Should we talk to our acne patients about diet?
by Emily Altman, MD, Dermatology
For years I sat in exam rooms with parents and teens and told them there was no relationship between diet and acne to the great delight of the kids. Parents begged me to tell their kids that too much of potato chips, pizza, chocolate, soda or any junk food at all was what was causing the kids to break out. But from what I knew at that point, there was no scientific evidence of a link between diet and acne. Well, little did I know!
Acne vulgaris, the most common skin condition, is a highly prevalent, multifactorial disorder of the pilosebaceous unit. The epidemiology data from 2001 showed that approximately 45 million people in the United States have acne, with an estimated prevalence of 85% in those between ages 15 and 24 (1).Acne affects 60-70% of Americans at some time during their lives. Twenty percent have severe acne with permanent physical and possibly psychological scarring (2).
Acne forms as a result of obstruction and inflammation of hair follicles and their accompanying sebaceous glands (pilosebaceous units). There are multiple factors involved, including the biology of the sebaceous gland itself, sebum production, hyperkeratinization of the hair follicle, bacterial influences, the immune functions of the sebaceous gland, neuropeptides, cytokines and toll-like receptors, hormones and nutritional factors (3).
Although familial studies have demonstrated that hereditary factors are important in determining susceptibility to acne (4), twin studies have suggested that developing clinical acne is partially under environmental control (5).
Nutrition is one of those environmental factors that can and should be controlled in any acne treatment regimen. So what is the evidence for the role of nutrition in the pathogenesis of acne?
In one of the first papers to be published on the subject of the relationship of acne and diet, Cordain et al examined the prevalence of acne in two nonwesternized societies: The Kitavan Islanders of Papua New Guinea and the Ache hunter-gatherers of Paraguay (6). No cases of acne were found among the 1200 Kitavan (including 300 15-25 year olds) or 115 Ache (15 15-25 year olds) examined. The authors observed that both the Ache and Kitavan diets were composed of minimally processed plant and animal foods, virtually devoid of typical Western-diet high glycemic loads that may acutely or chronically elevate insulin levels. Neither society had any evidence of insulin resistance. Kitavans were also not found to be overweight or hypertensive. Previous studies have demonstrated that diet-induced hyperinsulinemia elicits an endocrine response that promotes unregulated tissue growth and enhanced androgen synthesis. Based on that the authors concluded that dietary interventions with low glycemic loads may have a therapeutic benefit in acne treatment.
Interestingly, in the Eskimo and Zulu populations, acne was absent when they were living and eating in traditional manner, but became a problem when these populations moved from their villages to the cities (7).
A 2006 prospective cohort study by Adebamowo et al. that examined 6094 girls aged 9-15 years showed that a greater consumption of milk was associated with a higher prevalence of acne (8). The results were not associated with the fat content of the milk. The authors postulated that the milk intake affected acne though the insulin-like growth factor-1 pathway and through the bioactive molecules milk contains, such as androgens, 5 alpha reduced steroids and other steroid hormones. The sebaceous gland has a full complement of enzymes that can produce testosterone from cholesterol or from its precursors found in milk. Similar results were shown when the Adebamowo team looked at dairy consumption and acne in teenage boys (9).
In 2007 Smith et al. compared the effect of an experimental low glycemic-load diet with a conventional high glycemic-load diet on clinical and endocrine aspects of acne vulgaris. In that study 43 male patients with acne completed a 12-week, parallel, dietary intervention study with investigator-masked dermatology assessments. Primary outcomes measures were changes in lesion counts, sex hormone binding globulin, free androgen index, insulin-like growth factor-I, and insulin-like growth factor binding proteins. The study found that at 12 weeks, total lesion counts had decreased more in the experimental group compared with the control group. The experimental diet also reduced weight, reduced the free androgen index, and increased insulin-like growth factor binding protein-1 (which reduced the bioavailability of IGF-1) when compared with a high glycemic-load diet. The study suggested that nutrition-related lifestyle factors play a role in acne pathogenesis (10).
The evidence for the role of insulin, insulin-like growth factor-1, hyperglycemic food and milk consumption in the pathogenesis of acne was summarized in a viewpoint paper by Melnik and Schmitz (11). Authors wrote, "A growing body of evidence underlies the role of insulin resistance with increased insulin/IGF-1 signalling in the pathogenesis of acne. IGF-1 is the key hormonal mediator regulating adreno-gonadal androgen synthesis, amplifying cutaneous androgen activity and stimulating proliferation of sebaceous follicle."The authors provided an overview of conditions associated with increased IGF-1 serum levels. Many of these conditions are frequently associated with acne.
- Large for gestational age newborns of mothers with milk consumption during pregnancy
- Large for gestational age newborns of mothers with diabetes during pregnancy
- Cow milk formula-fed newborn infants
- Recombinant IGF-1 therapy for dwarfism
- Precocious pubarche
- Puberty
- Adolescents or adults who were small for gestational age or had low birth weight
- PCOS
- Milk and milk protein consumption
- High glycemic foods
- Acromegaly
- Obesity
- States of hyperinsulinemia and insulin resistance
- IGF-1 gene variations like absence of IGF-1 CA 19/19 allele
References:
Agency for Healthcare Research and Quality. Management
of acne. Summary, evidence report D technology assessment: number 17. AHRQ publication no. 01-E018, March 2001.http://archive.ahrq.gov/clinic/epcsums/acnesum.htm
Fulton J. Acne Vulgaris. eMedicine 2011 http://emedicine.medscape.com/article/1069804-overview#a0101
Kurokawa I et al. New developments in our understanding of acne pathogenesis and treatment. Experimental Dermatology 2009;18:821-832
Goulden V, McGeown CH, Cunliffe WJ. The familial risk of adult acne: a comparison between first-degree relatives of affected and unaffected individuals. Br J Dermatol. 1999;141:297-300.
Walton S, Wyat EH, Cunliffe WJ. Genetic control of sebum excretion and acne: a twin study. Br J Dermatol. 1989;121:144-145.
Cordain et al. Acne Vulgaris. A Disease of Western Civilization.Arch Dermatol. 2002;138:1584-1590
Ghodsi SZ et al. Prevalence, severity, and severity risk factors of acne in high school pupils: a community-based study. J Invest Dermatol. 2009 Sep;129(9):2136-41
Adebanowo CA et al. Milk consumption and acne in adolescent girls. Dermatol Online J. 2006 May 30;12(4):1.
Adebamowo CA. Milk consumption and acne in teenaged boys.J Am Acad Dermatol. 2008 May;58(5):787-93.
Smith RN et al. 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):247-56
Melnik BC, Schmitz G. Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Experimental Dermatology2009;18:833-41.
Veith WB, Silverberg NB. The Association of Acne Vulgaris With Diet. Cutis 2011;88:84-91
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