Almost everyone develops acne during their teenage years, and some people continue to suffer from it through early adulthood. For some, it is a debilitating condition, leading to lowered self-esteem and sometimes depression. It is characterised by the presence of blackheads and whiteheads, also known as comedones, increased production of sebum, and is sometimes accompanied by inflammation, redness, nodules and cysts.
What is happening in the skin
It is easier to understand acne when you can picture the structures involved, most particularly, what is know as the pilosebaceous unit, which is made up of the hair follicle and sebaceous gland. The sebaceous gland normally secretes sebum onto the hair and skin through ducts in the side of the hair follicle. See image below left.
The first stage in the development of acne is the formation of a ‘microcomedo’ - seen in the image above right. This forms when epithelial cells lining the hair follicle proliferate and develop abnormally, forming a plug made of keratin and dead cells. The plug prevents the flow of sebum from the follicle, causing the build-up of sebum, dead cells, and inflammatory cells. The resulting enlargement of the pilosebaeous unit is signalled by the formation of visible comedones. A closed comedo, (the singular for ‘comedones’), sometimes called a whitehead, is covered by a thin layer of epithelium. An open comedo, commonly known as a blackhead, looks dark because the keratin plug oxidises after it is exposed to air. Recent studies suggest that inflammation occurs before the keratin plug develops, and may even be the trigger for the formation of the plug.
From here, more severe inflammation may begin, and is signalled by the appearance of visible redness on the skin surface. The presence of bacteria, particularly Propionibacterium acnes, is sometimes but not always associated with the presence of inflammation. In severe cases, enlarged and inflamed follicles may rupture into the deeper layer of the skin, the dermis. These ruptured follicles cause chronic inflammation in the dermis and the formation of nodules and cysts which may cause fibrosis and visible scarring.
What factors trigger acne?
1) Changes in the sebaceous gland and production of sebum
The onset of acne is almost always associated with an increased level of androgens (such as testosterone) in the bloodstream, which coincides with puberty in males and females. High levels of androgens cause enlargement of the sebaceous glands and trigger increased production of sebum. In addition, the sebaceous glands possess the enzyme 5α-reductase, which converts testosterone to the more potent 5-α-dihydrotestosterone, which results in more sebum production and additional growth of the sebaceous glands. This means that the sebaceous glands themselves can be pro-active in scaling up their output of sebum.
It has been noted that the sebum of patients with acne differs from that of non acne sufferers in a number of ways:
Amount of sebum:
Acne sufferers produce up to 60% more sebum than unaffected individuals. One lipid component, squalene, is produced at around twice the amount found in controls - its significance is discussed below. (summarised in 1)
Amount of linoleic acid:
Linoleic acid is one of the essential fatty acids (read more about the role of essential fatty acids in skin in our blog here) that is critical for the proper formation of the skin’s barrier. Acne sufferers have a reduced level of linoleic acid in their skin, and it seems that a deficiency of linoleic acid in sebum can result in the abnormal formation of keratin. This abnormal keratinisation could contribute to the formation of the keratin plug that precedes comedo formation.
Because linoleic acid has a critical role in the skin’s barrier function, a reduction can make the pilosebaceous unit more permeable to inflammatory substances - so these is some evidence that a linoleic acid deficiency makes the pilosebaceous unit more prone to inflammation. (summarised in 2).
Finally, linoleic acid has an inhibitory effect on the enzyme 5-α-reductase (3), which converts testosterone to its more active form 5-α-dihydrotestosterone. Therefore a deficiency of linoleic acid in the pilosebaceous unit could result in increased androgen activity in the sebaceous gland, and therefore lead to increased sebum production. Interestingly, in one study (4), the application of linoleic acid to the skin of patients with mild acne over the period of a month was associated with a 25% reduction in the size of microcomedones.
This means that a linoleic acid deficiency in the skin can contribute to the development of acne via 3 different mechanisms.
