Russianstar
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We all know it works, weve seen the logs and read the reviews!!!!!
So whats new?
Forma Stanzol Reviews: 9/10
Thats just one users unbiased review, without any reps adding their bit... but what makes it so special, well this table will help explain..
Relative Potency of Type 1 and Type 2 Aromatase Inhibitors
Product Aromatese inhibition% Residual aromatase %
Formestane (91.9) ( 8.1)
Aromasin ( 97.9) ( 2.1)
Cytadren ( 90.6 ) (9.4 )
Arimadex (96.7) ( 3.1)
Femara/Letro (98.7) ( 1.3)
You can see how well it compares against some of the well known A.I's that are available, and because it leaves some residual Aromatase the hances of rebound gyno are reduced greatly, also its effects on lipids are also minimised, which is a good thing when they are in all likely hood taking a battering.
You heard it reduces prolactin too?
You may have read this article i wrote some time back...
Anyone who knows anything about chemical structures will see that superdrol is not a progestin, and shouldnt cause prolactin like side effects.
The problem is everyone is different and eveyone has different amounts of progestin receptors, wich can cause worse sides in some users than others, one guy can use deca and get no bloat, another with the same dose will get bloat and gyno, because of this one reason alone. Now Beastsrol or superdrol is in itself not that androgenic, and as its structure suggests its not that different to other dht based steroids, now an action takes place that explains how it works... its doesnt act like a typical androgenic, but acts a little like oxymetholone, in that it doesnt show any real affinity for the 5AR enzyme, so you get weaker affinty for the androgen receptor than dht, but you get stronger androgenic effects as the enzyme 3beta hydroxysteroid dehydrogenase has little effect on the androgen affinity of superdrol.
The problem is this same enzyme 3beta hydroxysteroid dehydrogenase, is used in the conversion of many metaobiles in the body, superdrol produces a lot of metabolites that dont get bound by the androgen receptor like we just saw, it cant aromatize, so it doesnt bind to the estrogen receptor, but it circulates, as its also a di methyl, it is very biovailable so a lot of the product circulates in the blood, and these extra metabolites dont bind specificly...not in the way they should.. so i will explain in a detailed way then make it much easier to understand.
Prolactin is normaly caused by progestins, but can also be caused by dht, how?
For example, it is currently understood that when testosterone enters the cell cytoplasm it is subsequently converted to the more "active" androgen, dihydrotestosterone, DHT, by reduction at the 5alpha position, This is normal. Dihydrotestosterone is then either bound to a cytoplasmic "receptor" protein Rc, or is further metabolized to either 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol ,DIOL. The binding of DHT to its cytoplasmic receptor protein results in translocation of the steroid-receptor complex into the nucleus where presumably the complex dissociates and DHT exerts its androgenic effects. The transport of DHT to the nucleus can also result from the conversion of testosterone to DHT by nuclear membrane-bound 5alpha-reductase. Prolactin augmentation of DHT effects is envisioned as resulting from interaction of prolactin with its receptor, which due to the large size of the prolactin molecule is probably located in or on the plasma membrane.
Because superdrol is androgenic, but lacks the ability to show affinity via 5ar, it circulates, and this causes the large amounts of androgens to look for a transporter, so that it can bind to the androgen recptor, so it uses prolactin wich has a high affinity to cytoplasmic receptor protein, allowing the androgens, testosterone, to be carried and allowing them to convert to dht, only problem is prolactin hormone or luteotropic hormone is synthesised and secreted by sex binding lactotrope cells in the adenohypophysis (anterior pituitary gland, And this gland now produces more prolactin to help deal with the large amount of testosterone circulating that hasnt bound to the estrogen of androgen receptor, Part of the reason why superdol is so anabolic, So instead of binding to the androgen receptors in the scalp and the prostrate it converts to dht through this unique process, using prolactin to enter the cytoplasmic receptror protein, and allowing it to convert to dht and then bind to the androgen receptors in the muscle, causing its distinct hardening effects, it still cant bind to the scalp or prostrate via 5ar as the form of dht it has converted too doesnt allow for that affinity.
So more prolactin is produced to allow for the superdol to find a receptor ,this excess prolactin triggers a process that fills the breast with milk via a process called lactogenesis, in men however it causes a distinct enlargment of the mammary gland and can even cause a man to lactate.
If superdrol had better binding to the androgen receptor via 5AR then this problem would be prevented, the other thing is that prolactin production can remain elevated for months after a cycle has finished, and once the androgen has been removed, ( the cycle is over) the cytoplasmic receptor proteins have nothing to do other than to allow the prolactin to proceed with its hormonal action within the body, causing the male mammary gland to enlarge ready to produce milk... Hence the REBOUND gyno, this is why proper pct is needed for superdrol, and the use of something to prevent prolactin.
I suggest using topical Formestane.
Now the best bit is this, There are references as that show that DHT applied in areas with high prolactin can reduce gyno. Here is one:
Benveniste O, Simon A and Herson S. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature. Clinical Infectious Diseases 2001;33:891-893.
This shows that when in this case dht, but anything strongly androgenic in its actions is applied to gyno where high levels of prolactin are found then gyno can be reduced!!! Now this will work with prolactin induced gyno, as this and at least 6 other studies show.
So not only can Formastane improve gyno the same way masteron can, by preventing estrogen from binding to the estrogen receptor, it can also reduce the size of prolactin induced gyno, as it lowers the amount of progestin receptors available, and seems to act as a slight dopmamin agonist.
Now you will see many companies add pregenelone to formestane to reduce the androgenic activity, but it aslo reduces it effects considerably.
