Diet and acne: a review of the evidence

Acne vulgaris is the most common dermatologic condition in the USA, affecting more than 17 million Americans of all ages, although it is especially common in adolescents.1 Moreover, approximately 80–90% of American adolescents experience acne.2 Severe acne is associated with low self-esteem, poor body image, social withdrawal, and depression.3 Pharmaceutical acne treatments are costly and have potentially severe side-effects. Adolescent acne is typically the result of clogged, infected, pilosebaceous follicles. Adults may experience fewer comedones and more inflammatory lesions.1 Normally, sebum travels up the follicle to the skin surface. Hormones may increase sebum production and cause follicular cells to hyperproliferate and block the follicular opening, forming a comedo.4 Complete follicle blockage results in closed comedones (i.e. “whiteheads”), whereas incomplete blockage results in open comedones (“blackheads”). Comedo formation typically occurs over the course of 2–3 weeks. Acne may manifest in the form of noninflammatory comedones, superficial inflammatory lesions (papules, pustules), and/or deeper inflammatory lesions (nodules, cysts). Inflammatory lesion formation occurs most commonly when Propionibacterium acnes colonizes the pilosebaceous unit, triggering follicular rupture and a neutrophil cascade.5 Rarely, acne may have nonbacterial causes.6 In studies of diverse populations, individuals with acne commonly attribute the condition3, 7-9 or its exacerbation3, 7, 8, 10 to diet. Chocolate and oily or fatty foods are commonly implicated;7, 10-12 however, reviews prior to 2007 have concluded that diet plays no important role in acne and that the condition is primarily attributable to genetic predisposition and hormonal influences.13-15 Two large twin studies16, 17 have reported on the heritability of acne. Estimated heritability (genetic variance/phenotypic variance) ratios for acne risk and severity range from 0.5 to 0.9 among adolescent16 and adult17 pairs of monozygous and dizygous twins. Walton et al.18 reported that sebum excretion is influenced by genetic factors, but that the development of clinical disease is mediated by environmental factors. These studies suggest that genetic factors alone do not fully account for the acne risk. Despite the genetic regulation of sebum excretion and other determinants of acne, environmental influences, such as diet, may act as modifiers of gene expression. Recently, well-designed, controlled, prospective studies have supported the association between specific dietary factors and acne. We therefore critically examined the quality and strength of the published literature examining the association between diet and acne. We conducted a review of the relationship between diet and acne using the following keywords: “acne,”“acne vulgaris,”“diet,”“nutrition,”“food,”“food allergy,”“vitamin,” and “chocolate.” The following databases and periods were included: Medline since 1949; Embase-Medicine & Embase-Psychology (EMBASE) since 1980; the Cochrane Central Register of Controlled Trials (Cochrane) since 1898; Database of Abstracts on Reviews and Effectiveness (DARE) since 1990; PsycInfo since 1967; and the Cumulative Index to Nursing and Allied Health Literature (CINAHL) since 1982. Articles were also obtained by bibliography review. Articles published in languages other than English were reviewed if English translations were available. Observational and interventional human studies with participants of any age, sex, or health status were included. Articles were excluded if they reported only on the potential effects of topical, herbal, or vitamin preparations, or on the diagnosis, treatment, or pathogenesis of acne. A small sample size, a lack of a control group, and unclear statistical methods were not reasons for exclusion. The primary author (EHS) reviewed the titles and abstracts of all potentially relevant articles to determine whether they met the eligibility criteria. Of the 59 abstracts and full articles retrieved, 31 articles were excluded for reporting only on the potential effects of topical, herbal, or vitamin preparations, or on the diagnosis, treatment, or pathogenesis of acne. The remaining 28 articles were included. We excluded one study that did not report on diet. Of the 27 relevant articles, 21 were observational studies and six were clinical trials (Table 1). We found 15 cross-sectional,3, 7-12, 19-26 two case–control,27, 28 and four prospective cohort29-32 studies, as summarized in Table 1. Population-based studies suggest that acne prevalence is lower in rural societies than in industrialized populations. Cordain et al.19 studied the Kitavan islanders of Papua New Guinea (n = 1200) and the Aché hunter-gatherers of Paraguay (n = 115). The islanders subsisted mainly on root vegetables, fruit, fish, and coconut. Their intake of dairy products, coffee, alcohol, cereals, oils, sugar, and salt was minimal. An estimated two-thirds of the Aché hunter-gatherer diet consisted of sweet manioc, peanuts, maize, and rice. Approximately one-quarter of their diet consisted of flour, sugar, and meat. No cases of acne were detected in either population. The authors suggested that the low fat intake and the absence of high-glycemic-index foods may explain