientific Consensus Summit from the International Carbohydrate Quality Consortium (ICQC). Nutr Metab Cardiovasc Dis. 2015;25(9):795-815. [PMID:26160327]
- Rostami Mogaddam M, Safavi Ardabili N, Maleki N, et al. Correlation between the severity and type of acne lesions with serum zinc levels in patients with acne vulgaris. Biomed Res Int. 2014;2014:474108. [PMID:25157359]
- Gupta M, Mahajan VK, Mehta KS, et al. Zinc therapy in dermatology: a review. Dermatol Res Pract. 2014;2014:709152. [PMID:25120566]
- Bakry OA, El Shazly RM, El Farargy SM, et al. Role of hormones and blood lipids in the pathogenesis of acne vulgaris in non-obese, non-hirsute females. Indian Dermatol Online J. 2014;5(Suppl 1):S9-S16. [PMID:25506579]
- Melnik BC. Linking diet to acne metabolomics, inflammation, and comedogenesis: an update. Clin Cosmet Investig Dermatol. 2015;8:371-88. [PMID:26203267]