Acne: therapeutic interventions

Acne is a common condition that affects many people at some point in their life, particularly those in their teens and early 20s.  Although often perceived as a self-limited disease of adolescence, its prevalence remains high into adulthood. In the UK nearly 90% of teenagers have acne and half of them continue to experience symptoms as adults. By the age of 40, 1% of men and 5% of women still have lesions and currently acne is becoming more prevalent in children.

Although it may seem like a non-life threatening, superficial condition it can have a significant effect on self-esteem and contribute to mental health conditions such as depression and anxiety.

A key aspect of the pathogenesis is the increase in sex hormones at the onset of puberty but there can be many other underlying causes. Acne is an inflammatory skin condition characterised by excessive sebum production, follicular hyperkeratinisation of sebaceous ducts, and an increased release of inflammatory mediators. Additionally, research has shown that androgens and microbial colonisation with Propionibacterium acnes contribute to the pathogenesis of acne. These influences and potential therapeutic interventions will be discussed in this blog.

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Sebum production and hyperkeratinisation

Sebum is an oily secretion, produced by the sebaceous glands in the skin. It is used to lubricate, moisturise and prevent water loss from the skin surface. Excessive production of sebum is associated with acne as it provides a moist and nutritious environment for the growth of bacteria. If pores become blocked and sebum production continues both sebum and bacteria become trapped in the sebaceous gland which allow bacteria to replicate, this then creates inflammation. Sebum production is affected by sex hormones, particularly testosterone and oestrogen, as well as insulin. The increase in testosterone in males and oestrogen in females at puberty stimulates an increased production of sebum which can lead to the onset of acne.

The over production of keratinocytes in the skin is also associated with the onset of acne. Keratinocytes are cells which are found in the epidermis of the skin, they produce a keratin protected layer of cells with a waterproof protective layer. These cells are continuously being replaced and therefore keratinocytes are constantly replicating. Hyperkeratinisation occurs when the cells of the follicle become cohesive and do not shed normally onto the skin’s surface. This can lead to blockages of the sebaceous gland pores as mentioned above and the formation of comedones – the primary sign of acne, consisting of a dilated hair follicle filled with keratin squamae (skin debris), bacteria, and sebum^1,2.

Poor blood sugar regulation can lead to an increase in both insulin and insulin-like growth factors including IGF-1. High levels of these, particularly IGF-1, are associated with increased sebum production and also hyperkeratinisation and in addition stimulate sex hormone production. Therefore, stabilising blood sugar levels and improving insulin sensitivity are essential for addressing acne progression. In one study of forty-three males, aged 15–25 with moderate acne, fed a low-glycaemic load diet for 12 weeks, the number of acne lesions, sex hormone levels, and insulin markers were compared at baseline and after intervention. Normalisation of the insulin response and sex hormone levels were associated with a reduction in acne lesions.  The patients both lost weight and showed improvement of acne compared to a conventional Western, high-glycaemic load, diet^2,3.

Bacteria

Research has shown that acne is associated with the overgrowth of the specific bacteria strain Propionibacterium acnes. This bacteria is found naturally on the skin and can become opportunistic and overgrow when conditions are out of balance. It grows well in anaerobic conditions as occur when sebaceous pores become blocked and provide the perfect environment for P. acnes to replicate. Recent studies have suggested that P. acnes is also associated with chronic inflammatory conditions including aortic valve endocardiosis, sarcoidosis and sciatica. Avoiding hyperkeratinisation and excess sebum is a priority for preventing the overgrowth of P. acnes. It is also essential to recognise that the skin has its own specific microbiome and disturbances to the homeostasis of this microbiome may contribute to opportunistic overgrowth and a possible detrimental effect to skin health generally.  It is also important to consider that the skin microbiome is strongly associated with the gut microbiome. Therefore supporting the microbiome of the gut may have a positive impact on  the skin^4,5.

One study identified that changes in the gut microbiota were associated with acne. When comparing 31 moderate to severe acne vulgaris patients and 31 healthy controls, acne patients had lower levels of Actinobacteria and higher levels of Proteobacteria than healthy controls. At the genus level, Bifidobacterium, Butyricicoccus, Coprobacillus, Lactobacillus and Allobaculum were all decreased in acne patients. Another study showed that Bifidobacteria and Lactobacilli (lactic acid-producing bacteria normally found in the gut) may assist with  inflammatory skin diseases, such as acne^2,6.

Inflammation

As with so many conditions, inflammation is a major factor in acne and modulating the inflammatory response is crucial when providing therapeutic support. It is now thought that keratinocytes within the skin are involved in controlling a local inflammatory response as well as generating a variety of hormones and neurotransmitters that affect whole-body states and even emotions. For example skin dryness and barrier disruption have been shown to stimulate cutaneous cortisol production, and this may be mediated by activation of inflammatory cytokines such as IL-1β with systemic implications². These have also been shown to interact with the local skin microbiome and influence adhesion, growth and virulence. Studies have shown that psychological stress can induce the local release of substance P, a peptide produced by nerve endings in the skin and a mediator of pro-inflammatory mechanisms. Substance P can cause changes in skin microbiota and increased levels are linked to eczema, acne and barrier dysfunction⁷.

