Diet and Acne Dairy and Sleep from folklore to science
Summary Points
Summary Points
• Acne is the 8th most prevalent disease globally. It commonly impacts 85% of teenagers but can persist into adulthood.
• Acne is a chronic inflammatory condition resulting from excessive sebum production, abnormal skin cell growth, and bacterial overgrowth. Hormonal changes, particularly during puberty, play a major role in its development.
• Sleep is a modifiable factor that supports health, contributing to both physiological and psychological functions. Insufficient sleep is a largely unrecognised public health problem globally. The circadian system responds to many signals including the light-dark cycle, food intake, temperature, physical activity, drugs and stress.
• The link between diet and acne has been debated for years, with various foods like dairy, high-fat foods, chocolate, and high-glycaemicindex (GI) foods all being studied as potential triggers.
Dietary components can act on neurotransmitters which influence sleep, and likewise, sleep deprivation can influence metabolic hormones and appetite. This relationship between food and the internal circadian clock is referred to as chrononutrition.
• Current research indicates that dairy has positive effects on sleep. Cow’s milk protein is rich in tryptophan, which is a precursor for both serotonin and melatonin. These hormones play important roles in the regulation of sleep. Small amounts of melatonin also occur naturally in cow’s milk.
• Insulin resistance and increased levels of Insulin-like Growth Factor 1 (IGF-1) may contribute to acne development by stimulating sebum production. High GI diets that lead to increased insulin and IGF-1, are associated with acne. Some studies show that low-GI diets may improve acne by reducing inflammation and sebum production, though evidence is still limited.
• Dairy consumption has been linked to acne through the relationship with IGF-1, but there is insufficient evidence from experimental studies. Observational studies suggest that skimmed milk may have a stronger association with acne than whole milk.
Editorial
Editorial
This issue explores the science behind dairy’s role in skin health, specifically acne. Acne affects 8 in 10 people aged 11-30, and many sufferers wonder if diet is a contributing factor.
Warm milk before going to bed is a tradition that has been passed down through generations as a practice to facilitate a restful night’s sleep.
As with other bedtime routines, it may be the ritual itself that helps to induce the anticipation of sleep. Also, drinking milk before falling asleep could be associated with soothing, early childhood memories that evoke calmness. However, it is also believed that naturally occurring components in milk can support the process of sleep.
While the link between diet and acne has been debated for years, there is little scientific evidence supporting any specific food as a direct cause. In fact, nutrients in milk, such as vitamin B2 and iodine, are essential for healthy skin. Misinformation, especially on social media, adds to the confusion, particularly for vulnerable young people.
• Fermented milk has been shown to significantly improve sleep efficiency. Lactic acid bacteria present in fermented dairy produce gammaaminobutyric acid, a neurotransmitter which is associated with sleep. Calcium inadequacy is associated with poor sleep and therefore, the calcium component of dairy may be another factor which influences sleep.
• While there is no strong evidence linking any specific food to acne, a healthy diet (high in fibre, fruits, vegetables, and omega-3 fatty acids, with reduced high-GI foods) may benefit acne sufferers. Restrictive diets should be avoided unless supervised by a dietitian to prevent nutrient deficiencies.
• The UK National Institute for Health and Care Excellence (NICE) does not recommend a specific dietary approach for treating acne due to limited evidence and potential risks of nutrient deficiencies.
• The overall composition of milk also makes it a nutritious bed-time drink. It provides casein-rich protein, which is encouraged as a pre-sleep intervention strategy to increase muscle protein synthesis overnight for both athletes and older people.
In this edition of DN Forum, we introduce the science of sleep and explore the research on how food interacts with sleep and the circadian system. We will focus specifically on the scientific evidence which examines the role of milk and dairy products.
Thanks to our expert authors for providing a deep dive into the evidence and clarity on this topic. We hope this issue helps debunk common myths and equips health professionals with the facts.