the low prevalence of acne in these populations. Freyre et al.20 compared acne prevalence in three Peruvian populations, including indigenous and white populations (n = 2214). Among 12–18-year-olds, the indigenous population showed a significantly (P < 0.001) lower acne prevalence (28%) than the white population (45%) or those of mixed ancestry (43%). Each adolescent group had a lower prevalence of acne than that reported in 12–18-year-old Americans.20 Bechelli et al.21 assessed the prevalence of acne in 9955 Brazilian schoolchildren: 8980 were impoverished urban children, whereas 975 were from rural areas. Less than 3% of the combined population (2.7%) demonstrated evidence of acne. Two reports have suggested that acne prevalence increases as populations adopt a Western diet through migration or cultural change. Reports of northern Canadian Inuits made no mention of acne until acculturation with their southern neighbors and subsequent increases in soda, beef, dairy products, and processed foods, after which the acne prevalence increased.22 Pre-World War II Okinawans, who traditionally followed a diet of sweet potatoes, rice, and vegetables, together with some soybeans, but little meat, reported an increase in acne prevalence after adopting a diet high in animal products.23 Seven studies have assessed the perceptions of factors believed to affect acne.3, 7-12 In a 2007 study, Rigopoulos et al.7 assessed the beliefs about acne among 13–18-year-old Greek students with and without acne. Self-reported acne was present among 59% of students. Among 316 students with and without acne, 62% cited diet as a causal factor, and 66% believed chocolate was an exacerbating factor. In 2006, El-Akawi et al.10 reported that, of 166 Jordanian male and female untreated clinic patients with acne, participants believed that their acne was aggravated by nuts (89%), chocolate (85%), cakes/biscuits (57%), oily food (53%), fried food (52%), eggs (42%), or milk, yogurt, and cheese (23%). Nearly one-fifth (19%) believed that consuming fruits and vegetables improved their acne. A survey administered by Ikaraoha et al.11 to 174 Nigerian students aged 18–32 years demonstrated that 75% of participants believed that an oily or fatty diet contributed to their acne. Of 130 male and female Saudi Arabian patients attending an acne clinic, more than one-quarter of participants believed that diet caused (26%) or exacerbated (32%) their acne.8 A 2003 study9 of Saudi Arabian high school and college students (n = 517), aged 15–29 years, demonstrated that 72% of students with and without acne (and 79% of 217 students with acne) believed that diet contributed to acne. In a 2001 study in the Journal of the American Academy of Dermatology, Tan et al.3 reported that acne was believed to be caused by diet less frequently than by hormonal or genetic factors. Although 32% of acne patients believed that diet caused their acne, 64% believed that hormones and 38% believed that genetics were responsible. In addition, 44% of participants believed that diet aggravated their acne. In 2001, Green and Sinclair12 reported that almost half of 215 sixth-year Australian medical students believed that diet aggravated their patients’ acne, citing chocolate and oily or fatty foods as the most common dietary factors. Kaymak et al.24 examined the association between acne and the glycemic index and glycemic load of the daily diet, insulin sensitivity, and insulin-like growth factor (IGF) levels in 91 university students (n = 49 acne patients, n = 42 control patients). Participants completed a food frequency questionnaire from which the authors calculated the glycemic index using published reports. Physicians assessed acne as well as insulin resistance through the calculation of the homeostatic model assessment (HOMA) index: [fasting insulin (microU/mL) × fasting blood glucose (mmol/L)/22.5]. There were no significant differences in fasting glucose or insulin levels, and none of the participants had insulin resistance. In patients with acne, levels of IGF-1 were higher and levels of IGF-binding protein-3 were significantly lower than those of controls. Participants with acne of more than 2 years’ duration ate a diet with a significantly higher glycemic index than did participants with acne of less than 2 years’ duration. Khanna et al.25 studied energy, carbohydrate, protein, and fat intake among 200 students in India with and without acne. They compared the diets of those with severe, moderate, mild, and no acne, and reported no dietary differences (P > 0.05) among the four groups; however, the researchers used a t-test, intended for the comparison of two groups, rather than the appropriate analysis of variance statistical test to compare the four groups. It is unclear whether the results from appropriate statistical tests would have differed from those reported. In a 1956 study published in the British Medical Journal, Bourne26 found that adult British soldiers, aged 20–40 years, with acne were significantly heavier than those without acne (73.2 kg vs. 67.5 kg; P = 0.013). Adolescent British soldiers aged 15–19 years with acne weighed more than those without acne (62.7 kg vs. 60.5 kg), although the differences were not significant. In a 2005 study, Adebamowo et al.27 tested the hypothesis that milk (whole, powdered, low-fat, and skimmed) intake was associated with a risk of teenage acne. More than 47,000 nurses were questioned about their adolescent diets and whether they had experienced “physician-diagnosed severe acne” during their teenage years. Prevalence ratios (PRs), comparing acne prevalence at the highest (more than three servings per day) to lowest (one serving or less per week) intake categories, were computed. In multivariate models adjusted for energy, present age, age of menarche, and body mass index, total milk intake was associated with severe acne [PR = 1.22; 95% confidence interval (CI), 1.03–1.44]. Severe acne prevalence increased as the milk fat content decreased: PR = 1.12 (CI, 1.00–1.25) for whole milk; PR = 1.16 (CI, 1.01–1.34) for low-fat milk; PR = 1.44 (CI, 1.21–1.72) for skimmed milk. Trend tests were significant for total milk [P(trend) = 0.002] and skimmed milk [P(trend) = 0.003]. The only nutrients significantly and positively associated with acne were vitamin D supplementation and total energy intake. High saturated fat intake was inversely associated with acne risk (PR = 0.88; CI, 0.80–0.94). There were no associations between acne and soda, French fries, pizza, or chocolate. The authors hypothesized that the hormones found in milk products were responsible for milk's association with acne. Bett et al.28 tested the hypothesis that acne patients consumed more sugar than age- and sex-matched controls. They compared the sugar consumption in 16 patients with acne with that in 16 patient controls with warts and 16 healthy age- and sex-matched office and factory worker controls. Diet was assessed by food frequency questionnaire. There were no significant differences in sugar consumption among the groups (121 g/day for acne patients vs. 111 g/day for wart patients and 120 g/day for healthy controls; P > 0.05). Four prospective cohort studies have evaluated the associations between diet and acne.29-32 Adebamowo et al. followed 4273 boys29 and 6094 girls,30 aged 9–15 years, in 1996. Information on dietary intake was collected between 1996 and 1998, and acne prevalence and severity were assessed in 1999. The authors investigated the association between self-reported acne severity and cow's milk (whole/2%, 1%, skimmed, chocolate) intake. PRs, comparing acne prevalence at the highest (two or more servings per day) to lowest (one serving or less per week) intake categories, were computed. After adjustment for baseline age, height, and energy intake, acne severity in girls30 was significantly associated with the intake of all categories of cow's milk: PR = 1.20 [CI, 1.09–1.31; P(trend) < 0.001] for total milk; PR = 1.19 [CI, 1.06–1.32; P(trend) < 0.001] for whole milk; PR = 1.17 [CI, 1.04–1.31; P(trend) = 0.002] for low-fat milk; PR = 1.19 [CI, 1.08–1.31; P(trend) < 0.001] for skimmed milk; PR = 1.29 [CI, 1.08–1.53; P(trend) = 0.02] for chocolate milk. In boys,29 the association between milk intake and acne was significant for total milk (PR = 1.16; CI, 1.01–1.34) and skimmed milk (PR = 1.19; CI, 1.01–1.40) intake. The test for trend was significant only for skimmed milk intake [P(trend) = 0.02]. Among both boys and girls, there were no significant associations between acne and the intake of nonmilk dairy foods, French fries, pizza, or chocolate. In a 2003 study, 22 university students were followed for one semester by Chiu et al.31“Dietary quality” was determined by the number of meals eaten per day and subjective self-ranking of “diet quality” on a four-point scale. Descriptive dietary data were not provided. Perceived dietary quality was inversely associated with acne exacerbation and severity (r = –0.48, P = 0.02). During the course of a study on radiation treatment for acne in 2083 patients between 1925 and 1949, Robinson32 collected 1–2 weeks of dietary records in a subset of patients. The number of dietary records was not reported. Milk products were the most frequently cited acne-causing food. Patients were subsequently advised to follow a low-fat, dairy-free diet; however, postintervention follow-up results were not published. Table 1 summarizes the results of six dietary intervention studies.33-38 Three33, 34, 36 of the six studies included control groups. Smith et al.34 assessed the effect of a low-glycemic-load diet (25% energy from protein and 45% energy from low-glycemic-index carbohydrates) on acne and insulin sensitivity. Participants (n = 43, all male, aged 15–25 years) were randomly assigned in a parallel design to the dietary intervention or control group urged to regularly include carbohydrates without receiving information on the glycemic index. Participants were followed for 12 weeks. Blind dermatologists assessed the number of acne lesions every four weeks, starting at baseline. Relative to those on the control diet, participants on the low-glycemic-load diet experienced greater reductions in counts of all lesions (51% vs. 31%; P = 0.03) and inflammatory lesions (45% vs. 23%; P = 0.02). Participants in the intervention group experienced a significant improvement (i.e. increase) in insulin sensitivity and significant changes in androgen levels, compared with participants in the control group.39 A positive correlation was observed between the in total lesion counts and the in insulin sensitivity as by