Why Formestane is needed.

This helps show its efficiacy at preventing estrogen and prolactin. http://www.ncbi.nlm.nih.gov/pubmed/20491779
“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. Formastat(tm) 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. Formastat(tm) 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.

Formestane (4-hydroxyandrostenedione)
Suicide Aromatase Inhibitor
Formastat is in many regards similar to a competitive steroidal aromatase inhibitor like Viratase. Both are steroidal compounds that work by attaching to the active binding site of the aromatase enzyme, preventing it from interacting with other steroids (such as testosterone) that are capable of being converted to estrogen. With the enzyme binding site occupied, it is for all intents and purposes inactive. If the inhibitor is present in a high enough level it will dramatically suppress estrogen concentrations in the blood. The difference between a competitive inhibitor like Viratase, and Formastat, is that the former will detach after some time, rendering the enzyme active again. Formastat on the other hand binds permanently with the aromatase enzyme, making it useless until the body actually replaces it through the normal metabolic attrition of enzymes. This type of compound is called a suicide or irreversible aromatase inhibitor, and has the benefit of being both highly selective in its action on estrogen and long-lasting in effect.
Because of its potent estrogen-suppressing action, 4-hydroxyandrostenedione has been successfully used on breast cancer patients in many other countries including England, Germany, Switzerland, Spain, Australia, New Zealand, Italy and Malaysia12345678 It has been shown to be an effective option as a second line of defense after tamoxifen, an estrogen receptor antagonist, has failed to elicit a positive response with patients, and to produce an overall response statistically similar to tamoxifen when administered as the first-line therapy . Those of us in the bodybuilding world looking to mitigate the physiological effects of estrogen for other purposes have likewise been confronted for the first time with a legal supplement that has all the actions and potency of a pharmaceutical agent, which would normally be obtained only with a doctor’s prescription! .
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 day12 . 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.
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 to 2-3 caps per day, at times when increasing testosterone levels is a primary focus of use.

Figure 1. Mean testosterone increase in 6 normal men given 500mg of oral 4-hydroxyandrostenedione. Source: Comparison of the pharmacokinetics and pharmacodynamics of unformulated and formulated 4-hydroxyandrostenedione taken orally by healthy men. Cancer Chemother Pharmacol 1990;27(1):67-71
Post-Cycle Use
When used during the recovery window after a cycle of prohormones, or even steroids for that matter, Formastat 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 Formastat 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, however will continue to investigate this possible activity.
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, enhances growth hormone output, 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.
A Naturally Occurring Hormone
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

Relative Potency of Type 1 and Type 2 Aromatase Inhibitors

Product

Aromatase Inhibition (%)

Residual Aromatase (%)

Formestane/

4-Androstenoldione

91.9

8.1

Aromasin/Exemestane

97.9

2.1

Cytadren/

Aminoglutethimide

90.6

9.4

Arimidex/Anastrozole

96.7

3.1

Femara/Letrozole

98.7

1.3

Anti-estrogens and IGF production.

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.

Product Effect Percentage

Formestane/

 

4-Androstenoldione

 

Increases IGF-1

26%

Femara/Letrozol

Increases IGF-1

24%

Arimidex/Anastrozole

Decreases IGF-1

18%

Nolvadex/Tamoxifen

Decreases IGF-1

23.5%

Faslodex/Fulvestrant

Decreases IGF-1

70%

Cytadren/

Aminoglutethimide

Increases IGF-1

27%

Aromasin/Exemestane

Increases IGF-1

28%

Superdrol and prolactin sides. Why Formestane is the answer.

Written by Russianstar, this information is copyrited

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.

 

 

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
  • Kindest regards RS

R.S

#UFC ,TUF 18 episode 4 Rousey gets blousey.

I am a huge fan of Rhonda, especially all that she has done in helping make female MMA a sport to be taken seriously. I must admit that her little displays of macho behaviour are somewhat underwhelming her respectability as a UFC fighter, and a champion at that. I think though that instead of going to see guest coach Dennis Hallman and getting in his face, Maybe she should have stopped her own coach, from making such a fool of himself for the second week running… Making ridiculous comments like we will do this when there are no cameras, and he was saying it with his heart in his mouth, just look at the video again, Typical body language of someone who was already realising this was a very bad idea.

