Free-IGF-1 lowers SHBG | Acne, Polycystic Ovarian Syndrome, Hyperinsulinemia and Diet

1)

Arch Dermatol. 2002 Dec;138(12):1584-90.
Acne vulgaris: a disease of Western civilization.

Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J.
Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. cordain@cahs.colostate.edu
Comment in:
* Arch Dermatol. 2002 Dec;138(12):1591-2.
* Arch Dermatol. 2003 Jul;139(7):941; author reply 942-3.
* Arch Dermatol. 2003 Jul;139(7):941-2; author reply 942-3.

Abstract

BACKGROUND: In westernized societies, acne vulgaris is a nearly universal skin disease afflicting 79% to 95% of the adolescent population. In men and women older than 25 years, 40% to 54% have some degree of facial acne, and clinical facial acne persists into middle age in 12% of women and 3% of men. Epidemiological evidence suggests that acne incidence rates are considerably lower in nonwesternized societies. Herein we report the prevalence of acne in 2 nonwesternized populations: the Kitavan Islanders of Papua New Guinea and the Aché hunter-gatherers of Paraguay. Additionally, we analyze how elements in nonwesternized environments may influence the development of acne.

OBSERVATIONS: Of 1200 Kitavan subjects examined (including 300 aged 15-25 years), no case of acne (grade 1 with multiple comedones or grades 2-4) was observed. Of 115 Aché subjects examined (including 15 aged 15-25 years) over 843 days, no case of active acne (grades 1-4) was observed.

CONCLUSIONS: The astonishing difference in acne incidence rates between nonwesternized and fully modernized societies cannot be solely attributed to genetic differences among populations but likely results from differing environmental factors. Identification of these factors may be useful in the treatment of acne in Western populations.

PMID: 12472346 [PubMed - indexed for MEDLINE]

Source: http://www.ncbi.nlm.nih.gov/pubmed/12472346

Quote from full article below:
DIET AND HYPERINSULINEMIA

Although diet is infrequently considered as an etiologic agent in the development of acne,34 it represents a well-recognized factor in acute35 and chronic36-37 hyperinsulinemia. Recent evidence has demonstrated that the hormonal cascade triggered by diet-induced hyperinsulinemia elicits an endocrine response that simultaneously promotes unregulated tissue growth and enhanced androgen synthesis. Hence, hyperinsulinemic diets may represent a previously unrecognized environmental factor in the development of acne via their influence on follicular epithelial growth and keratinization and on androgen-mediated sebum secretion.

HYPERINSULINEMIA AND FREE IGF-1 AND IGFBP-3

Chronic and acute hyperinsulinemia initiate a hormonal cascade that favors unregulated tissue growth by simultaneously elevating levels of free insulinlike growth factor 1 (IGF-1) and reducing levels of insulinlike growth factor binding protein 3 (IGFBP-3).38-41 Because free IGF-1 is a potent mitogen for virtually all body tissues,42 elevated concentrations of free IGF-1 have a high potential for stimulating growth in all tissues, including the follicle.

In support of the notion that insulin-triggered elevations in free IGF-1 levels may promote acne via hyperkeratinization are data showing that IGF-1 is required for keratinocyte proliferation in humans43 and that in transgenic mice, overexpression of IGF-1 results in hyperkeratosis and epidermal hyperplasia.44 Furthermore, women with postadolescent acne maintain elevated serum concentrations of IGF-145 and are mildly insulin resistant.46

The reductions in IGFBP-3 levels stimulated by elevated serum insulin levels38-39 or by acute ingestion of high–glycemic load carbohydrates47 also may contribute to unregulated cell proliferation in the follicle. In murine knockout cells lacking the IGF receptor, IGFBP-3 acts as a growth inhibitory factor.48 Accordingly, IGFBP-3 is inhibitory to growth by preventing IGF-1 from binding to its receptor. Hyperinsulinemia indirectly increases the number of epidermal growth factor receptors by elevating levels of plasma nonesterified fatty acids,49 and it also induces production of transforming growth factor {beta}1.50 Increased concentrations of these cytokines depress localized keratinocyte synthesis of IGFBP-3, thereby increasing the availability of free IGF-1 to its keratinocyte receptors,51 which in turn promotes keratinocyte proliferation. Consequently, hyperkeratinization of sebaceous follicles may result synergistically from elevations in free IGF-1 levels and/or reductions in concentrations of IGFBP-3.

