If there’s something I’ve learned during several years of helping acne patients, it’s how utterly confused many are. Confused about what causes acne and how to get over it. Partly because of all the bad advice online, but mostly because nobody has ever properly explained acne to them. We are going to fix that now.
After reading well over a thousand studies I’ve learned that acne is not that complicated. That every single case of acne follows the same model, or happens the same way. Understanding this is critical in getting over acne. A mechanic couldn’t fix your car unless he understood how cars work. Armed with that knowledge he can figure out what’s wrong with your car and how to fix it. It’s the same here.
I can promise that after about 10 minutes (the time it takes you to read these 2 articles) you’ll understand acne like never before, and you’ll understand how to boot it out of your life for good.
About terminology. I use terms inflammation and oxidation interchangeably. Technically they mean different things, but in this context we can use them to refer to the same thing. So oxidative damage is the same as inflammatory damage. Inflammation, of course, is how your body responds to injury. Inflammation is what turns your thumb red after you hit it with a hammer, and it’s inflammation that makes big pimples so painful.
Sebum oxidation, the trigger that starts acne
Science on the past decade has quite conclusive shown that every single 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 conditions for sebum oxidation to happen.
This masterpiece of PowerPoint art helps to explain acne.
Sebum is made of many fatty acids, one of them is called squalene. Squalene is very important for skin health and that’s why it’s part of many skincare 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 in the area. And the severity of acne was linked to the degree of oxidative damage squalene suffered. In other words, if squalene only suffered minor damage it caused little bit of acne, but squalene that was badly damaged caused severe cystic acne.
Here’s what a 2010 review had to say:
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. In addition, the treatment of ear skin with squalene peroxidation by-products caused marked hyperplasia and hyperkeratosis of the epithelium in follicular infundibulum, and increased the proliferation of the sebaceous glands.
Lipid Mediators in Acne. Monica Ottaviani, Emanuela Camera, Mauro Picardo. Mediators Inflamm. 2010; 2010: 858176. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943135/
Vitamin E to the rescue
Because damaged squalene is so harmful, your skin does everything it can to protect squalene. It does this with vitamin E. Vitamin E is a strong antioxidant that can protect squalene from oxidative damage. It’s also fat soluble, which makes it one of the main antioxidants in sebum.
Studies have shown a tight correlation between squalene and vitamin E secretion. So the more squalene your skin produces the more vitamin E it also secretes.
The next bit explains what squalene peroxide does to the skin. It explains why acne is more about inflammation than about bacteria, and how oxidative damage creates ideal conditions for bacteria to colonize the blocked pores. It’s more about details and not absolutely necessary for you to understand. Click the link below to expand the text, but you can also skip it if you want.
Click to expand
How squalene causes acne
Other studies have shown that squalene peroxide stimulates keratin and sebum producing cells in the skin. Keratin is a tough protein that binds the skin cells together. When the skin produces too much keratin, a condition known as hyperkeratosis, dead skin cells have difficulties in separating. So your skin pores get filled with big lumps of dead cells, instead of individual cells. Hyperkeratosis is a common feature in many skin conditions and is the reason why retinoids work so well in acne – they prevent hyperkeratosis.
Sebum of course is the oil your skin produces.
The combination of excess keratin and sebum production creates ideal conditions for blocked pores. Much like logs in a river, big lumps of dead skin cells get tangled, and combined with excessive sebum production, easily obstruct the narrow openings in the skin pores.
It’s not bacteria
A blocked pore is the first stage of a pimple. It’s important to note that this blocking of skin pores has nothing to do with bacteria. Studies have shown that these earliest forms of pimples don’t even contain bacteria.
Noninflamed lesions, which are first visible during the adrenarche in acne-prone individuals, do not contain propionibacteria. Comedogenesis appears to be independent of bacterial infection and may be driven by high levels of bioactive interleukin-1α derived from ductal hyperkeratinocytes.
Is Acne an Infection of Blocked Pilosebaceous Follicles? Anne Eady, Jonathan H. Cove. American Journal of Clinical Dermatology. July 2000, Volume 1, Issue 4, pp 201-209. http://link.springer.com/article/10.2165/00128071-200001040-00001
Why is this important?
Because the vast majority of current acne therapies are aimed at controlling bacteria. Yes, controlling bacteria can help, but you can get better results by attacking acne before it even gets started. This is why topical antioxidants can be so effective in acne. They can prevent this initial oxidative damage to sebum and stop acne before it even gets started. You’ll see this in studies that show topical vitamin B3 (and some other antioxidants) are more effective than topical antibiotics or benzoyl peroxide – not to mention topical antioxidants don’t have any side-effects.
Studies have also shown that the initial oxidative damage to sebum alters the environment within a blocked pore to be suitable to bacterial colonization. And if you can prevent the initial damage the bacteria could not colonize the blocked pore.
P. acnes, once thought to be the initiating factor of inflammatory acne, might never make the pilosebaceous unit its home were it not for this initial inflammatory insult to the sebum. Oxidation of sebum alters oxygen tension in the follicle, resulting in the micro-aerophilic environment required for P. acnes to survive. Apparently, inflammation and oxidative stress might set the stage for all subsequent pathogenic factors leading to acne.
Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles. Whitney P Bowe, Alan C Logan. Lipids in Health and Disease 2010, 9:141. http://www.lipidworld.com/content/9/1/141
Bacteria of course also play a role in acne. Once oxidative damage has blocked a pore and changed the environment within, the bacteria take over it and multiply rapidly. They produce toxins that irritate the skin. The immune system attacks the bacteria and this exponentially increases inflammation in the area. This is what turns invisible blocked pores into red and painful pimples.
But the important point is that none of this would happen without the initial oxidative damage to sebum. Let me say that one more time. Science has clearly shown there can be no acne without initial oxidative damage to sebum. It’s the match that lights the fire and sets the stage for acne.
That’s why most of your efforts should be aimed at preventing sebum oxidation. A case can also be made for antibacterial agents to control those pimples you cannot completely prevent – it happens because of genetics (say hi to your parents).
Setting the stage for sebum oxidation
So far we’ve only talked about what happens at your skin. Cliché as it may be, but acne goes deeper than the skin. Here’s where things like diet, stress, hormones and gut problems come into play.
If you look at the image above, you’ll see the two arrows that lead to sebum oxidation: hormones and inflammation. The combination of hormones and inflammation is what creates the conditions for sebum oxidation to happen and for acne to get started.
- Hormones affect how much sebum your skin produces and also the composition of sebum. Studies have shown that acne-prone skin produces about 3 times more sebum than normal skin. As if that’s not bad enough, sebum from acne-prone skin also has proportionally more squalene. This means that acne-prone skin has a lot more squalene than normal skin. Treatments that affect acne-hormones (such as diet) can reverse this.
- Inflammation affects acne by depleting antioxidant stores. Here’s a simple analogy. If you think of inflammation as fire, then antioxidants are like the fire brigade. The fire brigade has a limited capacity to put out fires. If there are too many fires at one time, then the fire brigade may not have time to put out all the fires. Studies have shown that something like this happens in acne. That excessive sebum production causes so much demand that the antioxidant system cannot keep up.
There are several lines of evidence to show the antioxidant system cannot cope with the oxidative stress (medical term for inflammation) acne causes.
For example, a study published in 2012 measured antioxidant and inflammation levels in skin scrapings from acne-prone and healthy skin. The study found 2 to 4 fold more inflammation in acne-prone skin.
Compared to people with healthy skin acne patients have lower blood levels of antioxidants and more inflammation. There’s even a dose-response curve; people with severe acne show higher levels of inflammation than people with mild or no acne. Here’s a graph I produced from a study published in January 2013.
Several studies show topical antioxidants reduce acne more than topical antibiotics or benzoyl peroxide.
Then there’s the 2012 study that showed 50% reduction in acne with antioxidant supplements. The researchers randomly assigned the participants into one of four groups: N-Acetyl Cysteine (NAC), sillymarin (found in milk thistle), selenium or placebo. Each participant took the supplement daily for 2 months. This graph shows average pimple count in each group:
Apologies if it seems like I’m laboring over this too much. I just want to make sure you understand how critical inflammation is to acne. I don’t mean to imply that inflammation is more important than hormones, but people are more familiar with the role hormones play in acne, and that’s why I focused more on the less well-known aspect.
The skin is constantly exposed to inflammation; think UV rays, air pollution, bacteria and pathogens, harsh chemicals you apply on your face, and chlorine in swimming pools. Humans have an effective system protecting us from the harmful effects of excessive oxidative damage: antioxidants.
Due to genetics and hormones acne-prone skin produces up to 3 times more sebum than normal skin. Excessive sebum production increases the demand for antioxidant protection. If the antioxidant system cannot meet the demand sebum is left vulnerable to oxidative damage. Following oxidative damage squalene forms squalene peroxide, a massively comedogenic substance that causes blocked pores and sets the stage for acne.
And that is why you get acne.
Next, how to use this to get permanently clear skin, or
- Monica Ottaviani, et al. Lipid Mediators in Acne. Mediators Inflamm. 2010; 2010: 858176. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943135/
- Anne Eady, Jonathan H. Cove. Is Acne an Infection of Blocked Pilosebaceous Follicles? American Journal of Clinical Dermatology. July 2000, Volume 1, Issue 4, pp 201-209. http://link.springer.com/article/10.2165/00128071-200001040-00001
- Whitney P Bowe, Alan C Logan. Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles. Lipids in Health and Disease 2010, 9:141. http://www.lipidworld.com/content/9/1/141
- Ozturk Perihan et al. The activity of adenosine deaminase and oxidative stress biomarkers in scraping samples of acne lesions. Journal of Cosmetic Dermatology.Volume 11, Issue 4, pages 323–328, December 2012. http://onlinelibrary.wiley.com/doi/10.1111/jocd.12011/abstract
- Hani A. Al-Shobaili, et al. Biochemical Markers of Oxidative and Nitrosative Stress in Acne Vulgaris: Correlation With Disease Activity. Journal of Clinical Laboratory Analysis. Volume 27, Issue 1, pages 45–52, January 2013. http://onlinelibrary.wiley.com/doi/10.1002/jcla.21560/full
- Bowe WP, Patel N, Logan AC. 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. http://www.ncbi.nlm.nih.gov/pubmed/22648222
- Ahmed Salih Sahib, et al. Effects of Oral Antioxidants on Lesion Counts Associated with Oxidative Stress and Inflammation in Patients with Papulopustular Acne. J Clin Exp Dermatol Res 3:163. http://www.omicsonline.org/2155-9554/2155-9554-3-163.php?aid=10078