acne in adolescence: a role for nutrition?
TRANSCRIPT
![Page 1: Acne in adolescence: A role for nutrition?](https://reader036.vdocuments.mx/reader036/viewer/2022073109/575081421a28abf34f8e38ce/html5/thumbnails/1.jpg)
Acne in adolescence: A role for nutrition?
Robyn SMITH and Neil MANNSchool of Applied Sciences, RMIT University, Melbourne, Victoria, Australia
KEY POINTS
• Acne prevalence varies substantially between populationsand is low in non-Westernised societies consuming tradi-tional diets.
• A unifying feature of traditional diets is low glycaemicload.
• High-glycaemic-load diets have recently been implicatedin acne aetiology due to their ability to affect insulindemand, androgen bioavailability and insulin-like growthfactor-I activity.
• The beneficial results of a low-glycaemic-load diet on acneobserved in a recent trial require confirmation in largerstudies.
During the past century, much controversy has surroundedthe subject of diet in acne management. In the 1930s, majordermatology textbooks advocated dietary restrictions foracne patients based upon ‘clinical experience . . . that [sug-gests] a diet high in carbohydrates and sweets seems to makesome acne cases worse’. 1 However, apart from the individualimpressions of physicians, there was little evidence tosupport dietary practices for the control of acne. Forty yearslater, dietary advice was removed from standard texts, andthe consensus has since been that ‘diet plays no role in acnetreatment in most patients’.2 Nonetheless, many acnepatients continue to believe that acne is exacerbated bydiet,3,4 and a recent survey found that 41% of final-yearmedical students at Melbourne University regarded diet asan aggravating factor.5
Few studies have examined the diet and acne connection,and those that have, show major design faults. Fulton et al.in a crossover single-blind study found no effect of chocolateon acne when compared with a placebo bar.6 However, alater examination of the ingredients in the placebo barrevealed that the fatty acid composition and sugar contentswere virtually identical to that found in the experimentaltreatment.7 Anderson examined the effect of the daily con-sumption of chocolate, milk or nuts and found no effect onacne.8 However, the present study has been criticised for itssmall sample size (minimum of 3 subjects per food), its shortduration (7 days) and its lack of controls.9 Although theexperiments of Fulton et al.6 and Anderson8 are frequentlycited as evidence that diet plays no role in acne development,a major limitation of both studies was that they concentratedon single foods with no background dietary analysis.
Variations in acne prevalence worldwide have promptedresearchers to question the natural development of thedisease. For instance, rates of acne in Kenya,10 Zambia11 and
Peru12 are reportedly lower than in the black13,14 andHispanic14 populations of Western countries. In a recentobservational report, Cordain et al. attributed that theabsence of acne in two non-Westernised societies (theKitavan Islanders of Papua New Guinea and the Ache’hunter-gatherers of Paraguay) to environmental factors,mainly local diets, which are devoid of high-GI (glycaemic-index) carbohydrates.15 This concept is an extension of anearlier hypothesis put forward by Schaefer,16 who reportedthe emergence of acne in the Eskimos of North Americafollowing the adoption of a Western lifestyle. Schaefer pro-posed that the increase in acne prevalence in Eskimo groupswas the result of the ‘shift to refined, ... rapidly absorbablecarbohydrates’. This is in stark contrast to their earlier diet,which was composed primarily of meat and fish.17 AlthoughRussian settlers introduced the Eskimos to basic agricultureand carbohydrate foods (e.g. barley, buckwheat, cabbage andpotatoes) some 70–100 years ago, these carbohydrates weregenerally low in GI and did not replace animal protein as themain source of energy.18 The emergence of acne to varyingdegrees in Eskimo groups appeared to coincide with theincrease in the annual per capita consumption of refinedsugar and flour, while the per capita consumption of proteinderived from animal sources showed an inverse relation-ship.16,19 Since the relatively recent introduction of refinedcarbohydrates to the diet, the Eskimos have also demon-strated faster growth (increased final height), earlier pubertyand dramatic increases in the incidence of obesity, diabetesand heart disease.16,19,20
