Acne, dietary and lifestyle influences. How do we treat it?
When the skin is functioning properly, it protects, regulates temperature, retains water, among other things. It is constantly in a state of renewal being completely renewed every 27 days. Epidermal cells originate from stem cells that are in the basal layer of the epidermis. They undergo changes as they migrate to the skin surface. They become 3 different types of cells before eventually becoming corneocytes that make up the outermost layer of the epidermis and stratum corneum (7).
Acne vulgaris is a extremely common skin condition that majority of the population come into contact with at some point in their lives. It is generally worst seen in parts of the body that contain the densest population of sebaceous glands which is the upper chest, back and face. Acne pathogenesis is characterized by increased colonization of P. acne anaerobic bacteria, increased sebum production, inflammation and hyper-keratinization.
Skin anatomy.
There are a number of probable factors involved in the pathogenesis of acne including:
Genetics
Bacteria - Propionibacterium acnes (abovementioned)
IGF-1 (insulin like growth factor-1)
Androgens (hormonal)
Cortisol (stimulated by stress)
Stress (Skin-brain axis)
Barrier dysfunction (Psoriasis, Atopic Dermatitis)
Toxic over burden (compromised detoxification processes)
Diet – high refined carbohydrates (predominant and typical western diet), dairy consumption, low fruits & vegetables, dehydration
Inflammation
HOW AND WHATS INVOLVED:
Well, I’m glad you asked,
The sebaceous glands in our skin are the oil producing glands, and are situated alongside hair follicles and lies in the dermis (lower layer) of the skin and extends to the surface epidermal layer (Tortora & Derrikson) .
Sebaceous glands are absent in the palms and soles of our feet, generally small in most areas of the trunk and limbs and usually larger in the skin of the breasts, face, neck and back.
Sebum (oil) is secreted by these cells and production begins to increase from the age of 9.
Hormones & The Brain-Skin axis (stress)
These sebaceous glands are stimulated by sex hormones (androgens ie. Testosterone) from the testes, ovaries and adrenal glands to increase production of sebum. Major players involved affecting hormonal acne are:
Dihydrotestosterone (the more potent form of testosterone).
Dihydrotestosterone is 5-10 x more potent then testosterone.
Dihydrotestosterone is synthesised from testosterone in the presence of 5α-reductase. Zinc is a primary inhibitor of 5α-reductase (1).
Oestrogen is known to inhibit excessive sebum production possibly by the mechanism androgen binding to its binding protein. When androgen levels are higher, this can present an imbalance in the androgen: oestrogen ratio.
Prolactin is the hormone involved in stimulating lactation. It is almost immediately induced by psychological stress. Prolactin stimulates keratinocytes to proliferate and regulates keratin expression. It also stimulates sebum production. This displays a mechanism of the skin-brain axis (2).
corticotropin-releasing hormone (CRH), glucocorticoids (Adrenocorticotropin ACTH – stimulates the adrenal glands to make cortisol) , and catecholamines (adrenaline) are released when we are under mental, physical and emotional stress. Our skin has a fully functioning HPA (hypothalamic pituitary adrenal) system that is responsive to CRH & ACTH and stimulates a cascade of physiological affects in moments of perceived stress (2).
CRH and its receptors have been detected on sebocytes (sebum producing cells) and stimulates lipogenesis through upregulation of key enzymes. Furthermore, it induces the production of proinflammatory cytokines IL-6 and IL-11) in keratinocytes (2).
CRH inhibits the secretion of gonadotropic releasing hormone, that can in turn reduce the production of oestrogen from the ovaries and contribute to the androgen:oestrogen imbalance.
The excess sebum then feeds the P. Acnes bacteria and exacerbates the inflammatory response.
Stress can also interfere with the wound healing process and the skins barrier function reducing the protective barrier essential for maintenance of hydration and protection against microbial infection.
Stress (epinephrine, norepinephrine and cortisol) were found to increase DNA damage, and interfere with repair contributing to premature aging of the skin.
Stress and the neuropeptide substance P has also been linked to acne, and interestingly can increase the virulence of some skin microflora (bacteria) (2).
The gut-skin axis
The gut microflora can influence the skin via cross talk through a pathway known as the mTOR pathway (just another confusing name for a pathway). Metabolites produced by our microbiota have been shown to regulate cell proliferation, lipid metabolism and other metabolic functions. This relationship between the gut and skin is bidirectional and can in turn, affect the diversity of the intestinal microbiome through the regulation of the intestinal barrier.