Maybe we could see a match up at the TUF final, between Dennis Hallman 52 wins and 14 losses, And Mr im going to eyeball everyone Edmond  Taverdyan, 2 wins against 2 unknowns. Brilliant how Edmond was telling Dennis, they would get kicked off the show as they walk to the octagon, reminded me of a dog with its tale between his legs. Hilarious, and it was real TV gold.

Rhonda’s word choices are just crazy,I love the “you act tough behind twitter, we are tough all the time” Comment from the last episode, but she out does herself in this episode.  I quote “If your team disrespect us, we are going to find a way to let you know that’s a bad idea, I’m the only one who can fight officially” And Rhonda, You did start it, and you will probably keep starting it, even after you fight Meisha. Rhonda get over it, or jealousy will eat you up and consume you, and your not a guy, so don’t swagger.

The fight was between Jessica Rakoczy vs. Roxanne Modafferi

Despite sharing her name with a Porn star, Jessica is no joke, she is real hardcore,  don’t let her Motherly persona fool you, She lost her mother at 15, Then just as things started to pick up in her boxing , she was involved in a pile up, a multi-car accident that injured her neck, shoulder, back and knee prevented her from competing, And just after recovering from that, and making a solid claim for the Canadian national Boxing team, an ill timed punch broke her wrist on her opponents head. Despite all that, She won major boxing titles at lightweight, mainly because her speed and technique were far beyond most of her more experienced peers, and she developed K.O power, knocking out one opponent in 38 seconds. When she turned to MMA the change seemed to cause Jessica problems with 3 straight losses, and a ban followed because of taking painkillers and not informing the Arena Doctors. However she rebounded by returning to boxing, rising to 33 wins 3 losses and 12 k’0s. Her boxing is superb, and mentally as well as physically she has all the attributes to win this season of TUF.

Roxanne is a bit of an Oxy-Moron, she looks like a Geek, and is very intelligent, she can speak a few languages, she has a lovely friendly disposition, but.. she knows Jujitsu, and despite her stand up being pretty weak, her ground game certainly isn’t, One of the pioneers of Womens MMA her record may look a little weak, but she has vast experience, however fighting Jessica was not a clever move by Meisha Tate.

The fight really was always out of Roxanne’s reach, Jessica’s foot work and strength made life very difficult for Roxanne, and even when she got it to the ground, Jessica showed a vastly improved ground game an was able to escape any potential submission attempts from Roxanne, Great coaching by Rhonda’s team. In round 2 Roxy attempted an armbar, Jessica lifter her up and slammed her, and it looked like Roxy was already unconscious to me, But she rallied and survived a few more moments and then a huge right hand, and a couple more shots landing flush, the ref stops the fight.

You can see how well liked Roxanne is, as there were no real cheers until very sportman like behaviour, or sportladly like behaviour from Roxanne asking for Jessica who was celebrating, though somewhat subdued, to come over. Jessica hugged Roxanne who seem inconsolable, and everyone cheered glad that she was ok. Some really sweet comments from other in house fighters saying how protective they felt for Roxanne really showed the calibre of person she is, and how well respected.. Her stand up needs serious work if she is ever to be a top level MMA artist, but I do not doubt she has the heart to put in the effort needed.

A win for Jessica, who despite an injury was able to show a great ground defence, and high level standup, she could be a real contender for winning this season, her athleticism is probably the best in the house, and she has fire to win, and great coaching.

Thanks for following my blog, MMA in the UK is growing, and I want to be a part of that.

Kindest regards Russianstar.

A few Tweets.

          @arielhelwani

Amazing. No nonsense, all great. RT @wahly22: @arielhelwani This is such a great episode. These two women are genuinely likable.

11 Retweets      10 favorites
Chris Holdsworth          @holdsworth135

Wow! These girls went hard. Congrats to @JessRakoczy. @Roxyfighter fought her heart out. Very touching after the fight. @TUFonFS1

18 Retweets

Cody Bollinger          @CodyBollinger    

Crazy finish and great fight! Both TUF as nails

2 Retweets      3 favorites

Russianstar: Experiences with Ipamorelin

Ipamorelin profile.

