Much confusion exists as to which anabolic-androgenic steroids (AAS) should be used to achieve given goals, how they should be combined and why, and their relative advantages and disadvantages. While many individual points discussed here have been discussed in previous columns, this is the first time I have brought this information together into a single place for easy reference, and some new material is introduced as well.
Comparing Anabolic Steroids
Comparison of different drugs must be made in a rational manner. Unfortunately, in bodybuilding that is rarely done. I have had people tell me, “Winstrol is useless! If I inject two amps per week of Sustanon, I get good results every time. I tried two amps per week of Winstrol and got very little from it. It is no good.”
But let’s look at this comparison a little more closely: two amps of Sustanon is 500 mg of testosterone esters. Two amps of Winstrol is 100 mg of stanozolol. Should one necessarily be surprised that 500 mg of one drug outperformed 100 mg of another? Does this mean that the latter drug is useless? Of course not.
Three forms of comparison are reasonable – one of them being economic, one being from the medicinal chemistry viewpoint, and the third being from the clinical viewpoint.
First, we might compare these drugs dollar for dollar. If price is our main concern, then it is reasonable to compare the results of using say $27 per week of Sustanon vs. $27 per week of Winstrol Depot. In this comparison, given typical market prices, Winstrol loses, at least for mass cycles.
Secondly, we might compare equal amounts of the drugs. Really we would prefer to correct for molecular weight (esters add weight to a drug) but here we shall neglect that and compare milligram for milligram. Thus, one might compare 350 mg/week Sustanon with 350 mg/week Winstrol Depot. In this comparison, Winstrol is a real competitor, and certainly wins if we are comparing adding these amounts to certain stacks rather than in isolation.
Lastly, we might compare side effects of equally-effective doses of each drug, and the drug with the least side effects for the same therapeutic effect is considered superior. In this comparison, Winstrol would indisputably win, at least in the moderate dose regime.
The latter two types of comparison are the types I shall make in this article. The types of comparison seen in many steroid books, where low doses of oxandrolone are compared with 50 mg of Anadrol®, or a moderate amount of testosterone propionate is compared with a much larger amount of enanthate, etc., shall not be made here since they are useless and uninformative.
The Reference Drug: Testosterone
Testosterone, as the natural product drug and one of the most widely used AAS, is the most convenient choice for a reference drug to which all others will be compared.
Particular properties of testosterone that are of note include that it converts enzymatically both to DHT and to estradiol (estrogen). While with normal levels of testosterone these conversions are in fact desirable, with supraphysiological levels caused by drug adminstration they can be undesirable. DHT is at least three times more potent (effective per milligram) than testosterone at the androgen receptor (AR): therefore, in those tissues which convert testosterone to DHT, there is effectively three times as much androgen as elsewhere in the body. Thus, whatever level of androgen is experienced by the muscle tissue is multiplied threefold or more in the skin and in the prostate. This can be excessive. Proscar could be used to keep DHT levels more or less normalized despite heavy testosterone use, however.
Excess conversion to estrogen is also undesirable since it contributes to inhibition of the hypothalamic/pituitary/testicular axis (HPTA), can cause or aggravate gynecomastia, can cause bloating, and can give unfavorable fat pattern distribution. This conversion can be somewhat reduced by use of aromatase inhibitors such as Cytadren, and/or the effects of the estradiol produced may be blocked in many tissues, including the hypothalamus and breast tissue, by Clomid.
Among the most significant differences of synthetic AAS compared to testosterone is that they may avoid either or both of these enzymatic conversions. Another difference results from the fact that not all activity caused by androgens is mediated by the androgen receptor, and not all AAS are comparably effective in these other activities.
Testosterone used alone is capable of giving very effective results, particularly with doses over one gram per week, and can give substantial results with only 500 mg/week. If no other drugs are used, however, side effects such as gynecomastia are fairly likely. Prostate enlargement, worsening of acne, and acceleration of male pattern baldness (for those genetically susceptible to it) are particularly severe because of the effectively-higher androgen levels seen in these tissues as a result of local conversion to the more-potent DHT. Synthetics which do not convert to DHT give only the same effective level of androgen in these tissues as in the body as a whole, rather than effectively three times the level. This is a significant advantage.
A particularly interesting property of testosterone is its low toxicity, exclusive of the above-mentioned side effects. Doses of two grams or four grams per week are hardly unknown in bodybuilding, and are not particularly hard on the liver. No one seems to want to take doses of any other single steroid at comparably-effective doses, and it seems that if one tried, they might be more toxic. E.g., the hepatotoxicity of Winstrol Depot resulting from its 17a-methyl group is not severe at doses of say 350 mg/week, but might well be problematic at a dose of two grams per week – though that is speculation, since no one I have heard of uses such doses of Winstrol. Thus, at the higher dosage regimes testosterone appears to have an advantage in terms of toxicity vs. effectiveness over many of the synthetics. These doses, however, are in the pro bodybuilder range. In the dosage range more appropriate for most individuals, the reverse is often the case.
