Acne is a common plague of adolescents going through puberty, however, adult acne is currently on the rise. There are many different types of acne, but this piece will focus on acne vulgaris as it is the most common type in the world.
Many factors go into the development of acne; it can be negatively by family history, being overweight, obesity, stress, oily or mixed skin, irregular menstrual cycles, diet, smoking, the improper use of cosmetics, the long-term use of electronics, poor quality of sleep, high temperature, sun exposure, air pollution, mineral oils and halogenated hydrocarbons.
The result of many of these factors lead to the internal mechanisms of increased sebum production, negative hormonal fluctuations, and inflammatory reactions. This piece will mainly focus on the role of stress and diet in acne.
Acne Basics – Sex Differences, Western Medicine’s Approach, and Taking a Look at Indigenous Cultures
There’s a lot of sexual dimorphism in disease states between men and women; women are more prone to developing autoimmune disease than men, for example. However, with acne, both women and men are affected equally, but the most severe form more often appears in men, probably due to the influence of androgens, which we’ll chat on more in depth later. Acne is also more common in caucasian populations than African American, Asian, Indian, and others.
Nowadays it has been shown that acne is caused by different factors such as increased production of sebum, the release of inflammatory mediators in the skin, hyperkeratosis, and the skin microbiome; particularly colonization by anaerobic Propionibacterium acnes.
Moreover, the factors contributing to the formation of acne also include genetic predispositions, hormonal abnormalities (androgens play the key role), immunological disorders, psychological, environmental and even iatrogenic factors.
The typical western medicine drugs for acne usually come with a host of side effects; we talk about accutane and its myriad problems later (under Vitamin A), but another typical treatment is doxycycline, which is an antibiotic. Chronic use of antibiotics is only going to make things significantly worse; dysregulating the gut microbiome and potentially driving the issue long term.
Studies on the effects of diet on acne vulgaris have shown that occurrence of acne is lower in rural and non-industrialized areas than in Western populations. It is believed that it may be a result of differences between both specific food choice and glycemic loads of diets of both populations.
In 2002, Cordain et al. conducted a study among two non-Western populations – the Kitavan Islanders of Papua New Guinea and the Aché hunter-gatherers of Paraguay. Among approximately 1300 subjects, no cases of acne were reported. Cordain et al. suggested that the absence of acne in these societies may have been a direct consequence of their diets.
Both populations subsist on low inflammatory, low glycemic load diets devoid of Western refined foods such as cereals, chips, cookies and bread. The diet of the Kitavan people consisted of tubers, fruits, fish, and coconuts. Intake of dairy products, coffee, alcohol, cereal, sugar, and refined oils was minimal to none.
Here are a list of some key factors within the diet may contribute to acne, which we’ll chat more in depth about as we go along:
- Glycemic index of foods and overall glycemic load of the diet
- Milk and dairy products
- Dietary fiber
- Fatty acid ratios
- Vitamin A and zinc
Let’s go ahead and break down each of the above aspects individually.
Glycemic Index of Foods and Overall Glycemic Load of the Diet
Let’s define glycemic index vs. glycemic load. The glycemic index of a food is how impactful it is on your blood sugar per gram of carbohydrate. The glycemic load of a diet is the overall impact of the entire diet on blood sugar control, which seems to have more of the effect here.
The crux of how glycemic load can affect acne is through hyperinsulinemia, increased IGF-1, and downstream effects of that that can result from a high GL diet. When we’re eating a high glycemic load, this stimulates insulin production and release, and if the glycemic load of the diet is chronically high, we’re going to have more insulin around as well, potentially resulting in hyperinsulinemia.
Chronic hyperinsulinemia can have the potential to increase androgens as well as decrease SHBG, particularly in females, making these androgens significantly more available. DHT and testosterone are the major androgens that interact with the androgen receptors on sebaceous glands, with DHT being 5 to 10 times more potent than testosterone. These androgens increase sebum production in the skin as well as induce changes in skin cell proliferation, and increased likelihood of over-colonization by Propionibacterium acnes.
Hyperinsulinemia increases serum levels of IGF-1 and reduces serum levels of insulin-like growth factor binding protein 3 (IGFBP3). These two factors directly increase proliferation and decrease apoptosis of keratinocytes (a type of skin cell) as well as increase sebum production. When someone has acne, the hair, sebum, and keratinocytes stick together inside the pore, so this could lead to increased acne production. This increased keratinocyte proliferation combined with increased sebum production from both androgens and IGF-1 leads to a less than ideal situation for skin health.
