How to effectively manage acne

Acne is no longer a skin condition reserved for the young. Acne effects teenagers, adults, men and women of all generations and ethnicities. The British Journal of Dermatology estimates 85% of people between the ages of 12-24 are currently experiencing at least minor acne[1].

Symptoms range from whiteheads to blackheads, from pustules to papules, from an oily skin type to an often dry underlying skin tone.

An industry which in the past focused on ‘the spotty teenager’ is now being forced to re-assess. Acne has reached epidemic rates with a tellingly high prevalence in Western countries, posing the question – just which lifestyle factors are responsible for its rise?

What is acne?

Acne is a skin disease characterised by the clogging of a person’s pores by a mixture of sebum and dead skin cells. Clogged pores or hair follicles trigger an immune reaction causing consequential inflammation. It is this inflammatory immune reaction which is responsible for the visual signs of acne.

Acne has traditionally been a skin condition associated with puberty. During this time it effects men more so than women with rising androgen and testosterone levels triggering an increased production of sebum. Acne most commonly effects the lower third of a person’s face, however other androgen effected areas such as a person’s chest and back are also frequently effected.

In the western world, the association of acne to puberty is being diluted by a rising rate of adult acne.  The referral of patients aged 25 and over is steadily increasing[2] and 90% of acne presentations in women aged 25 and over share the familial symptoms of adolescent acne[3].

The cause of acne

Understanding the causes of acne help patients and doctors alike to treat each presentation of the condition effectively. Acne can rear differently for every patient. Some forms affect only the jawline, others spread to the chest and back. Some experience only open comedones, others have a combination of both open and closed. Some presentations sync with monthly hormone fluctuations and others remain consistent regardless of time.

For acne lesions to form, 3 factors need to combine;

  1. Increased sebum production
  2. Dead skin/ hyperkeratinisation
  3. An increase in Propionibacterium acnes bacteria

Oily, combination skin types are prone to acne outbreaks because of the above acne triangle. Sebum is an important cofactor. All skin types create a protective layer of sebum – a natural oil, however, oily skin types make more than most. This often visible layer provides a sticking point for dead skin cells.

Skin is in a constant state of flux with a healthy person’s skin turning over, almost fully every 30 days[4]. Top layers of skin visible to the naked eye are technically dead, enabling them to pack tightly together forming a defensive barrier against hydration loss and bacterial invasion. Oily skin types find shedding these layers of skin troublesome, with debris often becoming entrapped in sticky sebum plugs. This process is described as hyperkeratinisation – a condition where the inner cell lining of hair follicles fails to desquamate (exfoliate) effectively[5].

Plugs of sebum and dead skin cells pose an attractive feeding ground for bacteria. Healthy skin has a microflora of bacteria present at regulated concentrations. In the condition of acne, a naturally present bacteria – Propionibacterium acnes, overgrows as a consequence of hyperkeratinisation and increased sebum production.

As Propionibacterium acnes (p.acnes) populations increase, they consume ‘sebum: skin’ plugs and in doing so excrete an irritating protein nicknamed CAMP[6]. It’s the excretion of CAMP proteins that provoke inflammation causing visible acne cysts, papules, and pustules.

Effective treatments for acne

Acne although not health impairing often has significantly negative effects psychologically. Effective management of the condition can bring great relief for sufferers. Although scientists have not yet evolved a cure for the condition, there are several changes a person can make to their diet and skincare regimen that show positive effects.

A collection of the most effective are detailed below, as all presentations of acne are unique, some may be more effective than others. Trialling each will help evolve a treatment and maintenance plan that works individualistically.

  1. Diet – trial elimination of dairy

Diary is one example of a food now widely available in the west and not as commonly consumed in the east. Dairy can be described as an insulinotropic food meaning it contains several ingredients that stimulate the release of insulin and associated hormones e.g. insulin-like-growth factor-1 (IGF-1).

Milk is designed to be nutrient dense for supplying young humans and, or mammals with a calorie intensive food that enables growth. The introduction of milk and dairy into western diets post-infancy is a relatively new dietary concept.

