Sunday, March 17, 2013

Is Acne a Disease?

The Prevalence of Acne 

Acne affects between 40-50 million in the US, which in 1998 was between 14.8-18.5% of the population [1].  Acne is more common during adolescence, but it also affects a smaller proportion of adults (see table) [2] and even about 36% of 4-7 year olds have acne [3] 

Prevalence of Acne
Middle Age

Acne is considered a fairly normal part of adolescence as it is so common at that age, and is one of those things that apparently, just happens. 

Being considered a normal part of adolescence may have led to studies such as the one quoted below, which suggest acne is not a disease, but rather an evolutionarily adaptive, physiological process. 

“…adolescent acne is a normal physiological process - a high-order psychoneuroimmune interaction - that functions to ward off potential mates until the afflicted individual is some years past the age of reproductive maturity, and thus emotionally, intellectually, and physically fit to be a parent.” [4] 

There are two major flaws with that idea: 

1.      Many people who aren’t adolescents have acne (see table)
2.      Hunter-gatherers don’t seem to get acne 

There have been no reports of acne among the Inuit, Okinawans, Aché (hunter-gatherer tribe in Paraguay) and Kitavans.  It’s possible that these people are genetically resistant to acne, but that doesn’t really explain their absence of acne as other South American Indians and Pacific Islanders have acne when they adopt a western lifestyle [3] [5] 

How Acne Happens 

The development of acne seems to have a few key steps: 

1) Hyperkeratinisation of the Hair Follicle 

Dead skin cells in the hair follicle would normally detach (desquamate) and be forced out of the follicle, mainly by the growing hair.  In hyperkeratinisation that process is blocked and many dead skin cells don’t leave the follicle due to an excess of keratin, which is the main protein of skin.  Keratin sticks the dead skin cells together and blocks the hair follicle or the sebaceous duct (where sebum comes from).  When the normal flow of sebum onto the skin surface is obstructed the comedones (blackheads and whiteheads) are formed which starts the process of acne [6] [7]. 

People with acne have abnormal keratinisation that that obstructs the pilosebaceous unit (hair follicle + sebaceous gland + arrector pili muscle (small muscles that cause goosebumps)) [6]. 

2) Androgen-mediated Increases in Sebum Production 

Sebum is an oily substance that consists of triglycerides, wax esters, squalene and sterol (mostly cholesterol) esters.  Sebum is produced by sebocytes in the sebaceous gland and the main function of sebum is to keep the skin and hair supple. 

Acne cannot occur without sebum [7] and people with acne secrete about 2.2 times more sebum [8].  Acne occurs mainly on the face, upper chest and upper back, which are the parts of the body that produce the most sebum [9].  Androgens are largely responsible for sebum production. 

3) Colonization of the Follicle by Propionibacterium acnes (P. acnes) 

P. acnes are commensal anaerobic gram-positive bacteria that live mainly on the skin.  They are normally harmless, but are generally implicated in acne (hence their name) (see the table below) [10] and are pretty strongly associated with acne [9]: 

  • People with acne have more P. acnes
  • P. acnes progressively increases from pre-adolescence to early adulthood 
  • P. acnes correlates with sebum excretion
  • The face, upper chest and upper back have more P. acnes and sebum 
  • P. acnes can induce a T cell reaction
  • Antibiotics are used as a treatment for acne and antibiotic resistance is associated with treatment failure (although may also be due to biofilms and poor penetration of biofilms) 

However, the incidence and severity of doesn’t always correlate with P. acnes, and improving acne doesn’t always reduce P. acnes.  Although this could be because some treatments are anti-inflammatory [9], which may also explain the lack of correlation. 

4) Hyperinflammatory Immune Response

Inflammation is a major part of acne.  Acne patients mount an immune response to P. acnes that is not seen in normal patients [9].  There are several sources of inflammation in acne (also see the table below): 

  • P. acnes generate lipases that can break down the triglycerides in sebum into glycerol and free fatty acids.  FFA (particularly medium chain C8 to C14*) are comedogenic, irritate the follicular lining and can lead to rupture of the follicle with release of the follicular contents into the surrounding dermis, which leads to inflammatory lesions (people with acne also tend to be more sensitive to FFA) [6]. 
  • P. acnes releases pro-inflammatory enzymes and cytokines 
  • P. acnes can bind to toll-like receptors, which initiates an inflammatory response 

* Which may explain how coconut oil and MCT oil can be a trigger for acne in some people.


So we have four main questions: 

1.      What are the causes of hyperkeratinisation of the hair follicle?
2.      What are the causes of excessive sebum production?
3.      If there is, is there any way to avoid colonisation by P. acnes?
4.      What are the causes of the hyperinflammatory immune response?


  1. The acne posts are very interesting and useful, many thanks, keep it up!

  2. Consuming coconut products breaks me out like you wouldn't believe. Consistent coconut consumption transforms me into half human, half p acne. It really is horrible and painful. I discovered this the long hard way.