We hope you enjoy this edition of DN Forum and look forward to any feedback or comments you wish to share: nutrition@ndc.ie
We welcome any feedback or comments to: nutrition@ndc.ie
Dr. Marianne Walsh Nutrition Manager
Dr Mary Harrington Senior Nutritionist
The National Dairy Council (NDC)
Diet and Acne
INTRODUCTION
Acne is one of the most common skin conditions worldwide, indeed the 8th most prevalent disease affecting humans1,2. It affects 9.4% of the global population or at least 850 million people. Although acne affects approximately 85% of teenagers, it can occur in most age groups and can persist into adulthood3,4,5
Different aspects of diet have been investigated as possible triggers of acne. Micronutrients, fruits, vegetables, high-fat foods, saturated fat, eggs, dairy, carbohydrates, fish, and chocolate have all been linked to either an increased or decreased risk of acne6,7
ACNE VULGARIS
Acne vulgaris (acne) is a chronic inflammatory skin disease defined by lesions that result from the inflammation of plugged pilosebaceous units (consisting of the hair follicle and attached sebumproducing sebaceous gland) in the skin5, 7. The grading of acne remains poorly defined, with NICE guidelines (updated Dec, 2023) grading according to number of lesions8. Approximately 20% of those with acne will have significant disease. Mild disease can last 4-6 years, while severe disease can last up to 12 years or longer. The severity of acne correlates with the duration of the disease.
Risk factors for acne development include the increasing of age during adolescence, family history of acne, and oily skintype1, 10. There may also be an association with cigarette smoking and increasing body mass index (BMI)3,11
Acne in Western Populations
There appears to be an increased risk of acne in Western populations with lower prevalence of acne observed in non-western populations7. This may reflect differences in geographic ancestry-related genetics, diet, lifestyle, body weight and physical activity. Cordain et al. carried out a study looking at a non-westernised population (1,200 Kitavan Islanders of Papua New Guinea and 115 Aché hunter-gatherers of Paraguay) and observed no cases of active acne4. The development of acne in some populations after the adoption of a Western diet and lifestyle suggests that diet may play a role however, genetic differences are also important7,12,13
Sarah Keogh Founder of Eatwell and Registered Dietitian with the Coeliac Society
Desmond J. Tobin
Full Professor of Dermatological Science & Director, Charles Institute of Dermatology, University College Dublin
There are several pathophysiological factors involved in the development of acne:
• Excessive sebum production, in response to hormonal stimulation (e.g. increasing androgen levels at puberty).
• Increased proliferation and abnormal maturation of keratinocyte in the upper hair follicle leading to intra-follicular hyperkeratinization.
• Overgrowth of so-called acneic strains of cutibacterium acnes bacteria (previously called Propionibacterium acnes), which release factors that attract and activate many inflammatory cells of the immune system.
• Complex inflammatory mechanisms 1,5,9 Recent data suggests that a sub-clinical autoimmunity-like inflammation predates abnormal keratinization and comedogenesis.
DIET AND ACNE
Diet has been implicated in the development of acne for decades, although lacking robust evidence14. Early studies examined the potential role of carbohydrate (i.e. sugars) and chocolate in acne development and severity with mixed results15. Increased attention has been paid to diet and acne in recent years with studies examining the potential effects of milk; the role of glycaemic index diets, omega-3 fats and other nutrients6
Before examining individual foods or dietary patterns, it is important to understand some of the mechanisms that may be involved in the association between diet and acne.
MECHANISMS IN DIET & ACNE ASSOCIATIONS
Insulin and Insulin-like Growth Factor 1 (IGF-1) in Acne Vulgaris
Insulin resistance and IGF-1 may play a role in the pathogenesis of acne6. In patients with acne, associations with incidence and severity of acne and serum levels of IGF-1 have been reported16
IGF-1 levels rise sharply during childhood, with maximum levels reached in the mid-teens in response to growth hormone, stimulating the synthesis of androgens13. However, IGF-1 levels fall sharply over the following 10-15 years. Once IGF-1 levels fall below a certain point it may no longer trigger acne, Androgen hormones (e.g. testosterone, dihydrotestosterone) and IGF-1 influence sebum production14. IGF-1 correlates with the clinical course of acne in adolescents and has been shown to stimulate sebum production and sebocyte growth5, 7,16, 17. Increased sebum production influences colonisation by Cutibacterium acnes, the bacteria associated with acne lesions, although the presence of this bacterium alone is not indicative of risk, as there are acneic (e.g. 1A1) and non-acneic strains of this bacterium18,19
Ben-Amitai et al. found that acne was absent in individuals with Laron syndrome, which is characterised by IGF-1 deficiency20. Several studies report a correlation between IGF-1 levels and acne lesions in women, and higher levels of IGF-1 have been observed in women with acne than in controls21
High glycaemic index (GI) diets but also milk consumption have been reported to increase insulin and IGF-1, leading to the possibility that diet may contribute to an increase in acne incidence and severity15,16. However, circulating levels of IGF-1 are also genetically determined. Tasli et al. examined IGF-1 polymorphisms and found that the frequency of the IGF-1 (CA) polymorphism was significantly different between control and acne patients22. This polymorphism results in higher circulating levels of IGF-1 and is significantly associated with severity of acne compared to other polymorphisms in the same gene19, 22. This suggests that the patient’s intrinsic IGF-1 gene status (primarily produced by the liver) is likely to dominate, especially as calorie restriction has been found to have no effect on IGF-1 levels 23
Glycaemic Index (GI) and Acne
Cordain et al. postulated that high GI diets may contribute to the prevalence of acne in Western countries4. High GI diets are known to increase insulin and IGF-1. For this reason, several studies have investigated a possible link between high GI diets and acne. Frequent consumption of high GI carbohydrate foods may expose adolescents to acute hyperinsulimaemia, thereby increasing IGF-1 levels and acne16. High glycaemic index diets have been shown to increase reactive hyperinsulinaemia and increase formation of IGF-124. As discussed above, increased IGF-1 is associated with a higher risk of acne.
