The A/A (Androgenic/Anabolic ratio) thing was done in the 30s in Germany. This is from an old meso article:
"For you to fully appreciate the things I am going to discuss in this article you have to have a background on how anabolic steroids are screened for activity. As you know, anabolic steroids are derivatives of testosterone which share two types of activity – muscle building (deemed anabolic) and non muscle male sex hormone related activity (deemed androgenic).
The goal of researchers in the golden age of anabolic steroid research (1935-1965) was to synthesize a compound which retained a high degree of anabolic activity coupled with a vastly diminished androgenic activity. This property was quantified using what is known as the Anabolic / Androgenic ratio (A/A ratio). The goal was not so much to produce a compound that was strongly anabolic, but rather the goal was to produce a compound with the highest possible A/A ratio. You must understand that the market for anabolic steroids was not bodybuilders / athletes but geriatric patients, patients recovering from surgery or injury, or those suffering from weakness or catabolism secondary to some other disease. These can include men and women, and even children. It was therefore paramount to avoid any virilizing effects when providing such people anabolic treatment, and so an anabolic agent with a very low A/A ratio was needed.
To determine the A/A ratio, scientists utilized a test called the Rat Levator Ani Assay. In this test, scientists use two groups of castrated rats. The rats are castrated to remove any interfering influence from fluctuating natural androgen levels. The first group of rats are a control group that receives a placebo, while the second group receives the steroid (either by injection or orally). After a period of time (several days to weeks) the rats are sacrificed. Researchers then isolate three organs from each of the rats – the seminal vesicles, ventral prostate, and levator ani muscle. These organs are all weighed and a comparison of the active group to the placebo groups is made. The differences in weights for the seminal vesicles and ventral prostate represent androgenic activity, while the difference in the weight of the levator ani muscles in the control and active group represent anabolic activity.
To give a landmark against which to gauge the relative activities of each steroid in this assay, a standard is used in some of the rats in the active group. This standard is usually testosterone, testosterone propionate, or 17alpha-methyltestosterone (MT) and the results obtained from the rats given this standard are designated an arbitrary number of 1 for anabolic activity and 1 for androgenic activity. Therefore these standard androgens are said to have an A/A ratio of 1."
A/A ratios are listed on the meso profiles.
Interestingly, later research showed that the drug ester affected the A/A ratio.
"The ester bond is fairly easily broken under the right conditions. If the molecule is dissolved in water, this can occur by a simple chemical reaction, yielding the parent drug and a carboxylic acid. For example, if the steroid used is testosterone propionate, testosterone and propionic acid are released. Carboxylic acids are safe and natural in the body in reasonable amounts. It should not be thought that these are strong acids because they are not: they are acids in the same sense that, e.g., Vitamin C or lactic acid are acids. Furthermore, the amount of carboxylic acid present at any time is extremely low.
The carboxylic acids do not have any activities of interest. Once the ester group is removed, it has done its job, and the parent drug acts in its normal manner.
Besides the simple chemical hydrolysis described above, the esters can be removed by enzymes in the blood called esterases, though water still is required for the reaction. The great majority of hydrolysis occurs with the help of these enzymes or by non-specific reactions with proteins. These reaction cannot take place while the esterified steroid is dissolved in fat. Thus, while the esterified steroids are dissolved in fat, they are protected from hydrolyis, and thus serve as a depot for the drug, giving extended duration of action.
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What is the significance of the partition coefficient?
Differences in partition coefficient seem to account almost fully for the differences between various esters of anabolic steroids, as shown by Chaudry and James.1,2 To understand their work, though, it is necessary first to consider the methods they used to obtain their data on the anabolic and androgenic effects of the drugs tested.
These scientists are not using those terms in the manner which many bodybuilding authors do. The anabolic effect is measured by increase in weight of the levator ani muscle in the rat, and the androgenic effect is measured by increase in weight of the seminal vesicles and prostate. These measurements are neither perfectly indicative of muscle-building value to bodybuilders nor to any particular undesired side effect except perhaps prostate enlargement. Despite the limitations of the method, this was the assay method available.
A number of esters of nandrolone were studied, using various single doses, but only the results from a single dose of 1 mg are given here. The results are as follows:
Parent Drug
Ester
# of Carbons
Anabolic Effect
Anabolic / Androgenic Ratio PRC** (P) x10-3
Nandrolone formate 1 1176 13:1 15*
acetate 2 1594 11:1 25*
propionate 3 1880 10:1 41*
butyrate 4 1488 7:1 69
valerate 5 2526 9:1 115*
hexanoate 6 3731 9:1 192
heptanoate 7 6559 13:1 269
octanoate 8 5557 15:1 611
nonanoate 9 5080 19:1 455
decanoate 10 7735 25:1 802
undecanoate 11 6576 32:1 1460 "
In short the longer ester had higher A/A ratios. This goes against common sense, showing that A/A ratios are not so useful. God only knows what they are measuring.
In short, we now know that anabolic activity is caused by differences in activity at the androgen receptor (AR) in muscle. Androgenic activity is caused by increasing activity, directly or indirectly, on the androgen receptor (AR) in sexual tissues. There is no mystery here. Its mostly a matter of metabolism when strong drugs like deca aren't too androgenic, and otherwise, strong AR agonists like tren and very androgenic and anabolic.
There's no sense confusing things with outdated myths.
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