IGFBP-3 AND RETINOID RECEPTORS

Insulin-mediated reductions in IGFBP-3 levels may further promote unregulated follicular growth by affecting the nuclear retinoid signaling pathway. Retinoids are natural and synthetic analogues of vitamin A that inhibit cell proliferation and promote apoptosis.52 The body’s natural retinoids (trans retinoic acid and 9-cis-retinoic acid) act by binding 2 families of nuclear receptors: retinoic acid receptors (RARs) and retinoid X receptors (RXRs). Retinoid receptors, in turn, activate gene transcription by binding as RAR-RXR heterodimers or RXR-RXR homodimers to retinoic acid response elements located in the promoter regions of target genes whose function is to limit growth in many cell types.53

Insulinlike growth factor binding protein 3 is a ligand for the RXR{alpha} nuclear receptor and enhances RXR-RXR homodimer–mediated signaling.54 Studies in knockout rodents show that the RXR{alpha} gene is required for actions of the 2 endogenous retinoic acid ligands (trans retinoic acid and 9-cis-retinoic acid),55-56 and RXR{alpha} agonists and IGFBP-3 are growth inhibitory in many cell lines.57 Additionally, RXR{alpha} is the major RXR receptor in skin.58 Consequently, low plasma levels of IGFBP-3 induced by hyperinsulinemia may reduce the effectiveness of the body’s natural retinoids to activate genes that normally would limit follicular cell proliferation.

HYPERINSULINEMIA, IGF-1, ANDROGENESIS, AND SEBUM PRODUCTION

Sebum production, essential to the development of acne,32 is stimulated by androgens.31-32 Consequently, hyperinsulinemia may promote acne by its well-established androgenic effect. Insulin and IGF-1 stimulate the synthesis of androgens in ovarian59-60 and testicular61-62 tissues. Furthermore, insulin and IGF-1 inhibit the hepatic synthesis of sex hormone binding globulin (SHBG),63-64 thereby increasing the bioavailability of circulating androgens to tissues. Cross-sectional studies demonstrate inverse relationships between serum SHBG and insulin65 and IGF-1.66-68 Additionally, sebum production is stimulated not only by androgens,31-32 but also by insulin69 and IGF-1.70 Direct injections of recombinant IGF-1 in humans elicit androgenesis and acne.71 Higher serum androgen,72 insulin,45 and IGF-146 concentrations are associated with the presence of acne in women. Taken together, these data suggest that the endocrine cascade induced by hyperinsulinemia enhances sebum synthesis and the development of acne.

POLYCYSTIC OVARY SYNDROME

Acne is a characteristic feature in patients with polycystic ovary syndrome, who are also frequently hyperinsulinemic, insulin resistant, and hyperandrogenic.73 These patients typically maintain elevated serum concentrations of androgens and IGF-1 and lower concentrations of SHBG.73-75 Androgen levels can be lowered and disease symptoms alleviated by improving insulin sensitivity through weight loss76 or by use of pharmaceuticals such as metformin77 that improve insulin metabolism. Numerous studies78-80 have reported that tolbutamide, an antihyperglycemic drug similar to metformin, is therapeutically effective in treating acne.

DIETARY CHARACTERISTICS AND INSULIN RESISTANCE IN NONWESTERNIZED SOCIETIES

Both the Aché and Kitavan diets are composed of minimally processed plant and animal foods and are virtually devoid of typical Western carbohydrates that yield high glycemic loads that may acutely35 or chronically36-37 elevate insulin levels (Table 1). Recently acculturated hunter-gatherer populations who have adopted Western diets frequently are hyperinsulinemic and insulin resistant and have high rates of type 2 diabetes,81-82 whereas hunter-gatherer and less westernized populations living in their native environments rarely exhibit these symptoms,83-85 including other unacculturated South American Indian tribes.86 Neither the Kitavan islanders nor the Aché hunter-gatherers manifest the classic symptoms of insulin resistance. The Kitavans are not overweight or hypertensive,14-15 and they maintain low serum concentrations of insulin,16 plasminogen activator inhibitor 1,17 and leptin,18 which are indicators of high insulin sensitivity.

