Diet Does Affect Acne

Alternative Medicine

 


Effect of Diet on Acne

Health care professional in the fields of alternative medicine have been proposing that diet does affect acne and that food will have an effect on the health of the skin. Naturopathic medicine (as practiced in traditional form) promotes the use of diet to address virtually all types of health disorders, be they acne, heart disease or any other health problem.

As pointed out by the article below, the effect food has on the skin may not always be a direct one. Diet may well affect a metabolic pathway which then has an effect on the skin. The following is an article published in the scientific literature that clearly demonstrates the effect diet has on acne.

Organic Skin Care Products
Get nature's best to care for your skin. Wildcrafted's range of products only contain fresh, safe & effective certified organic ingredients.




Diet and Acne

by

Jonette E Keri; Rajiv I Nijhawan

Published in: Expert Rev Dermatol. 2008;3(4):437-440. ©2008 Expert Reviews Ltd.
Posted: 09/16/2008

Abstract and Introduction

Abstract

Acne is a common dermatologic condition that affects many individuals in different decades of life. The specific role of diet in the development of acne has been a topic of debate for many decades, but this controversy has come to the forefront in recent years with new studies indicating the potential role of diet, contradicting historical studies. This article reviews past and more recent data regarding the link between diet and acne, commenting on areas where new investigations many help to elucidate the true contribution of diet to the pathogenesis of acne.

Introduction

Acne is a common condition affecting 40-50 million people in the USA.[1] Although classically thought of as a disease of teenagers, it can affect patients into their fourth and fifth decades of life.[2] The role of diet with regard to acne has been a controversial subject revisited many times by the dermatologic community. A recent 2007 article outlining the 'Guidelines of care for acne vulgaris management' evaluated the basis of dietary restriction in the medical literature and graded the information based upon the quality of methodology.[3] The evidence for the role of dietary restrictions in acne treatment was listed as "limited quality patient-oriented evidence," and the recommendations on dietary restrictions were based on "inconsistent or limited quality patient-oriented evidence". This report stimulated comments to the editor[4] and has, along with other new evidence,[5-10] brought the controversy again to the forefront.

Does Diet Affect Acne?

The belief that diet affects acne is widely held. When acne patients were surveyed, 32% felt that diet caused acne and 44% felt diet aggravated acne.[11] Over the last 30 years, most dermatologists have told patients that acne is not caused by what they eat. These previously widely accepted concepts came from two studies evaluating chocolate[12] and chocolate bars, milk, peanuts and Coca-Cola™,[13] and their roles in causing acne. The landmark study by Fulton et al. used chocolate as the food of choice in which 65 patients showed no difference in their acne when comparing those who ate chocolate bars with those who ate bars lacking chocolate.[12]

However, it must be noted that there was minimal difference between the sugar and fat content of the chocolate bars and that of the placebo bars, and the chocolate bars contained no milk while the control bar contained some nonfat milk solids. These bars were also consumed in addition to their normal diets. Owing to the lack of a significant difference between the bars in terms of glycemic load or milk content, both areas have recently been studied further in depth. There were numerous study limitations in Anderson's study, including a lack of a clear grading system, data reflecting the numbers of lesions both before and after the trial period, a control group, investigator blinding and baseline diet determination, which makes the validity of the results questionable.[13]

Although the two previous studies have been referenced the most in regards to refuting diet's contribution to acne, they cannot be used as conclusive evidence. Additional historical studies shared similar shortcomings in their conclusions.[14-16] Recently, after a long hiatus, there has been more interest in determining the role of diet in acne. In 2002, Cordain et al. reported the lack of acne in certain non-Westernized populations, the Ache hunter-gatherers of Paraguay and the Kitavan Islanders of Papua New Guinea, and hypothesized that the lack of acne was in relation to the low glycemic loads of their diet.[17] However, it is difficult to differentiate the contribution of the environment (diet) versus genetics.

