i disagree--and using caps will not make your point any more viable--if the prohormone requires some sort of action to convert it to a usable substance how is that not a precusor? heck, from peer reviewed research journal look at the damn title:
Journal of Athletic Training 2002;37(3):300–305by the National Athletic Trainers’ Association, "The Safety and Efficacy of Anabolic Steroid
Precursors".....whichh found "Whenever an athlete is considering using steroid precursorsor any ergogenic supplement, 3 questions must be asked: is itsafe, does it work, and is it legal? At this time, scientific sup-port for the ergogenic or anabolic use of steroid precursorsdoes not exist"
or e.g, as noted by Bill Roberts "where testosterone has a hydroxyl group in a certain position, androstene has a keto group. All the rest of the steroid is exactly the same. So the body can convert testosterone to androstene back and forth by using the enzyme that can make this change. We already mentioned the first way an enzyme can change one steroid into another. This was interchanging the keto that androstene has at the 17th position with a hydroxyl by 17b -HSD. Both of the diones (androstene and norandrostene) rely on this conversion. Both use this enzyme, and a small fraction of each is converted to testosterone or to nandrolone, respectively.
The second way is interchanging the hydroxyl that a diol has at the 3rdposition with the keto that testosterone has by another enzyme, 3b -HSD. Both of the diol products rely on this. So androdiol and norandrodiol both use this enzyme, and again, a small fraction is converted to testosterone or nandrolone, respectively.
The third way involves changing bonds as well as groups. While testosterone has a double bond (a chemical bond between carbon atoms using two pairs of electrons rather than just one pair) between the 4- and 5- carbons, the 5- prohormones have their double bond between the 5- and 6- carbons. These, such as 5-androstenediol, can only be converted to testosterone if this bond is changed in the process. This is more complex, and requires 3b -HSD/5,4 isomerase. The net result though is the same thing: conversion to testosterone.
But it is not testosterone---and lets not ignore the King et al study--
King, D.S., R.L. Sharp, M.D. Vukovich, G.A. Brown, T.A. Reifenrath, N.L. Uhl, and K.A. Parsons. Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: a randomized controlled trial. JAMA. 281:2020-2028, 1999
found at
http://jama.ama-assn.org/cgi/content/abstract/281/21/2020?maxtoshow=&HITS=10&hits=10&RESULTFORMAT
the crap did not work. period.
'Serum free and total testosterone concentrations were not affected by short- or long-term androstenedione administration. Serum estradiol concentration (mean [SEM]) was higher (P<.05) in the androstenedione group after 2 (310 [20] pmol/L), 5 (300 [30] pmol/L), and 8 (280 [20] pmol/L) weeks compared with presupplementation values (220 [20] pmol/L). The serum estrone concentration was significantly higher (P<.05) after 2 (153 [12] pmol/L) and 5 (142 [15] pmol/L) weeks of androstenedione supplementation compared with baseline (106 [11] pmol/L). Knee extension strength increased significantly (P<.05) and similarly in the placebo (770 [55] N vs 1095 [52] N) and androstenedione (717 [46] N vs 1024 [57] N) groups. The increase of the mean cross-sectional area of type 2 muscle fibers was also similar in androstenedione (4703 [471] vs 5307 [604] mm2; P<.05) and placebo (5271 [485] vs 5728 [451] mm2; P<.05) groups. The significant (P<.05) increases in lean body mass and decreases in fat mass were also not different in the androstenedione and placebo groups. In the androstenedione group, the serum high-density lipoprotein cholesterol concentration was reduced after 2 weeks (1.09 [0.08] mmol/L [42 (3) mg/dL] vs 0.96 [0.08] mmol/L [37 (3) mg/dL]; P<.05) and remained low after 5 and 8 weeks of training and supplementation.
Conclusions
Androstenedione supplementation does not increase serum testosterone concentrations or enhance skeletal muscle adaptations to resistance training in normotestosterogenic young men and may result in adverse health consequences.