A unifying feature of traditional diets is that they arenaturally low in glycaemic load. As the GI can only be usedto compare foods of equal carbohydrate content, the glycae-mic load was later developed to characterise the glycaemiceffect of whole meals or diets (GI ¥ available dietary carbo-hydrate). The glycaemic load may be interpreted as ameasure of the blood glucose- and insulin-raising potential,as it represents the rate of carbohydrate absorption (indi-cated by the GI) and the quantity of carbohydrate con-sumed.21 The glycaemic load may be modulated by alteringthe absolute amount of carbohydrate consumed or by select-ing foods using the GI concept. Accumulating evidence sug-gests that the glycaemic load of Western diets has increasedover recent years: (i) due to an increase in carbohydrateconsumption as a consequence of dietary recommendationsto decrease dietary fat; and (ii) as dietary trends appear tofavour high-GI foods.22
High-glycaemic-load diets have recently been implicatedin acne aetiology due to their ability to increase insulin
Nutrition & Dietetics 2007; 64 (Suppl. 4): S147–S149 DOI: 10.1111/j.1747-0080.2007.00211.x
© 2007 The AuthorsJournal compilation © 2007 Dietitians Association of Australia
S147
![Page 2: Acne in adolescence: A role for nutrition?](https://reader036.vdocuments.mx/reader036/viewer/2022073109/575081421a28abf34f8e38ce/html5/thumbnails/2.jpg)
demand and other factors associated with insulin resistance(e.g. hyperphagia, elevated non-esterified fatty acids,obesity).15 Clinical and experimental evidence suggeststhat insulin may increase androgen production and effect,through its influence upon steroidogenic enzymes,23
gonadotrophin-releasing hormone secretion24 and sexhormone-binding globulin (SHBG) production.25–27 Further-more, insulin has been shown to decrease a binding proteinfor insulin-like growth factor-I (IGF-I), which may facilitatethe effect of IGF-I on cell proliferation.28 Altogether, theseevents may influence one or more of the four underlyingcauses of acne: (i) increased proliferation of basal kera-tinocytes within the pilosebaceous duct; (ii) abnormaldesquamation of follicular corneocytes; (iii) androgen-mediated increases in sebum production; and (iv) colonisa-tion and inflammation of the comedo by Propionibacteriumacnes. 15
Support for a role of insulin in acne development can alsobe found in the high prevalence of acne in women withpolycystic ovary syndrome (PCOS), a condition associatedwith insulin resistance, hyperinsulinaemia and hyperan-dogenism.29 Insulin resistance is believed to be the underly-ing disturbance in PCOS, as it generally precedes and givesrise to the cluster of endocrine abnormalities that charac-terise PCOS (increased androgens, increased IGF-I anddecreased SHBG).30 Treatments for PCOS now include oralhypoglycaemic agents which improve insulin sensitivity,restore fertility and alleviate acne.31,32
The extent to which acne is related to the typical Westerndiet is controversial, but the future holds promise of a shift inparadigm. A recent study by the authors33 has demonstratedthat a low-glycaemic-load diet, which mimics the diets ofacne-free populations, significantly reduced acne lesioncounts and hormonal aspects of acne (e.g. insulin, androgenbioavailability, free IGF-I). Furthermore, the improvement inclinical and endocrine parameters was significantly greaterthan the control arm, which followed a high-glycaemic-loadWestern diet. Although confirmation of the diet–acnehypothesis will require larger-scale experiments, the presentstudy suggests that the institution of a non-Westernised diet,adapted for modern times, may have a therapeutic effect onacne. As a basic principle, this type of diet should containminimally processed carbohydrate-based foods, includinga wide variety of fresh fruits, vegetables, wholegrains, leanmeats, fish and seafood.
REFERENCES
1 Wise F, Sulzberger M. The role of the general practitioner in themodern treatment of acne vulgaris. In: Wise F, Sulzberger MB,eds. The 1933 Year Book of Dermatology and Syphilology. Chicago,IL: The Year Book Publishers, 1933; 7–12.
2 Kaminester L. Acne. JAMA 1978; 239: 2171–2.3 Tan J, Vasey K, Fung K. Beliefs and perceptions of patients with
acne. J Am Acad Dermatol 2001; 44: 439–45.4 Rasmussen J, Smith S. Patient concepts and misconceptions
about acne. Arch Dermatol 1983; 119: 570–72.
5 Green J, Sinclair R. Perceptions of acne vulgaris in final yearmedical student written examination answers. Aust J Dermatol2001; 42: 98–101.
6 Fulton J, Plewig G, Kligman A. Effect of chocolate on acnevulgaris. JAMA 1969; 210: 2071–4.
7 Mackie B, Mackie L. Chocolate and acne. Aust J Dermatol 1974;15: 103–9.
8 Anderson P. Foods as the cause of acne. Am J Fam Pract 1971;3: 102–3.
9 Treloar V. Diet and acne redux. Arch Dermatol 2003; 139:941.
10 Verhagen A, Koten J, Chaddah V, Patel R. Skin diseases inKenya. A clinical and histopathological study of 3168 patients.Arch Dermatol 1968; 98: 577–86.