Taken oraly it has little effect, but transdermaly it is extremely potent, in fact its used to treat breast cancer as It is available as an intramuscular depot injection , some of you maybe aware called lentaron.
So how does it work exactly, Aromatase is an enzyme that synthesizes estrogen. Aromatase inhibitors block the synthesis of estrogen. This lowers the estrogen level, and slows the growth of cancers, And transdermaly formestane is one of the strongest products for this, so that means lean ROCK HARD gains on cycle. This is because the androgens can no longer convert into estrogen.. thats good news as it doesnt act like exemestane wich form a permanent bond with the aromatase enzyme, so preventing any estrogen wich is bad for your joints and tendons.
So why does gyno happen on cycle?
Bodybuilders who use steroids may experience an increase in estrogen levels , and this has undesirable consequences for a bodybuilder, such as gynecomastia. This is often the case when a natural aromatase inhibitor 4-OHAD has itself been inhibited. 4-OHAD is a metabolite of testosterone, which can mean 4-OHAD remains inhibited whilst aromatase levels are allowed high, so you actualy get even less androgens than normal and higher estrogen levels, so using Forma-Stanozolol can change the ratios allowing the enzyme 4-OHAD to remain active, so limiting estrogen, by increasing testosterone itself through its AI activity, And by preventing estrogen from binding to receptors so preventing gyno, but as it allows some estrogen to circulate, tendons and ligaments are kept strong and healthy.
It has a 12 hour half life wich is great as when used just morning and night it will build up even plasma levels in the blood and be constantly active, so getting full benefits of its AI properties, And through its special abilty to stimulate the dopaminergic system, it can prevent prolactin.. so it actualy can PREVENT GYNO BOTH FROM PROLACTIN AND ESTROGEN, and be used to TREAT GYNO FROM PROLACTIN through its abilty to act as a dopamine agonist, its ability to lower progestin receptor count, and its androgenic properties, And be used to TREAT GYNO CAUSED BY HIGH AROMATISATION.
Yes Formastane could even be used to treat and prevent DECA droopiness.
But i havent finished, one more thing makes this perfect not only alone or on cycle but especialy through PCT when estrogen levels rise, problem is if you block estrogen off you get low igf-1 levels... formestane can increase igf1 levels by a whopping 26 percent!!!
And you know i said it was androgenic... well it is, but it also can reduce BPH, so it even protects your prostrate!!!
And as its a transdermal, you may want to rub it all over your nips for improved action, you see i love milk, but i dont want to make my own, in fact i like boobies but i dont want to grow my own, and FORMASTANE can reduce your chances of either of these ever happening, and believe me for those whove experienced both the former happening, its not nice!!!
So not only is formastane perfect for any cycles using aromatizing compounds, but its perfect for anything that produces prolactin or is progestenic.. It will reduce any sides, or bloat and allow pct to be much easier and more effective.
Well there is more...
Combined inhibitory effect of formestane and herc... [Cancer Sci. 2010] - PubMed - NCBI
"In cells which expressed ERalpha, formestane/herceptin combination suppressed the mRNA expression of aromatase and HER2 and decreased cyclin D1 expression"
So you know HER2 is to do with prolactin expression.
Forma-stanzol contains the suicide aromatase inhibitor formestane (4-hydroxyandrostenedione), a clinically proven anti-estrogen exceedingly more potent than any supplement to come before it. 6-oxo-androstenedione, chrysin, indole-3-carbinol, calcium d-glucarate, trihydroxystilbene, not even our old Viratase (5-alpha-androstanedione) can come close. All of them combined in one capsule still wouldn't even have a shot. Forma-stanzol is such a revolutionary advance in the area of estrogen suppression because it contains the only agent backed by not one but numerous placebo-controlled human medical studies, and so effective it is actually a prescription breast cancer drug in other countries.
What other benefits apart from estrogen and prolactin control does it offer?
The Need for Estrogen Maintenance
Estrogen has both positive and negative effects that you should be aware of. On the positive it supports good high density cholesterol, increases muscle glucose utilization for tissue growth and repair, and even increases androgen receptor concentrations in various tissues. It is now understood that estrogen serves many useful purposes in men, particularly if we are looking for rapid muscle mass gain. If bulk is the goal it is therefore usually advised to hold off on estrogen maintenance compounds until there is a clear need for them. This brings us to the negative side of estrogen, namely that it can work to hide muscle definition by increasing water retention and fat buildup. It can also promote gynecomastia (the development of female breast tissue) in men if levels get too high. Since androgens and estrogens playing opposing roles on the disposition of body fat and the growth of mammary tissues, maximizing the ratio between these two hormones is often an important objective, particularly at times when dieting and cutting are key goals or gynecomastia is a worry because strongly aromatized hormones such as testosterone are being supplemented.
Testosterone Stimulation
To spite that fact that 4-hydroxyandrostenedione is also a weak prohormone to the anabolic steroid 4-hydroxytestosterone, as an aromatase inhibitor it also possesses notable testosterone stimulating properties. Whatever weak androgenic activity it may have is more than compensated for by its strong ability to lower estrogen levels. This action of course reduces the suppressive signal estrogen sends to your brain (estrogen is a main feedback signal to control the release of testosterone), increasing the testicular output of testosterone. In-vivo human studies show clearly that 4-hydroxyandrostenedione will suppress estrogen concentrations at levels that were not high enough to suppress gonadotropins13 . Even studies using 250mg to 500mg of 4-hydroxyandrostenedione injected every 2 weeks, or oral doses as high as 1000mg daily, have failed to show any notable suppressive effect towards testosterone concentrations14 . When the drug was given to men, including oral doses as high as 500mg (double the maximum recommended dose), we have seen measurable increases in serum testosterone concentrations 15 16 17. Due to the theoretical potential for androgenic feedback inhibition at high doses we do recommend, however, keeping within the recommended dosage range, and perhaps even limiting the dose at times when increasing testosterone levels is a primary focus of you the user.