The low glycemic-load theory postulates that a state of elevated insulin is prevented, which is also noted to inhibit the initiation of a cascade that increases androgens. More specifically, foods with high glycemic loads are known to give rise to hyperinsulinemia, which can then lead to an increase in plasma concentrations of insulin-like growth factor (IGF)-1.[18] Free IGF-1 may promote acne by inducing hyperkeratosis and epidermal hyperplasia,[19,20] which is an initial step in the formation of a follicular obstruction. IGF-1, in addition to insulin, can also stimulate androgens, which are known to cause an increase in sebum production.[21] Clinically, there is evidence that patients with acne have higher serum levels of IGF-1, as seen in the Cappel et al. study evaluating postadolescent women aged 20-25 years.[18]

Young men with acne have also been studied with respect to dietary glycemic load and hormonal concentrations.[5] A total of 43 men aged 15-25 years with acne, were divided into either control or low glycemic-load diet groups and followed their respective diets for 12 weeks. Those in the low glycemic-load group not only lost weight and had a greater decrease in total lesion count,[6] but also had a reduced free androgen index and an increase in IGF-binding protein (IGFBP)-1,[5] probably indicating an increase in insulin sensitivity. Individuals with insulin resistance have been observed previously to have low IGFBP-1 concentrations.[22]

However, IGFBP-3, not IGFBP-1 is the primary binding protein of IGF-1. Kaymak et al. demonstrated that patients with acne had significantly higher IGF-1 and lower IGFBP-3 blood concentrations than the unaffected control subjects.[8] IGFBP-3 essentially binds IGF-1 and thereby blocks it, but any unbound or free IGF-1 is still capable of promoting its action,[9] thus the free IGF-1-IGFBP-3 ratio appears to be a better indicator of keratinocyte proliferation.[23] Both chronic and acute hyperinsulinemia also appear to increase free IGF-1 and reduce IGFBP-3.[23] Interestingly, IGFBP-3 is also a ligand for retinoid X nuclear receptor-α, which is the receptor that pharmaceutical retinoids therapeutically bind in the treatment of acne.[23,24] Since diet has a direct impact on insulin levels, which further influence IGF-1, IGFBP-1 and IGFBP-3, diet has been proven to play some role in the pathogenesis of acne.

There is an intricate pathway involving androgens, insulin and IGF-1, which all appear to provide positive feedback perpetuating the pathway. The specifics of such interactions have yet to be delineated but some of the best evidence for the role of diet in the development of acne comes from patients with polycystic ovarian syndrome (PCOS). PCOS is a disease of young women characterized by irregular menses, hirsutism, obesity and acne. Such patients are known to have increased plasma concentrations of insulin, IGF-1 and androgens,[25] and lower concentrations of sex hormone-binding globulin.[23] Interestingly, acne in patients with this disease improves with medications such as metformin, acarbose and pioglitazone, which are prescribed to enhance insulin metabolism,[26-28] but there have been no randomized, controlled studies evaluating their therapeutic effects on acne patients without PCOS.

Milk and Acne

Milk's contribution to the development of acne has often been debated, but two recent studies implicate its role. The Nurses Health Study II retrospectively evaluated 47,355 women, who completed questionnaires regarding diet and teenage acne, and found a positive correlation between milk (both whole and skim) in teenage acne.[29] These women's teenage sons were studied in the Growing Up Today Study (GUTS), which also found a positive association between the intake of skim milk and acne.[10] Interestingly, a genetic association was not mentioned. The authors do recognize their studies' limitations, such as the retrospective design of the first study and the self-assessment of acne in the second.

Although the association of dairy and acne remains unclear, similar studies and additional nutritional research are invaluable steps to help delineate diet's potential role in the pathogenesis of acne. According to Holmes et al., milk, which has been associated with increased IGF-1 concentrations, may have a specific correlation to the development of acne similar to the role IGF-1 may have in the previously mentioned high glycemic diets. Furthermore, there is a hypothesis that cow's milk has endogenous hormones that may also stimulate comedogenesis.[30] Milk contains several components that may affect the pilosebaceous unit, such as estrogens, progesterone, androgens, androgen precursors (including dehydroepiandrosterone-sulfate and androstenedione), 5-α-reduced steroids (including dihydrotestosterone, 5-α-pregnanedione and 5-α-androstanedione) and bioactive molecules (such as glucocorticoids and IGF-1).[31-33] Additionally, iodine in milk has been reported to possibly exacerbate acne.[34]

