Acne – are dietary factors relevant?

25th August 2020, Dr Chee L Khoo

diet and acne

Moderately severe to severe acne can have significant psychological harm associated with low self-esteem, poor perception of one’s body, social isolation, and depressive symptoms. Patients often believe that consumption of various food contribute to their acne development and severity. Although chocolate, fatty foods, and milk are frequently thought to be responsible is there any evidence on the role of nutrition in acne? If there is, what are the mechanisms linking acne and diet? Perhaps, by understanding the mechanisms involved, we may be able to reduce the severity of the acne with minimal medications.

As you can imagine, randomised controlled trials can be difficult when investigating multiple food exposures. Observational studies frequently focus on teenage acne and are based on  frequency questionnaires for previous food exposure, which lead to both a lack of precision in food records and a recall bias without taking into account various potential confounding factors, such as depression, energy intake and smoking.

So, what do we know about diets and acne? Before we delve into the possible effect of diet on acne development and severity, we should look at the pathophysiology of acne. Acne pathogenesis is thought to be attributed to four key factors:

  1. Excess sebum production
  2. Hyperproliferation of Cutibacterium acnes (C. acne) bacteria
  3. Hyper-keratinisation of the pilosebaceous follicles and
  4. Inflammatory mechanisms

The role of mTORC1

Mammalian target of rapamycin complex 1 (mTORC1) is a protein complex that functions as a nutrient/energy/redox sensor and controls protein synthesis. It is involved in cell proliferation and metabolism. In particular, it mediates sebaceous gland hyperproliferation, lipid synthesis and hyperplasia of keratinocytes (hyperkeratinisation).

A number of factors activates mTORC1:

  • Insulin growth factor -1 (IGF1) – also increases androgen levels
  • Leucine, a common amino acid in meat and dairy proteins  
  • Androgen which also increases mTORC1
  • Stress, inflammation and growth – via increase in mTORC1
  • Hyperinsulinaemia e.g. PCOS, obesity, high GI/GL diet

The role of diet

Glycaemic Index/Glycaemic Load

The glycaemic index (GI) of a food refers to the rise in the blood glucose level, relative to pure glucose, 2 h after consumption of that food. Glycaemic load (GL) is a measure of a food’s ability to raise blood glucose levels, which accounts for carbohydrate in the food.

Low-GL diets have been shown to reduce the free androgen index (FAI) and increases insulin-growth factor binding protein-3 (leading to reduce IGF1 activity), whereas a low-GI and low-GL diet also decreases IGF-1 levels [1,2]. In one study involving 31 male patients with acne (aged 15–25 years), a low-GL diet was compared with a control diet for 12 weeks.  There was an increased ratio of saturated-to-mono-unsaturated fatty acids of skin surface triglycerides and a reduction in acne lesions [3].

Daily consumption of chocolate and confectionaries were independently and highly associated with acne in other studies [4-6]. This was confirmed in a recent prospective cohort NutriNet-Santé study involving 24,452 participants. The consumption of milk chocolate and sugary beverages was highly associated with current acne (odds ratio of 1.28 and 2.19, respectively) [6].

Ketogenic diets, which rely on a near-total reduction in carbohydrate and increased consumption of fat and protein, cause the body to source energy from ketones rather than glucose. Ketogenic diets have been shown to reduce markers of inflammation and levels of IGF-1 [7-9].

Dairy

Eighty percent of cow’s milk protein is casein, and the remaining 20% is whey proteins. Whey proteins are predominantly responsible for the insulinotropic effects of milk, whereas casein stimulates IGF-1 to a greater extent than whey. Perhaps, this can explain why body builders on protein supplements (which are primarily dairy protein) aggravate their acne.

A 3-year prospective study involving 6094 girls aged 9–15 years found a positive association between acne prevalence and consumption of full-fat, skimmed, and low-fat milk but no association with non-milk dairy foods, chocolate, and pizza [10].

The most likely cause for the association of dairy with acne is thought to be the insulin index, defined as the elevation of insulin levels in the blood during the 2-h period after food is ingested [11]. Milk has a very high insulin index, irrespective of fat content [11]. By comparison, cheese has a low insulin index, whereas ice cream has a high insulin index due to added sugar.

Fats and fatty acids

Omega-3 fatty acids have been shown to decrease IGF-1, which is implicated in sebum production and follicular occlusion. Omega-3 fatty acids inhibit synthesis of inflammatory leukotriene B4, which in turn reduces inflammatory acne lesions. Increased trans-fat and saturated fat consumption was associated with increased acne severity [12]. Adding an omega-3 fatty acid supplement or α-linoleic acid supplement significantly reduced inflammatory and non-inflammatory lesion counts (13).