IGF-1 influences comedogenic (acne-causing) factors such as androgens, growth hormone and glucocorticoids. It has been shown that androgens increase the endogenous levels of IGF-1 in blood and this further increases levels of androgens. A vicious circle is thus created in effect contributing to an increased production of sebum.
Milk and Dairy Products
We’ve already talked about IGF-1, and according to research it seems that this is one of the main culprits behind dairy’s effect on acne as well. Milk and dairy products contain a cow-analogue of human IGF-1 that is identical to it, and dairy also disproportionately (relative to the amount of carbohydrates it contains) stimulates production of our own endogenous IGF-1 as well.
Milk that is available in stores is not only rich in placenta-derived progesterone but also other precursors of dihydrotestosterone (DHT), such as 5α-pregnanedione and 5α-androstanedione. These compounds are easily enzymatically modified to DHT and the enzymes required for this process are available in the pilosebaceous unit, which is basically the collection of hair shaft, follicle, and sebaceous gland.
In addition to those factors, immunologic sensitivity to A1 casein in cow’s dairy is a rather common sensitivity, and if one is sensitive to A1 casein in cow dairy products, this could cause a systemic inflammatory response which could further contribute.
Many studies have shown that skim milk and low-fat dairy products cause significantly more acne than whole milk and less processed, whole-fat dairy products. It is believed that during the production of skim milk and other low fat dairy products, there are changes in the bioactivity of biologically active molecules such as glucocorticoids and transforming growth factor β (TGF-β), which changes their interaction with receptors in the body.
There is also a possibility that the hormonal balance of skim milk and low fat dairy may be impaired. As a result, consumption of skim milk, low fat dairy, and processed dairy products may cause increased acne. In order to maintain the proper consistency of skim milk, manufacturers sometimes add whey protein factors, such as α-lactalbumin, whose role in acne formation is also not negligible. This also occurs in other processed dairy products as well.
For a little bit of data: In 2006, Adebamowo et al. conducted a cohort, prospective 3-year observation study. It included more than 6,000 girls aged from 9 to 15 years. A positive correlation between the consumption of milk with varying fat contents and the occurrence of acne vulgaris was shown; meaning, significantly more acne in low-fat milk products. In 2008, Adebamowo et al. conducted a prospective study that included more than 4,000 boys. A positive correlation between consumption of skim milk and acne vulgaris was shown, but the association was not present with whole milk.
This one might be painful to read, but the data is the data! Many of the studies on chocolate’s effect on the skin are controversial and inaccurate because of additional ingredients (milk, sugar, etc.) in bars and other products.
For one example of a poor study, the Journal of American Academy of Dermatology conducted a study with chocolate and acne and found that significant changes in severity of acne occurred among respondents even after a single ingestion of chocolate. This allowed the authors to hypothesize that chocolate can exacerbate acne lesions. However, in this particular study, there is no information about the type of chocolate consumed by subjects and the percentage of cocoa in consumed samples, which is certainly going to influence results. Was it the actual cocoa, or was it the milk and sugar that was added?
However, since then there have been a few double-blind, placebo-controlled RCTs using 100% unsweetened cacao in capsule form, which would be the real test.
Caperton et al did a one week study where fourteen men with a history of acne vulgaris between the ages of 18 and 35 were assigned to swallow capsules filled with either unsweetened 100-percent cocoa, hydrolyzed gelatin powder, or a combination of the two. All of the men had increases in acne lesions compared to placebo, leading the authors to conclude that chocolate may influence acne production in those prone or with a history.
In another RCT, twenty-five acne prone male subjects were asked to consume 25 g of 99% dark chocolate daily for 4 weeks. Statistically significant changes of acne scores and numbers of inflammatory papules were detected as early as 2 weeks into the study.
As far as mechanism, there is limited research, but one study connects it back to insulin levels as well. Brand-Miller et al conducted an RCT comparing six pairs of food. One of each pair was flavored with cocoa powder, otherwise the foods within the pairs were exactly the same.
The subjects consumed the different pairs of foods on different occasions, and although the GI of the food did not differ within each pair, the insulin response of the chocolate-dusted food of the pair was always higher, by an average of 28%. The greatest difference occurred within the flavored milk category in which the chocolate version elicited 45% greater insulinemia than the strawberry flavored milk.
Several studies show that when dietary fiber is increased at most meals, acne improves. Most of these studies used average individuals eating a standard american diet; therefore the authors attribute the increase in dietary fiber helping acne to an overall decrease in glycemic index and load of the diet.