Inflamed comedones have been shown to contain higher levels of lipid peroxidation products, which are formed by the oxidation of lipids. In particular, squalene, a polyunsaturated lipid that is abundant in sebum, is readily oxidised. Oxidised squalene has been shown to cause proliferation of epithelial cells and the release of pro-inflammatory molecules, both of which could initiate comedo formation, possibly through generation of free radicals. The skin naturally produces vitamin E, a potent antioxidant, in response to the presence of oxidised squalene, most likely as a protective measure. Sebum from acne sufferers has been shown to contain both higher levels of oxidised squalene and reduced levels of vitamin E when compared to sebum from unaffected individuals. (summarised in 2).
In recent studies, systemic levels of antioxidants, including vitamins A and E, as well as beta-carotene and vitamin C, were lower in acne patients than in healthy controls. It was not clear whether the lower circulating levels of antioxidants was a result of a higher demand for antioxidants in acne patients, or whether the lower levels of antioxidants predisposed them to acne in the first place. Topical and systemic antioxidants have been proposed as a means of treating acne, but to date there is no clear evidence of a role for this approach in treatment (summarised in 1).
2) The role of bacteria in acne
Although the bacterium Propionibacterium acnes was once thought to be the initiating cause of acne, it is now considered that P. acnes invades only after the early changes in the pilosebaceous unit have taken place. Once the process of inflammation and oxidative changes in the sebum have begun, it seems that the anaerobic conditions are in place for P. acnes to survive and proliferate within the comedo.
Once it has colonised the pilosebaceous unit, P. acnes stimulates the production of inflammatory molecules, including free radicals, further increasing the inflammatory response. Different strains of P. acnes are known to cause different types of inflammation and varying damage to the cells within the pilosebaceous unit. (summarised 1 and 5).
3) Can Diet influence acne?
A link between diet and acne has long been controversial, but the fact that acne is more prevalent in western cultures has led to the investigation of potential links between the two.
The strongest link between diet and acne is the high glycemic diet, which is common in the west. High glycemic diets include those containing high carbohydrate, starchy, sugary foods that cause high blood sugar and a corresponding increase in insulin levels. These diets have two important hormonal effects: they raise insulin levels, which may also stimulate sebaceous gland growth and sebum production; and they lower sex hormone binding globulin (SHBG) levels, which increases androgen concentrations, thereby increasing the activity of the sebaceous glands. (reviewed in 6).
In one study, acne sufferers were placed on either a high or a low glycemic diet for 12 weeks, and their acne symptoms were compared. Those on the low glycemic diet had significantly fewer acne symptoms than those on the high glycemic diet. They also showed a more normal sensitivity to insulin and reduced levels of androgens. Although only a preliminary study, it suggests that low glycemic diets could help control acne symptoms (7).
Another area that deserves consideration is the fact that western diets tend to have a higher omega-6/omega-3 fatty acid ratio, which is linked to a greater tendency for inflammation, and potentially the development of inflammatory acne. If so, an increased consumption of omega-3 fatty acids, for example those found in oily fish, could create a healthier fatty acid balance, and potentially reduce inflammation. A link between acne and the frequent consumption of dairy products has also been made, and this may be related to either the glycaemic effect of dairy products, or their hormonal content (summarised in 11).
4) The role of genetics in acne
Studies have shown that acne is a highly heritable disease, but to date no candidate genes have been identified. Possible candidates proposed to date include genes that relate to androgen and steroid metabolism (8).
Current treatments for acne
Substances that reduce the load of P. acnes include oral and topical antibiotics, some of which also have some anti-inflammatory properties. Benzoyl peroxide is also commonly prescribed for its antimicrobial activity and its possible action in helping break down comedones. There are antibiotic resistance problems with some commonly used antibiotics, and negative side effects are not uncommon. Benzoyl peroxide may cause contact dermatitis and has also been shown to reduce skin surface levels of vitamin E by 90% and vitamin C by up to 70% (summarised in 1). This reduction in vitamin E could potentially increase the rate of oxidation of lipids, which in itself is a factor that increases inflammation and could contribute to the progress of acne (see above).
