We all want clearer skin, right?
So, in the name of clearing up acne and associated acne myths, let’s get nerdy with a deep dive into the science of zits. After all, once we know our enemy, it’s easier to fight back!
Let’s consider the three main causes of acne 1:
- Increased levels of androgens
- Bacterial overgrowth and related local inflammation
- Blocked sebum glands (typically caused by follicular hyperkeratinisation and overproduction of sebum).
That’s right, chocolate doesn’t make this list… but that doesn’t mean it’s entirely off the hook. Why? Because chocolate is often made with ingredients that can play a big role in acne, such as dairy and processed sugar, by way of those three processes listed above.
Before we look at how each of these processes contributes to acne, I should clarify that this article is about acne vulgaris, or common acne.
Other types of acne, such as acne rosacea, have some shared factors but are distinct conditions with their own mechanisms.
OK, without further ado, let’s get to know our androgens.
Hormones and acne
Androgens are a group of sex hormones, including testosterone. Levels of these hormones vary between individuals and within the same individual at different times during life. When androgen balance is disrupted, especially if this situation persists, chances are you’ll see some symptoms such as acne, excessive hair growth, and even changes in mood. Sound familiar? Yup, a sudden rise in androgens is normal in teenage males and helps give rise to secondary sexual characteristics and to sperm production.
Around 85% of teens suffer with acne to some degree. Acne also tends to strike during perimenopause and in trans men beginning testosterone shots. The common theme here is major sex hormone upheaval, particularly periods of hyperandrogenism 2.
These are not the only conditions where a person might have high levels of circulating androgens, however. For some, androgen imbalance or disruption can be caused by repeated excessive consumption of foods high on the glycemic index (GI) and by endocrine disrupting chemicals (more on this below).
Numerous studies have found that those suffering from acne tend to have some degree of insulin resistance 3. High GI foods can lead to hyperinsulinemia, a decrease in insulin like growth factor protein-1 (IGFP-1) and a resultant increase in insulin like growth factor-1 (IGF-1) itself. IGF-1 then goes on to stimulate androgen synthesis in the ovaries and testes but reduces the liver’s production of sex hormone binding globulin (SHBG).
In fact, even a high sugar intake by itself (independent of insulin levels) can decrease SHBG synthesis. This is because all that sugar has to be converted to fat in the liver, which detracts from the liver’s other jobs, such as producing SHBG.
As you might imagine, other things that upset liver function can also contribute to acne. This means high alcohol intake, drugs, and environmental pollutants, as well as a diet high in troublesome fats.
Genetic factors can also affect the synthesis of androgens, estrogens, and SHBG. For example, several studies have found that the TA repeat polymorphism [(TA)n] of the SRD5A2 gene is associated with increased activity of dihydrotestosterone, which then increases sebum secretion and acne 6. In addition, over-activated mTORC1 increases androgen hormone synthesis and exogenous testosterone directly activates mTORC1 (more on this below). This means that animal-derived foods, which are often a source of testosterone, can lead to excessive lipogenesis, increased fat, oily skin, and, potentially, acne.
Interestingly, northern Canadian Inuits don’t appear to have suffered much, if at all, with acne prior to the rapid increase or inclusion of dietary items such as soda, beef, dairy products, and processed foods 7. Similarly, prior to the second world war, Okinawans, who traditionally eat a diet of sweet potatoes, rice, and vegetables, together with some soybeans and fish, but little meat, reported little experience with acne. This changed after the war as diets high in animal products became more common; similar patterns were also seen in indigenous populations in Mali 89.
Many other things also act as endocrine disruptors, including bisphenol-A, a chemical often used to line cans and in water bottles. Chemical pollutants can also become concentrated in fatty animal-derived foods, especially oily fish. So, if you’ve noticed your acne get worse after taking an omega-3 fish oil, check the quality of the supplement. Low quality oil laced with contaminants might make your acne worse even if you’re taking it to try to combat the next trigger for acne, inflammation connected to bacterial overgrowth.
Bacterial growth, inflammation, and acne
The idea persists that acne is a result of poor hygiene, but is that really true? Turns out, not really. We all carry the bacterium responsible for acne, Propionibacterium acnes, on our skin and, for the most part, this doesn’t lead to breakouts. As usual, something else tips the balance.
For example, localized inflammation can cause changes in keratin synthesis and the behavior of keratinocytes in the skin. Meanwhile, androgen disruption might alter sebum (oil) production in the skin. The combination of factors can lead to blocked pores, in which P. acnes can thrive. In turn, bacterial overgrowth can cause more localized inflammation that triggers acne all over again.
Some research from 2014 suggests that not everyone will respond in quite the same way to P. acnes, however. The expression of the gene NLRP3 (which is involved in immune system activity) appears to be significant in determining P. acnes-induced IL-1β production in sebocytes. As such, those with greater expression of this gene may have greater activation of the NLRP3 inflammasome by P. acnes and, thus, more sebum and acne 13.
Once you understand the possible vicious cycle behind acne, it’s easier to understand why ‘curing’ acne isn’t as simple as using an antibacterial face wash.
Indeed, follicular hyperkeratinization, our second major contributing factor for acne, is quite complex and is a key target for many acne treatments such as retinoid therapy.
Sebum, follicular hyperkeratinization, and acne
Yes, that is quite the mouthful, but read on, there are nuggets of wisdom below.
Follicular hyperkeratinization is a key element in the development of acne. Hyperkeratinization is, as the name suggests, an overabundance of keratin in skin cells. This causes cells to stick together rather than shedding normally. The result? Blocked pores. Or, in dermatological parlance, a microcomedone, which can lead to acne lesions.
Top tip: Many types of make-up can cause comedones and acne. If you notice your acne gets worse when you use make-up, consider switching to a non-comedogenic cosmetics range.
Retinoids (drugs commonly used to treat acne) work by normalizing keratinization and inhibiting microcomedone formation. Thus, they help prevent the formation of inflammatory acne lesions. But what causes hyperkeratinization in the first place?
Some researchers have posited that low levels of linoleic acid (omega-6) may increase follicular hyperkeratosis and vulnerability to acne lesions 32. However, this may not be due to a dietary deficiency of linoleic acid at all. Instead, the problem seems to be that the essential fatty acid is diluted by excessive sebum production.
Excess sebum leads to abnormal keratinocyte differentiation and, you guessed it, blocked pores. Low levels of linoleic acid can also impair the skin’s natural barrier function, making it more susceptible to infection with P. acnes and to inflammatory molecules.
Hyperkeratinization has also been linked to issues with the 5-alpha-reductase type 1 enzyme. And here’s the really fun part, the steroid 5-alpha-reductase catalyzes the reduction of testosterone into the much more potent androgen dihydrotestosterone (DHT). Research shows that areas of skin more prone to acne have higher activity of type I 5α-reductase and that people of all genders with acne tend to have increased expression of 5α-reductase 14.
So, undesirable changes in circulating androgens could be contributing to excessive shedding and clumping of keratinized skin cells that block pores, increase vulnerability to bacterial infection and… lead to acne.
Keratinocytes also produce inflammatory cytokines such as interleukin-1alpha. And both inflammation and androgen hormones can stimulate the differentiation of keratinocytes, with the help of IL-1alpha and other growth factors. This, in turn, leads to hyperkeratinization and the development of comedones.
All this science is well and good, but what does it mean if you are trying to prevent or relieve acne? To find out, check out the sister post to this article: Want Clear Skin? Avoid These 5 Acne Causing Foods.
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