Omega 3-6 Fatty Acid Ratios
As I’ve talked about numerous times before, the ratio of omega-6 to omega-3 fatty acids resulting from diet is one of the factors that modulate the inflammatory mechanism. A high intake of omega-3 fatty acids can inhibit the production of proinflammatory cytokines which can have a therapeutic effect on acne vulgaris.
Leukotriene B4 (LTB4) is widely known as a substance that regulates sebum production. Omega-3 fatty acids, and particularly eicosapentaenoic acid (EPA) derived from fish oils inhibit conversion of arachidonic acid into LTB4. Every pilosebaceous unit has the ability to produce proinflammatory substances, including LTB4, using substances that come from decomposition of fat originated from diet.
Fish oil, especially EPA, can inhibit production of LTB4 and prevent inflammatory processes. Omega-3 fatty acids have the ability to lower IGF-1 levels as well, which also suggests that they may have a beneficial effect in treatment of acne.
The research on omega-3’s for acne is slightly sparse, however:
A study conducted in 1961 in North Carolina among over 1000 teenagers showed that people who consume large amounts of fish and seafood, have less symptoms of acne (blackheads, papules, pustules, oily skin).
A small study of 5 patients, published in 2008, showed that among patients who consumed dietary supplements based on omega-3 fatty acids (it consisted of: EPA, selenium, zinc and chromium) a reduced number of acne lesions was observed.
Another study from 2012 gave 930 mg of EPA to 13 individuals over 12 weeks. Pooled results from the cohort as a whole indicated that there was no association between supplementation and acne improving. However when you look at the individuals within the study instead of just pooled averages, you see that 7 of them improved significantly, 4 actually got worse, and 2 remained unchanged. The 7 that improved were classified as having “severe” acne at baseline of the study, therefore the authors conclude that omega 3 supplementation may be efficacious in severe acne.
It has been suggested that oxidative stress may be implicated in the inflammatory origin of acne and that supplements containing antioxidants may be valuable adjuvants in acne treatment.
In 2008, El-Akawi et al. conducted a study comparing blood levels of lipid-soluble antioxidants (vitamin A and E) in 100 patients with acne and in 100 healthy control subjects without acne. They found that patients with acne had significantly lower plasma concentrations of these antioxidants as compared with the control subjects.
Low levels of blood selenium have also been documented in patients with acne. It’s been shown that the selenium-dependent glutathione peroxidase enzyme activity is low in patients with acne, so it is possible that selenium supplementation may be of value in acne, particularly if dietary intake is low.
In a study of 47 women and 42 men with acne vulgaris, it was shown that after 12-week supplementation of vitamin E and selenium, the skin condition improved.
Studies in mice and hamsters show that EGCG and resveratrol may exhibit anti-acne effects, however these results have yet to be replicated in humans.
Vitamin A and Zinc
A study conducted in 1998 by Kligman et al. showed that oral supplementation of vitamin A (retinol) is effective in acne treatment when used in high doses (300,000 U/day for women and 400,000–500,000 U/day for men).
More studies mirror this, and this led to the creation of accutane, one of the most effective pharmacological treatments for acne, which is simply a very high dose of a naturally occurring derivative of vitamin A.
However, given its fat soluble nature, it builds up in tissues rather quickly and can cause a gamut of side effects, some mild and some serious. Everyone taking accutane will experience extremely dry and peeling skin.
The worst part is that long term use has been connected to damage of the liver, pancreas, and intestines, as well as development of Ulcerative Colitis, Crohn’s Disease, and Inflammatory Bowel Syndrome (IBS), so I would not recommend this approach.
Zinc is a micronutrient that is essential for the development and functioning of the human skin, amongst many other roles. It has been shown to be bacteriostatic against Propionibacterium acnes, to inhibit chemotaxis, and to reduce production of pro-inflammatory cytokine – tumor necrosis factor α (TNF-α).
In early studies on the influence of zinc on human skin conducted by Michaelsson and Fitzherbert in 1970’s, it has been shown that acne improved with oral zinc supplementation in zinc-deficient patients.
Later studies have confirmed that patients with acne often are deficient in zinc, and its oral supplementation has a positive effect on treatment of acne vulgaris.
However, doses used in the studies that were efficacious were rather huge; between 400-600 mg of zinc sulfate per day. If someone is supplementing this much for acne, they most certainly need to be supplementing copper alongside as even supplementing 50mg of zinc per day over time can induce a copper deficiency.
