http://www.pnas.org/cgi/reprint/88/18/8044.pdf
My question is, do you think methyl-DHT would have the same effect? If so I have some M-5AA that I could take along with some M1,4ADD. If my theory is correct this would be an amazing stack. M1,4 converts to Dbol plus the activity on its own, size and strength. M-5AA for more strength and aggression. Now the kicker, extra 5a-reductase coupled with Dbol would have some M1T floating around in my system. Couple this possibly with topical Form to control estrogen we have:
M1,4Add ---> Dbol
M-5AA ---> M-DHT
Dbol ---> M1T
Formestane ---> decreased estrogen, increased IGF-1
Thoughts?
and at the endFeed-forward control of prostate growth: Dihydrotestosterone
induces expression of its own biosynthetic enzyme,
steroid 5a-reductase
(androgen action/testosterone metabolism/4-azasteroid inhibitors)
FREDRICK W. GEORGE*t, DAVID W. RUSSELLt, AND JEAN D. WILSONt
Departments of *Cell Biology and Neuroscience, tMolecular Genetics, and tInternal Medicine, The University of Texas Southwestern Medical Center at
Dallas, Dallas, TX 75235
Contributed by Jean D. Wilson, June 21, 1991
ABSTRACT Dihydrotestosterone, the primary mediator
of prostate growth, is synthesized in target tissues from the
circulating androgen testosterone through the action of steroid
Sa-reductase (EC 1.3.99.5). The expression of 5a-reductase
and the level of 5a-reductase messenger RNA in rat ventral
prostate are regulated by androgens. To determine whether
this control is mediated by dihydrotestosterone or testosterone,
we investigated the effect of rmasteride, a potent inhibitor of
steroid 5a-reductase, on the expression of 5a-reductase in the
prostate. The administration of rmasteride to intact rats for 7
days caused a 55% decrease in prostate weight and an 87%
decrease in 5a-reductase enzyme activity. Furthermore, the
restoration of prostate growth after castration and the enhancement
in 5a-reductase enzyme activity and 5a-reductase messenger
RNA level by testosterone administration were blocked
by finasteride, whereas the inhibitor had no effect on dihydrotestosterone-
mediated increases in 5a-reductase activity or
messengerRNAlevel. Thesefindingsindicatethatdihydrotestosterone
itself controls prostate growth and Sa-reductase activity.
They further suggest that prostate growth is controlled by
a feed-forward mechanism by which formation of trace
amounts of dihydrotestosterone induces 5a-reductase, thereby
increasing dihydrotestosterone synthesis and triggering a positive
developmental cascade.
So what I'm getting out of this is that taking in DHT increases the amount of 5a-reductase our body makes (this may be a well known fact, doesn't matter).Thus, the
presence of dihydrotestosterone, but not testosterone, increases
the quantity of 5a-reductase mRNA
My question is, do you think methyl-DHT would have the same effect? If so I have some M-5AA that I could take along with some M1,4ADD. If my theory is correct this would be an amazing stack. M1,4 converts to Dbol plus the activity on its own, size and strength. M-5AA for more strength and aggression. Now the kicker, extra 5a-reductase coupled with Dbol would have some M1T floating around in my system. Couple this possibly with topical Form to control estrogen we have:
M1,4Add ---> Dbol
M-5AA ---> M-DHT
Dbol ---> M1T
Formestane ---> decreased estrogen, increased IGF-1
Thoughts?