This month’s article is put together a little differently from usual: rather than holding to any one topic, I will focus on some errors published in World Anabolic Review 1996 (WAR) and offer corrected information in those areas. WAR is probably the best book available to the bodybuilder on the use of anabolic steroids, but is not always correct. While many MESO-Rx readers will own this book, others will not, but the information given will still be useful. Generally, the errors are not unique to WAR, but are commonly believed, and furthermore, the correct information is of value.
This oral anabolic/androgenic steroid (AAS) is actually a prodrug of boldenone. It is the exact same molecule, but with a cyclopentenyl ether modification at position 17 (recall that injectable AAS often use ester modifications at 17). This allows for some degree of oral effectiveness. The prodrug is not active until it is converted to the parent drug in the body, by removal of this group.
Quinbolone is not very potent (effective per milligram) compared to injected boldenone undecylenate (Equipoise), which itself is not particularly potent. Contrary, however, to the claim in World Anabolic Review, this compound should aromatize comparably to Equipoise, based on its chemical structure. However, I know of no athletes who use it, so I cannot say that this is demonstrated.
Although this anabolic steroid can indeed lead to estrogenic side effects, it is very questionable, as Pat Arnold has pointed out, if it itself converts to estrogen at all. There is no evidence in the scientific literature for that, and if it does do so, it is not by a mechanism known for other steroids. Aromatase would be required but would not be sufficient. It may be the case that oxymetholone affects estrogen metabolism, perhaps either by slowing its rate of elimination, or by upregulating aromatase production. Whatever the cause, antiestrogens should be employed with this drug unless the user simply does not care about estrogenic side effects.
Oxymetholone does not convert to DHT. However, it is a potent androgen in the skin and scalp nonetheless. Use of a 5-alpha reductase inhibitor, such as Proscar, would be of no use, since the compound cannot be 5-alpha reduced.
There is no support for the claim that nandrolones require more protein intake than is needed with other anabolic steroids. There is, in my opinion, a tendency on the part of the WAR authors to see a statement concerning a particular steroid, and if they have not seen it for other steroids, to then assume that the property is unique to that steroid. Here, because the information packet with the drug says that the patient must be sure to consume sufficient protein, they imagine this is peculiar to the drug. It is, however, true for all anabolic steroids.
The claim that aromatization is less than with Deca Durabolin is unlikely to be correct. Because of the longer half life, for the same dose, there will be less drug in the blood during the first few weeks of use, thus creating this illusion. If blood nandrolone levels are the same, giving comparable effectiveness, rate of aromatization would be the same.
This is true for all claims made for varying rates of aromatization according to ester. I do not think such claims are ever correct given equal blood levels of drug, and they certainly are not substantiated in the scientific literature.
The claim that 50-100 mg per 10 days will normally result in no virilization symptoms for women will be over-optimistic for many female users. Only a few weeks of such use will result in some irreversible virilization for some women. This is true for substantial doses of any anabolic steroid. If a drug is an agonist (activator) of the androgen receptor it will have virilization activity if given at a high enough dose. That dose will vary according to the individual’s susceptibility, and according to the specific tissue.
This compound actually is dihydrotestosterone (DHT), not “almost identical” to it.
The claim that clenbuterol is an anabolic in humans comparable to milder AAS is not correct. Clenbuterol should be considered to be merely a potent and long-lasting version of ephedrine. The dosing schedule given (two days on, two days off) makes no sense because the half life of the drug is long enough that the “off” days still have high levels of drug in the system: thus receptor desensitization will not be avoided. Aside from that theoretical reason, it is also observation that the scheme simply does not work to prolong the effectiveness of the drug.
Clomid’s activity is achieved not by stimulation of the hypothalamus, but by blocking inhibition of the hypothalamus by estrogen.
Clomid is a mixed estrogen agonist/antagonist (activator/blocker) not because it is a “weak estrogen” but because it puts the estrogen receptor in a somewhat different conformation (shape) than does estradiol. The result is that in some tissues Clomid acts as an antagonist, and in others as an agonist, depending on what cofactors are used in that tissue in combination with the estrogen receptor.