When we see intestinal dysbiosis (bacteria imbalance) and disrupted intestinal lining integrity this can cause a feedback cycle of metabolic inflammation leading to the exacerbation and development of acne (7).
The complex bidirectional relationship between the GI track and skin may also be directly correlated with psychological comorbidities depression and anxiety, as the stress response can cause GI distress (abovementioned). Stress has been postulated to cause the intestinal flora to produce different neurotransmitters (serotonin, norepinephrine and acetylcholine or influence the endocrine cells to release neuropeptides. These neurotransmitters can increase intestinal permeability increasing inflammation locally and systemically (7).
Interestingly substance P (SP) has been mutually noted in both acne vulgaris and intestinal dysbiosis. Substance P can trigger pro-inflammatory mediators implicated in the pathogensis of acne (7).
Detoxification
The skin has also been found to possess detoxification enzymes for phase I and phase II detoxification in the liver. This can imply that the skin has an important role in detoxification and that compromised liver detoxification may exhibit further burden on the skin aggravating dermal conditions such as acne (3).
Diet & Acne:
A high glycemic load and glycemic index diet.
High glycaemic load and index diets (generally speaking, a westernised diet consisting of high amounts of processed foods, sweetened beverages, refined and simple carbohydrates and alcohol and low in fruits and vegetables) consistently raise our blood sugar levels, that in turn raise our insulin levels. Excessive repeated exposure to insulin can desensitises our cells causing hyperinsulinemia (4).
Elevated insulin levels stimulate the secretion of circulating androgens that increase the production of sebum (4).
Elevated insulin levels also increase the production of Insulin like Growth Factor-1 IGF-1), and decrease its corresponding binding protein, increasing the level of circulating IFG-1 creating an imbalance. IGF-1 increases proliferation of keratinocytes that build up and block pores increasing acne risk factors (4).
IGF-1 also can influence increasing comedogenic (acne) factors such as androgens and glucocorticoids that can fuel the vicious cycle (4).
IGF-1 can influence development of acne by increasing proliferation of the skins epidermis in the hair follicle, hyperkeratinisation, and stimulate androgen fuelled sebum production(4).
Finally, research suggests that increased serum levels of IGF-1 has been correlated with acne patients is comparison to healthy patients with no acne (5).
(6).
The gut-skin axis
The gut microflora can influence the skin via cross talk through a pathway known as the mTOR pathway (just another confusing name for a pathway). Metabolites produced by our microbiota have been shown to regulate cell proliferation, lipid metabolism and other metabolic functions. This relationship between the gut and skin is bidirectional and can in turn, affect the diversity of the intestinal microbiome through the regulation of the intestinal barrier.
When we see intestinal dysbiosis (bacteria imbalance) and disrupted intestinal lining integrity this can cause a feedback cycle of metabolic inflammation leading to the exacerbation and development of acne (7).
The complex bidirectional relationship between the GI track and skin may also be directly correlated with psychological comorbidities depression and anxiety, as the stress response can cause GI distress (abovementioned). Stress has been postulated to cause the intestinal flora to produce different neurotransmitters (serotonin, norepinephrine and acetylcholine or influence the endocrine cells to release neuropeptides. These neurotransmitters can increase intestinal permeability increasing inflammation locally and systemically (7).
Interestingly substance P (SP) has been mutually noted in both acne vulgaris and intestinal dysbiosis. Substance P can trigger pro-inflammatory mediators implicated in the pathogenesis of acne (7).
Dairy consumption & acne:
Dairy, in particular milk, has been a controversial topic within the condition of acne vulgaris.
The consumption of milk gave rise to an insulin response that far exceeds the GI rating. It is presumed that a fraction of a milk protein is involved in stimulating the insulin response.
The consumption of milk has been associated with increasing circulating (possibly via the increasing insulin stimulus) IGF-1 levels by 10-20% in adults. This has been proposed because 1, milk contains active levels of hormones and IGF-1 itself. Whether or not the molecule survives digestion and enters the plasma is at this stage not definitive.
The general composition of milk proteins is 80% casein and 20% whey protein. In one trial, a group of 57 people received either casein or whey proteins in amounts similar to found in milk. The casein group, serum IGF-1 increased by 15% however no changes in insulin were observed. In the whey group, fasting insulin increased by 21% however no changes in IGF-1 were noted. The subjects however in this study did consume amounts equivalent to what is found in 1.5L of cows milk, which is quite a high amount that most people would not consume in a day.
Therefore typical western diets consisting of the consumption of dairy, may have an agonising effect on serum insulin + IGF-1 levels therefore contributing to the development and progression of acne.