Several studies have shown associations between insulin resistance, glycaemic load (GL) and acne vulgaris5,25. However, not all studies show these associations26,27.
Emiroglu et al. measured blood levels of insulin and glucose in 243 acne vulgaris patients and 156 healthy controls15. They found no difference in fasting blood glucose between the two groups. However, fasting insulin levels were significantly higher in the patient group.
Smith at al. examined 43 male acne patients for 12 weeks 28. Participants followed either a low GI diet or
a standard diet. After 12 weeks on a low GI diet, total lesion counts decreased significantly compared to controls.
Conversely, Kaymak et al. found no association between acne, self-reported GI and GL in a study of 49 patients with acne and 42 healthy controls27
Kwon at al. investigated 32 patients with mild to moderate acne who were randomly assigned to either a low GL or control diet, and completed a 10-week, intervention trial29. The low GL group demonstrated significant clinical improvement in acne lesions, reduced inflammation, and reduced size of sebaceous glands.
Ismail at al. found that young adults with acne had higher GI diets and higher consumption of milk and icecream compared to controls30. Smith et al. investigated a low GI, high protein diet in male acne patients with a control group 31. Patients following the diet for 12 weeks, showed significant improvements in acne scores. IGF-1 levels also fell significantly in the diet group. However, participants did lose weight and this may be a factor in observed improvements in acne scores.
In a further study in males, Smith et al. examined the effect of a low GL diet on sebum outflow and sebum composition28. The low GL diet led to changes in saturated to monounsaturated fatty acid ratios in sebum, which negatively correlated with acne lesion counts and reduced sebum outflow. They concluded that a low GL diet may alter several factors associated with acne development in males.
Reynolds et al. randomised acne patients to either a high or low GI diet for 8 weeks32. Acne improved on both diets, with only slightly greater improvement in the low GI diet. However, differences did not reach significance. The authors concluded that a longer time frame may be required.
Overall, evidence suggests that a low GI/low GL diet may help improve acne in some patients7. However, there is a limited number of studies, and many are observational with few intervention studies. A low GI/ GL load diet is also typically higher in fibre and lower in fat, and participants frequently lose weight on these diets. Therefore, observed effects of a low GI diet may be related to other dietary and body composition factors33
The UK-based NICE guidelines on the management of acne concluded that there was some evidence that a low-glycaemic load diet may improve acne. However, the loss of weight and greater attention to the details of food raised concerns about eating disorders, especially as most people with acne are young and the onset of eating disorders is most common in adolescence8,34. For these reasons, no recommendation for a low GI or low GL diet was made.
PCOS Insulin resistance and acne – skewing results for diet and acne?
Polycystic ovary syndrome (PCOS) affects 5-20% of women of reproductive age worldwide. Metabolic dysfunction characterized by insulin resistance and compensatory hyperinsulinaemia is evident in the vast majority of affected individuals35. There is a significantly increased risk of acne in women with PCOS, which responds to a low GI/GL diet29,35. There have been no studies investigating low GI diets and acne in the general population that have considered the role PCOS may play in the response to the low GI diet in patients with acne.
Family History and Acne
Family history of acne strongly predicts acne in patients36. Familial hypercholesterolaemia, diabetes, and hypertension are also strong risk factors for acne36,37.
