Anabolic-androgenic steroids are a fairly wide family of compounds that began to be used in the 1950s, and on a large scale in the following decades. The history of modern androgen therapy did not begin until 1935 in Amsterdam, when Ernest Lacquer isolated testosterone from bull’s testicles.
It should be added that he isolated only 10 mg of testosterone from 100 kg of bull’s testicles. Researchers working with Lacquer found that the new compound has greater potential compared to androsterone and called it testosterone.
Testosterone was synthesized in 1935. In the same year, Adolf Butenandt in Göttingen and Leopold Ruzicka in Basel independently synthesized testosterone. Methylated testosterone was the first of 3 synthetic AAS, in addition to mestanolone and metandriol. All of them are examples of C17 alpha alkylated SAAs (methyl group at the C17 position), which immunize these agents against the first-pass effect (little of the active substance is lost in the first contact with the liver), while increasing their toxicity.
The abbreviation SAA stands for “anabolic androgenic steroids”, ie agents that affect anabolism (eg, muscle growth) and androgenicity, that is, male sexual characteristics (testes, body hair, voice timbre, effect on the prostate, seminal vesicles, etc.). Strong androgenic agents in women cause clitoral hyperplasia, voice deepening, breast and uterine reduction, muscle gain, acne, etc.
Testosterone affects both parameters equally, and other AAS have different proportions of androgenicity and anabolicity. Immediately correcting the common myth: tables with ratios circulating in the network are mostly based on research on rats or mice (or even on cell lines) – their impact on humans is negligible or none. For example, how does a study of anabolic effects on the levator ani muscle in rats relate to humans? Some theoretically powerful agents (according to the table) do not work so well on human muscle growth. An agent that is strongly anabolic and weakly or not androgenic would be ideal. Unfortunately, it was not possible to create it. In addition, deeper structural modifications of the AAS carry other possible complications, such as effects on the liver – which will be discussed in a moment.