The (Re-)Discovery of 17{beta}-hydroxyestra-4,9,11-trien-3-one: Low Dose Trenbolone Safely Promotes Myotrophic Actions in Skeletal Muscle and Provides Partial Protection Against Bone Loss and Visceral Fat Accumulation

Sometimes it is interesting to see how agents that have been around all along reappear back on the medical scene, all of a sudden. A recent study conducted by a group of scientists from Florida (Yarrow. 2011) that compared the effect of different doses of 17{beta}-hydroxyestra-4,9,11-trien-3-one aka Trenbolone on muscle hypertrophy and prostate health of testosterone seems to have the potential to trigger such a "revival":

In both intact and orchiectomized animals, all TREN doses and supraphysiologic testosterone-enanthate augmented androgen-sensitive levator ani/bulbocavernosus muscle mass by 35-40% above Shams (p≤0.001), and produced a dose-dependent partial protection against orchiectomy-induced total and trabecular bone mineral density losses (<0.05) and visceral fat accumulation (<0.05). The lowest doses of TREN successfully maintained prostate mass and hemoglobin concentrations at Sham levels in both intact and orchiectomized animals; whereas supraphysiologic testosterone-enanthate and high-dose TREN elevated prostate mass by 84% and 68%, respectively (<0.01). 

Whether this indicates that "trenbolone therapy" in men would actually be an alternative to the traditional androgen therapy to counter muscle wasting and other medical conditions remains to be elucidated. This is especially valid in view of the fact that the variables controlled in this study did not encompass any of the side-effects steroid (ab-)users tend to report on injectable trenbolone. In other words: Just because it does not enlarge your prostate, this does not mean that it is safe.

Viscous Circle: Low Testosterone > Increased Visceral Fat > Insulin Resistance > Even Lower Testosterone

E.J. Hamilton and colleges (Hamilton. 2010) investigated the effect of androgen deprivation therapy (ADT) in prostate cancer patients on subcutaneous and visceral fat. There results are far from being surprising:

Twelve months ADT increased visceral abdominal fat area by 22% (from 160.8 ± 61.7 to 195.9 ± 69.7 cm²; p<0.01) and subcutaneous abdominal fat area by 13% (from 240.7 ± 107.5 to 271.3 ± 92.8 cm²; p<0.01). Fat mass increased by 14% (+3.4 kg; p<0.001) and lean tissue mass decreased by 3.6% (-1.9 kg; p<0.001). Insulin resistance (HOMA-IR) increased by 12% (2.50 ± 1.12 to 2.79 ± 1.31, p<0.05).

All that by itself is bad enough, but in the end, by the medical suppression of androgens doctors put their poor patients in a viscous circle, from which it will be very difficult to escape, as obesity and insulin resistance will further reduce testosterone production and overall metabolic health regardless of whether they are secondary to low testosterone, come from bad eating habits or whatever.