Dose and Pharmacokinetics
After oral administration peak levels of 4-hydroxyandrostenedione are reached in the blood at approximately 1.5 hours , and the drug is cleared from the body with a half-life of approximately 3 hours . Due to its nature as an irreversible inhibitor, its estrogen-suppressing activity outlives it actual active lifespan in the bloodstream. Studies have demonstrated that maximum estrogen suppression is achieved with an oral dose of only 250mg per day 12 . Doubling this dose to 500mg, or even quadrupling it to 1000mg, was shown to have no effect on aromatase inhibition or estrogen levels appreciably different from the 250mg dose.. So topicaly with the advanced system Forma-stanzol offers, the dosing is not how muh you use thats important, its how much you need, and that varies on your own individual goals, General health, a lower dose, Estrogen suppression on a cycle a higher dose.... It really is dependent on many variables.
It doesnt stop there....
Post-Cycle use
When used during the recovery window after a cycle of prohormones, or even steroids for that matter, Formastane can offer a very unique additional benefit. The main focus at this time is of course minimizing the post-cycle hypoandrogenic (low androgen) state, mainly by trying to restore the natural production of testosterone, which in many cases has been suppressed by the cycle of hormones. In most cases some type of anti-estrogen is incorporated into an athlete's recovery program, due to the effect they can have on testosterone release (discussed above). Because Formastane is also a prohormone to 4-hydroxytestosterone, however, it allows for some small level of continued supplementation of exogenous androgen during this window. Normally this would be considered a very bad idea, as androgens are usually suppressive towards testosterone release. But with this product its weak androgenic activity is compensated for by its estrogen suppressing action, so provided reasonable doses are used it can essentially serve as a small bridge to full testosterone recovery. Regular aromatase-inhibitors, of course, cannot offer this benefit.
searl and bell formestat research Cancer Chemother Pharmacol 1990;27(1):99-130
DHT Inhibition
This compound has also demonstrated some ability to inhibit the 5-alpha reductase enzyme in certain in-vitro studies , which would seem to suggest it could offer some benefit by reducing androgenic activity in sensitive target tissues with high concentrations of 5-alpha reductase. At least one study in Scotland, however, suggests that this trait of 4-hydroxyandrostenedione is not strong enough to offer much of a physiological effect . Another makes note of both testosterone and DHT increases in some male patients taking the compound, not testosterone alone, which clearly does not support a strong DHT inhibiting role . We therefore at this time do not have enough evidence to conclude that 4-hydroxyandrostenedione is a potent 5-alpha-reductase inhibiting compound, But it holds promise in this area, One user applied Formastane to his prostate area and found relief from the pain he had been feeling... But more research needs to be done.
A Point to remember...
4-hydroxylated androgens such as 4-hydroxyandrostenedione have been shown to be naturally occurring, and therefore can be legally sold as nutritional supplements.
REFERENCES:
1 Treatment of advanced breast cancer with formestane. Murray R, Pitt P. Ann Oncol 1994;5 Suppl 7:S11-3
2 Pilot study of formestane in postmenopausal women with breast cancer. Joseph JK, Lim AK. Med J Malaysia 1998 Mar;53(1):37-41
3 Formestane is feasible and effective in elderly breast cancer patients with comorbidity and disability. Venturino A, Comandini D. Breast Cancer Res Treat 2000 Aug;62(3):217-22
4 Formestane versus megestrol acetate in postmenopausal breast cancer patients after failure of tamoxifen: a phase III prospective randomised cross over trial of second-line hormonal treatment (SAKK 20/90). Swiss Group for Clinical Cancer Research (SAKK). Thurlimann B, Castiglione M. Eur J Cancer 1997 Jun;33(7):1017-24
5 Formestane in the treatment of advanced postmenopausal breast cancer. Possinger K, Jonat W, Hoffken K. Ann Oncol 1994;5 Suppl 7:S7-10
6 Comparison of the selective aromatase inhibitor formestane with tamoxifen as first-line hormonal therapy in postmenopausal women with advanced breast cancer. Perez Carrion R, Alberola Candel V. Ann Oncol 1994;5 Suppl 7:S19-24
7 An endocrine and pharmacokinetic study of four oral doses of formestane in postmenopausal breast cancer patients. Dowsett M, Mehta A. et al. Eur J Cancer 1992;28(2-3):415-20
8 Formestane is feasible and effective in elderly breast cancer patients with comorbidity and disability. Venturino A, Comandini D. et al. Breast Cancer Res Treat 2000 Aug;62(3):217-22
9 Formestane. A review of its pharmacological properties and clinical efficacy in the treatment of postmenopausal breast cancer. Wiseman LR, Goa KL. Drugs Aging 1996 Oct;9(4):292-306
10 Comparison of the pharmacokinetics and pharmacodynamics of unformulated and formulated 4-hydroxyandrostenedione taken orally by healthy men. Dowsett M, Lloyd P. Cancer Chemother Pharmacol 1990;27(1):67-71
11 Dose-related endocrine effects and pharmacokinetics of oral and intramuscular 4-hydroxyandrostenedione in postmenopausal breast cancer patients. Dowsett M, Cunningham DC et al. Cancer Res 1989 Mar 1;49(5):1306-12