Dietary interventions using low–glycemic load carbohydrates may have therapeutic potential in the treatment of acne because of the beneficial endocrine effects of these diets. Low–glycemic load diets are associated with a reduced risk for type 2 diabetes,87  and dietary interventions using low–glycemic load carbohydrates  improve insulin sensitivity.88  Furthermore, a large-scale intervention89  has demonstrated that diets rich in low–glycemic load foods reduced serum testosterone and fasting glucose levels while improving insulin metabolism and increasing concentrations of SHBG.89  These endocrine changes are consistent with those known to promote normal follicular cell proliferation and to reduce sebum production. It is possible that low–glycemic load diets may have therapeutic potential in reducing symptoms of acne, a disease virtually unknown to the Aché and Kitavans.

Full article: http://archderm.ama-assn.org/cgi/content/full/138/12/1584
File: Arch Dermatol-Acne Vulgaris.pdf

2)

Clin Dermatol. 2008 Jan-Feb;26(1):93-6.
Diet and acne.
Danby FW.

Dartmouth Medical School, Hanover, New Hampshire, Manchester, NH 03104, USA. fwdljm@tds.net <fwdljm@tds.net>
Abstract

Acne is caused by the action of dihydrotestosterone, derived from endogenous and exogenous precursors, likely acting synergistically with insulin-like growth factor-1. These sources and interactions are discussed. Both a mechanism of action and recommended dietary changes that limit ingestion and production of these hormones are proposed.

PMID: 18280909 [PubMed - indexed for MEDLINE]

Source: http://www.ncbi.nlm.nih.gov/pubmed/18280909

3)

Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):95-112.
Hyperinsulinemic diseases of civilization: more than just Syndrome X.

Cordain L, Eades MR, Eades MD.

Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. cordain@cahs.colostate.edu
Abstract

Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor alpha, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body’s endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.

PMID: 14527633 [PubMed - indexed for MEDLINE]

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Source: http://www.ncbi.nlm.nih.gov/pubmed/14527633

4)
Eur J Dermatol. 2010 Sep 7. [Epub ahead of print]
The influence of dietary patterns on acne vulgaris in Koreans.

Jung JY, Yoon MY, Min SU, Hong JS, Choi YS, Suh DH.
Abstract

The association between acne and food has been evaluated with inconsistent results. We enrolled 783 patients with acne and 502 control subjects. For the patients with acne, blood tests for insulin, insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), post prandial 2 hours blood glucose (PP2), and dehydroepiandrosterone sulphate (DHEAS) were performed. The acne patients were divided into an “aggravated by food” group (AF) and a “not aggravated by food” group (NAF). All participants were asked to fill out a questionnaire. The frequency of vegetables (yellow, green leafy, cruciferous) (P = .001) and fish (white flesh and green fish, blue tuna) ((P = .03) intake was significantly higher in the control group than in the acne group. Intake of instant noodles (P = .01), junk food (P = .002), carbonated drinks (P = .005), snacks (P = .001), processed cheeses (P = .04), pork (braised) (P = .02), pork (roast) (P < .001), chicken (fried) (P = .001), chicken (stewed) (P = .001), nuts (P = .002) and seaweed (P = .003) were significantly higher in the acne patients than in the controls. Intake of roast pork (P = .02), fried chicken (P < .02), and nuts (P = .03) was significantly higher in the AF than NAF. In addition, the regularity of inter-meal intervals (P < .001) and breakfast intake (P < .001) were significantly lower in the acne patients. IGF-1 and IGFBP-3 showed sexual differences. This study also showed that a high glycemic load diet, dairy food intake, high fat diet, and iodine in Korean foods appear to play a role in acne exacerbation. In addition, irregular dietary patterns were found to aggravate acne.

