Acne is the most common skin disorder in the United States, affecting more than 17 million Americans. Most adolescents 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.
Common acne, as it appears in adolescents, is associated with many factors, including genetic predisposition, hormonal abnormalities, and clogged pilosebaceous follicles. Plugs found in follicles of patients with acne are composed of a mixture of lipids secreted by sebaceous glands and keratin that accumulates from surrounding keratinocytes.
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 cause the darkened appearance of open comedones. Increased production of androgens during puberty leads to sebaceous gland growth and increased sebum production, providing an anaerobic lipid-rich medium that is optimal for bacterial growth. Propionibacterium acnes (an anaerobic diptheroid) proliferates and can incite an inflammatory reaction that results in the characteristic acne lesions.
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 P. acnes), and the release of lysosomal enzymes from neutrophils attracted by chemotactic factors released by P. 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, usually in patients with darker complexions.
Risk Factors and Diagnosis
Cosmetics. Skin and hair products that contain oils or dyes can exacerbate acne lesions. Water-based cosmetics are less comedogenic.
Repetitive skin trauma. Rubbing (even with cleansing agents), scrubbing, or occlusive clothing (eg, bra straps, helmets, turtlenecks) can promote inflammatory reactions in the lesions.
Environmental exposures. Humidity and sweating can exacerbate acne. Exposure to certain chemicals (eg, dioxin and other halogenated hydrocarbons) that are found in herbicides and other industrial products can cause severe inflammatory acne and scarring.
Drugs. Certain drugs are likely to cause acne, including corticosteroids, phenytoin, isoniazid, disulfiram, lithium, and B vitamins.
Diet. Milk intake, in particular, has been linked to acne (see Nutritional Considerations).
Climate. Humidity and heavy sweating may lead to acne.
Genetics. Genetics likely plays a role in the manifestation of acne, especially in persistent and late-onset cases.1
Stress. Stress is believed to be associated with acne exacerbations, but further study is required to establish this connection.
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 suggests acne fulminans, a serious disease that requires immediate treatment with systemic corticosteroids and isotretinoin (see Acne Treatment).
Women with oligomenorrhea should be evaluated for hyperandrogenism, which may occur due to 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 to treat acne in the future.
A number of topical therapies are used to treat noninflammatory acne.
- Retinoids (eg, tretinoin, adapalene, tazarotene) decrease follicle hyperkeratinization. Treatment for 8 weeks is required before assessing efficacy, and acne may initially worsen. Retinoids are available in various preparations, including creams, gels, and microgels (which are less irritating), solutions, and pads. Skin irritation and photosensitivity may occur. Tazarotene is contraindicated during pregnancy.
- Acid preparations (eg, salicylic acid, azelaic acid, glycolic 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 erythromycin, or a topical retinoid.
Extraction of comedones may be performed by a trained clinician after first treating the patient with a retinoid.
Inflammatory acne is often treated with multiple topical therapies. Benzoyl peroxide, topical antibiotics (eg, erythromycin, tetracycline, azealic acid, clindamycin), retinoids, and acids are commonly used.
Antibiotics attack the proprionibacterium in the hair follicles. Bacterial resistance may occur, but is reduced by combination therapy with benzoyl peroxide.2
Severe acne can be treated with intensive topical treatment, but may require oral therapy.
Oral antibiotics are usually prescribed for 6 months and then tapered. 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 6 months.
Systemic corticosteroids should be added if the acne worsens with initiation of isotretinoin.
Some studies suggest that acne occurs more commonly in countries following Westernized diets. 3-5 However, the role of nutritional factors remains unclear. For years, dermatologists advised patients to avoid chocolate, fried foods, and fatty foods, although proof of their pathogenic role was lacking. Acne may not be worse in individuals with a higher intake of table sugar or chocolate,4 although recent evidence suggests that diet may indeed contribute to hormone-related acne.