The bacteria P. acnes can accumulate in the hair follicles of the face, neck, chest, and back. This bacteria is present in normal amounts in most people and is considered a symbiont, but when the body and skin have a more inflammatory disposition, it can cause overgrowth and accumulation to pathogenic levels. This bacteria can drive inflammatory acne lesion formation.
Kang et al. (2009) examined the effect of a probiotic lotion on P. acnes. This lotion contained Enterococcus faecalis SL-5 as a species of Lactobacillus genus. They tested 70 patients with moderate acne over 8 weeks. At the end of the study, the treatment group experienced significantly reduced inflammatory acne lesions vs. the control group.
Another RCT by Muizzuddin et al. tested Lactobacillus Plantarum in 1% and 5% topical solutions. The lesions were evaluated after treating 10 volunteers aged 18–50 years with the formulation once a day for 4 days. The formulation with a 5% concentration of the bacteria significantly reduced the lesion size and erythema, whereas the formulation with a 1% concentration exerted no significant effects after 4 days.
We do have a few studies on oral probiotics as well. Jung et al. randomly assigned 45 female patients aged 18–25 years to a group that only received probiotics (the probiotic in this case was a Lacto/bifido blend with two different lactobacillus strains at 5 billion CFU each, and bifidobacterium bifidum at 20 billion CFU), a group that received probiotics and minocycline (an antibiotic) and a group that only received minocycline.
The total number of lesions significantly decreased in all the patients after 4 weeks, and the improvement continued during a 12-week follow-up. A significant decrease was observed in the total number of lesions in the group receiving probiotics and minocycline compared to in the other two groups, whereas the group receiving minocycline alone developed candidal vaginitis.
In this study, while the combo group responded the best, you also have to consider the negative far-reaching effects of antibiotics on the whole-body microbiome, which manifested in the development of candidal vaginitis here, but also impacts cognitive health, metabolic health, and other systems. The group getting only probiotics still responded well and had significant reductions.
For those unfamiliar with the HPA axis, when we experience stress, CRH is released from the hypothalamus, communicates to the pituitary to release ACTH, which then communicates to the adrenal cortex to produce cortisol.
Interestingly, the skin also developed a fully functional peripheral HPA system where CRH, ACTH, and their receptors are produced in skin cells.
Skin-expressed CRH itself stimulates sebaceous gland lipid production and steroidogenesis, which contributes to acne.
Studies have also shown an increase of CRH expression in the sebaceous glands of individuals with acne, compared to a low expression in normal skin. This upregulation of CRH expression in acne-involved skin may influence the inflammatory processes that lead to stress-induced acne lesions. CRH also induces cytokines IL-6 and IL-11 production in keratinocytes, contributing to inflammation, which is regarded as a key component in the pathogenesis of acne.
Prolactin has been shown to be induced by psychological stress and stimulates keratinocyte proliferation and regulates keratin expression in keratinocytes, as well as stimulating sebum production in sebaceous glands. The combination of these two, just like androgens and IGF-1, can lead to increased acne.
If you’ve been following me for a while, you’ll already have an idea of how important getting good quality and quantity of sleep is. Significant amounts of studies have associated lack of sleep and poor sleep quality with increased incidence of acne.
The mechanism here is less elucidated, however, authors hypothesize changes in global inflammatory status, changes in the skin microbiome, and increased expression of CRH in skin, therefore driving skin inflammation, may be possible causes.
Conclusion: Bringing it All Together
We have the potential for stress and poor sleep to induce skin inflammation, and then the vicious interactions and feedback loops of hyperinsulinemia, androgens, and IGF-1 driven by a high GI diet and milk/dairy products in those that are prone. Chocolate may also be contributing through either an elevated insulin response or another unknown mechanism.
The best course of action would be to optimize foundational aspects first: Get good sleep and manage your stress levels through meditation, breathwork, or other means.
Increase fiber and lower the GI of your diet in general, and do a 1 month experiment of removing the culprits to see if it makes a difference: Dairy and chocolate being the main ones.
If you’re absolutely die-hard dairy, but notice that when you took it out, your acne improved, then you can still try to reintroduce high fat dairy to see if it makes a difference. As we highlighted before, full-fat dairy doesn’t seem to have the same association with acne as low fat dairy.
I would avoid extremely high dose vitamin A as it has significant and long term side effects. High dose zinc may be applicable here for a limited time period, just be sure to supplement copper alongside.
Probiotics, both topical and oral, seem to have a modest effect in the reduction of inflammation-related acne, so giving this a try could be helpful as well.
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