The insulin cascade created by foods like dairy initiate a pathway of biological reactions associated with androgen receptor activation, comedogenesis, increased sebum production and follicular inflammation[7] – all factors commonly noted in the pathogenesis of acne.

  1. Diet – eliminate high glycaemic index (GI) foods

The GI of a food measures the effect consuming it will have on a person’s blood sugar and therefore release of hormones such as insulin. High GI diets have been positively linked to the pathogenesis of acne[8], with studies showing a well-designed, low GI diet positively reduces the risk of acne[9][10].

The GI scale rises from 0-100, with 100 having the same blood-sugar effect as consuming pure glucose. Foods with a low GI rate from 0-55, foods with a medium GI from 56-69 and foods with a high GI from 70-100.

Examples of high GI foods include;

  • Baked russet potato (111[11])

  • Boiled white potato (82)

  • Pizza, plain baked dough, served with parmesan cheese and tomato sauce (80)

  • Pretzels (83)

  • Rice cakes (82)

  • White rice, boiled, type non-specified (72)

  • Cornflakes (81)

  • Baguette, white, plain (95)

The westernised diet is laden with high GI foods, both naturally available (russet potatoes) and highly processed (pretzels and rice cakes), studies show just a 3 month conversion to a low GI diet has a beneficial effect on acne severity and incidence.

  1. Exfoliate regularly to prevent hyperkeratinisation

The formation of acne lesions depends on the collision of 3 factors – increased sebum production, hyperkeratinisation and the prevalence of p.acnes bacteria. Tackling any one of these 3 factors helps to alleviate the symptoms of acne.

Hyperkeratinisation is the inability of hair follicle skin cells to exfoliate readily. This change in squamation encourages the collection of sebum which in turn encourages the congregation and proliferation of p.acnes.

Exfoliating regularly increases a person’s skin cell turnover rate, reducing the severity of hyperkeratinisation. There are 2 ways this can be achieved, by either;

  1. Physical exfoliation e.g. muslin cloth, facial scrub or brush.
  2. Chemical exfoliation e.g. salicylic acid.

Physical exfoliation works most effectively on the very outer layer of skin whereas chemical exfoliation is able to dissolve into hair follicle sebum plugs, where over time, skin cell adhesion is weakened.

Chemical exfoliants such as salicylic acid are known keratolytic agents – ingredients which soften keratin, the predominant protein available within the skin. In addition to being keratolytic, salicylic acid also lends antibacterial properties useful in the fight against acne.

  1. Use linoleic high oils or linoleic high moisturisers

A noted and proposed contributor to the development of acne is a changed sebum biology. The sebum of acne prone individuals has been noted as fatty acid deficient. Sebum is a complex mixture of ingredients including squalene, wax esters, cholesterol esters, free cholesterol, and triglycerides. Sebum composition rather than sebum amount is proposed as a primary driver in the formation of acne[12].

Essential fatty acids such as linoleic acid show promise for protecting against the development of comedonal acne[13] with other studies showing its topical application can help to reduce the size and severity of microcomedones[14].

Linoleic acid is an essential fatty acid the body is unable to self-synthesise. Dermatological studies show this omega fatty acid plays a vital role in signalling the normal desquamation of skin and therefore helping to re-adjust hyperkeratinisation.

Linoleic acid is the predominant ingredient in natural oils such as rosehip, grapeseed and evening primrose oil.

  1. Daily use of antioxidant-rich skincare and sun protection

In addition to the essential fatty acid deficiency detected in the sebum of acne patients, an increased oxidant: antioxidant ratio has been noted. The oxidation of sebum transforms native species into new non-native, non-skin identical species[15].

Lipid peroxide markers have been shown significantly higher in the contents of acne lesions than those found naturally present in non-acne affected areas of skin. It is proposed that the by-products of sebum oxidation are cytotoxic or irritant, resulting in hyperkeratosis and comedone formation.

Topically applied antioxidants such as vitamin E can help resist the oxidation of native sebum species.

UV light is a common trigger of oxidation, specifically, studies have shown the oxidation of squalene to cause irritation. Additional studies show a mixture of squalene oxidation by-products with oxidised triglyceride oils (free-fatty acids) pose comedogenic potential to skin[16].

