Faculty Peer Reviewed
A 17-year-old female comes into the clinic for an annual health checkup. During the visit she reveals that she has been dealing with acne so severe that she is often embarrassed to go to school. She states that her diet often consists of lots of candy, fast food, and soft drinks. She asks, “Am I getting acne because of what I eat?”
Introduction
Acne is a common skin disorder that affects more than 17 million people in the United States. While most people equate acne with the teenage years, acne can occur in adults too. The prevalence of acne in adolescents has been found to be anywhere from 35 to 90 percent compared to 7 to 51 percent found in post-adolescents.[1,2] Unfortunately, what remains the same is the psychosocial burden that acne imposes on those who suffer from it. Many people who have acne often experience low self-esteem, feelings of inferiority, social withdrawal, anxiety, and depression, making the management of the disease important to both physicians and patients.
Pathogenesis of Acne
The pathogenesis of acne originates within the pilosebaceous follicles found predominately in the skin of the face, upper back, and upper chest. For unknown reasons, abnormal keratinization and desquamation of the infundibular epithelium occur, plugging the ducts with keratinocytes and sebum to form invisible microcomedones.[3] With the onset of adrenarche and the rise of androgen levels, hormones such as dihydrotestosterone (DHT) act on androgen receptors to stimulate excess sebum that is unable to reach the surface of the skin, resulting in the formation of comedones. Propionibacterium acnes, an anaerobic normal constituent of skin flora, is then able to proliferate in this anaerobic, lipid-rich environment, colonizing the pilosebaceous unit and eventually triggering follicular rupture and a neutrophil cascade.[4]
Presentation of Acne
The clinical presentation of acne can be divided into noninflammatory and inflammatory lesions. Noninflammatory lesions include closed and open comedones. Closed comedones, or whiteheads, result from the accumulation of sebum and keratinous material in plugged follicles. Open comedones, or blackheads, result when continued distention opens the follicular orifice, allowing the sebaceous material to become oxidized at the surface of the skin. In contrast, inflammatory lesions arise when the comedones rupture into the surrounding dermis rather than the surface of the skin. The keratin-, hair- and lipid-containing material then initiates an inflammatory response leading to the formation of erythematous papules, pustules, and cysts.
Diet and Acne
The association between diet and acne has always been a highly controversial issue. Before the 1960s, standard treatment for acne included dietary restriction of chocolate, fats, sweets, and carbonated beverages. Studies done by Fulton and colleagues [5] and Anderson [6] were the first to dispel these ideas as myths, as they found no association between the consumption of chocolate, milk, and cola and the development of acne. Until the past decade, most dermatologists practiced and counseled patients under these beliefs, dismissing any idea of a relationship between diet and acne as unscientific. However, recent studies have surfaced that revisit the notion of a link between food intake and the development of acne.
Dairy and Acne
In 2005, a large case-control study conducted by Adebamowo and colleagues [7] evaluated the association between milk and acne in the adolescent diets of 47 355 nurses. Results showed that among participants diagnosed with severe acne, those with the highest level of total milk intake had acne more frequently than those with low levels of milk intake, particularly with skim milk. This is thought to be due to the testosterone and DHT precursors found in milk that contribute to the comedogenicity of milk by stimulating the androgen receptors of the pilosebaceous units. Furthermore, the positive correlation with skim milk and increased plasma levels of insulin-like growth factor 1 (IGF-1) is also thought to contribute to the formation of acne. IGF-1 also stimulates the synthesis of androgens and inhibits the production of sex hormone-binding globulin (SHBG), increasing the overall bioavailability of androgens to stimulate the production of sebum and the formation of acne.
Carbohydrates and Acne
Stronger evidence supports the notion that a low glycemic diet is helpful for improving acne. Studies were performed on two rural non-westernized populations known for their low glycemic diet, the Kitavan of Papua New Guinea and Aché of Paraguay.[8] Results found no cases of acne in either population, which suggested the idea that diet was the reason for the absence of acne. Another randomized controlled trial conducted by Smith and colleagues [9] demonstrated that individuals assigned to a low glycemic-load diet experienced improvement in acne severity, decreased weight, and an increase in SHBG levels. With the increase in SHBG, free androgen levels would be expected to decrease, consequently reducing comedone production.
Fat and Acne
While no large, well controlled studies that examine the effect of fat intake on acne risk have been published, there has been speculation regarding the involvement of omega-6 and omega-3 fatty acids with acne. The pro-inflammatory properties of omega-6 acids and the anti-inflammatory properties of omega-3 acids are thought to play a role in the inflammation of pilosebaceous units.[10] Similarly, diets high in fat have been linked with increased IGF-1 levels, while diets low in fat are thought to be associated with decreased IGF-1 levels.
Conclusion
The topic of dietary intake and its influence on acne will continue to be controversial and it is clear that further research is needed in order to fully elucidate its precise role. However, we can no longer discredit the association as a mere myth. Although we cannot treat acne solely with nutrition, we can certainly shape its outcome. Even if no single food directly causes acne or effectively decreases its symptoms, we can still stress to patients that diet can lessen or increase its severity. In the case of the 17-year-old female who wonders if her diet is the reason for her breakouts, we can advise her that certain foods may not be the exact cause of her acne but rather a factor that may affect the severity of her symptoms.
Dr. Wu is a 3rd year resident at NYU Langone Medical Center
Peer reviewed by Vicki Levine, MD Clinical Assistant Professor; Department of Dermatology, Chief Dermatology Dept. Veterans Affairs
References:
1. Dreno B, Poli F. Epidemiology of acne. Dermatology. 2003;206(1):7-10. http://www.ncbi.nlm.nih.gov/pubmed/12566799
2. Collier C, Harper JC, Cafardi JA, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol. 2008;58(1):56-59.
3. Morohashi M, Toyoda M. Pathogenesis of acne. Med Electron Microsc. 2001;34(1):29-40. http://www.ncbi.nlm.nih.gov/pubmed/11479771
4. Kurokawa I, Danby FW, Ju Q, et al. New developments in our understanding of acne pathogenesis and treatment. Exp Dermatol. 2009;18(10):821-832.
5. Fulton JE Jr, Plewig G, Kligman AM. Effect of chocolate on acne vulgaris. JAMA. 1969;210(11):2071–2074. http://jama.ama-assn.org/content/210/11/2071.refs
6. P.C. Anderson, Foods as the cause of acne, Am Fam Physician 3 (1971), pp. 102–103. P.C. Anderson, Foods as the cause of acne, Am Fam Physician 3 (1971), pp. 102–103.Anderson PC. Foods as the cause of acne. Am Fam Physician. 1971;3(3):102–103.
7. 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(2):207–214.
8. Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. Acne vulgaris: a disease of Western civilization. Arch Dermatol. 2002;138(12):1584-1590. http://archderm.ama-assn.org/cgi/content/full/138/12/1584
9. 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(2):247-256.
10. Cordain L. Implications for the role of diet in acne. Semin Cutan Med Surg. 2005;24(2):84–91. http://thepaleodiet.com/cordain-l-implications-for-the-role-of-diet-in-acne-semin-cutan-med-surg-20052484-91/
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