Clomid is an effective antagonist in the hypothalamus and in breast tissue. It is an effective agonist in bone tissue, and for improving blood cholesterol.
The claim that duration of intake should not exceed 10-14 days is incorrect. Clinical studies with male patients have been for periods of a year or longer. This error probably originates from the fact that, for use in women, due to the menstrual cycle there would obviously be no point in trying to stimulate ovulation all four weeks of the month. Thus, use in women is limited to 10-14 days. That limitation is not because of toxicity.
Clomid is in fact useful throughout a cycle if aromatizable drugs are being used.
Cytadren, at moderate doses, is a fairly effective inhibitor of aromatase and a weak inhibitor of desmolase (an enzyme needed for the production of all steroids), and at higher doses becomes an effective inhibitor of desmolase.
Inhibition of desmolase will lead, at least temporarily, to decreased production of cortisol. Contrary to the claim in World Anabolic Review, there is no evidence, nor good reason to believe, that reducing cortisol below normal would be of benefit to the weight training athlete, and considerable evidence that it is a bad idea. Thus, desmolase inhibition is to be avoided.
The claim that Cytadren significantly inhibits natural production of testosterone is not correct. The desmolase step is rate limiting for the production of cortisol, but not for testosterone: thus, a slowing of desmolase activity does not slow production of testosterone significantly. However, the conclusion that natural athletes should not use Cytadren is correct, but for a different reason. Natural athletes have no need of the antiaromatase activity, and the anti-desmolase activity, reducing cortisol below normal, is not desirable. It would only be desirable if cortisol levels were abnormally high, which should not be the case.
The claim that 2-4 tablets per day (500-1000 mg) should be taken is extraordinarily bad advice. I do not believe that more than 250 mg/day should be taken, and that should be taken very carefully, divided into 125 mg (half a tab) in the morning, and 62.5 mg (quarter tab) six and twelve hours after that. The two on, two off idea is also not a good one, since that gives no antiaromatase activity half of the time.
It has been demonstrated that 250 mg/day is not much less effective than 1000 mg/day in inhibiting aromatase, but the smaller dose results in much less desmolase inhibition.
If the drug is suddenly discontinued, cortisol rebound may occur. Thus, the drug should be tapered down.
Deca has no peculiar property in terms of enhancing protein synthesis besides that which all anabolic steroids have. The claim that it does not aromatize at doses below a given threshold (400 mg/week is stated) is not correct. It aromatizes at any dose, but at a lower rate than testosterone does. This phenomenon of aromatization occurring at any dose with an aromatizable steroid is true for all aromatizable steroids.
Antiaromatases will be of no effect in avoiding this aromatization, since the aromatase enzyme is not used.
The claim that women will usually experience no problems with doses of 100 mg/week will often not be true for long term use, and sometimes not true even for short term use.
The claim that shorter acting nandrolones, such as Durabolin, will avoid virilization problems is also not correct.
This anabolic steroid was not developed by Dr John Ziegler: that is a myth. Rather, after its development, he was the first physician to give this steroid to weightlifters.
Dianabol does not convert to DHT, but is itself a potent androgen in skin and scalp.
The claim that this substance is more potent than Deca is not correct. The potency is comparable or slightly less.
This anabolic steroid has no unusual anabolic properties and is largely comparable to Deca. Possibly, besides AR agonist activity, it has etiocholanolone-like activity; if so, this would account for the slight fever some users report from it.
While Finaject itself is no longer available, in some cases injectable preparations from Finaplix have been made. The substance is the same: trenbolone acetate.
There is no evidence in the literature, nor I think practical evidence, that trenbolone acetate has a “special role” in burning fat. Rather, it is an extraordinarily potent AAS, being about three times as effective per milligram as testosterone esters. For this reason, any property which anabolic steroids have, trenbolone acetate will demonstrate more strongly per milligram.
I have found no indication in the scientific literature of particular kidney toxicity with trenbolone. I know of a number of users, at doses of typically 50 mg/day, who have experienced no problems. There are however anecdotal claims of kidney problems. It seems to me, however, that this is occurring only with athletes stacking an incredible amount of drugs, and how the blame can fairly be laid at trenbolone (actually at Parabolan, not trenbolone acetate) is not clear.