PMID: 20822969 [PubMed - as supplied by publisher]
Source: http://www.ncbi.nlm.nih.gov/pubmed/20822969

5)

Hautarzt. 2010 Feb;61(2):115-25.
[Acne vulgaris. Role of diet]

[Article in German]

Melnik B.

Fachgebiet Dermatologie, Umweltmedizin und Gesundheitstheorie, Universität Osnabrück, Sedanstr. 115, 49090 Osnabrück. Melnik@t-online.de
Abstract

The epidemic-like high prevalence of acne of more than 85% of adolescents exposed to westernized life style points to the role of nutritional factors. Insulinotropic foods, especially milk, dairy products and carbohydrates with high glycemic index and smoking lead to pathological exaggeration of already physiologically increased growth factor signaling of puberty. Food-derived growth factors activate the oncogenic phosphoinositide-3-kinase/Akt signaling pathway, which increases androgen receptor transcriptional activity and de-represses FoxO1-suppressed target genes of follicular keratinocyte proliferation and sebaceous lipogenesis. Thus, acne is the visible metabolic syndrome of skin exaggerated by growth factor signaling of westernized malnutrition. These insights allow a new classification of western life style acne as acne alimentaris and provide the rationale for dietary intervention. All efforts should be undertaken to eliminate the insulinotropic effector mechanism of milk in order to reduce the prevalence of acne and even more serious civilization diseases associated with malnutrition-dependent oncogenic signal transduction.

PMID: 20107753 [PubMed - indexed for MEDLINE]

Source: http://www.ncbi.nlm.nih.gov/pubmed/20107753

6)

Skin Therapy Lett. 2010 Mar;15(3):1-2, 5.
Does diet really affect acne?

Ferdowsian HR, Levin S.
Physicians Committee for Responsible Medicine, Washington, DC, USA.

Abstract

Acne vulgaris has anecdotally been attributed to diet by individuals affected by this skin condition. In a 2009 systematic literature review of 21 observational studies and 6 clinical trials, the association between acne and diet was evaluated. Observational studies, including 2 large controlled prospective trials, reported that cow’s milk intake increased acne prevalence and severity. Furthermore, prospective studies, including randomized controlled trials, demonstrated a positive association between a high-glycemic-load diet, hormonal mediators, and acne risk. Based on these findings, there exists convincing data supporting the role of dairy products and high-glycemic-index foods in influencing hormonal and inflammatory factors, which can increase acne prevalence and severity. Studies have been inconclusive regarding the association between acne and other foods.

PMID: 20361171 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/20361171

Full article: http://www.skintherapyletter.com/2010/15.3/1.html

Full article:
More than 17 million Americans suffer from acne vulgaris.1 Approximately 80-90% of all adolescents experience some degree of acne.2  Adults are also affected. Acne has been associated with other clinically relevant issues, including depression.3 While studies have demonstrated patients’ perceptions about a link between diet and acne,3-7  reviews published in or prior to 2005 have not shown a conclusive correlation.8-10 In addition, methodological issues have limited conclusions that could be drawn from the literature before 2005. A 2009 review evaluated the published literature on the association between diet and acne risk and severity. Authors showed that dairy products and high-glycemic-index foods increased the risk for acne, whereas the studies did not conclusively demonstrate an association between acne and other foods, such as chocolate or salt.11
Pathophysiology

Acne forms as a result of obstruction and inflammation of hair follicles and their accompanying sebaceous glands (pilosebaceous units). Acne can be inflammatory or noninflammatory and may involve colonization of the follicle with bacteria (most commonly Propionibacterium acnes). With increased hormonal activity, sebum production and blocking of follicles also increase; the latter leading to closed comedones (whiteheads) or open comedones (blackheads).
Dairy Products

Migration studies have demonstrated that as populations shifted toward a more Westernized diet, either through relocation or a local cultural change, the prevalence of acne increased. This trend was observed in Canadian Inuit12 who increased their consumption of soda, beef, dairy products, and processed foods, as well as among Okinawan Japanese13 who decreased their starch intake and increased their total animal product intake.

