Feeling utterly confused? Don’t know what you can do to get over acne?
Don’t worry. You are in the right place. My name is Seppo Puusa, and for the past 5 years I’ve read just about every single scientific paper on acne I managed to get my hands on – well over 1000 by now.
On this page, I’ll explain some of the most important things you have to understand, if you want to get over acne. By the time you are done, you should feel like you finally understand what’s going on in your skin.
It took me over 15 years of living with acne to figure this out. I wrote this page so that others don’t have to wait that long.
Sebum oxidation, the trigger that starts acne
Science on the past decade has conclusively shown that every pimple starts with inflammatory damage to sebum; or sebum oxidation. Everything else you may have heard that causes acne; things like diet, stress, hormones and what not, only create the conditions for sebum oxidation to happen.
This masterpiece of PowerPoint art helps to explain this.
Sebum is a waxy substance composed of triglycerides, fatty acids, and other fatty substance. Out of these, squalene and linoleic acid seem to be the most relevant for acne.
Squalene is critical for skin health, and that’s why it’s part of many skin care formulations. However, it comes with a rather nasty downside.
When squalene suffers oxidative damage, it turns into squalene peroxide. Squalene peroxide is massively comedogenic.Animal studies have shown that applying squalene peroxide to rabbit ears causes acne. And the severity of acne is linked to the degree of oxidative damage squalene suffered. In other words, if squalene only suffered minor damage it caused a little bit of acne, but squalene that was badly damaged caused severe cystic acne.
A 2010 review concluded the following:
Comedogenicity of squalene peroxides has been demonstrated in animal experiments in which comedones have been induced by exposing rabbit ears to irradiated squalene. The degree of squalene peroxidation was found to correlate positively with the size of the comedones elicited.
Lipid Mediators in Acne. Monica Ottaviani, Emanuela Camera, Mauro Picardo. Mediators Inflamm. 2010; 2010: 858176. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943135/
Nobody has studied what happens when you apply squalene peroxide on human skin. However, studies as far back as 50 years found increased levels of squalene peroxides in acne patients. Modern studies have confirmed this (source).
A 2014 study showed that people with mild acne had 79% more squalene peroxide in sebum than people with clear skin. After four weeks of treatment with retinol and vitamin E cream, squalene peroxide levels dropped by 56%. Similarly, the treated areas showed much less hyperkeratinization and inflammation.
Linoleic acid (LA) is another important fatty acid. There’s an inverse relationship between sebum production and linoleic acid concentrations; i.e. the more sebum is produced, the lower the LA concentration is. This could explain why people with acne have less LA in sebum. One study showed that people with acne had 65% less LA in sebum than those without acne.
Deficiency in LA causes barrier problems in the follicular duct. Think of the skin pore (follicle) as a tube; LA deficiency causes holes to appear in the wall of the tube and consequently makes them weaker. This makes the follicle more prone to rupture and may result in leakage of substances inside the follicle into the surrounding area. Some of these substances are inflammatory, like bacterial toxins, and likely cause inflammation in the area.
Acne cannot happen without this initial oxidative damage
This oxidative damage to sebum, or lipid peroxidation, is what kicks off a new pimple.
In 2010, Drs. Bowe and Logan wrote a fantastic paper on the role lipid peroxidation plays in acne. They concluded with following:
Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne.
Bowe, W. P. & Logan, A. C. Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles. Lipids Health Dis 9, 141 (2010). https://www.ncbi.nlm.nih.gov/pubmed/21143923
Everything else you’ve read about acne (blocked pores, bacteria, too much keratin, etc.) follows this initial oxidative damage.
Exposed to squalene peroxide, the cells in the skin drastically increase the production of keratin – a tough protein that binds the skin cells together. Normally dead skin cells are shed off and pushed out of the skin pore one by one. Excess keratin prevents the dead cells from separating properly – so the pore fills up with chunks of dead cells. Too much keratin also makes the pore walls rigid.
Combined with sticky sebum, you have the perfect recipe for blocked pores and the first stage of a pimple. The blocked pore becomes a breeding ground for bacteria. The number of bacteria in the blocked pore grows exponentially, and they start to irritate the skin and cause drastically more inflammation. This is when a pimple starts to get red and painful.
As more sebum and dead skin cells flow into the blocked pore, it eventually bursts – much like a water balloon. The inflammatory material spills out to the surrounding area. This is how big nodules and cysts form.
It’s important to keep in mind that none of this would happen without the initial oxidative damage to sebum.
Understanding how diet and lifestyle affect this
All this talk about microscopic events in the skin does not mean diet and lifestyle wouldn’t affect acne.
Let’s take another look at that masterpiece of PowerPoint art I showed you earlier.
Inflammation and hormonal issues are what sets the stage for sebum oxidation to happen. Briefly, here’s the role each plays.
Androgens (male sex hormones, like testosterone) and insulin boost the amount of sebum the skin produces. As the skin produces more sebum, it also produces more squalene.
A 2009 study showed squalene makes up 15% of sebum, while the average for acne patients was 20%. The study also showed acne patients produced 59% more sebum. Putting these two figures together, acne patients had 112% more oxidation-prone squalene than people without acne.