12 An endocrine and pharmacokinetic study of four oral doses of formestane in postmenopausal breast cancer patients. Dowsett M, Mehta A, King N, Smith IE, Powles TJ, Stein RC, Coombes RC. Eur J Cancer 1992;28(2-3):415-20
13 Aromatase inhibitors and hormone-dependent cancers. Brodie AM, Banks PK, Inkster SE, Dowsett M, Coombes RC. J Steroid Biochem Mol Biol 1990 Nov 20;37(3):327-33
14 Dose-related endocrine effects and pharmacokinetics of oral and intramuscular 4-hydroxyandrostenedione in postmenopausal breast cancer patients. Dowsett M, Cunningham DC et al. Cancer Res 1989 Mar 1;49(5):1306-12
15 Aromatase inhibition: 4-hydroxyandrostenedione (4-OHA, CGP 32349) in advanced prostatic cancer. Davies JH, Dowsett M, Jacobs S, Coombes RC, Hedley A, Shearer RJ. Br J Cancer 1992 Jul;66(1):139-42
16 Comparison of the pharmacokinetics and pharmacodynamics of unformulated and formulated 4-hydroxyandrostenedione taken orally by healthy men. Dowsett M, Lloyd P. Cancer Chemother Pharmacol 1990;27(1):67-71
17 Pharmacokinetics of 4-hydroxyandrostenedione in man after intramuscular injection of different formulations and the effect of this drug on plasma aromatizable androgens and 17beta-estradiol concentrations. Danza G, Muratori M, Guarna A, Occhiato EG, Sadri R, Serio M. J Steroid Biochem Mol Biol 1993 Sep;46(3):373-9
18 Aromatase and other inhibitors in breast and prostatic cancer. Brodie AM, Banks PK, Inkster SE, Son C, Koos RD. Steroid Biochem Mol Biol 1990 Dec 20;37(6):1043-8
19 Effects of 4-hydroxyandrost-4-ene-3,17-dione and its metabolites on 5 alpha-reductase activity and the androgen receptor. Davies JH, Shearer RJ et al. J Enzyme Inhib 1992;6(2):141-7
20 A kinetic analysis of the inhibition of human prostatic 5 alpha-reductase by 4-hydroxyandrostenedione and related steroids. Houston B, Habib FK Steroids 1988 Sep;52(3):237-47
21 Aromatase inhibition: 4-hydroxyandrostenedione (4-OHA, CGP 32349) in advanced prostatic cancer. Davies JH, Dowsett M. Br J Cancer 1992 Jul;66(1):139-42
22 Sexual specific C-4 hydroxylation of 5 -androstane-3,17-dione in rats and the influence of the antiandrogen cyproteron acetate. Wenzel M, Pitzel L, Bollert B. Hoppe Seylers Z Physiol Chem 1972 Jun;353(6):861-8
We havent finished just yet!!
Anti-Estrogens And IGF-1 Production
GH (Growth Hormone) is like a master hormone for tissue growth and fat regulation due to its own intrinsic qualities and its propensity to be converted into or trigger the production and release of Growth Factors. Of these Growth Factors, one of the best known in regard to muscle growth is IGF-1 (Insulin-Like Growth Factor-1).
As most are aware by now, IGF-1 is a powerful anabolic and anti-catabolic hormone. Whether in pre-contest mode or packing on the mass, the amount of circulating and stored IGF-1 an athlete maintains plays a powerful role in the results achieved. Obviously as IGF-1 levels decrease so does the potential for packing on the beef, and the amount of lean tissue lost during calorie-restricted periods increases as well. (Not good)
Estrogen, and more so estradiol, can trigger GH release from the pituitary gland. Aromatase inhibitors decrease the amount of circulating estrogen/estradiol and estrogen receptor antagonist keep estrogen out of the specific pituitary receptors. So in many regards the use of anti-estrogens can effect IGF-1 production and in some cases affect the number of IGF-1 receptors our tissues posses
In the case of Forma its all good... take a look below.
Product effect percentage
Forma-stanzol increases igf-1 26%
Letro increases Igf-1 24%
Arimadex decreases igf-1 18%
Nolvadex decreases igf-1 23.5%
Faslodex decreases igf-1 70%
Cytadren increases igf-1 27%
Aromasin increases igf-1 28%
This again shows what an affective PCT aid Forma-stanzol can be, and it also means it can be used even after PCT to continue to promote gains, and an anabolic masculine state.
As IGF is the main marker in checking HGH levels, You can be sure that Forma-stanzol doesnt suppress but rather increases glycogensis and promotes with synergy that fat burning effects of your own GH.
Now finaly consider this....
From these studies and all the logs of formestane available on the internet these are the facts.
?Formestane increases IGF-1 secretion and activity.
?Formestane decreases the number of progesterone receptors (inhibits the trenbolone and "deca-dick" type side effects and increases fat loss)
?Formestane inhibits 91.9% of aromatase enzyme production
?Formestane increases HPTA activity similar to hcg and Clomid together
?Formestane is anabolic and androgenic
?Formestane is a "suicide inhibitor" of aromatase. Specifically this means that it will irreversibly bind to the aromatase enzyme and permanently deactivate it
?Formestane (The sterile injectable form) possesses a 4-day half-life
?Formestane decreases SHBG 34% thus increasing androgen activity.
?Formestane inhibits DHT (dehydrotestosterone) formation and activity.
?Formestane possesses 1% of the binding affinity of DHT to DHT receptors
?Formestane has been shown to decrease prostate concerns such as BPH.
?Formestane has been shown to continue to increase HPTA function above natural levels even after 22 weeks of continuous administration
So choose your weapon carefully!!