Authors of a large case-control study14 evaluated the association between milk and acne in the adolescent diets of more than 47,000 nurses. Among participants who had been diagnosed with severe acne as teenagers, those with the highest level of total milk intake (>3 servings per day) reported having acne more frequently, when compared with individuals with the lowest level of intake (=1 serving per week). This association was strongest (a 44% increase) for skim milk intake, suggesting fat content was not the determining factor for acne risk. Researchers hypothesized that the hormones found in milk played a role in acne risk.

Two large prospective cohort studies examined the association between diet and acne among 9-15 year-old children, including 6094 girls15 and 4273 boys.16 For girls, there was a significant association with acne severity for all categories of cow’s milk (total, whole, low-fat, skimmed, and chocolate). For boys, the association was significant for total and skimmed milk. Girls were approximately 20% more likely to experience severe acne if they consumed =2 servings of milk per day, when compared with girls who consumed =1 serving of milk per week. Boys were approximately 16% more likely to experience severe acne if they consumed =2 servings of milk per day, when compared with boys who consumed =1 serving of milk per week.

A study from 2005 showed that components of milk, other than lipids, have insulin-stimulating abilities.17 Insulin drives insulin-like growth factor 1 (IGF-1), which in turn increases testosterone and decreases the production of sex hormone- binding globulin (SHBG). Another study observed a positive correlation between levels of IGF-1 and acne.18
High-Glycemic-Index Foods

Authors of 2 large cross-sectional studies19 in Papua New Guinea (n=1200) and Paraguay (n=115) found no cases of acne in either population. Researchers speculated that the rural populations’ low-fat and low-glycemic-index diets could be the reason for the absence of acne in these groups.

Authors of a randomized controlled trial20 examined the effect of low-glycemic-load diets on acne risk and insulin sensitivity. Individuals assigned to the low-glycemic-load diet experienced improvement in the mean number of acne lesions, when compared with the control group. In addition, the low-glycemic-load diet group’s mean weight decreased, and insulin sensitivity and SHBG levels increased.21 Increases in SHBG levels correlated with decreased lesion counts. As SHBG levels increase, free androgen levels would be expected to decrease accordingly. These investigative findings support the role of low-glycemic-load diets in influencing hormonal levels, as well as improving insulin sensitivity and acne.20-22
Fat and Fatty Acid Intake

Although there have been no published, large, well-controlled studies that examine the effect of fat or fatty acid intake on acne risk, omega-6 fatty acids are pro-inflammatory and their pro-inflammatory mediators have been associated with acne.23 By contrast, omega-3 fatty acids have anti-inflammatory properties24 and may be associated with decreased risk of acne by decreasing IGF-1 levels and follicle inflammation. Typically, Western diets have a low ratio of omega-3 to omega-6 fatty acids, as compared with diets observed in non- industrialized nations.25

Additionally, diets high in saturated fats have been associated with increased IGF-1 levels, while diets that are low-fat and high in fiber have been linked with decreased IGF-1 levels.26

Chocolate

In a crossover trial examining the effect of chocolate intake on acne, 65 participants consumed 112g of dairy-free cocoa- enriched bars of chocolate each day for 4 months. Researchers compared the results to the same group’s consumption of chocolate bars without the cocoa enrichment and found no significant difference between the groups.27 Similarly, other intervention trials showed no effect of chocolate on acne.28,29 However, these trials had no control groups and the results were not quantified.

Conclusion

Population-based and migration studies have suggested a correlation between diet and acne. Large, well-controlled, observational studies have demonstrated that diets high in dairy products are associated with an increase in the risk for and severity of acne. Researchers have found significant associations between all varieties of cow’s milk and acne. The relationship between milk and acne severity may be explained by the presence in dairy of normal reproductive steroid hormones or the enhanced production of polypeptide hormones such as IGF-1, which can increase androgen exposure, and thus, acne risk. Recent findings also describe an association between a high-glycemic-index diet and longer acne duration. In addition, randomized clinical trials have demonstrated that a low-glycemic-load diet can influence hormonal levels and improve insulin sensitivity and acne. No study has established a positive association between acne and chocolate, saturated fat, or salt intake.