Firstly just so everyone knows what we are talking about here is a look at one of the best peptides available.

Ipamorelin is a GHRP (growth hormone releasing peptide) receptor-active GH secretagogue, it doesnt significanly effect cortisol or prolactin, so this makes it highly specific for GH release.

Aib-His-D-2-Nal-DPhe-Lys-NH2

It has also been found that 12 weeks of treatment with ipamorelin increased bone mass in young adult female rats in one study that can be found on pubmed.

It is important to remember that Ipamorelin is a ghrelin mimetic, and an analog to ghrelin.
However it doesnt cause the kind of hunger feelings caused by ghrp-6.
Ipamorelin acts with synergy when used during your own GHRH (growth-hormone releasing hormone) pulse or when coadministered with GHRH or a GHRH analog such as Sermorelin or cjc.
The synergy comes about due to both the obvious suppression of somatostatin and the increases in GH release per-somatotrope, while GHRH increases the number of somatotropes that release GH.
Due to the fact that its selective and doesnt really alter cortisol or prolactin levels, this makes Ipamorelin a very exciting peptide, it is as effective as ghrp-6 without the increase in hunger or cortisol or prolactin serum levels, and it has another property unique to Ipamorelin.
A mega-dose of ipamorelin results in a mega-release of GH (up to the entire amount that is actualy present in the pituitary), whereas GHRP-2 and GHRP-6 have limits of approximately 1mcg/kg in humans for their maximal GH release.
I find this very exciting when used directly after training to increase recovery and in the maturation of satelite muscle cells.

Results and experiences.

I used 100mcg 3 times a day, i used it exactly as GHRP-6 in my experiences thread… i used it injected directly in to joints and areas that i have damaged and found over just a 2 week period a massive amount of improvement, in particular in my elbow where i was suffering from a strained ligament.. the pain subsided totaly and full strength returned within 4 weeks.. this was after it hurting on and off for over 3 months. The pain has never returned,

As for its anabolic properties i used 300mcg straight after training to get a much larger pulse in GH, and found recovery improved vastly… over 12 weeks on this protocol i lost about 2 lbs in bodyfat.. but as my BF is very low i think had i been bigger this number would have been considerably higher.
I saw an increase in vascularity.. improved skin texture.. very deep sleep, in fact i was feeling sleepy quite a bith through the day.. minimal water retention and about 3lb gain in mass… sadly i am at my genetic max i feel for size and find it nearly impossible to hold on to anything over my current weight, however 2lb has lasted over 3 months, with the obvious fluctuations in glycogen retention etc… i use an average weight based on 14 readings through the week to get a correct measurement.

If i combined this with something like CJC, wich i hope to do very shortly i feel this could be an incredible combination.. and currently the best peptide combination.. although i still love the effects of ghrp-6, i love the hunger stimulation.
The selective effects of ipamorelin make this a very special peptide..

Russians peptide rating..

10/10

This is a must buy and perfect to get to grips with peptides if you are a first time user.

Russianstar : Experiences with GHRP-6

Written by Russianstar, This information is copyright.

Firstly to get things clear GHRP-6 is a peptide a Growth Hormone Releasing hexapeptide , its a 28 amino acid peptide, and it works by signaling to the pitruitary gland to begin secreting Growth Hormone.

2SMolecular Formula C46H56N12O6
Molecular Weight 873.01
CAS Registry Number 87616

6-amino-2-[[2-[[(2S)-2-[[(2S)-2-[[(2R)-2-[[(2S)-2-amino-3-(3H-imidazol-4-yl)propanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]propanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-phenyl-propanoyl]amino]hexanamide

GHRP-6 lackS opioid activity, but you get a huge pulse, (dose dependant) in your own GH levels, and you get the effects of the increased IGF-1 secreted by the liver.
Now both the increased GH and IGF-1 are highly desirable for atheletes, bodybuilders and those looking to improve their own physique.
Now you may have heard many tell you that when they take GHRP-6 the best GHRP i have used, that they get a huge and very intense increase in appetite, about 20 mins after the initial injection, Well this is caused by the GHRP-6 antagonising the peptide Ghrelin, it mimicks it, but actualy fights against it causing the signal for gastric emptying and hunger. Ghrelin is what many believes causes obesity, and insulin resistance amongst other things, and i believe this is one way by wich GHRP-6 may help reduce fat, by fighting against it in effect … but, and there is always a but, if you take more than 150mcg the effects of the gastric emptying can be so strong that you may have the urge to severely stuff yourself with foods, so if your on a bulk this is a great side effect, and considering the price its a very good one, so on a bulk i rate this as the number one aid in increasing appetite, as you get very good anabolic effect too and increased strength.

