Androgenetic alopecia is the most common form of hair loss in men and women alike. It is especially common in males, and more than 50% of the population will notice it by the age of 50. As its name signifies, androgenetic alopecia involves the interplay of both androgenic hormones and genetic factors. Individuals with this condition appear to be more locally sensitive to androgens, and have higher levels of androgen receptor protein and dihydrotestosterone in the scalp, in comparison to those unaffected. Although dihydrotestosterone is identified as the primary hormone involved in the progress of androgenetic alopecia, it does not possess a unique ability to influence this condition. All anabolic/androgenic steroids stimulate the same cellular receptor, and as a result are capable of providing the necessary androgenic stimulation. Baldness can result from steroid use, even in the absence of steroids that convert to, or are derived from, dihydrotestosterone.
The genetics of androgenetic alopecia are not fully understood. At one time it was believed this condition could be inherited solely from the maternal grandfather. More recent evidence contradicts this notion, however, showing strong support for father-to-son transmission in many cases. A number of genes have been identified as having a potential link to the disorder, including certain variants (polymorphisms) of the androgen receptor gene. No single genetic variant alone has yet been able to explain all cases of androgenetic alopecia, however. AGA is now believed to involve several genes (polygenic). The way these genes combine, and the level of androgens in the scalp, may ultimately work together to control the onset and severity of androgenetic alopecia. Estrogen is also known to lengthen the anagen phase, and the pathogenesis of this condition may ultimately involve genes that alter both androgen and estrogen activity.
Treatment for androgenetic alopecia in men usually involves topical minoxidil and oral finasteride, a 5-alpha reductase enzyme inhibitor. Women are typically prescribed antiandrogens and estrogen/progestin drugs. The focus in both cases is on reducing relative androgenic action in the scalp, which may (at least temporarily) stall the condition. With this in mind, many steroid users concerned with hair loss will tailor their drug intake to minimize unnecessary androgenic activity. This usually involves moderate dosing and the careful selection of drugs with high anabolic-to-androgenic ratios, such as oxandrolone, methenolone, or nandrolone. Alternatively, some may choose to use injectable testosterone esters combined with finasteride to reduce scalp DHT conversion. These strategies are met with varying degrees of success.
There has been no study on the role of genetics in baldness linked to steroid abuse. Anecdotally, individuals with existing visible androgenetic alopecia appear to be those most susceptible to the effects of anabolic/androgenic steroids on the scalp. For many of these people, the loss of hair appears significantly accelerated when taking these drugs. On the other hand, this side effect is generally a much less significant issue with individuals that have not noticed thinning beforehand. Many go on to abuse steroids for years without any visible effect at all, making it clear that there is more to this disorder than local androgen levels. It is well understood that androgens play a role in the progression of androgenetic alopecia for those genetically prone. Steroid use can, therefore, coincide with the first noticeable onset of this condition. It is unknown, however, if anabolic/androgenic steroid abuse can cause baldness in an individual that does not carry any genetic susceptibility.
Wlliam Llewellyn (2011) - Anabolics