As the answers are not definitive, if acne is a problem for you and you have not yet tried to eliminate dairy, I would suggest removing it from your diet for a trial period.
So, What the heck do we do???
MY TIPS FOR YOU:
EAT MORE fruits, vegetables, grains, nuts, seeds and occasionally lean meats. I know it sounds simple, but it really is that simple. Mother nature will always surpass supplements and consuming wholefoods will ensure our microbiome diversity is, well, diverse and well fed. You don’t want to experience a hungry microbiome, it will cause you all kinds of grief. Aim for 30-40 different plants every single week!! Fruits and vegetables contain an abundance of vitamins, minerals, antioxidants and phytochemicals all of which play a functional role in our cellular health.
A low GI/GL diet that is high in fibre: diets that contain 30g of fibre per day showed significant improvements in skin condition. A low glycaemic load diet also showed an improvement in skin composition, this was thought to be attributed to the dietary fiber, which in-turn will also support the microbiome, thus the gut -skin axis (4).
Omega 3 fatty acids (consume oily fish) the ratio of omega 6: omega 3 in a western diet is roughly 30:1, and is either a agonist or antagonist inflammatory mediator. High intakes of omega 3 (in particular EPA) from marine sources can inhibit the production of proinflammatory cytokines and can therefore reduce inflammation associated with acne. One cytokine in particular (leukotriene – LTB4) is a regulator of sebum production and EPA and γ-linolenic acid (GLA) found in plant sources (borage oil) inhibits the conversion of arachidonic acid > LTB4 (4).
Found in: oily fish, salmon, mackerel, sardines, flaxseeds, walnuts.
Zinc: Zinc is an essential mineral involved in the formation of collagen, wound healing and has been shown to be bacteriostatic (antibacterial) against Propionibacterium acnes and reduce inflammatory mediators. Zinc possesses antioxidant properties and is also an inhibitor of the 5 a-reductase enzyme that converts testosterone to dihydrotestosterone, a driver of acne (9). Zinc deficiency has also been notable in acne patients.
Found in: oysters, seafood, red meats, liver (chicken, lamb, beef), nuts (brazil, almond, cashew, chestnuts, peanuts, pecan, pine nuts, walnuts), seeds (pepitas, sesame seeds, sunflower seeds) nutritional yeast, cheese especially blue vein, broad and butter beans.
Vitamin A (retinol): is involved in cellular differentiation of epidermal cells, increasing thickness in skin structure and also increases the production of glycosaminoglycans that are responsible for retaining water and increasing collagen that begins to decline from the age of roughly 28. In one study, Vitamin A & Vitamin E concentrations were significantly lower then the control groups. Topical and oral vitamin A can improve and modify acne severity (10). Vitamin A has an inhibitory effect on the sebaceous glands which leads to a decrease in P. acnes (10).
Found in: liver (beef, lamb, chicken), egg yolk, butter, (provitamin A – beta carotene) carrots, tomatoes rockmelon, apricots, mangoes pumpkin, peaches, spinach, sweat potato.
Vitamin E: is a natural lipid soluble antioxidant that is involved in fighting lipid peroxidation. Vitamin E is a major protector of cell membranes as these are comprised of phospholipids. Vitamin E protects the cell membranes from oxidative damage, lipid peroxidation and also plays a roll in enhancing immune function.
Found in: wheat germ, sesame seeds, safflower oil, olive oil, almonds, egg yolk, sunflower seeds, olives.
Vitamin C: Vitamin C is involved in the hydroxylation of proline & glycine which is an required step in the formation of collagen reducing fine lines and firming skin. conditions such as stress, smoking, viral illness, fever and antibiotic use can lead to diminished vitamin C level.
Found in: Kiwi fruit, blackcurrants, red chilli peppers, broccoli, watercress, strawberries, papaya, rockmelon, citrus fruits, green peppers, cauliflower, parsley, cabbage, banana, guava, snow peas.
REDUCE/MANAGE YOUR STRESS: in this day and age, it is so hard to disconnect, however reducing stress and practicing mindfulness is imperative to support hormonal harmony, avoid GIT distress and support our mental health that ultimately can effect our skin. There are many fabulous meditation apps such as; insight timer and headspace have some great guided meditations.
Avoid processed foods: high GI and high GL foods has been linked to acne in some people, focusing on a wholefoods will increase your intakes of necessary fibre, vitamins and minerals and plant chemicals to reduce inflammation, support a healthy digestive tract, balance hormones and blood sugar levels and support a healthy immune function.