11 Ratnam A, Jayaraju K. Skin diseases in Zambia. Br J Dermatol1979; 101: 449–53.
12 Freyre E, Rebaza R, Sami D, Lozada C. The prevalence of facialacne in peruvian adolescents and its relation to their ethnicity.J Adolesc Health 1998; 22: 480–84.
13 Wilkins J, Voorhees J. Prevalence of nodulocystic acne in whiteand negro males. Arch Dermatol 1970; 102: 631–4.
14 Taylor S, Cook-Bolden F, Rahman Z, Strachan D. Acne vulgarisin skin of color. J Am Acad Dermatol 2002; 46: S98–106.
15 Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton B, Brand-Miller B. Acne vulgaris—a disease of Western civilization. ArchDermatol 2002; 138: 1584–90.
16 Schaefer O. When the Eskimo comes to town. Nutr Today 1971;6: 8–16.
17 Nestle M. Animal v. plant foods in human diets and health: isthe historical record unequivocal? Proc Nutr Soc 1999; 58: 211–18.
18 Smith A. The Oxford Encyclopedia of Food and Drink in America.New York: Oxford University Press, 2004.
19 Schaefer O. Pre- and post-natal growth acceleration andincrease sugar consumption in Canadian Eskimos. Can MedAssoc J 1970; 103: 1059–68.
20 Bendiner E. Disastrous trade-off: Eskimo health for whitecivilization. Hosp Pract 1974; 9: 156–89.
21 Brand-Miller J, Thomas M, Swan V, Ahmad Z, Petocz P,Colagiuri S. Physiological validation of the concept of glycemicload in lean young adults. J Nutr 2003; 133: 2695–6.
22 Slyper A. The pediatric obesity epidemic: causes and contro-versies. J Clin Endocrinol Metab 2004; 89: 2540–47.
23 Kristiansen S, Endoh A, Casson P, Buster J, Hornsby P. Induc-tion of steroidogenic enzyme genes by insulin and IGF-I incultured adult human adrenocortical cells. Steroids 1997; 62:258–65.
24 Willis D, Mason H, Gilling-Smith C, Franks S. Modulation byinsulin of follicle stimulating and luteinizing hormone action inhuman granulosa cells of normal and polycystic ovaries. J ClinEndocrinol Metab 1996; 81: 302–9.
25 Plymate S, Matej L, Jones R, Friedl K. Inhibition of sexhormone-binding globulin production in the human hepatoma(HepG2) cell line by insulin and prolactin. J Clin EndocrinolMetab 1995; 67: 460–64.
26 Haffner S. Sex hormone-binding protein, hyperinsulinemia,insulin resistance and non-insulin-dependent diabetes. HormRes 1996; 45: 233–7.
27 Goodman-Gruen D, Barret-Connor E. Sex hormone-bindingglobulin and glucose tolerance in postmenopausal women. TheRancho Bernardo study. Diabetes Care 1997; 20: 645–9.
28 Powell D, Suwanichkul A, Cubbage M, DePaolis L, Snuggs M,Lee P. Insulin inhibits transcription of the human gene for
Robyn Smith and Neil Mann
© 2007 The AuthorsJournal compilation © 2007 Dietitians Association of Australia
S148
![Page 3: Acne in adolescence: A role for nutrition?](https://reader036.vdocuments.mx/reader036/viewer/2022073109/575081421a28abf34f8e38ce/html5/thumbnails/3.jpg)
insulin-like growth factor-binding protein-1. J Biol Chem 1991;266: 18868–76.
29 Franks S. Polycystic ovary syndrome. N Engl J Med 2003; 13:853–61.
30 Dunaif A, Segal K, Futterweit W, Dobrjansky A. Profoundperipheral insulin resistance independent of obesity in poly-cystic ovary syndrome. Diabetes 1989; 38: 1165–74.
31 Kazerooni T, Dehghan-Kooshkghazi M. Effect of metformintherapy on hyperandrogenism in women with polycystic ovarysyndrome. Gynecol Endocrinol 2003; 17: 51–6.
32 Ciotta L, Calogero AE, Farina M, De Leo V, La Marca A, CianciA. Clinical, endocrine and metabolic effects of acarbose, an
a-glucosidase inhibitor, in PCOS patients with increased insulinresponse and normal glucose tolerance. Human Reprod 2001;16: 2066–72.
33 Smith R, Mann N, Braue A, Mäkeläinen H, Varigos G. The effectof a high protein, low glycemic load diet versus a conventional,high glycemic load diet on biochemical parameters associatedwith acne vulgaris. A randomized, investigator-masked, con-trolled trial. J Am Acad Dermatol 2007; 57: 247–56. EPub aheadof print.
Acne in adolescence
© 2007 The AuthorsJournal compilation © 2007 Dietitians Association of Australia
S149