Therapies aimed at reducing androgen levels and therefore sebum levels include oestrogen therapy and the combined contraceptives. Spironolactone is another anti-androgen therapy which may have significant side effects. (10)
Topical retinoids, which are related to vitamin A, have been shown to help normalise keratinisation within the pilosebaceous unit, thereby reducing comedo formation, and are anti-inflammatory. They cause thinning of the stratum corneum, the outermost layer of the skin, and may result in peeling, irritation and sun sensitivity.
Oral retinoids, in the form of isotretinoin (Roaccutane, Accutane), is the most clinically effective therapy to date for the treatment of severe acne, usually resulting in either long term remission or significant improvement. Isotretinoin is a synthetic drug related to vitamin A which has anti-inflammatory properties, reduces sebum production, reduces keratin formation in the pilosebaceous unit, thereby reducing the formation of comedones, and reduces the burden of P. acnes. Treatment with isotretinoin is not without risks and is recommended only when other treatments fail. It can cause severe foetal abnormalities and so the risk of pregnancy must be avoided. In adolescents, mood changes and depression are also risk factors, and other effects include increased skin sensitivity, dermatitis, headache, tiredness and many others (summarised in 9). Altered healing of skin wounds with excessive granulation tissue is also a consideration while on tretinoin (10).
A variety of treatments including injection of steroids into lesions, has been considered beneficial for large inflammatory lesions. Surgical peels with glycolic acid or salicylic acid have been beneficial for some patients. Phototherapy, which results in destruction of sebaceous glands, has been considered useful for some forms of acne.
Severe acne should be managed by a doctor or dermatologist to reduce the risk of scarring, and to manage any potential psychological effects of the condition.
When acne is less severe, and in light of recent advances in the understanding of acne, it is worth considering both dietary changes and the non-medical management of the skin.
There is now fairly strong evidence that low glycemic diets may reduce the severity of acne (see above), and they also offer other health benefits, including reducing the risk of developing insulin resistance and type-II diabetes. A shift towards this kind of diet is considered by to be safe for most people. Increasing the intake of omega-3 fatty acids for their possible anti-inflammatory benefits, and fresh fruit and vegetables for their high antioxidant levels would also seem a safe and beneficial dietary adjustment.
The Mokosh approach to care of acne-prone skin
In our view it is important to treat acne-prone skin gently, without the use of harsh abrasives or strong detergents, which can damage the skin’s barrier and exacerbate the severity of acne. (Read our blog here about our views on skin cleansing).
Our approach includes the use of ingredients that are free of synthetics, preservatives and emulsifiers, helping to preserve the skin’s biome and barrier function. Mokosh certified organic skin care products are rich in natural antioxidants, including pro-vitamin A and vitamin E, which may help prevent lipid peroxidation, which as we describe above, can initiate or worsen the inflammatory response, one of the earliest changes in acne. In addition they contain a range of known anti-inflammatory botanicals, which can help dampen the inflammatory response in the skin. They are enriched for linoleic acid, which has been found to be deficient in the sebum of acne-prone skin. As described above, topical application of linoleic acid has been shown to reduce the size of microcomedones and may help prevent formation of the keratin plug that precedes microcomedo formation. Finally our Facial Cleanser, Exfoliator and Mask helps keep the skin clear of superficial debris which can block the opening of the pilosebaceous unit, and helps remove excess sebum without the use of skin barrier-damaging detergents.
Key Mokosh products for gentle cleansing:
We offer two products for cleansing acne-prone skin. Neither of these is a detergent or an abrasive.
Makeup Remover & Cleansing Oil - This is made using a blend of pumpkin seed, jojoba, baobab and sesame oils. Massage of the face with this oil delivers pro-vitamin A, vitamin E, a range of other antioxidants and linoleic acid to the skin, whilst dissolving excess sebum and dirt. The oil is then removed using a cloth soaked in warm, not hot, water.