The inverse is true for linoleic acid. The more sebum the skin produces, the less linoleic acid there is in the sebum.
Here’s an easy way to think about this. Imagine a dimmer switch that’s connected to an old lightbulb. The more you open the dimmer switch, the more current goes through the bulb and the more likely it is to burn out.
The same is true for hormones and your skin. As hormone levels increase, so does your risk of getting acne.
Insulin increases sensitivity of the skin to acne causing hormones
Contrary to what most people think, the vast majority of people with acne don’t have abnormally high hormone levels. Some do, but they are a minority.
The difference seems to be in how the skin reacts to the hormones. Studies have shown that acne-prone skin is more sensitive to the androgen hormones that stimulate sebum production. The skin converts various precursor androgen hormones into more potent testosterone and DHT – the hormones that stimulate sebum production the most. All the enzymes required for the conversion are in the skin.
Without going into details, the hormone insulin is one of the keys here. High insulin levels stimulate the release of precursor androgens and increase the activity of the converting enzymes in the skin. Insulin delivers a deadly one-two punch to the skin.
Your diet and lifestyle choices have a huge impact on your hormone levels – and especially on insulin levels. This is why studies have shown that diets that cut sugar and quickly digested carbohydrates can reduce acne.
The skin uses antioxidants to protect sebum from oxidative damage. Antioxidants can neutralize free radicals before they have a chance to damage squalene.
Vitamin E is a major antioxidant in the skin. It’s transported to the skin via sebum. Studies have shown a continuous and much higher flow of vitamin E to the areas of skin that produce more sebum. For example, the sebum collected from the cheeks contained 20 times more vitamin E than the sebum collected from the forearms (source).
Researchers believe that the primary task of vitamin E in the skin is to protect squalene from oxidative damage. There is a very tight correlation between squalene and vitamin E secretion, such that when squalene secretion increases, so does vitamin E secretion.
Shortage of antioxidants is going to leave sebum unprotected and exposed to acne-triggering oxidative damage.
Failure of antioxidant protection in acne patients
Studies comparing antioxidant levels in people prone to acne and those with healthy skin show that the antioxidant protection is overwhelmed in acne patients. For example, one study showed 30% more squalene peroxide and 20% less vitamin E in sebum taken from acne-prone skin (source).
To compensate for the higher demand of antioxidants in the skin, acne patients draw from the body’s antioxidant reserves at a much higher rate than individuals with clear skin. We can see this from studies comparing blood antioxidant and oxidant values between acne patients and people with clear skin. One study showed:
- Vitamin A: 33% lower in acne patients
- Vitamin C: 40% lower
- Vitamin E: 45% lower
- Beta-carotene: 65% lower
This means that the antioxidant system can’t cope with the demand in acne patients. Furthermore, anything that increases inflammation further depletes the antioxidant stores and leaves the sebum even more vulnerable to oxidative damage.
Here’s a list of common things that can cause inflammation and aggravate acne:
- Gut problems
- Food allergies and sensitivities
- Allergic reactions
Acne types – The first step towards permanently clear skin
So far everything we’ve talked about applies to everyone with acne. However, no two people with acne are the same. What works for one person with acne often doesn’t work for another.
This is where the idea of acne types comes in. Having read a well over 1000 scientific papers on acne and related topics, I’ve come to realize we don’t all suffer from the same acne.
Let me explain.
Yes, hormones and inflammation play a role in everyone with acne. But many different things cause inflammation and hormonal imbalance; such as poor diet, stress, and gut problems.
Regardless of whether it’s caused by stress or gut problems, inflammation still causes acne. But you can’t tell the difference just looking at the skin. In both cases, the person just has ‘acne’.
This is what I mean when I say we don’t all suffer from the same acne. And this is why following what worked for someone else often does nothing for you.
To get over acne, you have to identify the ultimate cause(s) behind your acne – the things that cause hormonal issues and inflammation for you.
You can do that by identifying your acne type.
Not everyone gets acne from drinking milk. Not everyone is stressed because of acne. And not everyone with acne has gut problems. But some do and are.
Acne types help you to identify the cause(s) that are the most likely culprits behind your acne. And guess what? When you look for solutions to those issues, then you are likely to make much more progress with your skin.
Acne types also help to make sense of acne by breaking it down into manageable chunks. For most people, there’s a combination of causes that leads to acne.
The first step towards permanently clear skin
Instead of trying to solve this big and fussy problem called acne, you can solve it in small pieces. For example, it’s common for women to show signs of hormonal and emotional/stress types. So you would go, “OK, I have to make some adjustments to my diet to keep hormones under control, and I should try yoga or meditation to manage stress.”
Much easier and simpler. Because now you have an action plan that’s tailored to your unique situation.
This is why I say that identifying your acne type is the first step towards permanently clear skin.