So what can you use it for?
Well personaly i used 150mcg injected directly into the joints or areas that ive had any niggling injuries, the localised effect it has on collagen growth is nothing short of astounding, and i have personaly recovered from a full pectoral tendon tear, where the tendon ripped right of the humerous bone, its now in even better shape than it was prior to the injury, and 5g of the GHRP-6 will last ages when used accordingly, even at this dose fat loss is noticeable and the anabolic effects of increased muscle size and strength can be seen.
One of the other uses is to kick start your own GH after a cycle, a dose of 200-500mcg 2 x a day is sufficient to start your own GH, however it does not mean to say your own GH levels will be where they were before you carried out your cycle, this is user dependant, but it will certainly be a very usefull addition, and a usefull addition to any hormonal cycles PCT as the increased igf-1 levels it brings will greatly increase the chances of you holding on to any muscle you have gained.
Another thing i noticed was the improvement in my immune system, and my well being, this is partly because of the effect GHRP-6 can have on the increase again in IGF-1 wich plays an important role in the healthy function of your immune response. It also has a healthy protective effect on neurons and on the CNS (central nervous system).

In one study i saw recently it was shown that GHRP-6 GHRP-6 has a protective effect on the liver that seems to be mediated by IGF-I, TNF-alpha, and nitric oxide. Data also suggest that the anti-inflammatory effect of GHRP-6 in the liver is exerted on nonparenchymal cells, So again for pct this may prove an invaluable asset.

As for peptides they are fairly new as compared to other anabolics, but they i feel are far better, and have way more potential, just how much remains to be seen.
Just remember with GHRP-6 not to eat carbs or fats 50 mins each side of the dose so as not to interfere with the gh pulse it will cause, and 250mcg 3 x a day is the best dose i found to avoid overly mimicking ghrelin and still cause a large amount of muscle gain, tissue repair and fat loss.

Russianstars peptide rating 8/10.

Kind regards, and happy training. RS

Testosterone, its receptors, how it builds muscle, Cortisol, and Xenoestrogens.

How does testosterone build muscle?  what receptors does it activate and what does it tell them

