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.
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.reported that it reduces
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.