If this makes sense to you, I urge you to consider Clear for Life, my science-based natural acne treatment course. Clear for Life is built around the idea of acne types. It’s jam-packed with proven diet, lifestyle, and supplement suggestions specific to each acne type. Once you know your acne type, you just mix and match from the suggestions the ones that are relevant for your situation. All the recommendations are based on scientific studies, so you know the advice is proven and reliable. All the dietary advice is ‘real life compatible’ – meaning that you can still go out and have a life while doing this. If that’s something you are interested, you can check out Clear for Life here.
That’s all for now. I hope you found this useful, and that it feels like you are finally getting a handle on what’s going on in your skin.
Best of luck on your journey to clear skin!
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- Bowe, W. P. & Logan, A. C. Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles.Lipids Health Dis 9, 141 (2010). https://www.ncbi.nlm.nih.gov/pubmed/21143923
- Bowe WP, et al. Acne vulgaris: the role of oxidative stress and the potential therapeutic value of local and systemic antioxidants. J Drugs Dermatol. 2012 Jun;11(6):742-6. https://www.ncbi.nlm.nih.gov/pubmed/22648222
- Monica Ottaviani, et al. Lipid Mediators in Acne. Mediators Inflamm. 2010; 2010: 858176. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943135/
- Tochio, T., Tanaka, H., Nakata, S. & Ikeno, H. Accumulation of lipid peroxide in the content of comedones may be involved in the progression of comedogenesis and inflammatory changes in comedones. J Cosmet Dermatol 8, 152–8 (2009). https://www.ncbi.nlm.nih.gov/pubmed/19527342
- Apostolos Pappas, et al. Sebum analysis of individuals with and without acne. Dermatoendocrinol. 2009 May-Jun; 1(3): 157–161. https://www.ncbi.nlm.nih.gov/pubmed/20436883
- Saint-Leger D, et al. A possible role for squalene in the pathogenesis of acne. I. In vitro study of squalene oxidation. Br J Dermatol. 1986 May;114(5):535-42. https://www.ncbi.nlm.nih.gov/pubmed/2941049
- Saint-Leger D, et al. A possible role for squalene in the pathogenesis of acne. II. In vivo study of squalene oxides in skin sur- face and intra-comedonal lipids of acne patients. Br J Dermatol. 1986 May;114(5):543-52. https://www.ncbi.nlm.nih.gov/pubmed/2941050
- Chiba, K., Yoshizawa, K., Makino, I., Kawakami, K. & Onoue, M. Comedogenicity of squalene monohydroperoxide in the skin after topical application.J Toxicol Sci 25, 77–83 (2000). https://www.ncbi.nlm.nih.gov/pubmed/10845185
- Pappas, A., Johnsen, S., Liu, J.-C. C. & Eisinger, M. Sebum analysis of individuals with and without acne. Dermatoendocrinol 1,157–61 (2009). https://www.ncbi.nlm.nih.gov/pubmed/20436883
- Costa, A. et al. Evaluation of the Quantitative and Qualitative Alterations in the Fatty Acid Contents of the Sebum of Patients with Inflammatory Acne during Treatment with Systemic Lymecycline and/or Oral Fatty Acid Supplementation.Dermatol Res Pract 2013, 120475 (2013). https://www.ncbi.nlm.nih.gov/pubmed/24191156
- Thiboutot, D. et al. Activity of the type 1 5 alpha-reductase exhibits regional differences in isolated sebaceous glands and whole skin. J. Invest. Dermatol. 105,209–14 (1995). https://www.ncbi.nlm.nih.gov/pubmed/7636302
- Thiboutot D, et al. Androgen metabolism in sebaceous glands from subjects with and without acne. Arch Dermatol. 1999 Sep;135(9):1041-5. https://www.ncbi.nlm.nih.gov/pubmed/10490108
- Thiboutot D, et al. Activity of 5-alpha-reductase and 17-beta-hydroxysteroid dehydrogenase in the infrainfundibulum of subjects with and without acne vulgaris. Dermatology. 1998;196(1):38-42. https://www.ncbi.nlm.nih.gov/pubmed/9557222
- Peter E Pochi et al. Skin Surface Lipid Composition, Acne, Pubertal Development, And Urinary Excretion Of Testosterone And 17-Ketosteroids In Children. Journal of Investigative Dermatology (1977) 69, 485–489. https://www.ncbi.nlm.nih.gov/pubmed/143498
- Zouboulis, C. C., Chen, W.-C. C., Thornton, M. J., Qin, K. & Rosenfield, R. Sexual hormones in human skin. Horm. Metab. Res. 39, 85–95 (2007). https://www.ncbi.nlm.nih.gov/pubmed/17326004
- Thiele JJ, et al. Sebaceous gland secretion is a major physiologic route of vitamin E delivery to skin. J Invest Dermatol. 1999 Dec;113(6):1006-10. https://www.ncbi.nlm.nih.gov/pubmed/10594744
- Mauro Picardo, et al. Sebaceous gland lipids. Dermatoendocrinol. 2009 Mar-Apr; 1(2): 68–71. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835893/
- Khalid O Abulnaja. Oxidant/Antioxidant Status In Obese Adolescent Females With Acne Vulgaris. Indian J Dermatol. 2009 Jan-Mar; 54(1): 36–40. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2800868/