Other Popular Steroids
Deca Durabolin (Nandrolone Decanoate)
This drug is unique (so far as I know) in that 5a-reductase, the enzyme which converts testosterone to the more-potent DHT, actually converts nandrolone to a less-potent compound. Therefore this AAS is somewhat deactivated in the skin, scalp, and prostate, and these tissues experience an effectively-lower androgen level than the rest of the body. Therefore, for the same amount of activity as another drug at the androgen receptors (ARs) in muscle tissue, Deca gives less activity in the scalp, skin, and prostate. Thus, it is the best choice for those particularly concerned with these things.
Its effectiveness at the androgen receptor of muscle tissue is superior to that of testosterone: it binds better. Yet, it gives only about half the muscle-building results per milligram. This I think is a result of its being less effective or entirely ineffective in non-AR-mediated mechanisms for muscle growth.
It also appears less effective or entirely ineffective in activity on nerve cells, certainly on the nerve cells responsible for erectile function. Use of Deca as the sole AAS often results in complete inability to perform sexually.
These problems can be solved by combining with a drug that does supply the missing activity: e.g. testosterone.
To some extent, nandrolone aromatizes to estrogen, and it does not appear that this can be entirely blocked by use of aromatase inhibitors – indeed, aromatase may not be involved at all in this process (there is no evidence in humans that such occurs) with the enzyme CYP 2C11 being in my opinion the more likely candidate for this activity. In any case, Cytadren, an aromatase inhibitor, has not been found effective in avoiding aromatization of nandrolone.
The drug is moderately effective at doses of 400 mg/week. The long half-life of Deca-Durabolin makes it unsuited to short alternating cycles, but suitable for more traditional cycles, with a built-in self-tapering effect in the weeks following the last injection.
This drug appears to be comparable to nandrolone in its potency. It lacks nandrolone’s advantage of being metabolically deactivated by 5a-reductase. I cannot at the moment comment on whether the effect it does produce is owed to strong binding at the AR or to effectiveness in promoting non-AR-mediated mechanisms for growth.
This steroid is approximately comparable to nandrolone in anabolic potency, though it binds to the AR slightly less-well than that drug, and apparently is similarly ineffective in non-AR-mediated anabolic effects. On the other hand, it is pleasant to use at doses considerably higher than what is pleasant for nandrolone esters, and so therefore it is not necessarily less effective, provided that one can afford it. It appears to cause less inhibition than Deca or testosterone for any given degree of anabolic effect, perhaps because it does not convert to estrogen. Unlike Deca, it is not metabolically deactivated by 5a-reductase and therefore is not as kind to the skin and hair as that drug – however, by suppressing natural testosterone production and therefore the highly potent DHT, it can improve skin relative to using no AAS at all.
This substance is to be avoided by male bodybuilders unless they wish deliberately to use something that is estrogenic. An alternate estrogenic option would be Pentabol. This actually is the same compound, but without the ester, for oral use (at very low bioavailability.)
One obvious difference between Winstrol Depot and other injectables is that it is not esterified, being sold as aqueous stanozolol suspension. (It should not be called water-soluble: virtually none of it is dissolved in the water.) This means that it does not have a classical half-life, where at timexthe level is ½ the starting level, at time 2xthe level is ¼, at time 3xthe level is 1/8, etc. Instead, the microcrystals slowly dissolve, and when they have all dissolved levels of the drug then fall very rapidly.
For veterinary application, Upjohn claims that once-weekly doses supply constant levels. I am not sure if that is actually true or not – it might be true in terms of being clinically practical but not literally true. If true, then it may be that the observation of bodybuilders that frequent dosing is required has more to do with a significant dose being required, e.g. 350 mg/week, rather than an actual need for it to be injected daily. Unfortunately bodybuilders often make illogical comparisons, and will conclude that daily injections are needed, since a once a week injection of 50 mg did not do the job! Well, of course it didn’t: the dose was too low. For a future article, some urinalysis testing may be performed to come up with some more specific information on this matter, since it is of interest to many.
In some cases, women have had virilization problems with oral Winstrol at only 2 mg/day. Thus, it cannot be assumed that even a single tab per day is necessarily safe for all women concerned about maintaining their natural voice, avoiding hirsutism, etc.
Stanozolol has some unique biochemical properties which we will discuss in a later article.
Contrary to what many would expect, this compound is actually only a weak agonist of the AR, with poor binding. It follows, then, that its value must come from non-AR-mediated effects. Since it is not very effective in activating ARs, it should be stacked with an AAS that is effective in that regard. At moderate doses (20-50 mg/day) oral methandrostenolone appears (in my opinion) to be about twice as effective per milligram (twice as potent) as injectable testosterone esters.
It converts to estradiol via aromatase. The amount of this conversion may be reduced by use of Cytadren (see previous articles discussing dosage and dose pattern.)