Facial Cleanser, Exfoliator & Mask - This product comes in the form of a powder, to which water is added immediately before use to make a smooth paste. This is massaged over the face very gently, without the application of pressure, resulting in the gentlest physical exfoliation, which removes superficial dirt, excess oil and cellular debris. The ingredients include anti-inflammatory and skin-supporting aloe vera; oatmeal which contains natural saponins, antioxidants and anti-inflammatory substances; neem leaf powder which has both antimicrobial and anti-inflammatory effects; meadowsweet and pomegranate powder, which deliver alpha- and beta-hydroxyacids in tiny amounts to aid exfoliation; as well as calendula and tulsi, both of which are anti-inflammatory and antibacterial. This powder should be rinsed away very thoroughly after massage to ensure no powder is left on the skin. A moisturiser should be applied after use.
Key Mokosh product for moisturising acne-prone skin:
For acne-prone skin our recommended moisturiser is Elderberry & Chia Seed Beauty Serum which acts as a stand-alone moisturiser. It is enriched for linoleic acid which, as described above, is deficient in acne-prone skin. Linoleic acid has been shown to reduce the size of microcomedones, and helps restore the skin barrier. It also contains good levels of gamma linolenic acid, an essential fatty acid which is extremely important for a healthy skin barrier (see our blog about the role of essential fatty acids in skin here) and, like linoleic acid, can reduce the activity of the enzyme 5-α-reductase (3). As we describe above, reduced activity of this enzyme inhibits the conversion of testosterone to its more active form in the sebaceous gland, thereby reducing sebum production. It contains good levels of the antioxidants pro-vitamin A and vitamin E, as well as a range of other antioxidants.
Many acne advisory sites advise against using oils on acne-prone skin, but in our experience this blend is both non-comedogenic and beneficial when used sparingly (only a few drops is needed to moisturise the whole face), and when applied in a very thin layer over the skin. This is best achieved by applying our Pure Hydrosol Toner first, which allows dilution of the oil into a thin layer. It sinks readily into the skin helping to form a barrier against the environment.
For many people acne is a chronic disease which needs to be managed carefully and sympathetically. As there is such a strong genetic link, some people suffer from severe acne independent of diet and lifestyle. When acne is chronic or severe, it is imperative to seek medical help to limit the risk of scarring. A healthy diet and lifestyle and a sensible approach to managing acne is a good start in controlling acne. We hope this article has improved your understanding of the condition and will help you make appropriate decisions for your skin when dealing with it. Over the years we have received a lot of feedback from our customers relating how our certified organic skin care products have helped them manage their acne. We'd love to hear your what your experience has been so we can share the information with our readers!
1. Bowe, W.P. and Logan, A.C. (2010) Clinical implications of lipid per oxidation in acne vulgaris: old wine in new bottles. Lipids in Health and Disease 2010; 9: 141
2. Ottaviani, M. ., Camera E. and Picardo, M. (2010) Lipid Mediators in Acne. Mediators of Inflammation 2010. Article ID 858176
3. Liang, T. and Liao, S. (1992) Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids. Biochem J. 285 ( Pt 2):557-62.
4. Letawe C. Boone, M. Pierard G.E. (1998) Digital image analysis of the effect of topically applied linoleic acid on acne microcomedones. Clin Exp Dermatol. 23(2):56-8.
5. Makrantonaki, E., Ganceviciene R. and Zouboulis, C. Dermatoendocrinol. (2011) An update on the role of the sebaceous gland in the pathogenesis of acne. Dermatoendocrinology 3: 41–49.
6. Pappas, A. (2009) The relationship of diet and acne. A review. Dermatoendocrinol. 1: 262–267.
7. Smith RN, Mann NJ, Braue A, Mäkeläinen H, Varigos GA (2007) 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. 57:247-56.
8. Bataille, V., Snieder, H., MacGregor A.J., Sasieni, P., Spector,T.D. (2002) The Influence of Genetics and Environmental Factors in the Pathogenesis of Acne: A Twin Study of Acne in Women.
9. Layton, A. (2009) The use of isotretinoin in acne. Dermatoendocrinol. 1: 162–169
11. Katta, R. et al. (2014) Diet and Dermatology: The role of Dietary Intervention in Skin Disease. J Clin Aesthet Dermatol. 7: 46–51