Avoid dairy: the jury is still out on this one, however if you are an acne sufferer, its worth a try removing it from your diet for a period of time and observe any changes.
Drink more water: water is so important, yet often can be missed. Drinking enough water can be a challenge for a lot of people therefore making a conscious effort to consume 2-3L of water per day is advise to avoid dehydration, support detoxification, biochemical reactions and maintain fluid balance in and out of cells.
Supplements:
Lactoferrin is an iron-binding milk-derived protein that has shown antibacterial and anti- inflammatory. Lactoferrin supplementation of 100mg per day in combination with 5mg zinc and 11 IU vitamin E 2 x daily showed significant improvements in total acne lesions (inflammatory or non-inflammatory), will improvements noted as soon as 2 weeks (8). A brand that i use myself is Medlab. They have a product called lactoferrin enhance. This is by no means sponsored, I just love their brand and use their products for my clients myself.
Nordic naturals cod liver oil: Contains omega 3 fatty acids (EPA, DHA) vitamin A and Vitamin E to help reduce inflammation, fight oxidation and improve cell membrane fluidity and integrity.
Probiotics: Probiotic supplementation has been shown to be beneficial in some acne patients. Different strains produce different outcomes such as supplantation with Lactobacillus bulgaricus and Lactobacillus acidophilus can inhibit the production of P. acnes through secretion of anti-bacterial proteins (4). Other possible mechanisms involve inhibiting inflammation, intestinal membrane integrity and treating dysbiosis. Lactobacillus rhamnosus SPI in particular was shown to improve reducing IGF-1 and improving insulin signalling and improve acne in 12 weeks (11).
Diet is always superior to supplements however in some cases supplements can be required. It is always advised to gain health professional advice before beginning a supplement, as some minerals can be dangerous in high does and testing can be imperative before commencing nutritional supplementation. There is no one size fits all when it comes to acne and each individuals driving factors can differ. Still having trouble?? A nutritionist can help. There may be the requirement for testing and consecutive appointments, but a health professional will help to identify the underlying cause.
References
Słopień, R., Milewska, E., Rynio, P., & Męczekalski, B. (2018). Use of oral contraceptives for management of acne vulgaris and hirsutism in women of reproductive and late reproductive age. Przeglad menopauzalny= Menopause review, 17(1), 1.
Chen, Y., & Lyga, J. (2014). Brain-skin connection: stress, inflammation and skin aging. Inflammation & Allergy-Drug Targets (Formerly Current Drug Targets-Inflammation & Allergy), 13(3), 177-190.
Sarris, J. & Wardle, J. (2014) Clinical Naturopathy 2e - An evidence-based guide to practice. Chatswood: Churchill Livingstone.
Kucharska, A., Szmurło, A., & Sińska, B. (2016). Significance of diet in treated and untreated acne vulgaris. Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii, 33(2), 81.
Spencer, E. H., Ferdowsian, H. R., & Barnard, N. D. (2009). Diet and acne: a review of the evidence. International journal of dermatology, 48(4), 339-347.
Melnik, B. C., & Schmitz, G. (2009). Role of insulin, insulin‐like growth factor‐1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Experimental dermatology, 18(10), 833-841.
Salem, I., Ramser, A., Isham, N., & Ghannoum, M. A. (2018). The gut microbiome as a major regulator of the gut-skin axis. Frontiers in microbiology, 9.
Chan, H., Chan, G., Santos, J., Dee, K., & Co, J. K. (2017). A randomized, double‐blind, placebo‐controlled trial to determine the efficacy and safety of lactoferrin with vitamin E and zinc as an oral therapy for mild to moderate acne vulgaris. International journal of dermatology, 56(6), 686-690.
Gupta, M., Mahajan, V. K., Mehta, K. S., & Chauhan, P. S. (2014). Zinc therapy in dermatology: a review. Dermatology research and practice, 2014.
El‐Akawi, Z., Abdel‐Latif, N., & Abdul‐Razzak, K. (2006). Does the plasma level of vitamins A and E affect acne condition?. Clinical and Experimental Dermatology: Experimental dermatology, 31(3), 430-434.
Fabbrocini, G., Bertona, M., Picazo, O., Pareja-Galeano, H., Monfrecola, G., & Emanuele, E. (2016). Supplementation with Lactobacillus rhamnosus SP1 normalises skin expression of genes implicated in insulin signalling and improves adult acne. Beneficial microbes, 7(5), 625-630.
Disclaimer: this article does not take into account the individual and should not be taken as specific or definitive advice. Health status, current and past medical history, age, dietary and lifestyle factors all need to be taken into account when treating the individual.