Bataille et al. examined the influence of environment and genetics in acne in a twin study that included both identical and non-identical twins38. 14% of the twins reported a history of acne with 81% of the variance of the disease attributable to additive genetic effects. The remaining 19% was attributed to environmental factors. Family history of acne was significantly associated with an increased risk.
In 2020, Heng et al. in a review of the epidemiology of acne worldwide, concluded that the potential factors most likely to influence acne presentation and severity are family history and BMI11
EVIDENCE
FOR INDIVIDUAL FOODS AFFECTING ACNE
Milk and Acne
Milk and milk products have been implicated in the etiology of acne14. Observational studies have shown associations between dairy consumption and both acne frequency and severity. However, many studies do not find any associations14. It is very important to note that, unlike low GI diets, there are no intervention trials that have examined the effect of dairy and acne7
The potential association of dairy and acne is thought to be related to IGF-1 which may increase with dairy consumption7, 16. Frequent dairy consumers have higher levels of serum IGF-1 and insulin, compared with nondairy consumers7,16. However, several other foods and nutrients are associated with higher circulating IGF-1 levels including high protein, red meat, fish, seafood and zinc39,40. IGF-1 levels are also influenced by body weight and conditions such as polycystic ovary syndrome (PCOS)7,41. IGF-1 concentrations in blood also vary based on age, gender, BMI, and smoking7,42
IGF-1 is present in milk, however, the UK Committee on Carcinogenicity of Chemicals in Food, Consumer Products and the Environment state that it is unlikely there would be absorption of intact IGF-1 from foodstuffs by most consumers42
Data relating to intake of dairy products has been more nuanced. For example, intake of protein from milk and yogurt, but not cheese, has been positively associated with IGF-1 concentrations, which may relate to the removal of the whey fraction in cheese production43
It is unlikely that significant levels of intact IGF-1 from oral consumption of dairy products are absorbed, as ingested proteins will not survive digestion intact by gastric enzymes. So, milk-derived IGF-1 is unlikely to be active within the body in contrast to IGF-1 that is produced by the body itself (e.g., in the liver). Indeed, the US Food and Drug Administration reports that IGF-1 concentrations in milk are insignificant when compared to IGF-1 concentrations produced in the human body44. Interestingly, fermentation (commonly used in dairy processing) can significantly decrease IGF-1 concentrations45
Studies examining the effect of dairy on acne are so far only observational studies. This study type has a lower standard of evidence than experimental studies as they are more prone to bias and confounding factors. Thus, must not be used to demonstrate causality. Participants in the Women’s Health Study were asked to recall usual dietary intakes in high school and whether a physician had ever diagnosed them with acne. Acne prevalence was associated with dairy in this recall study46. The association appeared to be stronger for skimmed and low-fat milk than for whole milk. Adebamowo et al. conducted further retrospective studies on diet and acne finding small associations between milk consumption and risk of acne47,48. However, these studies asked participants to recall diets from more than 10 years previously. In these two latter studies, it was unclear if skimmed, low-fat or whole milk was more associated with acne.
A case-control study by Di Landro et al. found that frequent consumption of total milk and skimmed milk, but not whole milk or cheese, was positively associated with acne on 358 patients matched to 205 controls33.
However, a cross-sectional study among 714 adolescents found that semi-skimmed milk, cream cheese, low fat cheese, yoghurt and ice cream were not associated with acne although BMI was49. Likewise, Juhl et al. found no link between milk intake and acne in 20,416 adults from the Danish General Suburban Population Study50
In their meta-analysis, Meixiong et al. found that 70% of observational dairy/acne studies linked acne with intake of at least one dairy food7. Indeed, 14% of the studies reviewed found negative associations between dairy and acne. Despite the lack of any intervention studies, they concluded that increased dairy intake may exacerbate acne among people with a Western diet, as associations between dairy and acne is not observed in non-Western populations. Burris et al. also reviewed evidence for an association between dairy and acne and concluded that there is insufficient evidence to recommend milk restriction as a treatment for patients with acne14
In the UK’s NICE guidelines on acne the authors concluded that there was insufficient evidence to recommend restricting milk or dairy foods as part of the treatment for acne8
Milk and dairy foods are the major source of calcium and iodine in the diets of Irish adolescents, who need 1,150mg of calcium per day according to the European Food Safety Authority51. Thus, removing dairy products from the diets of adolescents, without substitution, may negatively affect calcium and iodine intakes. It is important that patients are referred to a registered dietitian if a milk-free diet is being trialled for acne patients to ensure their calcium, iodine and protein requirements are being met.