Western Diets and Acne
Indigenous populations that eat plant-based diets composed mainly (roughly 70%) of unprocessed or minimally processed foods high in carbohydrate and fiber, and emphasizing unsaturated, rather than saturated, fats (tubers, fruit, vegetables, peanuts, corn, rice), are largely free of acne. In contrast, the vast majority of teenagers and 40% to 54% of the adult (>25 years) population in Western societies have some degree of facial acne.3
Evidence also suggests that as immigrants become acculturated to a typical Western diet, their previously low incidence of acne rises to the levels found in Western societies.4 Aspects of diet under particular scrutiny are as follows:
Dietary fat contributes to sebum production, and excesses of both fat and carbohydrate contribute to increased lipid secretion in human skin. In contrast, restricting calories can reduce sebum production by as much as 40%.4
Diets high in saturated fat,6 meat,7 and milk5 increase blood concentrations of insulin-like growth factor (IGF-I), which, in turn, stimulates the production of androgens known to increase sebum production.3,4 Plant-based diets, low-fat diets, high-fiber diets, and vegetarian diets lower IGF-I and increase IGF-binding proteins.3,7,8
Dairy products may play a role in acne. In the Nurses Health Study II, more than 47,000 women completed questionnaires based on recalling their diet during high school in 1998, and associations were estimated between various food groups and diagnosis of teenage acne. Women who consumed more than 2 glasses of skim milk per day during their teen years (ie, ages 13-18) had a 40% greater prevalence of teenage acne, compared with those drinking less than 1 glass per week.5,9
Controlled trials testing this relationship are in progress. While mechanisms that might explain the association have not been established, several possibilities have been suggested. Milk contains both hormones and hormone-like chemicals (eg, IGF-I) that may survive processing and affect the pilosebaceous glands. Apart from the hormones found in milk, hormones or growth factors may be produced in the human body in response to milk ingestion. For instance, regular milk ingestion by adults is associated with an elevation of blood IGF-I concentrations,10 which may increase the risk for acne.
Low-fat, high-fiber, nondairy diet may be tried on a prospective basis.
What to Tell the Family
Acne is a 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. Moreover, following such a diet themselves may reduce their own risk for diet-related conditions.
1. Goulden V, Clark SM, Cunliffe WJ. Post-adolescent acne: a review of clinical features. Br J Dermatol. 1997;136:66-70.
2. Eady EA, Bojar RA, Jones CE, Cove JH, Holland KT, Cunliffe WJ. The effects of acne treatment with a combination of benzoyl peroxide and erythromycin on skin carriage of erythromycin-resistant propionibacteria. Br J Dermatol. 1996;134:107-113.
5. Adebamowo CA, Spiegelman D, Danby FW, Frazier AL, Willett WC, Holmes MD. High school dietary dairy intake and teenage acne. J Am Acad Dermatol. 2005;52:207-“214.
6. Heald AH, Cade JE, Cruickshank JK, Anderson S, White A, Gibson JM. The influence of dietary intake on the insulin-like growth factor (IGF) system across three ethnic groups: a population-based study. Public Health Nutr. 2003;6:175-180.
7. Allen NE, Appleby PN, Davey GK, Kaaks R, Rinaldi S, Key TJ. The associations of diet with serum insulin-like growth factor I and its main binding proteins in 292 women meat-eaters, vegetarians, and vegans. Cancer Epidemiol Biomarkers Prev. 2002;11:1441-1448.
8. Kaaks R, Bellati C, Venturelli E, et al. Effects of dietary intervention on IGF-I and IGF-binding proteins, and related alterations in sex steroid metabolism: the Diet and Androgens (DIANA) Randomised Trial. Eur J Clin Nutr. 2003;5:1079-1088.
9. Danby FW. Acne and milk, the diet myth, and beyond. J Am Acad Dermatol. 2005; 52:360-362.
10. Heaney RP, McCarron DA, Dawson-Hughes B, et al. Dietary changes favorably affect bone remodeling in older adults. J Am Dietetic Assoc. 1999;99:1228-1233.