References

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4. Rigopoulos D, Gregoriou S, Ifandi A, et al. Coping with acne: beliefs and perceptions in a sample of secondary school Greek pupils. J Eur Acad Dermatol Venereol 21(6):806-10 (2007 Jul).
5. Tallab TM. Beliefs, perceptions and psychological impact of acne vulgaris among patients in the Assir region of Saudi Arabia. West Afr J Med 23(1):85-7 (2004 Jan-Mar).
6. Al-Hoqail IA. Knowledge, beliefs and perception of youth toward acne vulgaris. Saudi Med J 24(7):765-8 (2003 Jul).
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8. Blau S, Kanof NB. Acne. From pimple to pit. N Y State J Med 65:417-24 (1965 Feb 1).
9. Wolf R, Matz H, Orion E. Acne and diet. Clin Dermatol 22(5):387-93 (2004 Sep-Oct).
10. Magin P, Pond D, Smith W, et al. A systematic review of the evidence for myths and misconceptions’ in acne management: diet, face-washing and sunlight. Fam Pract 22(1):62-70 (2005 Feb).
11. Spencer EH, Ferdowsian HR, Barnard ND. Diet and acne: a review of the evidence. Int J Dermatol 48(4):339-47 (2009 Apr).
12. Bendiner E. Disastrous trade-off: Eskimo health for white “civilization”. Hosp Pract 9:156-89 (1974).
13. Steiner PE. Necropsies on Okinawans: anatomic and pathologic observations. Arch Pathol 42:359-380 (1946).
14. Adebamowo CA, Spiegelman D, Danby FW, et al. High school dietary dairy intake and teenage acne. J Am Acad Dermatol 52(2):207-14 (2005 Feb).
15. Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in adolescent girls. Dermatol Online J 12(4):1 (2006).
16. Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in teenaged boys. J Am Acad Dermatol 58(5):787-93 (2008 May).
17. Hoyt G, Hickey MS, Cordain L. Dissociation of the glycaemic and insulinaemic responses to whole and skimmed milk. Br J Nutr 93(2):175-7 (2005 Feb).
18. Kaymak Y, Adisen E, Ilter N, et al. Dietary glycemic index and glucose, insulin, insulin-like growth factor-I, insulin-like growth factor binding protein 3, and leptin levels in patients with acne. J Am Acad atol 57(5):819-23 (2007 Nov). Cordain L, Lindeberg S, Hurtado M, et al. Acne vulgaris: a disease of Western civilization. Arch Dermatol 138(12):1584-90 (2002 Dec).
19. Smith RN, Mann NJ, Braue A, et al. A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Am J Clin Nutr 86(1):107-15 (2007 Jul).
20. Smith RN, Mann NJ, Braue A, 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 57(2):247-56 (2007 Aug).
21. Smith RN, Braue A, Varigos GA, et al. 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 Apr).
22. Zouboulis CC. Is acne vulgaris a genuine inflammatory disease? Dermatology 203(4):277-9 (2001).
23. James MJ, Gibson RA, Cleland LG. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr 71(1 Suppl):343S-8S (2000 Jan).
24. Simopoulos AP. Essential fatty acids in health and chronic disease. Am J Clin Nutr 70(3 Suppl):560S-9S (1999 Sep). 26. Kaaks R, Bellati C, Venturelli E, et al. Effects of dietary intervention on IGF-I and IGF-binding proteins, and related alterations in sex steroid metabolism: the Diet and Androgens (DIANA) Randomised Trial. Eur J Clin Nutr 57(9):1079-88 (2003 Sep).
25. Fulton JE, Jr., Plewig G, Kligman AM. Effect of chocolate on acne vulgaris. Jama 210(11):2071-4 (1969 Dec 15).
26. Anderson PC. Foods as the cause of acne. Am Fam Physician 3(3):102-3 (1971 Mar).
27. Grant JD, Anderson PC. Chocolate as a Cause of Acne: a Dissenting View. Mo Med 62:459-60 (1965 Jun).

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