 

Expert Commentary

Diet's influence on the pathogenesis of disease has become an area of increasing interest with reports often recommending specific foods for the prevention of, or therapeutic effect on, various medical conditions. While some studies have data validating their results, others do not. Since acne is so prevalent in our population and can often be debilitating, it is not surprising that researchers are further investigating the role of diet to help answer many of our unknown questions. Continued research in this area should be encouraged but investigators should keep in mind that the development of acne is most probably multifactorial, so a combination of interventions might provide the best therapy for this condition.

Five-year View

An increasing amount of recent evidence suggests a dietary contribution to the pathogenesis of acne but further investigation, especially nutritional research, is necessary to clearly delineate its role. Large, randomized, controlled trials of acne patients versus control subjects with selective glycemic load diets should be performed to help elucidate the link between diet and acne. Data already collected from patients with insulin resistance and PCOS may also help to identify possible treatment options.

References

Papers of special note have been highlighted as: o of interest

1. White GM. Recent findings in the epidemiologic evidence, classification, and subtypes of acne vulgaris. J. Am. Acad. Dermatol. 39(2 Pt 3), S34-S37 (1998).
2. Goulden V, Stables GI, Cunliffe WJ. Prevalence of facial acne in adults. J. Am. Acad. Dermatol. 41(4), 577-580 (1999).
3. Strauss JS, Krowchuk DP, Leyden JJ et al. Guidelines of care for acne vulgaris management. J. Am. Acad. Dermatol. 56(4), 651-663 (2007).
4. Treloar V. Comment on guidelines of care for acne vulgaris management. J. Am. Acad. Dermatol. 57(5), 900-901 (2007).
5. Smith RN, Mann NJ, Braue A, MŠkelŠinen 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. 57(2), 247-256 (2007).
1. o Randomized, controlled trial that investigates the effect of glycemic load on acne and correlates this to concentrations of androgens and IGF-binding proteins.
6. Smith RN, Mann NJ, Braue A, Makelainen H, Varigos GA. A low glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Am. J. Clin. Nutr. 86(1), 107-115 (2007).
7. Smith RN, Braue A, Varigos GA, Mann NJ. The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. J. Dermatol. Sci. 50(1), 41-52 (2008).
8. Kaymak Y, Adisen E, Ilter N, Bideci A, Gurler D, Celik B. Dietary glycemic index and glucose, insulin, insulin-like growth factor-1, insulin-like growth factor binding protein 3, and leptin levels in patients with acne. J. Am. Acad. Dermatol. 57(5), 819-823 (2007).
9. Treloar V, Logan AC, Danby FW, Cordain L, Mann NJ. Comment on acne and glycemic index. J. Am. Acad. Dermatol. 58(1), 175-177 (2008).
10. Adebamowo CA, Spiegelman D, Berkey CS et al. Milk consumption and acne in teenaged boys. J. Am. Acad. Dermatol. 58(5), 787-793 (2008).
11. Tan JK, Vasey K, Fung KY. Beliefs and perceptions of patients with acne. J. Am. Acad. Dermatol. 44(3), 439-445 (2001).
12. Fulton JE Jr, Plewig G, Kligman AM. Effect of chocolate on acne vulgaris. JAMA 210(11), 2071-2074 (1969).
13. Anderson PC. Foods as the cause of acne. Am. Fam. Physician 3(3), 102-103 (1971).
14. Grant JD, Anderson PC. Chocolate as a cause of acne: a dissenting view. Mo. Med. 62, 459-460 (1965).
15. Bett DG, Morland J, Yudkin J. Sugar consumption in acne vulgaris and seborrhoeic dermatitis. BMJ 3(5558), 153-155 (1967).
16. Bourne S, Jacobs A. Observations on acne, seborrhea, and obesity. BMJ 1(4978), 1268-1270 (1956).
17. Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. Acne vulgaris: a disease of Western civilization. Arch. Dermatol. 138(12), 1584-1590 (2002).
18. Cappel M, Mauger D, Thiboutot D. Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women. Arch. Dermatol. 141(3), 333-338 (2005).
2. o Correlated IGF-1 and androgen levels with the presence of acne with evidence suggesting increased levels of both may influence acne lesions in adults.
19. Bol DK, Kiguchi K, Gimenez-Conti I, Rupp T, DiGiovanni J. Overexpression of insulin-like growth factor-1 induces hyperplasia, dermal abnormalities, and spontaneous tumor formation in transgenic mice. Oncogene 14(14), 1725-1734 (1997).
20. Edmondson SR, Thumiger SP, Werther GA, Wraight CJ. Epidermal homeostasis: the role of the growth hormone and insulin-like growth factor systems. Endocr. Rev. 24(6), 737-764 (2003).
21. Deplewski D, Rosenfield RL. Role of hormones in pilosebaceous unit development. Endocr. Rev. 21(4), 363-392 (2000).
22. Attia N, Tamborlane WV, Heptulla R et al. The metabolic syndrome and insulin-like growth factor 1 regulation in adolescent obesity. J. Clin. Endocrinol. Metab. 83(5), 1467-1471 (1998).
23. Cordain L. Implications for the role of diet in acne. Semin. Cutan. Med. Surg. 24(2), 84-91 (2005).
24. Lee KW, Cohen P. Nuclear effects: unexpected intracellular actions of insulin-like growth factor binding protein-3. J. Endocrinol. 175(1), 33-40 (2002).
25. Franks S. Polycystic ovary syndrome. N. Engl. J. Med. 333(13), 853-861 (1995).
26. Kazerooni T, Deghan-Kooshkghazi M. Effects of metformin therapy on hyperandrogenism in women with polycystic ovarian syndrome. Gynecol. Endocrinol. 17(1), 51-56 (2003).
27. Ciotta L, Calogero AE, Farina M, De Leo V, La Marca A, Cianci A. Clinical, endocrine and metabolic effects of acarbose, an _-glucosidase inhibitor, in PCOS patients with increased insulin response and normal glucose tolerance. Hum. Reprod. 16(10), 2066-2072 (2001).
28. Lord JM, Flight IH, Norman RJ. Insulin-sensitising drugs (metformin, troglitazone, rosiglitazone, pioglitazone, D-chiro-inositol) for polycystic ovary syndrome. Cochrane Database Syst. Rev. 3, CD003053 (2003).
29. Adebamowo CA, Spiegelman D, Danby FW, Frazier AL, Willett WC, Holmes MD. High school dietary dairy intake and teenage acne. J. Am. Acad. Dermatol. 52(2), 207-214 (2005).
30. Holmes MD, Pollak MN, Willett WC, Hankinson SE. Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations. Cancer Epidemiol. Biomarkers Prev. 11(9), 852-861 (2002).
31. Harmann S, Lacorn M, Steinhart H. Natural occurrence of steroid hormones in food. Food Chemistry 62(1), 7-20 (1998).
32. Darling JA, Laing AH, Harkness RA. A survey of the steroids in cows' milk. J. Endocrinol. 62(2), 291-297 (1974).
33. Donnet-Hughes A, Duc N, Serrant P, Vidal K, Schiffrin EJ. Bioactive molecules in milk and their role in health and disease: the role of transforming growth factor-_. Immunol. Cell Biol. 78(1), 74-79 (2000).
34. Arbesman H. Dairy and acne - the iodine connection. J. Am. Acad. Dermatol. 53(6), 1102 (2005).

The information presented here is not to be used as or interpreted to be advice to treat acne, rather the information presented here is to inform the reader and is in no way intended to be interpreted as medical advice or recommendations for treatment. It is strongly suggested that readers seeking treatment for their acne, or any other health problem, consult a qualified and experienced health care professional for treatment advice of their condition.

Home | About Us | Site Map | Contact Us | Resource Library

©2008-2012 Wildcrafted Herbal Products Pty Ltd.

Alternative Medicine endorses Natural Organic Skin Care Products to Promote Healthy Skin, Naturally.


Site Design: Web Site Design for Small Business