Chocolate
Several studies have examined the link between chocolate and acne, with the majority finding a small (or no) association between milk chocolate, dark chocolate and cocoa and increased acne lesions in both observational and intervention studies13, 14, 52, 53 More research with larger groups, over longer periods is needed to determine links and to determine which components of chocolate may be relevant.
Fish and Omega-3 fats
Populations with higher intakes of omega-3 fatty acids and fish consumption have lower rates of acne33,54 Conversely, studies show that patients with acne are significantly more likely to have lower blood levels of eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)55
Omega-3 fatty acids EPA and DHA, are known for their anti-inflammatory properties, reducing proinflammatory cytokines, eicosanoids, and IGF-154 This suggests their potential to alleviate acne severity, especially when deficits are present.
Several studies have investigated the effect of EPA and DHA on acne54,55,56. Gamma linoleic acid (GLA) has also been shown to have anti-inflammatory effects on human skin epidermis56. Jung et al conducted a randomised controlled trial in 45 patients with acne56. Participants were allocated to a supplement of 2,000mg EPA and DHA or 400mg gamma linoleic acid or control group. After 10 weeks, acne lesions in both the fish oil and borage oil groups decreased significantly compared to the control group.
CONCLUSION
Changes in serum hormones predispose individuals to acne, beginning during adrenarche in both sexes (individuals insensitive to androgens do not develop acne). Androgens act in concert with IGF-1 to regulate the development of the pilosebaceous units – the target site for acne. The strongest risk factor for acne appears to be positive family history with several other factors including body, weight and smoking also playing a role3,11 Evidence from observational studies suggesting high GI diets and higher consumption of milk may increase risk and severity of acne is weak. Importantly, robust interventional-type studies of dairy and acne remain lacking. The omega-3 fats EPA and DHA may play a role in reducing acne incidence and severity.
References
1. Reynolds RV, Yeung H, Cheng CE et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2024 May;90(5):1006.e1-1006.e30.
2. Baldwin H, Tan J. Effects of Diet on Acne and Its Response to Treatment. Am J Clin Dermatol. 2021;22(1):55-65. Erratum in 22(1):67
3. Witkam WCAM, Dal Belo SE, Pourhamidi S et al. The epidemiology of acne vulgaris in a multiethnic adolescent population from Rotterdam, the Netherlands: A cross-sectional study. J Am Acad Dermatol. 2024 Mar;90(3):552-560.
4. Cordain L, Lindeberg S, Hurtado M et al. Acne Vulgaris: A Disease of Western Civilization. Arch Dermatol. 2002;138(12):1584–1590.
5. Pektas SD, Cinar N, Duman DD et al. The relationship among androgens, insulin resistance and ghrelin polymorphisms in post-adolescent male patients with severe acne vulgaris. Postepy Dermatol Alergol. 2020 Oct;37(5):800-809
6. Ryguła I, Pikiewicz W, Kaminiów K. Impact of Diet and Nutrition in Patients with Acne Vulgaris. Nutrients. 2024 May 14;16(10):1476.
7. Meixiong J, Ricco C, Vasavda C, Ho BK. Diet and acne: A systematic review. JAAD Int. 2022 Mar 29;7:95-112.
8. NICE Acne Vulgaris Management https://www.nice. org.uk/guidance/ng198 Accessed 27 March 2025
9. Cruz S, Vecerek N, Elbuluk N. Targeting Inflammation in Acne: Current Treatments and Future Prospects. Am J Clin Dermatol. 2023 Sep;24(5):681-694.
10. Rahaman SMA, De D, Handa S, Pal A et al. Association of insulin-like growth factor (IGF)-1 gene polymorphisms with plasma levels of IGF-1 and acne severity. J Am Acad Dermatol. 2016 Oct;75(4):768773
11. Heng AHS, Chew FT. Systematic review of the epidemiology of acne vulgaris. Sci Rep. 2020 Apr 1;10(1):5754.
12. Baldwin H, Tan J. Effects of Diet on Acne and Its Response to Treatment. Am J Clin Dermatol. 2021 Jan;22(1):55-65. Erratum in: 2021 Jan;22(1):67
13. Davidovici BB, Wolf R. The role of diet in acne: facts and controversies. Clin Dermatol. 2010 JanFeb;28(1):12-6
Overall, there is limited evidence of the effect of any one specific dietary factor on acne, although advice on healthy eating (increased fibre, fruits, vegetables and wholegrains, increased fish, and reduced consumption of high-GI foods) may benefit patients with acne.