To protect skin daily against sebum oxidation, a suitable SPF should be applied at regular intervals.


Sources and References

[1] Bhate K, Williams HC. Epidemiology of acne vulgaris. The British journal of dermatology 2013;168:474-85

[2] Seirafi, H., Farnaghi, F., Vasheghani-Farahani, A., Alirezaie, N.-S., Esfahanian, F., Firooz, A. and Ghodsi, S. Z. (2007), Assessment of androgens in women with adult-onset acne. International Journal of Dermatology, 46: 1188–1191. doi:10.1111/j.1365-4632.2007.03411.x

[3] Dréno, B., Thiboutot, D., Layton, A.M., Berson, D., Perez, M., Kang, S. and the Global Alliance to Improve Outcomes in Acne (2015), Large-scale international study enhances understanding of an emerging acne population: adult females. J Eur Acad Dermatol Venereol, 29: 1096–1106. doi:10.1111/jdv.12757

[4] Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Epidermis and Its Renewal by Stem Cells. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26865/

[5] Hyperkeratinization, corneocyte cohesion, and alpha hydroxy acids. E. J. Van Scott, R. J. Yu J Am Acad Dermatol. 1984 Nov; 11(5 Pt 1): 867–879.

[6] Liu P-F, Nakatsuji T, Zhu W, Gallo RL, Huang C-M. Passive Immunoprotection Targeting a Secreted CAMP Factor of Propionibacterium acnes as a Novel Immunotherapeutic for Acne Vulgaris. Vaccine. 2011;29(17):3230-3238. doi:10.1016/j.vaccine.2011.02.036.

[7] Nestlé Nutrition Institute Workshop Series, Vol. 67

Milk and Milk Products in Human Nutrition 67th Nestlé Nutrition Institute Workshop, Pediatric Program, Marrakech, March 2010 ISBN: 978-3-8055-9586-5 e-ISBN: 978-3-8055-9587-2 DOI:10.1159/isbn.978-3-8055-9587-2

[8] Spencer, E. H., Ferdowsian, H. R. and Barnard, N. D. (2009), Diet and acne: a review of the evidence. International Journal of Dermatology, 48: 339–347. doi:10.1111/j.1365-4632.2009.04002.x

[9] The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. Robyn N. Smith, Anna Braue, George A. Varigos, Neil J. Mann J Dermatol Sci. 2008 Apr; 50(1): 41–52. Published online 2008 Jan 4. doi: 10.1016/j.jdermsci.2007.11.005

[10] A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial.

Robyn N. Smith, Neil J. Mann, Anna Braue, Henna Mäkeläinen, George A. Varigos Am J Clin Nutr. 2007 Jul; 86(1): 107–115.

[11] Atkinson FS, Foster-Powell K, Brand-Miller JC. International Tables of Glycemic Index and Glycemic Load Values: 2008 . Diabetes Care. 2008;31(12):2281-2283. doi:10.2337/dc08-1239.

[12] Zouboulis, C.C., Jourdan, E. and Picardo, M. (2014), Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. J Eur Acad Dermatol Venereol, 28: 527–532. doi:10.1111/jdv.12298

[13] The fatty acids of wax esters and sterol esters from vernix caseosa and from human skin surface lipid.

  1. Nicolaides, H. C. Fu, M. N. Ansari, G. R. Rice

Lipids. 1972 Aug; 7(8): 506–517.

[14] LETAWE, BOONE and PIÉRARD (1998), Digital image analysis of the effect of topically applied linoleic acid on acne microcomedones. Clinical and Experimental Dermatology, 23: 56–58. doi:10.1046/j.1365-2230.1998.00315.x

[15] Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. C. C. Zouboulis, E. Jourdan, M. Picardo J Eur Acad Dermatol Venereol. 2014 May; 28(5): 527–532. Published online 2013 Oct 18. doi: 10.1111/jdv.12298

[16] Pappas A, Johnsen S, Liu J-C, Eisinger M. Sebum analysis of individuals with and without acne. Dermato-endocrinology. 2009;1(3):157-161.