When the laymen thinks of “anabolic steroids,” the first few words that come to mind are more than likely: aggression, testosterone, and muscles. While various steroidal compounds can mediate actions to perpetuate one or a number of muscle-building or male characteristic tropes, they are not mutually exclusive.
The actions that we attribute more so to certain anabolic-androgenic steroids (abbrev. AAS) than others in regards to cell growth (muscle, bone density, etc.) are regarded as being more anabolic. Their actions include increased protein synthesis from amino acids, increased nitrogen retention, increased appetite, increased bone remodeling and growth, and stimulation of bone marrow, which increases the production of red blood cells. Conversely, more androgenic compounds can be attributed towards perpetuating male characteristics. You can see them at work through increased sebaceous gland oil production, increased libido, testicular atrophy, changes in mental state including aggression, reduced sperm count, and central nervous system stimulation, among others.
This series will cover four different “classes” of steroids in which the author has dictated: anabolic, androgenic, DHT-derived, and “exotic” compounds (of which DHT-derived and exotic compounds can have vary degrees of anabolic/androgenic properties.) One thing to understand is that when looking at AAS compounds, it is unwise to think of them as mutually anabolic, or mutually androgenic. AAS compounds work in shades of grey in regards to all facets…for example, most DHT-derived compounds tend to be non-aromatizing (do not convert to estrogen), however Oxymetholone is a unique example. It has DHT actions but can actually perpetuate gynecomastia by being recognized within the body as progesterone, unlike other DHT derivatives. Thus, while I will be “classifying” compounds, the walls between these classifications are much more malleable that classifications seem to allude to.
Locks and Keys and Other Things:
To strengthen the above ideology, the reality is that ALL anabolic-androgenic compounds exert their effects through the same androgen receptors (…probably). All steroid compounds have a specific binding affinity to receptors within different physiological areas—I.e. Muscle tissue, reproductive regions, adipose tissue and even parts of the brain! That is to say that certain compounds are more likely to be bound within certain areas because they fit that specific “lock” better.
Once the “keys” are in the “locks”, they tell the receptor cell different messages in regards to how they fit into that receptor. This culminates in two ways: different AAS compounds tell the cell to turn on or keep quiet certain genes depending on their structure (and in turn their anabolic/androgenic ratio). This could mean increased protein synthesis from a strong anabolic compound, or heightened CNS activity from an androgenic compound. Also, different compounds act differently once taken in by the receptor– DHT would mediate its actions directly in the reproductive regions, while Testosterone would act as a pro-hormone, being readily converted by 5α-reductase to the more potent androgen DHT.
Seems pretty simple right? Not so fast. Note I said “probably,” after AR binding being the only mechanism by which AAS exerts its effects? This might not be the case. Let’s look at two black sheep to the binding affinity theory: Oxymetholone and Stanzolol.
It is well supported that both Oxymetholone’s and Stanzolol’s binding affinity is low that it is non-detectable. Obviously anadrol and winstrol certainly have their place in a user’s arsenal; these are not weaksauce drugs. So how then do they exert their effects? There are two theories: First, that while current procedures are not precise enough to detect it, they DO bind somewhat to the AR, but that once fitted they activate very specific genes whose products promote skeletal muscle anabolism while failing to activate genes which promote virilization, which other compounds do not. The other and as equally plausible is that all binding studies have been performed in vitro, or outside of the host. This leaves out the reality that there could be another physiological action at work that promotes the binding of Oxymetholone and Stanzolol in vivo.
If you want this author’s opinion, I believe it is the later of the two, and precisely the reason I bring the topic up: although this series will present some fancy science words and mechanisms of actions of different compounds, the reality is that research into AAS (hell, research into the human BODY for that matter) is in a fairly infant stage, and so there one must not get too terribly caught up in the science and disregard the anecdotal evidence; i.e. Test is a great base and one of the best compounds for putting on size while staying “safe” with health, and can be run for long periods of time. That tren, anadrol, and halotestin increase strength substantially, etc.
It also doesn’t mean you should base a cycle off of what you read. In short, androgen receptor sensitivity is HIGHLY variable in men. The androgen receptor has a few areas in its molecular structure where changes in the amino acid sequence can affect the sensitivity of that receptor for attaching to testosterone or other androgenic-anabolic drugs and attaching to the chromosomes — or relaying the receptor-stimulated gene messages to the rest of the cell. On average, humans are 99.9% biochemically similar to each other, but that .1% makes all the difference. So, read, learn, understand what works for the MAJORITY, but experiment. This series will be a guide, no more, no less.
- Saartok T, Dahlberg E, Gustafsson JA. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology. 1984 Jun;114 (6):2100-6.