If dietary treatment for acne is being considered, referral to a dietitian will allow a global review of diet including glycaemic index, dairy, omega-3 fatty acids. It is vital to ensure that patients (especially when actively growing) are not at risk of key nutrient deficiencies, such as calcium, from restrictive, non-evidence-based, dairyfree diets. Thus, the UK’s National Institute for Health and Care Excellence (NICE) have concluded that they would not recommend a specific dietary approach to the treatment for acne, as the limited evidence available for any potential benefit did not outweigh the risk of removing that element from the diet8
14. Burris J, Rietkerk W, Woolf K. Acne: the role of medical nutrition therapy. J Acad Nutr Diet. 2013 Mar;113(3):416-430.
15. Emiroğlu N, Cengiz FP, Kemeriz F. Insulin resistance in severe acne vulgaris. Postepy Dermatol Alergol. 2015 Aug;32(4):281-5
16. Melnik BC, Schmitz G. Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol. 2009 Oct;18(10):833-41
17. Davidovici BB, Wolf R. The role of diet in acne: facts and controversies. Clin Dermatol. 2010 JanFeb;28(1):12-6
18. Romańska-Gocka K, Woźniak M, KaczmarekSkamira E, Zegarska B. The possible role of diet in the pathogenesis of adult female acne. Postepy Dermatol Alergol. 2016 Dec;33(6):416-420
19. Borrel V, Gannesen AV, Barreau M et al. Adaptation of acneic and non acneic strains of Cutibacterium acnes to sebum-like environment. Microbiologyopen. 2019 Sep;8(9):e00841
20. Ben-Amitai D, Laron Z. Effect of insulin-like growth factor-1 deficiency or administration on the occurrence of acne. J Eur Acad Dermatol Venereol. 2011 Aug;25(8):950-4
21. 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. 2005 Mar;141(3):333-8
22. Tasli L, Turgut S, Kacar N et al. Insulin-like growth factor-I gene polymorphism in acne vulgaris. J Eur Acad Dermatol Venereol. 2013 Feb;27(2):254-7
23. Kazemi A, Speakman JR, Soltani S et al. Effect of calorie restriction or protein intake on circulating levels of insulin like growth factor I in humans: A systematic review and meta-analysis. Clinical Nutrition. 39 (6): 1705–1716
24. 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. 2007 Aug;57(2):247-56
25. Çerman AA, Aktaş E, Altunay İK et al. Dietary glycemic factors, insulin resistance, and adiponectin levels in acne vulgaris. J Am Acad Dermatol. 2016 Jul;75(1):155-62
26. Balta I, Ekiz O, Ozuguz P et al. Insulin resistance in patients with post-adolescent acne. Int J Dermatol. 2015 Jun;54(6):662-6
27. 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 Dermatol. 2007 Nov;57(5):819-23
28. 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. 2008 Apr;50(1):41-52
29. Kwon HH, Yoon JY, Hong JS et al. Clinical and histological effect of a low glycaemic load diet in treatment of acne vulgaris in Korean patients: a randomized, controlled trial. Acta Derm Venereol. 2012 May;92(3):241-6
30. Ismail NH, Manaf ZA, Azizan NZ. High glycemic load diet, milk and ice cream consumption are related to acne vulgaris in Malaysian young adults: a case control study. BMC Dermatol. 2012 Aug 16;12:13
31. Smith RN, Mann NJ, Braue A et al. A low-glycemicload diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Am J Clin Nutr. 2007 Jul;86(1):107-15.
32. Reynolds RC, Lee S, Choi JY et al. Effect of the glycemic index of carbohydrates on Acne vulgaris. Nutrients. 2010 Oct;2(10):1060-72
33. Di Landro A, Cazzaniga S, Parazzini F et al. Family history, body mass index, selected dietary factors, menstrual history, and risk of moderate to severe acne in adolescents and young adults. J Am Acad Dermatol. 2012 Dec;67(6):1129-35
34. NICE. Acne vulgaris: management [C] Dietary interventions for the treatment of acne vulgaris; Evidence review underpinning recommendations 1.3.1 and research recommendation 3 in the NICE guideline. June 2021.
35. Azziz R, Carmina E, Chen Z et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2016 Aug 11;2:16057