Sunday, April 28, 2013


If you read the pop media you’ll get the impression that the cause of acne is simply sebum >> clogged pore>> acne and that acne is largely inevitable and something that ‘just happens’ to adolescents.  Acne is so common that some researchers have proposed that acne is evolutionarily adaptive.  The problem with these ideas is that many people who aren’t adolescents have acne and hunter-gatherers have near population wide freedom from acne.
While excess sebum does strongly promote acne it’s a gross oversimplification to say sebum >> clogged pore>> acne.  There a few necessary pathological mechanisms involved in acne
  1. Hyperkeratinisation of the hair follicle
  2. Increases in sebum production
  3. P. acnes colonisation
  4. Hyperinflammatory immune response
There is strong evidence that androgens (T, DHT, DHEAS) and insulin/IGF-1 increase sebum production and can promote acne.  Androgens also promote hyperkeratinisation.  There are associations between milk consumption and high GL diets (both increase insulin and IGF-1) with acne
Sebum is made up of FFA, triglycerides, wax esters, squalene and cholesterol.  People with acne tend to secrete more sebum and a lot more squalene.  Squalene and wax esters are only found in sebum and sebum has two unique fatty acids: sapienic acid (16:1 cis n-10) and sebaleic acid (18:2 cis n-10).
High sebum production can dilute linoleic acid, which can compromise epidermal barrier function which then leads to water loss, hyperkeratinisation, inflammation and P. acnes colonisation.
MUFA in sebum seem to promote acne and a low GL diet increases the SFA:MUFA ratio in sebum and improves acne.
Squalene oxidisation promotes inflammation, hyperkeratinisation and sebum production and allows P. acnes colonisation by altering the oxygen tension of the follicle
People with acne show many signs of oxidative stress, which suggests a systemic source for the squalene oxidation
There are two main types of acne: inflammatory acne and non-inflammatory acne.  People are generally more concerned with inflammatory acne, which shows signs of immune activity (pus).
Perhaps the critical factor that separates inflammatory from non-inflammatory acne is a hyperinflammatory immune response to P. acnes as well as other things like FFA.  People with acne tend to have a hyperinflammatory immune response and GI related problems, which are a likely cause (but not the only one) of the hyperinflammatory immune response.
Prolactin promotes acne by increasing 5-alpha reductase and by promoting a hyperinflammatory immune response.  Many things that increase prolactin also seem to trigger acne, and a drug that reduces prolactin is therapeutic for acne
There is an association between acne with depression and anxiety.  Stress is a common cause of all three diseases.  Stress increases substance P and prolactin, promotes dysbiosis and may lead to glucocorticoid resistance, all of which promote acne.
The forums have two threads that are loaded with information, far more than I have on my blog.  Had I known about it earlier, I may have not done the blog posts at all.  See:
Some Strategies for Acne
This is for informational purposes only and is not meant to diagnose or treat any medical condition.
I have a speculation that if you broadly classify the mechanisms of acne as androgen/growth-based and immune related, then since men tend to have more androgen signalling and women tend to have a more inflammatory immune response.  So, for men the inflammatory immune response is more modifiable, whereas for women it’s the androgens.
Reduce Androgen Signalling if Female
A main cause of this is PCOS.  I don’t know much about it, but reducing insulin resistance seems to help.  See What Causes Insulin Resistance? Part VII
Reduce Sources of Oxidative Stress and Inflammation
Oxidative stress and inflammation underlie the hyperkeratinisation and the oxidised squalene in acne.  Since most people with acne are young you need to pretty much rule out causes of disease that are generally only found among older people, like mitochondrial dysfunction, insulin resistance and type 2 diabetes.  Some underlying problems in young people could include poor dental hygiene and gut health, food allergies and intolerances.
Reduce Stress
See Manage Your Stress.  Also look at some of the other things that increase prolactin.  See Prolactin and Stress
Improve Immune Regulation


  1. Great set of posts. Extremely useful. I wonder if it might be more precise to say that instead of inflammatory or non-inflammatory acne, there is "sufficiently-inflammatory-to-cause-rupture-of-follicle-wall acne" and "insufficiently-inflammatory-to-cause-rupture acne". Either way, looks like inflammation control may be key. Very thought provoking. Thanks.