the index (r = P = A in levels also with a in lesion counts (r = P = was completed by 31 participants (n = 16 intervention n = 15 control baseline and 12 weeks, follicular sebum and the of skin were sebum and the of sebum fatty did not between the groups. with baseline levels (P = however, participants in the intervention not the group demonstrated an increased of saturated to sebum fatty The in and significantly with the in acne lesion counts (r = P = The study authors concluded that the of sebum fatty may a role in acne tested the effect of four foods on acne. 1 medical students were to daily servings of a test food small chocolate of milk, of peanuts, or of participants acne lesions in 10 of the participants no The results were not by test foods, and the study was The authors reported that the foods were not associated with acne. Two studies tested the acne-causing of milk chocolate. In an intervention in university and participants a milk chocolate and to an the day four participants had but four had were not The concluded that large of chocolate did not acne. In a to test the effect of chocolate on acne, participants were to one dairy-free chocolate every day for weeks. The was with and During the control were to a chocolate with (i.e. fat in of the and A increase or in acne lesions was to be significant. between and control groups did not the clinical and were not reported. The authors concluded that large of chocolate did not significantly affect acne, sebum or sebum In a diet for acne patients with baseline excretion of at salt intake was not In four salt the number and severity of and and data for the other study participants were not reported. Population-based studies have suggested that, as diets acne prevalence Observational studies, including one and two large and prospective cohort have demonstrated an association between cow's milk intake and acne prevalence and severity (Table prospective cohort demonstrated an association between high-glycemic-index foods and acne whereas two demonstrated that a low-glycemic-index diet acne risk. have with to the association between acne and chocolate of and have to an association between acne and salt or intake. may have the that be from the literature to that two prospective to the follow-up only one a control group, and to the changes in acne. studies from a small sample size, lack of appropriate and incomplete reporting of published prospective have and appropriate statistical studies have the for an association between diet and acne. Acne typically results from sebum which follicular cells to hyperproliferate and block the follicle the and an results in production may be influenced by and hormonal such as and all of which may be influenced by dietary factors, as large studies reported a positive association between milk intake and acne. The studies of Adebamowo et demonstrated that higher levels of milk consumption were associated with acne risk in both boys and In the Health who consumed more milk as adolescents on showed a greater prevalence of severe acne than those with less These are supported by in which with consumption of dairy products had a low acne In observational studies, skimmed milk was associated with acne, that the fat content of milk not to affect its acne-causing authors have reported that the hormones in milk, such as and may milk and affect the pilosebaceous Milk consumption also increases IGF-1 which associated with androgen production in and acne in adult 42 from the studies of Smith et 34, have the between glycemic insulin sensitivity, hormonal and acne. consumption of foods with a high glycemic index insulin which may and sebum and androgen and to acne. low-glycemic-index foods have to increase and androgen higher levels have associated with lower acne participants in also and the low-glycemic-load diet was higher in fat and and lower in saturated compared with the comparison diet. These differences may be to and A study of followed for found that those with severe or acne had significantly higher androgen levels and significantly Although diets high in saturated fat increase the of low-fat, diets to the of and and increase the of The of to fatty in Western diets is commonly at 10 compared with ratios of 1 in and 2 1 in have suggested that inflammatory increase as are to and have associated with the development of inflammatory In high levels of fatty have to inflammatory and may acne risk by IGF-1 levels and of follicles. and and tested the acne-causing of milk chocolate and did not a control group, and study reported statistical et a control group and their Moreover, they tested rather than milk or however, the fat and sugar of treatment and control were the potential to the effects of or on the study did not evidence to whether acne that of Western dairy products, may be associated with acne. The hormonal effects of dietary such as glycemic index levels or fat or intake, may the effect of diet on acne risk. and clinical intervention studies to the relationship between diet and acne typically to and appropriate statistical prospective studies published since 2005 have the foods and dietary may acne risk and In to test the of dietary including controls for environmental acne age, and age at menarche, are

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