It is also not clear that trenbolone results in any greater degree of increased aggression for a given amount of anabolic effect than testosterone itself does. However, on a per milligram basis, it undoubtedly does. The substance does not cause uncontrollable “roid rage” despite the hype to that effect often seen.
The procedure given in WAR for making an injectable preparation from Finaplix is extremely poor and will result in injection not only of the trenbolone acetate, but of all the filler and binder, and in a nonsterile manner that is likely to lead to infection (as the authors of WAR point out.)
This substance is not a precursor of methyltestosterone, but is a distinct substance in its own right.
In my opinion this is a particularly harsh drug and not a good choice for an oral anabolic unless its particular properties of not aromatizing and being rather effective at increasing aggression are desired. It also is effective for endurance athletes in improving their ability to do maximum sustained work over a long period, a use not mentioned in WAR.
Use of this drug in the taper is rather counterproductive, since the resulting increased testosterone production is itself inhibitory to the hypothalamus and pituitary, delaying recovery. Thus, if this drug is used, it is preferably used during the cycle itself, to avoid testicular atrophy. Use every third week is sufficient for this.
HCG may upregulate aromatase. This is not demonstrated, but there is no doubt that it results in increased estrogen production, and this is a likely reason. Thus use of antiestrogens in conjunction with HCG is recommended.
The athlete wishing to pass a urinary testosterone/ epitestosterone ratio test, who would otherwise fail because of low epitestosterone resulting from low LH production, may find HCG useful in increasing epitestosterone, and therefore improving this ratio. It can also useful athletically by returning testosterone to normal levels should levels be low post-cycle, or, with care, to increase levels from normal to high normal.
This steroid appears to be approximately as effective as Primobolan per milligram or moderately more so. The primary reasons for not using this steroid are its excessive cost and low concentration per mL, requiring large injection volume. It may have antiaromatase activity.
There is no evidence whatsoever that this substance “magnifies” the effect of other steroids, or increases receptor sensitivity, or any such thing, nor is there any known mechanism by which it might do so. This appears to be strictly a myth, and it definitely cannot be substantiated in the scientific literature, nor from anecdotal evidence from experienced and methodical users.
The fact that it is used in combination veterinary steroids is rather irrelevant and proves nothing. Estradiol is also often used for steroids designed to increase the weight of animals being prepared for sale. Methandriol dipropionate has estrogenic activity, and it may be for this reason that it is effective in the veterinary steroids. Bodybuilders might just as well take a little estrogen, or avoid anti-estrogens, and could get the same effect (along with all the estrogenic side effects.)
This compound, once the ester is removed, is the same as 5-androstenediol, but not the same as 4-androstenediol, a superior compound.
This oral steroid is a poor choice for men, since it aromatizes easily and has some activity as a progestin (like progesterone.) The claim that Nilevar is unusually virilizing when used by women is borne out neither by (limited) anecdotal evidence, nor by a rather large body of scientific evidence. It should be considered comparable to Dianabol in this regard. That is to say, its virilizing effect is average for a synthetic anabolic steroid.
Nolvadex is very comparable to Clomid, behaves in the same manner in all tissues, and is a mixed estrogen agonist/antagonist of the same type as Clomid. The two molecules are also very similar in structure.
It is not correct that Nolvadex reduces levels of estrogen: rather, it blocks estrogen from estrogen receptors and, in those tissues where it is an antagonist, causes the receptor to do nothing.
The claim that Nolvadex reduces gains should not be taken too seriously. The fact is that any number of bodybuilders have made excellent gains while using Nolvadex. The belief that it reduces gains seems to stem from the fact that the scientific literature reports a slight reduction in IGF-1 (individuals using anabolic steroids were not studied though) from use of Nolvadex. Thus, reported that it reduces IGF-1 and therefore reduces gains. However, if this effect exists at all, it must be very minor, due to the excellent gains that many have made, and from the fact that no one has noticed any such thing from Clomid, which has the same activity profile.
