Acne, who isn’t familiar with it? Almost everyone ‘catches’ it to some degree or another around puberty. Even many people still suffer from it in adulthood, with the condition estimated to persist into the 20s and 30s in around 64% and 43% of individuals, respectively [1]. While the condition is easy to recognize clinically, its pathogenesis (the process by which it develops) is extensively complex and researchers worldwide are still deciphering it bit by bit.
Feel free to skip over to the final section of this article if you’re just looking for an example treatment regime.
In general, acne is thought to result from the following four pathogenic factors (in no particular order) [2, 3]:
- Increased sebum production
- Abnormal keratinization
- Release of inflammatory mediators into the skin
- Bacterial hypercolonization of the hair follicle by Cutibacterium acnes (C. acnes, formerly known as Propionibacterium acnes [P. acnes])
An increased sebum production per se isn’t much of a problem in the sense that it would just give a greasy skin. However, it’s thought to contribute to acne by providing a more comfortable environment for C. acnes and alteration of the composition of fatty acids in sebum. In particular, a decrease in its linoleic acid content. Taken together, this in turn might disturb the barrier function of the follicular walls of the keratinocytes (cells that make up the hair follicle) [4] and lead to an inflammatory cascade [5].
The abnormal keratinization refers to these cells not shedding normally like they should. Instead of sloughing off and being pushed onto the skin surface, they become cohesive and stick around in the hair follicle—essentially clogging it. It is thought this is an early event in the development of a comedone, yielding a microcomedone.
Androgens play a role in both of these. For example, androgen-insensitive men fail to produce demonstrable levels of sebum and don’t appear to develop acne [6]. This signifies that, at least some, androgenic activity is required for developing acne. A trial in which men first received ethinylestradiol (which would markedly suppress endogenous testosterone production), and subsequently received concurrent administration of testosterone, showed that the addition of testosterone led to a notable increase in sebum production [7]. Finally, the well-known testosterone researcher Shalender Bhasin and his group measured sebum production in men receiving graded dosages of testosterone (50, 125, 300, or 600 mg weekly) with or without the 5α-reductase inhibitor dutasteride for 20 weeks [8]. They found that sebum production in the forehead region, but not on the nose or back, was related to testosterone dose. However, the association was week and the 600 mg group even saw a, albeit non statistically significant, decrease in their sebum score. Sebum production might seemingly play a less important role in AAS-induced acne than expected. Indeed, oily skin was hardly reported by the subjects, whereas acne was more frequently reported.
Further interesting data with regard to the incidence of acne as a result of anabolic steroid use in high dosages comes from the HAARLEM trial [9]. Briefly, the HAARLEM trial was a prospective cohort study in which 100 anabolic steroid users were followed over time while they self-administered AAS [9]. Mean dosage, based on label information, was 898 mg per week, thus making their AAS cycle quite representative of common usage by bodybuilders. Measurements were taken before, during, as well as 3 months after the end of their cycle and 1 year after the start of their cycle. The researchers visually examined the skin for acne and at baseline 13% of the users were found to have acne. This increased to 29% at the end of the cycle, and dropped back to 23% 3 months after the cycle, and 10% 1 year after the start of the cycle. Self-reported acne was notably higher at the end of their cycle, with 10% at baseline, 52% at the end, 29% 3 months after, and 14% 1 year after the start of the cycle.
Clearly, acne is a common side effect of AAS usage in high dosages. But what can be done about it? In this article I’ll outline some treatment modalities. A word of caution is in place, however, as none of these trials evaluated the effects of these treatment modalities in AAS-induced acne specifically. However, it’s very reasonable to assume that they can work in this situation too.