Until next time, Take care all russianstar
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The best peptides are here!! PURCHASEPEPTIDES!!!!
So whats new?
Forma Stanzol Reviews: 9/10
Thats just one users unbiased review, without any reps adding their bit... but what makes it so special, well this table will help explain..
Relative Potency of Type 1 and Type 2 Aromatase Inhibitors
Product Aromatese inhibition% Residual aromatase %
Formestane (91.9) ( 8.1)
Aromasin ( 97.9) ( 2.1)
Cytadren ( 90.6 ) (9.4 )
Arimadex (96.7) ( 3.1)
Femara/Letro (98.7) ( 1.3)
You can see how well it compares against some of the well known A.I's that are available, and because it leaves some residual Aromatase the hances of rebound gyno are reduced greatly, also its effects on lipids are also minimised, which is a good thing when they are in all likely hood taking a battering.
You heard it reduces prolactin too?
You may have read this article i wrote some time back...
Anyone who knows anything about chemical structures will see that superdrol is not a progestin, and shouldnt cause prolactin like side effects.
The problem is everyone is different and eveyone has different amounts of progestin receptors, wich can cause worse sides in some users than others, one guy can use deca and get no bloat, another with the same dose will get bloat and gyno, because of this one reason alone. Now Beastsrol or superdrol is in itself not that androgenic, and as its structure suggests its not that different to other dht based steroids, now an action takes place that explains how it works... its doesnt act like a typical androgenic, but acts a little like oxymetholone, in that it doesnt show any real affinity for the 5AR enzyme, so you get weaker affinty for the androgen receptor than dht, but you get stronger androgenic effects as the enzyme 3beta hydroxysteroid dehydrogenase has little effect on the androgen affinity of superdrol.
The problem is this same enzyme 3beta hydroxysteroid dehydrogenase, is used in the conversion of many metaobiles in the body, superdrol produces a lot of metabolites that dont get bound by the androgen receptor like we just saw, it cant aromatize, so it doesnt bind to the estrogen receptor, but it circulates, as its also a di methyl, it is very biovailable so a lot of the product circulates in the blood, and these extra metabolites dont bind specificly...not in the way they should.. so i will explain in a detailed way then make it much easier to understand.
Prolactin is normaly caused by progestins, but can also be caused by dht, how?
For example, it is currently understood that when testosterone enters the cell cytoplasm it is subsequently converted to the more "active" androgen, dihydrotestosterone, DHT, by reduction at the 5alpha position, This is normal. Dihydrotestosterone is then either bound to a cytoplasmic "receptor" protein Rc, or is further metabolized to either 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol ,DIOL. The binding of DHT to its cytoplasmic receptor protein results in translocation of the steroid-receptor complex into the nucleus where presumably the complex dissociates and DHT exerts its androgenic effects. The transport of DHT to the nucleus can also result from the conversion of testosterone to DHT by nuclear membrane-bound 5alpha-reductase. Prolactin augmentation of DHT effects is envisioned as resulting from interaction of prolactin with its receptor, which due to the large size of the prolactin molecule is probably located in or on the plasma membrane.
Because superdrol is androgenic, but lacks the ability to show affinity via 5ar, it circulates, and this causes the large amounts of androgens to look for a transporter, so that it can bind to the androgen recptor, so it uses prolactin wich has a high affinity to cytoplasmic receptor protein, allowing the androgens, testosterone, to be carried and allowing them to convert to dht, only problem is prolactin hormone or luteotropic hormone is synthesised and secreted by sex binding lactotrope cells in the adenohypophysis (anterior pituitary gland, And this gland now produces more prolactin to help deal with the large amount of testosterone circulating that hasnt bound to the estrogen of androgen receptor, Part of the reason why superdol is so anabolic, So instead of binding to the androgen receptors in the scalp and the prostrate it converts to dht through this unique process, using prolactin to enter the cytoplasmic receptror protein, and allowing it to convert to dht and then bind to the androgen receptors in the muscle, causing its distinct hardening effects, it still cant bind to the scalp or prostrate via 5ar as the form of dht it has converted too doesnt allow for that affinity.
So more prolactin is produced to allow for the superdol to find a receptor ,this excess prolactin triggers a process that fills the breast with milk via a process called lactogenesis, in men however it causes a distinct enlargment of the mammary gland and can even cause a man to lactate.
If superdrol had better binding to the androgen receptor via 5AR then this problem would be prevented, the other thing is that prolactin production can remain elevated for months after a cycle has finished, and once the androgen has been removed, ( the cycle is over) the cytoplasmic receptor proteins have nothing to do other than to allow the prolactin to proceed with its hormonal action within the body, causing the male mammary gland to enlarge ready to produce milk... Hence the REBOUND gyno, this is why proper pct is needed for superdrol, and the use of something to prevent prolactin.
I suggest using topical Formestane.
Now the best bit is this, There are references as that show that DHT applied in areas with high prolactin can reduce gyno. Here is one:
Benveniste O, Simon A and Herson S. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature. Clinical Infectious Diseases 2001;33:891-893.
This shows that when in this case dht, but anything strongly androgenic in its actions is applied to gyno where high levels of prolactin are found then gyno can be reduced!!! Now this will work with prolactin induced gyno, as this and at least 6 other studies show.
So not only can Formastane improve gyno the same way masteron can, by preventing estrogen from binding to the estrogen receptor, it can also reduce the size of prolactin induced gyno, as it lowers the amount of progestin receptors available, and seems to act as a slight dopmamin agonist.
Now you will see many companies add pregenelone to formestane to reduce the androgenic activity, but it aslo reduces it effects considerably.