Vegetarian or vegan diets

Data on the effect of vegetarian or vegan diets is incomplete and inconclusive. Stewart and

Bazergy found the prevalence of vegan diets to not be significantly different between 453 patients with acne and 150 controls retrospectively screened from a family medical clinic (14). However, this study did not detail the contents of the vegan diets, which may have other factors, such as GL and GI, to explain the lack of difference.

Probiotics

The gut microbiota has also been implicated in acne pathophysiology. Metabolites produced by gut microbiota have been shown to interact with mTOR signaling pathways, which in turn affect intestinal microbiota composition and have implications in acne pathogenesis [15]. The role of C. acnes in acne, the balance of microbiota in the skin is of interest in acne pathogenesis and therapy. Coadministration of a probiotic mix, including Lactobacillus casei, Lactobacillus bulgaricus and Streptococcus thermophilus, with fatty acids, increases blood levels of anti-inflammatory fatty acids [16].

Despite limitations in studies investigating diet and acne, there is evidence that glycaemic index, dairy content, dietary fats, and probiotics may play a role in acne and its treatment. In addition to the usual acne therapy that we may prescribe, we should provide patients with information on how their choice of diet could enhance their therapeutic outcomes and possibly reduce the risk of relapse upon treatment cessation. There is evidence supporting this approach.

References:

  1. Smith R, Mann N, Braue A, Mäkeläinen H, Varigos G. 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. 
  2. Burris J, Shikany J, Rietkerk W, Woolf K. A low glycemic index and glycemic load diet decreases insulin-like growth factor-1 among adults with moderate and severe acne: a short-duration, 2-week randomized controlled trial. J Acad Nutri Diet. 2018;118(10):1874–85.  
  3. Smith R, Braue A, Varigos G, Mann N. The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. J Dermatol Sci. 2008;50(1):41–52
  4. Wolkenstein P, Misery L, Amici J, Maghia R, Branchoux S, Cazeau C, et al. Smoking and dietary factors associated with moderate-to-severe acne in French adolescents and young adults: results of a survey using a representative sample. Dermatology. 2015;230(1):34–9.
  5. Park S, Kwon H, Min S, Yoon J, Suh D. Epidemiology and risk factors of childhood acne in Korea: a cross-sectional community based study. Clin Exp Dermatol. 2015;40(8):844–50.
  6. Penso L, Touvier M, Deschasaux M, de Edelenyi FS, Hercberg S, Ezzedine K, et al. Association between adult acne and dietary behaviors: findings from the NutriNet-Santé Prospective Cohort Study. JAMA Dermatol. 2020;2020:201602. https ://doi.org/10.1001/jamadermatol.2020.1602
  7. Spulber G, Spulber S, Hagenäs L, Åmark P, Dahlin M. Growth dependence on insulin-like growth-factor-I during the ketogenic diet. Epilepsia. 2009;50(2):297–303.
  8. Forsythe C, Phinney S, Fernandez M, Quann E, Wood R, Bibus D, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids. 2008;42:65–77.
  9. Fraser D, Thoen J, Bondhus S, Haugen M, Reseland J, Djøseland O, et al. Reduction in serum leptin and IGF-1 but preserved T-lymphocyte numbers and activation after a ketogenic diet in rheumatoid arthritis patients. Clin Exp Rheumatol. 2000;18:209–14.
  10. Adebamowo C, Spiegelman D, Berkey C, Danby F, Rockett H, Colditz G, et al. Milk consumption and acne in adolescent girls. Dermatol Online J. 2006;12(4):1.
  11. Hoyt G, Hickey M, Cordain L. Dissociation of the glycaemic and insulinaemic responses to whole and skimmed milk. Br J Nutr. 2005;93:175–7.
  12. Burris J, Rietkerk W, Woolf K. Relationshps of self-reported dietary factors and perceived acne severity in a cohort of New York young adults. J Acad Nutri Diet. 2014;114(3):384–92.
  13. Jung J, Kwon H, Hong J, Yoon J, Park M, Jang M, et al. Effect of dietary supplementation with omega-3 fatty acid and gammalinolenic acid on acne vulgaris: a randomised, double-blind, controlled trial. Acta Derm Venereol. 2014;94:521–5.
  14. Stewart T, Bazergy C. Hormonal and dietary factors in acne vulgaris versus controls. Dermatoendocrinol. 2018;10(1):e1442160.
  15. Salem I, Ramser A, Isham N, Ghannoum M. The gut microbiome as a major regulator of the gut-skin axis. Front Microbiol. 2018;9:1459.
  16. Puch F, Samson-Villeger S, Guyonnet D, Blachon J, Rawlings A, Lassel T. Consumption of functional fermented milk containing borage oil, green tea and vitamin E enhances skin barrier function. Exp Dermatol. 2008;17(8):668–74.