Proscar and Winstrol

[hhajdo]

I was referring to dutasteride.

The study you posted was for finasteride.

Either way, I don't care enough to debate it. If you don't want to believe blocking DHT will raise estrogen, then don't. I don't care.

LOL, i didn't say that blocking DHT won't raise estrogen...

There is some evidence that DHT is an aromatase inhibitor & that it can antagonize ER.
Some people get gyno while on 5 ar inhibitors.


J Clin Endocrinol Metab 1984 Mar;58(3):467-72 Related Articles, Links


The intracellular control of aromatase activity by 5 alpha-reduced androgens in human breast carcinoma cells in culture.

Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW.

Four cell lines, each derived from a primary tumor from a patient with breast carcinoma, were grown to confluence in alpha-Minimum Essential Medium with 15% fetal calf serum and incubated for 24 h with [3H]androstenedione. The two lines (SA and PP) with the lowest formation of estrone and estradiol (less than 0.1% conversion) were the most active in the formation of the 5 alpha-reduced androgen metabolites androsterone (AND), 5 alpha-androstanedione (5 alpha-A-dione), and dihydrotestosterone (DHT). The two lines with the highest aromatase activity (DM and MD) had the lowest formation of 5 alpha-reduced metabolites. To determine if the 5 alpha-reduced androgen metabolites formed within the breast carcinoma cells could influence aromatase activity, the MD line was further studied.After 24-h preincubation with AND, DHT, or 5 alpha-A-dione at concentrations of 10(-6), 10(-7), and 10(-8) M, [3H]androstenedione was added to the culture medium, and aliquots were removed at 0, 4, 8, and 24 h. An 8-h incubation period was found to be optimum for inhibition studies. In comparison to control levels of estrone (2.5%) and estradiol (0.35%) formation, inhibition of aromatization was evident with all three compounds at 10(-8) M, with 5 alpha-A-dione producing the greatest inhibition (50%). At 10(-7) M, inhibition ranged from 45% (AND) to 70% (5 alpha-A-dione), and at 10(-6) M, inhibition was greater than 90% for each compound. 5 alpha-A-dione produced slightly greater inhibition than AND or DHT at each concentration tested. Since each of these compounds was capable of inhibiting aromatization, the cumulative effect of these 5 alpha-reduced metabolites could be an important factor in the intracellular regulation of aromatase activity.




Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.

Casey RW, Wilson JD.

Feminization in men occurs when the effective ratio of androgen to estrogen is lowered. Since sufficient estrogen is produced in normal men to induce breast enlargement in the absence of adequate amounts of circulating androgens, it has been generally assumed that androgens exert an antiestrogenic action to prevent feminization in normal men. We examined the mechanisms of this effect of androgens in the mouse breast. Administration of estradiol via silastic implants to castrated virgin CBA/J female mice results in a doubling in dry weight and DNA content of the breast. The effect of estradiol can be inhibited by implantation of 17 beta-hydroxy-5 alpha-androstan-3-one (dihydrotestosterone), whereas dihydrotestosterone alone had no effect on breast growth. Estradiol administration also enhances the level of progesterone receptor in mouse breast. Within 4 d of castration, the progesterone receptor virtually disappears and estradiol treatment causes a twofold increase above the level in intact animals. Dihydrotestosterone does not compete for binding to the progesterone receptor, but it does inhibit estrogen-mediated increases of progesterone receptor content of breast tissue cytosol from both control mice and mice with X-linked testicular feminization (tfm)/Y. Since tfm/Y mice lack a functional androgen receptor, we conclude that this antiestrogenic action of androgen is not mediated by the androgen receptor. Dihydrotestosterone competes with estradiol for binding to the cytosolic estrogen receptor of mouse breast, whereas 17 beta-hydroxy-5 beta-androstan-3-one (5 beta-dihydrotestosterone) neither competes for binding nor inhibits estradiol-mediated induction of the progesterone receptor. Dihydrotestosterone also promotes the translocation of estrogen receptor from cytoplasm to nucleus; the ratio of cytoplasmic-to-nuclear receptor changes from 3:1 in the castrate to 1:2 in dihydrotestosterone-treated mice. Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor.

 

[Essex boy]

Ifrit, how much dut are you taking and did you get any shedding from it or has it just been a continuous improvement in your hair? How long were you on finasteride before?

 

[GeneticalChallenge]

Thanks man!

I thought that the 30% increase seemed quite high (on paper) for this kind of drug and adding testosterone and dbol to that would increase it further and I really don´t need anymore estrogen floating around my nipples.

So basically it´s a safe bet to use Propecia along with test and d-bol?

Cheers!

Ps. I really like this board! Lots and lots of good info here!

Welcome to the board & happy birthday bro !

Finasteride may cause a sligt increase in test/estradiol but that's not really relevant on cycle since estrogen increase caused by Dbol/test will be much higher...
Just take Tamoxifen or an aromatase inhibitor if you're prone to gyno.

DHT contributes to gains due to its effect on central nervous system.
It doesn't have much effect in muscle because it gets deactivated by 3bHSD.

from:

DHT and the Athlete: Is it the Enemy?
By William Llewellyn

DHT and the neuromuscular system

It has been suggested that inhibiting the reduction of testosterone to DHT may not always be a good thing in terms of performance enhancement. It seems clear that DHT plays a vital role in the organization and functioning of the central nervous system, effects mediated by androgen receptors in neural cells. The specific importance of DHT in this area is evidenced by studies showing this hormone has a profoundly greater impact in neural cells compared to testosterone. In one such study it was demonstrated that both testosterone and DHT would result in increased androgen receptor proliferation in neural cells at 3 hours and 7 hours post administration, however only DHT sustained this increase at 21 hours. This strong difference lends support to suggestions that DHT and testosterone effect neural cells differently, perhaps such that the dihydrotestosterone-receptor complex and testosterone-receptor complex might even activate the transcription of different target genes. Others maintain that such a difference in effect would only be due to DHT forming a more stable and lasting complex with the androgen receptor, but the vital importance of DHT still remains evident.

The strong interaction between the central nervous system and skeletal muscles may be of key importance to the athlete, as these two areas interact to form what is referred to as the neuromuscular system. Clearly the ability of the body to adapt to training and better call upon nerve endings in muscle tissue is reliant on the functioning of the central nervous/neuromuscular system. Inhibiting the formation of DHT during a testosterone cycle may therefore inadvertently cause less to be achieved in terms of strength and muscle mass gains. We might also take note of the fact that while the anabolic steroid nandrolone is a stronger agonist of the androgen receptor than testosterone, it is much less effective at promoting strength and muscle mass increases in comparison. It seems logical that the loss of DHT (nandrolone actually reduces to a weaker steroid upon interaction with the 5-alpha reductase enzyme) may have something to do with this outcome. What is obvious is that were androgen receptor stimulation in muscle tissue solely responsible for strength and muscle growth, nandrolone would be a more potent drug than testosterone. Yet testosterone compounds remain the primary mass and strength agents among bodybuilders.

 

[frank5455]

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