Taken oraly it has little effect, but transdermaly it is extremely potent, in fact its used to treat breast cancer as It is available as an intramuscular depot injection , some of you maybe aware called lentaron.
So how does it work exactly, Aromatase is an enzyme that synthesizes estrogen. Aromatase inhibitors block the synthesis of estrogen. This lowers the estrogen level, and slows the growth of cancers, And transdermaly formestane is one of the strongest products for this, so that means lean ROCK HARD gains on cycle. This is because the androgens can no longer convert into estrogen.. thats good news as it doesnt act like exemestane wich form a permanent bond with the aromatase enzyme, so preventing any estrogen wich is bad for your joints and tendons.
So why does gyno happen on cycle?
Bodybuilders who use steroids may experience an increase in estrogen levels , and this has undesirable consequences for a bodybuilder, such as gynecomastia. This is often the case when a natural aromatase inhibitor 4-OHAD has itself been inhibited. 4-OHAD is a metabolite of testosterone, which can mean 4-OHAD remains inhibited whilst aromatase levels are allowed high, so you actualy get even less androgens than normal and higher estrogen levels, so using Forma-Stanozolol can change the ratios allowing the enzyme 4-OHAD to remain active, so limiting estrogen, by increasing testosterone itself through its AI activity, And by preventing estrogen from binding to receptors so preventing gyno, but as it allows some estrogen to circulate, tendons and ligaments are kept strong and healthy.
It has a 12 hour half life wich is great as when used just morning and night it will build up even plasma levels in the blood and be constantly active, so getting full benefits of its AI properties, And through its special abilty to stimulate the dopaminergic system, it can prevent prolactin.. so it actualy can PREVENT GYNO BOTH FROM PROLACTIN AND ESTROGEN, and be used to TREAT GYNO FROM PROLACTIN through its abilty to act as a dopamine agonist, its ability to lower progestin receptor count, and its androgenic properties, And be used to TREAT GYNO CAUSED BY HIGH AROMATISATION.
Yes Formastane could even be used to treat and prevent DECA droopiness.
But i havent finished, one more thing makes this perfect not only alone or on cycle but especialy through PCT when estrogen levels rise, problem is if you block estrogen off you get low igf-1 levels... formestane can increase igf1 levels by a whopping 26 percent!!!
And you know i said it was androgenic... well it is, but it also can reduce BPH, so it even protects your prostrate!!!
And as its a transdermal, you may want to rub it all over your nips for improved action, you see i love milk, but i dont want to make my own, in fact i like boobies but i dont want to grow my own, and FORMASTANE can reduce your chances of either of these ever happening, and believe me for those whove experienced both the former happening, its not nice!!!
So not only is formastane perfect for any cycles using aromatizing compounds, but its perfect for anything that produces prolactin or is progestenic.. It will reduce any sides, or bloat and allow pct to be much easier and more effective.
Well there is more...
Combined inhibitory effect of formestane and herc... [Cancer Sci. 2010] - PubMed - NCBI
"In cells which expressed ERalpha, formestane/herceptin combination suppressed the mRNA expression of aromatase and HER2 and decreased cyclin D1 expression"
So you know HER2 is to do with prolactin expression.
Forma-stanzol contains the suicide aromatase inhibitor formestane (4-hydroxyandrostenedione), a clinically proven anti-estrogen exceedingly more potent than any supplement to come before it. 6-oxo-androstenedione, chrysin, indole-3-carbinol, calcium d-glucarate, trihydroxystilbene, not even our old Viratase (5-alpha-androstanedione) can come close. All of them combined in one capsule still wouldn't even have a shot. Forma-stanzol is such a revolutionary advance in the area of estrogen suppression because it contains the only agent backed by not one but numerous placebo-controlled human medical studies, and so effective it is actually a prescription breast cancer drug in other countries.
What other benefits apart from estrogen and prolactin control does it offer?
The Need for Estrogen Maintenance
Estrogen has both positive and negative effects that you should be aware of. On the positive it supports good high density cholesterol, increases muscle glucose utilization for tissue growth and repair, and even increases androgen receptor concentrations in various tissues. It is now understood that estrogen serves many useful purposes in men, particularly if we are looking for rapid muscle mass gain. If bulk is the goal it is therefore usually advised to hold off on estrogen maintenance compounds until there is a clear need for them. This brings us to the negative side of estrogen, namely that it can work to hide muscle definition by increasing water retention and fat buildup. It can also promote gynecomastia (the development of female breast tissue) in men if levels get too high. Since androgens and estrogens playing opposing roles on the disposition of body fat and the growth of mammary tissues, maximizing the ratio between these two hormones is often an important objective, particularly at times when dieting and cutting are key goals or gynecomastia is a worry because strongly aromatized hormones such as testosterone are being supplemented.
Testosterone Stimulation
To spite that fact that 4-hydroxyandrostenedione is also a weak prohormone to the anabolic steroid 4-hydroxytestosterone, as an aromatase inhibitor it also possesses notable testosterone stimulating properties. Whatever weak androgenic activity it may have is more than compensated for by its strong ability to lower estrogen levels. This action of course reduces the suppressive signal estrogen sends to your brain (estrogen is a main feedback signal to control the release of testosterone), increasing the testicular output of testosterone. In-vivo human studies show clearly that 4-hydroxyandrostenedione will suppress estrogen concentrations at levels that were not high enough to suppress gonadotropins13 . Even studies using 250mg to 500mg of 4-hydroxyandrostenedione injected every 2 weeks, or oral doses as high as 1000mg daily, have failed to show any notable suppressive effect towards testosterone concentrations14 . When the drug was given to men, including oral doses as high as 500mg (double the maximum recommended dose), we have seen measurable increases in serum testosterone concentrations 15 16 17. Due to the theoretical potential for androgenic feedback inhibition at high doses we do recommend, however, keeping within the recommended dosage range, and perhaps even limiting the dose at times when increasing testosterone levels is a primary focus of you the user.