However, I would not be surprised if one were to tell a steroid user that Clomid reduced his gains, he would immediately become afraid that Clomid reduced his gains (please note that no one I have ever heard of has noticed this.) Not having been so misled, however, he would not conclude this from his results. But if an authority publishes that such an effect occurs, whether it does or not it can become self-fulfilling by biasing the user.
The fact that Nolvadex will reduce water retention may result in the user agreeing that gains are less, since weight gain is less, thus reinforcing the bias.
This preparation is quite similar to Sustanon, and is different only in that 100 mg/mL of it (of 250 mg/mL total) is testosterone hexanoate instead of the testosterone decanoate used in Sustanon. For this reason, Omnadren has a shorter half life, and will give a faster initial increase in blood level. This accounts for the claim of increased water retention and increased side effects, since levels, at first, are higher for the same dosage. As mentioned in WAR, the purity of Omnadren is questionable and other side effects may be caused by impurities.
The claim that Omnadren has a duration effect of “a good 2-3 weeks” is somewhat misleading since the half life of the longest lived component is only about 5 days. There is of course some effect 2 or 3 weeks after injection, but relatively little.
The hexanoate ester is quite similar to the well known enanthate ester, but is shorter by one carbon.
The isohexanoate ester in Omnadren is the same, only named differently, as the isocaproate ester in Sustanon. Thus, the hexanoate vs. decanoate difference is the only difference in the mixture of esters.
There is no reason to think that oxandrolone has any unique effect, unshared by other anabolics, with regard to increased phosphocreatine synthesis. All have this effect.
The claim that oxandrolone use “even in a very high dosage” does not influence the body’s own testosterone production is entirely incorrect. It most certainly does.
The fact that it does not convert to estrogen does not prevent this activity, because androgenic inhibition also exists and is well demonstrated. Oxandrolone, as an agonist of the androgen receptor, would be expected to inhibit testosterone production, and it is observed to do so. I am informed by Michael Mooney that this is particularly well noted with HIV patients who have been using Oxandrin, another brand name for oxandrolone. It also undoubtedly is the case generally. Only magic could result in that not being so.
Single dose use in the morning, however, instead of divided dose usage, would be expected to minimize this problem for pharmacokinetic and chronopharmacological reasons – relatively little of the drug would then be in the system at night, when LH production is highest. In the natural cycle of androgen production, androgen levels are highest in the morning, so this is the time at which artificially high levels of androgen will have the least possible inhibitory effect. This is true as well for other orals besides oxandrolone.
The claim that oxandrolone is liver toxic is mostly untrue, especially at lower doses. It is much less liver toxic than other 17-alpha alkylated steroids, probably because it is primarily metabolized outside of the liver, when metabolized, and much of it is excreted unchanged. At higher doses it can increase liver enzyme values, but I am not aware of any evidence that any cytotoxicity exists, as is the case with other 17-alpha alkylated steroids.
See Finaject for most discussion: the properties are the same except for longer half life.
The claim that acetate tablets help burn fat, as a result of being acetate esters, is purely a myth.
This AAS is entirely impractical for male bodybuilders, since the dose needed for significant effect would be cost prohibitive with the 5 mg tablets currently available.
Generally, claims of remarkably different behavior (other than differing half lives) between esters are unfounded. Comparisons made are often poor: for example, WAR compares the side effects of 350 mg/week of testosterone propionate with those seen with over a gram per week of testosterone enanthate. Not surprisingly, in that comparison propionate exhibits much less aromatization and other side effects. The comparison is, however, absurd.
Another falsehood which is quite commonly believed, thanks to Bill Phillips, is that Sustanon is particularly effective because the different esters bind different receptors. This is entirely false: the ester group is removed before the testosterone binds to the receptor, so there is no difference.
The theory that switching esters will somehow trick the androgen receptors is also not correct, for the same reason.
This compound is not a precursor of DHT, but is itself a potent agonist of the AR in skin and scalp.
This concludes our review of errors in World Anabolic Review. This article gives a somewhat unfair picture by discussing only the errors, rather than the many valuable and correct statements. Overall, this book is an excellent choice for the reader wishing to learn about anabolic steroids, but the above qualifications should be kept in mind.