AAS Half Lives and Anobolic/Androgenic Ratios

This thought/question was spawned after reading “Formestane vs Arimidex”. Bill Roberts wisely suggested learning the reasoning behind particular cycles. I think Bill and Brock would agree with Brian that half lives of AAS are important, as well as the androgenic/anabolic ratio of those AAS. That knowledge, per Brian’s reasoning (which also seems imminently reasonable), will enable a cycle design that approximately correctly predicts the amounts of the AAS in the system as a function of time. Brian also mentions there is quite a bit of disagreement between “authorities” on just what those half lives and anabolic/androgenic ratios are. But a cycle constructor needs something practical to go on. So here is my question: Where could one get a reasonable approximation (at least) of those two characteristics of AAS? Could Bill, Brian, and Brock possibly email those interested, or post that info (or where to obtain it) on this BB? I realize that AAS compete, which adds yet another variable into the formulation, but the above mentioned information would be of great benefit to those wishing to construct cycles that are effective, i.e., getting the “most bang for the least amount of buck”! T-Mag is in its own universe, and I feel extremely fortunate to be alive at the same time as all the contributers to this fantastic “meeting”!

I don’t have the info handy but I can tell you that
G&G’s or even the PDR (for what it lists) should have
half lives…any good pharmacology text book will also.
Merck Index too (maybe? Bill?). As for the ratio, I
don’t really view that as all that important WRT to time
kinetics (or even metabolism unless you’re interested in
5-AR and aromatization…and most of us know what aromatizes
and what is 5-AR’able).

The most important things, to me, in constructing a cycle
are (in order):

  1. Risk:reward (side effects).

  2. Availability

  3. Cost

So you need to know what you want to do and then see what
you can get to achieve what you want to do. You also
need to assess risk. How much are you willing to take?

The more androgenic steroids, as a rule, have a higher
incidence of deletarious physical side effects (but not
always lab side effects, because something “mild” but
17AA’ed, like stanozolol, in equipotent dosage to nandrolone
will have a higher incidence of liver toxicity).

I could go on and on about this forever, it would be a book.

And maybe with some prodding and Bill as a co-author, it
will be :slight_smile:

–Brock

Don’t worry about anabolic steroids “competing,” it’s not an issue. With drugs which are what is called “partial agonists” (estriol is an example like this) then competition is very important because the receptor doesn’t act the same when the partial agonist is bound as it does when a full agonist is bound.

So in that case, adding a partial agonist could actually give less total effect, because many of the receptors are now binding a partial agonist instead of a full one.

Not so with anabolic steroids! They are all full agonists. Adding a so-called “weak” steroid like Primobolan will still always add effect.

As for half-lives, they are very hard to find in the literature and I don’t have anythiing like a full list. The orals are unpredictable: you can’t look at the structure and guess. It’s a question of how well the steroid binds to metabolizing enzymes, which just cannot be determined except by experiment.

With the esters it’s another story, in the rat it has
been shown to be a very simple relationship: each added carbon in the chain adds about 1.5 days to the half life.
In these experiments, it was the same experimenter using
the same methods for different esters and getting this
consistent result. However, their consistent results were weird (though consistent!) since normally the rat shows shorter half lives for steroid esters than seen in man, while the values of these experimenters was longer. So I think they succeeded in proving that there is a consistent phenomonenon, as would be expected, that each added carbon adds to half life in a fairly smooth way, but their particular values are I think suspect at least as applied to man.

For values in man, the values reported in the literature often don’t agree with each other well and certainly aren’t consistent.
In man, you have different experimenters using different methods each time… things get messy and the relationship
is not as clear. Results are probably screwed up also by analytical methods not using only free steroid, as they should have done, but total including bound steroids, and by tracking the early part of the decay rather than the latter parts. What can I say, the data is not good and really would have to be redone.

Testosterone enanthate (7 added carbons) is claimed to be 4 days (unreasonably short I believe), while cypionate 9* carbons) is claimed to be 8 days (way too big a gap compared to enanthate) and nandrolone decanoate (10 carbons, but count it as 9 because nandrolone itself is missing a carbon) is claimed to be 8 days (too short compared to the claim for enanthate.)

Doing a regression with a reasonable value (3 days) selected for propionate, we obtain an estimate that the formula is, half life equals 1.5 days plus .67 days for each added carbon past 19 carbons.

So, the Roberts estimate for esters is testosterone propionate equals 3 days, T enanthate equals 6 days, T cypionate and methenolone enanthate equal 7 days, nandrolone decanoate equals 8 days,
and boldenone undecanoate or nandrolone laurate equals 9 days. For other steroids, plug in the formula…

Do I guarantee these values? No, but they represent a reasonable “best fit” of the data out there. To get correct values you would need to measure only the free steroid in the blood, and track this over quite a long period of time, not using the values for the first few days (which are influenced by effects other than half life.)

Bottom line? You really don’t need exact values anyway but having a ballpark figure is certainly useful. The numbers I am giving, if they are wrong, I think it’s probably in the direction of underestimating half life of the longest chain steroids. That is just an opinion, not what the published data yields on analysis or in any direct statements.

Also don’t worry about so-called “anabolic/androgenic ratios”… these are in fact the ratios of activity in the levator ani of the rat (a non-skeletal muscle, that doesn’t respond at all the same as skeletal muscle, which is analogous to the pubococcygeous (PCG) muscle in man) to the activity in the prostate and/or seminal vesicles of the rat.

As it happens, the “anabolic” value is not a very good predictor of efficacy for athletes in muscle anabolism, and the “androgenic” value is not a very good predictor of adverse side effects either.

So in other words, each number is a rather poor predictor, and the ratio is no better. I would forget about it completely.

Excellent! Thanks to both Bill and Brock!
You guys have enough “electricity” running through your brains to light New York city!
So, anabolic/androgenic ratios are nothing to get tied in a wad over (seems the tissues used to assess that ratio are inconsistent, anyway). Also, receptor competition is nothing to bother over as well. So that leaves half lives, in so far as what I asked.
Bill’s “Robert’s formula” is exactly what I was after: something in the ballpark to use as a practical guide. (“Doing a regression with a reasonable value (3 days) selected for propionate, we obtain an estimate that the formula is, half life equals 1.5 days plus .67 days for each added carbon past 19 carbons.”) Excellent. Thank you.
I know I’m a novice at the technicalities (and I LOVE technicalities!) of cycle construction, and Brock did give rock hard practical advice concerning Risk, Availability, and Cost, but could you tell me if you even think half-life assessment is as critical as, say, whether or not the chosen steroids are Type I or Type II?
I know, I know, cycle construction does warrant a book (you two, at least, GET ON IT!), but could you give me (Us) a “template” of guidelines (JUST on what flavors of juice to use) to consider when constructing a cycle for hypertrophy categorized by risk, i.e., “high”, “medium”, “low”? I know it’s extremely difficult to do so on other than a strictly personalized basis, but could you give us something along those lines, and hey, just attach a bunch of disclaimers so readers won’t go off half loaded thinking what you give us is anywhere near a tailored, personalized regimen, ready to use out of the box!
Do that and/or WRITE THE BOOK so a lot of us can trash the WAR and BP’s book! (Well, I trashed BP’s book a long, long time ago).