Testosterone builds muscle though a few different actions.
Firstly having a raised testosterone level, As normally you produce about 7mg a day, increases the anabolic state of the body.
Testosterone activates a process of protein synthesis in the muscles. It also stops the degradation of protein, which is an anti-catabolic effect. Together, both these factors along with increased Nitrogen retention help build muscle and hold on to it.
Intracellular androgen receptors cause protein synthesis to be speeded up, the increased Testosterone levels then cause Glycogen retention to take place within the muscle, repartitioning nutrients away from fat and into the muscle cell. These nutrients are then used to help build muscle.
The increased glycogen retention, and resulting water retention as carbohydrates hold water, causes the muscle cell to expand and stretch, also the muscle membrane, and this can also lead to muscle size increase.
These androgen receptors, Also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4, are also whats known as a Nuclear receptor.
Here is the science on how these Nuclear receptors determine the increase in muscle size through activation.
 These Androgen receptors have a direct regulatory effect on Gene transcription by binding  testosterone to the androgen receptor causing a conformational change in the receptor that, causes dissociation of (HSP) These are heat shock proteins, they are then transported from the Cytosol into the Cell nucleus, and dimerization. The androgen receptor dimer then binds to a specific sequence of DNA, This is what we call  a Hormone response element, and this causes the change within the muscle cell.. Androgen receptors interact with other proteins in the nucleus, resulting in up- or down-regulation of specific Gene transcription.
If Androgen receptors are up-regulated which they will be with increased Testosterone levels then through that mechanism of action, IGF-1 is activated within the muscle, increasing nutrient repartioning and muscle change, and Messenger RNA is produced, increasing protein synthesis.
Depending on your own personal Genes, will decide as to weather or not your increases in muscle size are large or small.
How does testosterone burn fat, what receptors are utilised..
Testosterone doesn’t burn fat, But it does increase metabolism. Increased IGF levels promote nutrient repartioning, Androgen receptor stimulation causes the calories you eat to be used as fuel for the muscle, and the increased Androgen receptor activation causes more Testosterone to be converted into DHT and less into Oestrogen, The higher the Test level of the subject, The greater the amount of Receptors activated, and in theory the less adipose tissue possessed, the greater the amount of Testosterone converted through some of these receptors into DHT. Yes Testosterone can have a direct interaction on some androgen receptors. in others its converted into DHT via the isoenzyme 5-Alpha reductase.
The increased DHT limits Oestrogen conversion, and so Oestrogen activated fat cell storage is decreased. Leading to Fat loss. This is how Weight loss actually can increase Testosterone levels as Fat cells synthesize the enzyme aromatase, which converts testosterone, the male sex hormone, into oestrogen, In particular Estradiol., the female sex hormone
other hormones that testosterone turns into and how they benefit
Testosterone can convert into Approximately 7% of testosterone is reduced to (DHT) by 5-AR  Approximately 0.4% of testosterone is converted into Estradiol by Aromatase an enzyme expressed in the brain, liver, and adipose tissues. Oestrogen is predominantly the female hormone, And DHT the hormone that makes men look like men, Harder muscles, hairier bodies, which is why you can tell some women have hormonal problems, its even a good way to tell if someone has polycystic ovaries, as it increases activation of facial hair follicles via 5-ar, and another enzyme 17-b.Low DHT and low Oestrogen can cause Libido problems, they need to be at a balanced level, DHT always being the more dominant of the 2, as you can see by the percentages they are converted into. But you need both, and if Oestrogen is too low, Muscle building will be very difficult as its also involved in protein synthesis, and mineral absorbtion, which are two very important factors in muscle growth.

How does stress lower testosterone what processes?
Cortisol is a well known stress hormone, released under high physical or mental stress.
Cortisol at high levels causes protein synthesis to halt, and it halts tissue growth and recovery.
It always seems if cortisol is high, Testosterone is lower, And if Testosterone is high Cortisol is lower, and I propose this as the reason.
This would be due to a negative feedback loop that causes the  down-regulation of transcripting genes either signaling the production of testosterone or that  signal it’s halt.  Exercise  naturally causes a  drop in cortisol (due to the stress of the exercise) total testosterone will  drop but free testosterone will always rise dramatically this is because of SHGB. sex hormone binding globulin releasing the testosterone so that it  becomes bioavailable (total testosterone =available + that bound to SHBG). 
Cortisol when its high binds up testosterone, and prevents it from being used for protein synthesis, when it drops, that bound test then becomes available.
Rather than go into all the enzymes involved, this seems the easiest way to explain a process that is very difficult to explain.
How does pollution and other factors lower testosterone?   plastic bottles and such?

Xenoestrogens are a type of xenohormone that imitates estrogen. Synthetic xenoestrogens are widely used industrial compounds, such as PCBs, BPA and phthalates, These are found in hair sprays, air fresheners, plastic bottles, plastic microwave meal containers, to name a few.

They have estrogenic effects on a living organism even though they differ chemically from the estrogenic substances produced internally by the endocrine system of any organism.

Xenoestrogens are clinically significant because they can mimic the effects of endogenous oestrogen, and the implications are huge, Lowered testosterone, increased feminisation, increased chance of prostate and other cancers, suppressed immune systems, to name just a few possible sides from thses parabens and horrible Xenoestrogens.

Limit your contact with them, Glass containers are best, Not only that, but the toxins in these containers can lower testosterone and cause oxidative stress on your organism. Why put all the effort in to eat healthy, and train hard, get the best supplements, to hamper your health and gains through this Testosterone poison

Until next time, enjoy my article, if you like it please share it or link it, Thank you. RS