Recent research has demonstrated that acne pathogenesis may be similar to that of atherosclerosis. Foam cells, a hallmark of atherosclerosis, are lipid-loaded macrophages and neutrophils that are generated from uptake of oxidised lipid. Foam cells have also been found in acne lesions. Therefore the same pathological processes which occur in atherosclerosis, including inflammation and oxidative stress, may be occurring in acne⁸.

Nutritional interventions

The aims of nutritional therapy support include:

• Supporting the health of the skin directly e.g. normal keratinocyte replication by providing nutrients which support skin health
• Blood sugar regulation and improved insulin resistance to help control sebum production
• Reducing and supporting a normal inflammatory response
• Supporting digestive health and a healthy microbiome

Skin supporting nutrients include

Regulating blood sugar Levels:

• Avoid sugar and refined carbohydrates
• Consume protein and healthy fats with each meal
• Opt for lower sugar fruits and vegetables, avoid bananas, grapes and mangoes in particular
• Aim for at least 12 hours overnight fast and avoid eating 3 hours before bed (fasting reduces insulin levels and helps to stabilise blood sugars)
• Consider supplementing magnesium, chromium, zinc and cinnamon
• Resistant starch, insoluble fibre, and fructooligosaccharides have been correlated with greater insulin sensitivity and reduced inflammation

Supporting a healthy microbiome:

• Consume fermented foods such as kefir, kombucha, sauerkraut and miso
• Include prebiotic foods (fuel for gut bacteria) and polyphenols from chicory, olives, baked apples and Jerusalem artichoke
• Consider a live bacteria supplement. Supplementation with both Lactobacillus acidophilus and Lactobacillus bulgaricus to 300 patients for 16 days showed clinical improvement in 80% of acne patients
• A prebiotic supplement containing inulin, β-glucan and blueberry polyphenols led to significantly improved glucose tolerance in adult humans

Reducing inflammation:

• Optimise gut health (orally-consumed pre- and probiotics have been shown to reduce systemic markers of inflammation and oxidative stress)³
• Reduce omega-6 fatty acids from meat, dairy and vegetable oils
• Increase omega-3 fatty acids from oily fish, chia and flax seeds and dark leafy green vegetables
• Use anti-inflammatory foods such as turmeric (curcumin) and ginger. Curcumin has shown promising results as an antimicrobial, anti-inflammatory and antidiabetic, all properties that may improve acne vulgaris.
• Increase vitamin E containing foods such as avocado

If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Helen) by phone or email at any time.

helen@cytoplan.co.uk, 01684 310099

Helen Drake and the Cytoplan Editorial Team

Relevant Cytoplan products

Acidophilus Plus – 9 strain live bacteria supplement. Alternative products Fos-A-Dophilus or Cytobiotic Active

Hair, Skin and Nails – contains vitamin C, pantothenic acid (B5), selenium, zinc, MSM and Pine Bark Extract

Krill Oil – Omega 3 supplement, naturally contains vitamin A (100IU) and asthaxanthin. Alternative products vegan omega 3, High Strength Fish Oil and Lem-0-3

Evening Primrose Oil – a natural source of gamma linolenic acid (GLA)

Tocopherols and Tocotrienol complex– full spectrum vitamin E supplement with 4 tocopherols and 4 tocotrienols

Vitamin A (Retinol Palmitate) – 5000IU of vitamin A.

Wholefood Zinc – 7.5mg zinc

Food State Selenium – 100ug selenium

Cell Active DIM – contains diiondlylmethane, calcium d-glucarate and phosphatidyl choline

Organic Turmeric Plus – contains Turmeric (providing curcumin), cat’s claw and gotu kola.

Cell-Active Curcumin Plus – contains liposomal curcumin and ginger

Blood Glucose Support – contains cinnamon, magnesium, chromium, zinc, manganese, copper, selenium and molybdenum

References

1. Murray JPM. Textbook of Natural Medicine. 4th Ed.; 2013.
2. Clark AK, Haas KN, Sivamani RK. Edible Plants and Their Influence on the Gut Microbiome and Acne. Int J Mol Sci. 2017;18(5). doi:10.3390/ijms18051070
3. Kumari R, Thappa D. Role of insulin resistance and diet in acne. Indian J Dermatology, Venereol Leprol. 2013;79(3):291. doi:10.4103/0378-6323.110753
4. Yan H-M, Zhao H-J, Guo D-Y, Zhu P-Q, Zhang C-L, Jiang W. Gut microbiota alterations in moderate to severe acne vulgaris patients. J Dermatol. August 2018. doi:10.1111/1346-8138.14586
5. Prescott SL, Larcombe D-L, Logan AC, et al. The skin microbiome: impact of modern environments on skin ecology, barrier integrity, and systemic immune programming. World Allergy Organ J. 2017;10(1):29. doi:10.1186/s40413-017-0160-5
6. Salem I, Ramser A, Isham N, Ghannoum MA. The Gut Microbiome as a Major Regulator of the Gut-Skin Axis. Front Microbiol. 2018;9:1459. doi:10.3389/fmicb.2018.01459
7. Harvey A, Huynh TT. Inflammation and acne: putting the pieces together. J Drugs Dermatol. 2014;13(4):459-463. http://www.ncbi.nlm.nih.gov/pubmed/24719066. Accessed March 28, 2018.
8. Jiang H, Li C. Common Pathogenesis of Acne Vulgaris and Atherosclerosis. Inflammation. August 2018. doi:10.1007/s10753-018-0863-y

Last updated on 20th November 2020 by cytoffice