by Bill Boborts by Bill Boborts
Different anabolio'androgenic steroids have differences in effects, and to understiind these differences, it is necessary to understand the structure of these molecules.
All AAS share structural similarities, and the framework of the molecules is always basically the same, as shown in the figure.
So how does structure affect activity?
First, let's consider the liver engyme 17-beta-hydroxysteroid dehydrogenase (17-HSD». This enzyme- inactivates oral steroids by converting the hydroxy (-0H) group at carbon 17 of oral steroids to a keto (=«0) group.
A methyl group added to carbon 17 blocks 17-HSD and solves the problem. Side effects of this methyl include reduced binding to U'BG (oka androgen binding globules -ed) and to aromatase. and some degree of liver toxirity, except in tlie case of oxandrolone.
Methyl groups added at carbons 1 or 2 also interfere with 17-HSD. This is why Primobolan can be used orally.
Aromatase acta to convert testosterone to estradiol. The enzyme does this by removing carbon 19 and removing hydrogen from carbons 1 and 2. This makes the A ring aromatic (three double bonds' and con veils the keto group to a hydroxy!, yielding estradiol.
How to defeat aromatase?
An elegant solution is to huve no carbon 19. Aromatase then cannot work at all. Nandrolone uses this approach. It isn't immune to aromatization. though, because of P450 desaturase. By the way, nandrolone is identical to testosterone except for the lack of carbon 19. (NOTE: 19-nors do not aromatize by the same mechanism that C-19 steroids do. What is thought to happen with them is that they are metabolized to 1-beta hydroxylatedTderivatives in vivo and then these are non-enzymatically converted [acid or base catalyzed] to the corresponding estrogens. — Patrick Arnold I
If the nandrolone« aren't aromatized by aromatase, then how could an anti-aromatase protect a nandrolone user from gyno?
I'd say that if can't and doesn't. An ER-antagonist drug like Nolvadex (undesirable.
because it reduces IGF-1) would be needed. Would Proviron bind enough to the ER to be of any help? (NOTE: A 1-beUi hydroxylase inhibitor would — Patrick Arnold).
Another solution is to add a methyl group at carbon 1, blocking the enzyme from removing a hydrogen from that location. This is Primobolan's approach. Proviron also uses this method, with the added advantage that it remains bound in aromatase molecules, thus blocking aromiiti-zation of other steroids. Masteron uses a methyl at carbon 2 to do the same thing.
5-alpha-DHT-3-beta-hydroxysteroid dehydrogenase (3-HSD) converts DHT to androstanediol, which doesn't bind well to the androgen receptor. Muscle tissue has quite a bit of 3-HSD, so not much DHT reaches the androgen receptors in muscle. The same is true of Proviron. for the same reason. Masteron. which is the same as DHT except for the added methyl, seems to avoid this problem.
Lastly, 5-alpha-reductase converts dou-hie bonds between carbons 4 and 5 to single-bowk Testosterone thus converts to DHT, and nandrolone to DHN. This enzyme is found in high concentration in the skin, scalp, and prostate, but not in muscle tissue. In these tissues, testosterone becomes more potent, since DHT binds to the AR more strongly th8n testosterone does. In contrast, nandrolone becomes less potent when it is converted to DHN, so nandrolone acts weakly in tissues with 5AR
Enough of the enzymes—let's move on to some steroids!
There are surprisingly few studies on the binding properties of popular anabolics. The data presented here is from Endocrinology, vlM, The results depend both on actual binding characteristics and on effects of enzyme metabolism; in other words, if enzymes deactivate a steroid, then reported binding values are lower. Fair enough.
First up is methyltrienolone. Don't ever use this stuff — it is hcpatotoxic even at 2.5 mg/day, and has never been approved for human use.
It is popular for scientific study because it is potent and cannot be metabolized to estradiol. (NOTE: See my conversion from trenbolone elsewhere in the issue. — Patrick Amoldi frnf The dfffk of
Methyltrienolone has double bonds in the 4,9. and 11 positions, and has a methyl on carbon 17. It binds to the AR about twice as well as DHT. and several times better than testosterone. It has extremely low binding to TeBG—most methyltrienolone is free.
Trenbolone is almost identical. The structural difference is that it has no methyl at 17; the practical difference is that it is far less toxic. Activities should be similar, except that binding to TeBG is probably not quite as low.
DHT binds to TeBG about 5 times better than testosterone does. In muscle tissue, however, most DHT is converted to androstanediol. so little reaches the AR. (1 speculate, though, that androstanediol probably has effects in muscle not mediated by thoAR.)
Proviron is like DHT, but with a methyl on carbon 1. It binds to TeBG about 20 times as strongly as testosterone docs.
Little nandrolone binds to TfeBG, but this steroid was found to bind to the AR as well as testosterone of even better. Nonetheless, in bodybuilding it'? not considered equally effective as a mass builder, but this could be for other reasons. For example, testosterone might be more potent in promoting GH or IGF-1 release.
Methenolonc (Primobolan) was a good performer. Its binding to AR was just as good as testosterone, and it bound to TeBG only 1/6 as much.
So what's the point of all this?
Strength of binding to the AR is not in itself important, but strong binding implies that an AAS will remain bound to the AR longer. Methenolone and nandrolone were shown to be excellent performers here, and trenbolone is probably even better.
The AR and other molecules *see" only-free AAS, so low binding to TeBG imparts an advantage here. On the other hand. TeBG is used to carry AAS into cells, and it would be more effective if saturated.
So I suggest that it is logical to stack both high-binding and low-binding steroids together in order to obtain both advantages. DC
HARD-HITTING DRUG FACT #2
(Editor's note: Every low years or so. you'll see an otter mail-order tor formulas to make steroids in your kitchen, usually from OHEA. There are very few steroids lliat can be made simply in your so-called kitchen. Next issue, we'll show you how to make testosterone (rom androslenedione. But (or now. I'd like to show you how difficult most steroid formulas are.)
Dan asked me to provide this synthesis ol melhyltrienolono with Ihe lull understanding lhat If Is loo difficult for all but the mosl experienced organic chemists, and certainly beyond the grasp ot ths average kitchen chemist. However, if it still quite Interesting as It shows how such things are certainly possible for someone with Die training and chutzpah to knock it oft.
Basically what we are talking about here is taking trenbolone acetate (Flnlplex pellets} and using it as the starting material for a series of reactions thai will produce the "super steroid" methyltrienolone. This steroid is In actuality 17-alpha-mothyliienbolone. the orally ocllve analog ot trenbolone (analogous to meihyltestosterone being the orally active analog ol testosterone) developed in Ihe sixtlES by Rousell-UCLAF. I call It a 'super steroid" because of lis outrageous reported oral anabolic activity (accumpanled by considerable andro-genldty. mind you) of over filly limes ijreator than melhyllestosterone. However, the stlcklc-r here is that methyl-Monotone is also VERY hepatotoxic and therefore you probably would not he able to stand the stuff In decern amounts. Bui this I; besides the point, since this is josi an exercise in tantasy. Right?
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