Although the exact cause of acne is intricate and sometimes confusing, most research points towards genetics to blame. It all comes down to there being one main difference between someone that is acne prone and someone that isn’t: retention hyperkeratosis. So, I’m here to break it down in simple terms.
The Process of Acne
- At puberty the body starts producing testosterone.
- An enzyme in the skin changes testosterone to dihydrotestosterone.
- Dihydrotestosterone stimulates the sebaceous glands to begin producing sebum.
- In the acne-prone follicle, sebum sets off retention hyperkeratosis
The first three mechanisms happen to everyone during puberty. It’s only in the susceptible individual that the fourth process happens known as retention hyperkeratosis. While this mostly happens in the early teenage years, it’s common for women in their forties to be triggered the same way due to an imbalance in hormones. The key factor here is the person becomes affected because they’re genetically predisposed.
Let me be clear, though: Acne sufferers do not produce more testosterone, nor does testosterone produce acne. Hormones simply trigger the process of acne in genetically prone skin. Also, oily skin doesn’t cause acne, it’s just a triggering component that affects genetically prone skin. As Dr. Fulton said it best, “sebum provides the match that ignites the acne fire which can rage out of control if not contained.”
What is retention hyperkeratosis, anyways?
Let’s talk anatomy real quick. The outermost layer of the skin is called the stratum corneum. On the surface of healthy skin, it’s about 14 cells thick, and inside a pore it narrows down to about 5 cells thick. The skin is always in a constant state of flux; shedding dead cells to make room for new cells. Typically the dead cells get pushed out the opening of the follicle with the flow of oil. This whole process happens differently in someone who is acne prone. Instead of the dead cells sloughing off and out of the pore, they instead stick together forming a mass with sebum, rudimentary hair, debris and bacteria. This is called an ‘impaction’ when it becomes retained inside the pore. This explains the first half of the term retention hyperkeratosis . As contents build up, the follicle wall becomes damaged from the pressure and inflammation begins.
As for the last part of the term… We all know ‘hyper’ means happening quickly, and keratin is a soft protein in dead skin cells that serve as the protective outer layer. Hyperkeratosis basically means keratin-containing skin cells (aka keratinocytes) are being produced at an abnormally fast rate. As more are produced, more are being shed and adding to an already developing impaction. Acne happens when your skin is growing faster than it can shed. And so the consequence is that you develop a very thick stratum corneum. The skin is out of balance and unhealthy at this point, and the thicker that layer becomes, the more room dead cells can contribute to impactions.
My goal in working with any clients who struggle with acne is to essentially thin out their skin a little bit, bringing it back down to a normal and healthier layer. This can be done by applying topical acids such as glycolic, lactic and salicylic acids. Acids enter the skin deeply and break apart those stubborn dead cells, encouraging them to slough off. I prefer this over scrubs, since scrubs tend to work on the skin too superficially. Another component in clearing the skin and controlling oil is to use benzoyl peroixde, sulphur, or resorcinol. These chemicals work by killing the bacteria that causes acne. When used together properly, they complement each other and you can see some amazing results. If you don’t use AHA’s/BHA’s and you go to apply a potent acne-killing cream, it’s mostly going to sit on top of the thick layer of dead cells, and so that product must work it’s way through that layer, on down to the healthy tissue, and then to the bottom of the zit. At that point, it’s not going to be very effective! By using chemical exfoliants, you’re getting 100% of the benefit from product since it can be applied much closer to the source! The trick to stopping retention hyperkeratosis is to always be one step ahead of the skin – shed the top layers faster than your skin can grow!