"There is an interesting paper about the effects of proviron on SHBG (1)
They gave men 150mg of proviron every day and looked at test and free test levels. The total testosterone went down about 30% but the free testosterone stayed the same. If you think about it or make a little bar graph, you will conclude that the only way this can happen is if the bound testosterone went down.
It turns out proviron binds more strongly to SHBG than does testosteone. So what they think is happening is that the proviron is either displacing test from SHBG and/or albumin, or lowering SHBG like androgens do, or both. Rather than increasing free test, this displaced test just acts back on the pituitary and/or hypothalamus to reduce test output. The net result is free test ends up unchanged but total test goes down via feedback inhibition. This exemplifies the futility of trying to raise free test levels by lowering SHBG.
(1) Aakvaag A, Stromme SB. The effect of mesterolone administration to normal men on the pituitary-testicular function.
Acta Endocrinol (Copenh). 1974 Oct;77(2):380-6."
also
It is unclear whether anabolic steroids act on skeletal muscle via the androgen receptor (AR) in this tissue, or whether there is a separate anabolic receptor. When several anabolic steroids were tested as competitors for the binding of [3H]methyltrienolone (MT; 17 beta-hydroxy-17 alpha-methyl-4,9,11-estratrien-3-one) to the AR in rat and rabbit skeletal muscle and rat prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone) greater than methenolone (17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one) greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05): stanozolol (17 alpha-methyl-5 alpha- androstano [3,2-c]pyrazol-17 beta-ol), methanedienone (17 beta-hydroxy-17 alpha-methyl-1,4-androstadien-3-one), and fluoxymesterolone (9 alpha-fluoro-11 beta-hydroxy-17 alpha-methyl-T). Other compounds had RBAs too low to be determined (e.g. oxymetholone (17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one) and ethylestrenol (17 alpha-ethyl-4- estren -17 beta-ol). The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction of its 3-keto function to metabolites, which did not bind to the AR [5 alpha-androstane-3 alpha, 17 beta-diol and its 3 beta-isomer (3 alpha- and 3 beta-adiol, respectively)]. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA in rat muscle to that in the prostate (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most cases.
So, whatever % DHT lowers SHBG levels, it does it 3x better.
And If you looked at the studies right, youll know as well that more aromasin is always better (if hoping to match proviron). Plus proviron is very supressive for its benefits.
All I know is i'm amped to get my Aromasin tabs in a week.
Please Scroll Down to See Forums Below 