Dose and Pharmacokinetics
After oral administration peak levels of 4-hydroxyandrostenedione are reached in the blood at approximately 1.5 hours , and the drug is cleared from the body with a half-life of approximately 3 hours . Due to its nature as an irreversible inhibitor, its estrogen-suppressing activity outlives it actual active lifespan in the bloodstream. Studies have demonstrated that maximum estrogen suppression is achieved with an oral dose of only 250mg per day 12 . Doubling this dose to 500mg, or even quadrupling it to 1000mg, was shown to have no effect on aromatase inhibition or estrogen levels appreciably different from the 250mg dose.. So topicaly with the advanced system Forma-stanzol offers, the dosing is not how muh you use thats important, its how much you need, and that varies on your own individual goals, General health, a lower dose, Estrogen suppression on a cycle a higher dose.... It really is dependent on many variables.
It doesnt stop there....
Post-Cycle use
When used during the recovery window after a cycle of prohormones, or even steroids for that matter, Formastane can offer a very unique additional benefit. The main focus at this time is of course minimizing the post-cycle hypoandrogenic (low androgen) state, mainly by trying to restore the natural production of testosterone, which in many cases has been suppressed by the cycle of hormones. In most cases some type of anti-estrogen is incorporated into an athlete's recovery program, due to the effect they can have on testosterone release (discussed above). Because Formastane is also a prohormone to 4-hydroxytestosterone, however, it allows for some small level of continued supplementation of exogenous androgen during this window. Normally this would be considered a very bad idea, as androgens are usually suppressive towards testosterone release. But with this product its weak androgenic activity is compensated for by its estrogen suppressing action, so provided reasonable doses are used it can essentially serve as a small bridge to full testosterone recovery. Regular aromatase-inhibitors, of course, cannot offer this benefit.
searl and bell formestat research Cancer Chemother Pharmacol 1990;27(1):99-130
DHT Inhibition
This compound has also demonstrated some ability to inhibit the 5-alpha reductase enzyme in certain in-vitro studies , which would seem to suggest it could offer some benefit by reducing androgenic activity in sensitive target tissues with high concentrations of 5-alpha reductase. At least one study in Scotland, however, suggests that this trait of 4-hydroxyandrostenedione is not strong enough to offer much of a physiological effect . Another makes note of both testosterone and DHT increases in some male patients taking the compound, not testosterone alone, which clearly does not support a strong DHT inhibiting role . We therefore at this time do not have enough evidence to conclude that 4-hydroxyandrostenedione is a potent 5-alpha-reductase inhibiting compound, But it holds promise in this area, One user applied Formastane to his prostate area and found relief from the pain he had been feeling... But more research needs to be done.
A Point to remember...
4-hydroxylated androgens such as 4-hydroxyandrostenedione have been shown to be naturally occurring, and therefore can be legally sold as nutritional supplements.
REFERENCES:
1 Treatment of advanced breast cancer with formestane. Murray R, Pitt P. Ann Oncol 1994;5 Suppl 7:S11-3
2 Pilot study of formestane in postmenopausal women with breast cancer. Joseph JK, Lim AK. Med J Malaysia 1998 Mar;53(1):37-41
3 Formestane is feasible and effective in elderly breast cancer patients with comorbidity and disability. Venturino A, Comandini D. Breast Cancer Res Treat 2000 Aug;62(3):217-22
4 Formestane versus megestrol acetate in postmenopausal breast cancer patients after failure of tamoxifen: a phase III prospective randomised cross over trial of second-line hormonal treatment (SAKK 20/90). Swiss Group for Clinical Cancer Research (SAKK). Thurlimann B, Castiglione M. Eur J Cancer 1997 Jun;33(7):1017-24
5 Formestane in the treatment of advanced postmenopausal breast cancer. Possinger K, Jonat W, Hoffken K. Ann Oncol 1994;5 Suppl 7:S7-10
6 Comparison of the selective aromatase inhibitor formestane with tamoxifen as first-line hormonal therapy in postmenopausal women with advanced breast cancer. Perez Carrion R, Alberola Candel V. Ann Oncol 1994;5 Suppl 7:S19-24
7 An endocrine and pharmacokinetic study of four oral doses of formestane in postmenopausal breast cancer patients. Dowsett M, Mehta A. et al. Eur J Cancer 1992;28(2-3):415-20
8 Formestane is feasible and effective in elderly breast cancer patients with comorbidity and disability. Venturino A, Comandini D. et al. Breast Cancer Res Treat 2000 Aug;62(3):217-22
9 Formestane. A review of its pharmacological properties and clinical efficacy in the treatment of postmenopausal breast cancer. Wiseman LR, Goa KL. Drugs Aging 1996 Oct;9(4):292-306
10 Comparison of the pharmacokinetics and pharmacodynamics of unformulated and formulated 4-hydroxyandrostenedione taken orally by healthy men. Dowsett M, Lloyd P. Cancer Chemother Pharmacol 1990;27(1):67-71
11 Dose-related endocrine effects and pharmacokinetics of oral and intramuscular 4-hydroxyandrostenedione in postmenopausal breast cancer patients. Dowsett M, Cunningham DC et al. Cancer Res 1989 Mar 1;49(5):1306-12