Irreversible hoarsening of the voice has been seen in some women from very few tablets of Dianabol: one per day for a few weeks. For this reason, in the 1960s doctors decided to end what had been a fairly common practice of prescribing this drug at one tab per day to women as a “tonic.”
As I have mentioned before, there is a great deal of individual variability, and some women are able to obtain desired anabolic activity prior to reaching their personal threshold for virilizing activity. Others are not.
Like methandrostenolone, oxymetholone does not bind well to the AR, and presumably exerts its anabolic effects via non-AR-mediated effects. It is not clear to me whether these effects are the same as those which Dianabol effectively induces. One difference does appear to exist: I suspect, though without evidence for or against it in the scientific literature, that oxymetholone is progestogenic. It has been observed to cause nipple soreness or to aggravate gynecomastia even in the presence of high dose antiestrogens, strongly suggesting that the effect is not estrogenic. Furthermore, that effect can be avoided by concurrent use of stanozolol, which is anti-progestogenic. It isn’t clear to me at this time whether the blocking of this progestogenic activity by Winstrol reduces gains or not.
Anadrol does not convert to estrogen, or at least there is absolutely no evidence and absolutely no plausible mechanism, and thus antiestrogens are not required if no aromatizable AAS are being used. However, in concert with drugs such as testosterone, Anadrol® is notorious for worsening “estrogenic” symptoms, possibly by producing progestogenic symptoms which the bodybuilder confuses as estrogenic, or by altering estrogen metabolism, or by upregulating aromatase.
Compared to what bodybuilders expect of it, the drug is reasonably mild when no aromatizing steroids are present. I consider its potency approximately comparable to Dianabol.
It would appear that, unlike oxymetholone and methandrostenolone, oxandrolone does have good binding to the AR. However, by itself it is considered to be a weak anabolic.
Part of the reason for this is that bodybuilders make unfortunate and unreasonable comparisons when judging AAS. If 20 mg/day oxandrolone (why, that’s 8 tablets, and isn’t that a lot?) does little, then the drug is pronounced useless or weak by the user. But that is only 140 mg/week. Does 140 mg/week testosterone give any tremendous results? No. Few AAS give dramatic results at that dose.
Because of its high price, very few bodybuilders have taken large doses of oxandrolone. There is a single case in the medical literature (Forbes et al.) where it is reported that a competitive athlete self-administered I believe 80 mg oxandrolone per day with remarkable gains. I never knew whether to give that credibility, because unless urinalysis was done to verify that no other steroids were taken, there is no way to be certain that the athlete did not actually take more drugs than he reported. In any case, at current prices, only the quite wealthy could afford such a dose.
Oxandrolone does not aromatize or convert to DHT, and has a longer half life than Dianabol – 8 hours vs. 4 hours. Thus, a moderate dose taken in the morning is largely out of the system by night, yet supplies reasonable levels of androgen during the day and early evening.
I find it difficult to make a potency comparison with any other steroid, because I know no male bodybuilders who have made substantial gains using oxandrolone alone.
This oral has progestogenic activity. I don’t have information on whether Winstrol counteracts this, as appears to be the case with Anadrol®, but in any case it is not considered a particularly useful drug for male bodybuilders. For female bodybuilders, it is probably an average synthetic, comparable to Dianabol.
Contrary to what one might expect, this drug has poor binding to the AR. Presumably its effects are largely non-AR mediated. It however is a rather toxic drug and I consider it to be a poor choice except perhaps pre-contest for those willing to suffer its toxicity, or for endurance athletes in non-tested competitions.
This drug has good binding to the AR, but in muscle tissue most of it never reaches the AR because it is enzymatically converted to the diol. Thus, it is not an effective anabolic. It is somewhat effective as an anti-gyno agent, however, and appears to reduce estrogenic bloating if that problem exists.
This is a topic which will have to be addressed in greater depth at a later time, particularly in regard to synergistic effects of certain combinations, where ½ x mg of A plus ½ y mg of B gives greater gains than either x mg of A or y mg of B.
But very briefly, so that you may obtain some information of practical use from this article, what should be done is to stack steroids that complement each other: where each is effective in ways that the other is not.
E.g., Dianabol alone has the problem that it does not bind the AR very well. Apparently though, it is very good in at least some non-AR-mediated effects. In contrast, nandrolone binds the AR very well, but apparently it is ineffective in most or all non-AR-mediated activities. If the two drugs are combined, the effect will be synergistic, since they complement one another. Not only does theory predict this, but it is observed.
Stacking Deca with Primo, however, would not be expected to be synergistic, and is not observed to be. Both have the same type of activity: both are good agonists of the AR and presumably ineffective in non-AR mediated activity. One might as well use all Deca or all Primo rather than combine the two.
These same principles will apply to other drugs described above. An area of particular interest is synergistic effects in combinations including testosterone, trenbolone, and/or stanozolol. I have the literature references to support the argument for non-AR-mediated effects, but observational evidence in bodybuilding sufficient to give reliable answers in this area is still incomplete. I expect, however, that future articles will answer these questions.