12 An endocrine and pharmacokinetic study of four oral doses of formestane in postmenopausal breast cancer patients. Dowsett M, Mehta A, King N, Smith IE, Powles TJ, Stein RC, Coombes RC. Eur J Cancer 1992;28(2-3):415-20
13 Aromatase inhibitors and hormone-dependent cancers. Brodie AM, Banks PK, Inkster SE, Dowsett M, Coombes RC. J Steroid Biochem Mol Biol 1990 Nov 20;37(3):327-33
14 Dose-related endocrine effects and pharmacokinetics of oral and intramuscular 4-hydroxyandrostenedione in postmenopausal breast cancer patients. Dowsett M, Cunningham DC et al. Cancer Res 1989 Mar 1;49(5):1306-12
15 Aromatase inhibition: 4-hydroxyandrostenedione (4-OHA, CGP 32349) in advanced prostatic cancer. Davies JH, Dowsett M, Jacobs S, Coombes RC, Hedley A, Shearer RJ. Br J Cancer 1992 Jul;66(1):139-42
16 Comparison of the pharmacokinetics and pharmacodynamics of unformulated and formulated 4-hydroxyandrostenedione taken orally by healthy men. Dowsett M, Lloyd P. Cancer Chemother Pharmacol 1990;27(1):67-71
17 Pharmacokinetics of 4-hydroxyandrostenedione in man after intramuscular injection of different formulations and the effect of this drug on plasma aromatizable androgens and 17beta-estradiol concentrations. Danza G, Muratori M, Guarna A, Occhiato EG, Sadri R, Serio M. J Steroid Biochem Mol Biol 1993 Sep;46(3):373-9
18 Aromatase and other inhibitors in breast and prostatic cancer. Brodie AM, Banks PK, Inkster SE, Son C, Koos RD. Steroid Biochem Mol Biol 1990 Dec 20;37(6):1043-8
19 Effects of 4-hydroxyandrost-4-ene-3,17-dione and its metabolites on 5 alpha-reductase activity and the androgen receptor. Davies JH, Shearer RJ et al. J Enzyme Inhib 1992;6(2):141-7
20 A kinetic analysis of the inhibition of human prostatic 5 alpha-reductase by 4-hydroxyandrostenedione and related steroids. Houston B, Habib FK Steroids 1988 Sep;52(3):237-47
21 Aromatase inhibition: 4-hydroxyandrostenedione (4-OHA, CGP 32349) in advanced prostatic cancer. Davies JH, Dowsett M. Br J Cancer 1992 Jul;66(1):139-42
22 Sexual specific C-4 hydroxylation of 5 -androstane-3,17-dione in rats and the influence of the antiandrogen cyproteron acetate. Wenzel M, Pitzel L, Bollert B. Hoppe Seylers Z Physiol Chem 1972 Jun;353(6):861-8
We havent finished just yet!!
Anti-Estrogens And IGF-1 Production
GH (Growth Hormone) is like a master hormone for tissue growth and fat regulation due to its own intrinsic qualities and its propensity to be converted into or trigger the production and release of Growth Factors. Of these Growth Factors, one of the best known in regard to muscle growth is IGF-1 (Insulin-Like Growth Factor-1).
As most are aware by now, IGF-1 is a powerful anabolic and anti-catabolic hormone. Whether in pre-contest mode or packing on the mass, the amount of circulating and stored IGF-1 an athlete maintains plays a powerful role in the results achieved. Obviously as IGF-1 levels decrease so does the potential for packing on the beef, and the amount of lean tissue lost during calorie-restricted periods increases as well. (Not good)
Estrogen, and more so estradiol, can trigger GH release from the pituitary gland. Aromatase inhibitors decrease the amount of circulating estrogen/estradiol and estrogen receptor antagonist keep estrogen out of the specific pituitary receptors. So in many regards the use of anti-estrogens can effect IGF-1 production and in some cases affect the number of IGF-1 receptors our tissues posses
In the case of Forma its all good... take a look below.
Product effect percentage
Forma-stanzol increases igf-1 26%
Letro increases Igf-1 24%
Arimadex decreases igf-1 18%
Nolvadex decreases igf-1 23.5%
Faslodex decreases igf-1 70%
Cytadren increases igf-1 27%
Aromasin increases igf-1 28%
This again shows what an affective PCT aid Forma-stanzol can be, and it also means it can be used even after PCT to continue to promote gains, and an anabolic masculine state.
As IGF is the main marker in checking HGH levels, You can be sure that Forma-stanzol doesnt suppress but rather increases glycogensis and promotes with synergy that fat burning effects of your own GH.
Now finaly consider this....
From these studies and all the logs of formestane available on the internet these are the facts.
?Formestane increases IGF-1 secretion and activity.
?Formestane decreases the number of progesterone receptors (inhibits the trenbolone and "deca-dick" type side effects and increases fat loss)
?Formestane inhibits 91.9% of aromatase enzyme production
?Formestane increases HPTA activity similar to hcg and Clomid together
?Formestane is anabolic and androgenic
?Formestane is a "suicide inhibitor" of aromatase. Specifically this means that it will irreversibly bind to the aromatase enzyme and permanently deactivate it
?Formestane (The sterile injectable form) possesses a 4-day half-life
?Formestane decreases SHBG 34% thus increasing androgen activity.
?Formestane inhibits DHT (dehydrotestosterone) formation and activity.
?Formestane possesses 1% of the binding affinity of DHT to DHT receptors
?Formestane has been shown to decrease prostate concerns such as BPH.
?Formestane has been shown to continue to increase HPTA function above natural levels even after 22 weeks of continuous administration
So choose your weapon carefully!!
Until next time, Take care all russianstar
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