I'll start Nolva at 20mg until it goes away. What would be a good maint dose after that????????

I'm in the middle of my 3rd week of...

And what scientific info do you have to back this claim up? Or is this what "everybody says" so you just believe it without question?

Point me towards a scientific article that claims that deca induces progesterone, I will gladly read it.

Now go off and read the merck index for tamoxifin citrate and look under Clinical Pharmacology and the Method of action, and wow you'll see that tamoxifin binds to and antagonizes ER's!!! NOT PR's!!!! WOW!!!!!

There is a ton of scientific research done on tamoxifin and we know that it only blocks the ER as it's meant to inhibit breast tumors which have an incredible abundance of ER's on them which stimulate growth. As well we know that gyno will also come from PR stimulation, we also know that deca will aromatize into a progesterone like molecule at doses of 400mg/week and higher bind to and STIMULATE the PR.

Obviously you're wrong again!

I can feel the Dark One stirring from his sleep 2Thick, he will not be pleased at twice in a week...LOL...

Deca has some androgenic qualities, and will aromatize into a simple estrogen, much the same as EQ.

This is not the same as an 17AA aromatization which has the ability to reside in the system for long peroids of time unaffected by the liver...

I agree with E2, and you know we share the same brain<wink>, in that...Deca has the affinity to bind to, and activate the PR recepters, and Nolvadex, Clomid, or Armidex will have little, or no effect on this stimulation of the PR recepters...

If it is in fact PR induced gyno, back off the dosage, and add winny...RU-486 is very hard to come by, if at all Bro...

I do love this argument though....and I would like to see, as well, any scientific proof you may have in reguards to Nolvadex, Armidex,...etc. Combatting PR induced gyno...

In other words....make me eat my belief's concerning Deca.....If ya dare ya circus midget....heh heh heh....

Human physiology goes beyond the obvious and just because Macro says it, does not make it gospel.

Once you finished a year of microbiology and biochemistry, you have the right to intelligently argue with my statement. Until then you do not know what you are talking about. You just assume that Deca will induce progesterone because it is progesterone-like. Sorry, but the human body is not that simple.

Must be hard.

Synthetic androgens exhibit estrogenic/antiestrogenic and progestational activities in addition to their androgenic effects. To investigate the pharmacological action of the synthetic androgen, 7alpha-methyl-19-nortestosterone (MENT), we examined its action in female rodents. The criteria employed for estrogenic/antiestrogenic effects were, uterine weight increase, vaginal cornification, induction of progesterone receptors (PR) synthesis and stimulation of peroxidase activity in the uteri of ovariectomized rats and mice....... The progestational activity of MENT in immature rabbits using the McPhail index assay was comparable to that of progesterone. Binding affinities of MENT and progesterone to PR were also comparable. However, the action of MENT on the uterus does not seem to be a progestational effect since mifepristone, an antiprogestin, had no effect on MENT-induced uterine growth. Specific androgen receptors (AR) in uterine cytosol were demonstrated. The involvement of AR in MENT action was confirmed by using an antiandrogen (flutamide) and an antiestrogen (ICI-182) in ovariectomized mice. Although MENT did not block the uterotropic effect of E2, it inhibited the E2-induced cornification of vaginal epithelium, induction of uterine PR synthesis and increase in uterine peroxidase activity in ovariectomized rats. The antiestrogenic effect of MENT was also blocked by flutamide. These results suggest that the uterotropic and antiestrogenic effects of androgens are mediated via AR. It is concluded that the increase in uterine weight caused by MENT is attributable to its anabolic effects.

And you have no clue as to what my educational background is. I've never stated what Macro says is gospel but he's right much more of the time then you ever are, that's an easy thing to see. IF you've ONLY finished one year of microbiology and biochemistry then you really are out of your league, better hit those books laddie.

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The effects of progesterone are totally different on females.

Good try, but you lose again. Next time try to cite th source too.

I'm sick of arguing with you, your ignorance is incredible.

Go take a little peak at this thread, and realize you're wrong again, must be hard eh???
http://www.elitefitness.com/ubb/Forum1/HTML/040002.html

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First, females naturally have much more progesterone and estrogen in their system than men. Of course they are going to react differently. Second, this research is being done on rats and rabbits. Third, the average dosage these animals recieve is about 12-15mg/kg of body weight. For you that equals out to about 1100mg-1500mg of Deca per week. I would assume something bad would happen with that much Deca in your system.

I think you are the one that needs to hit the books, my good firend.

Abstract

Plasma progesterone was raised in 36 of 50 (72%) men with liver disease compared with 20 healthy male control
subjects. Plasma progesterone was significantly higher in men with non-alcoholic cirrhosis with gynaecomastia than
those without, but no similar relationship was found in men with alcoholic fatty change and alcoholic cirrhosis.
Hyperprolactinaemia was found in 14% of men with liver disease but levels were unrelated to the presence of
gynaecomastia. Increased circulating levels of progesterone and prolactin alone do not explain the development of
gynaecomastia in patients with liver disease, but progesterone may be an additional factor acting in association with
the known disturbances of other sex steroids.

Progesterone, prolactin, and gynaecomastia in men with liver disease.
Farthing MJ, Green JR, Edwards CR, Dawson AM
Gut 1982 Apr 23:4 276-9

Abstract

Plasma progesterone was raised in 36 of 50 (72%) men with liver disease compared with 20 healthy male control
subjects. Plasma progesterone was significantly higher in men with non-alcoholic cirrhosis with gynaecomastia than
those without, but no similar relationship was found in men with alcoholic fatty change and alcoholic cirrhosis.
Hyperprolactinaemia was found in 14% of men with liver disease but levels were unrelated to the presence of
gynaecomastia. Increased circulating levels of progesterone and prolactin alone do not explain the development of
gynaecomastia in patients with liver disease, but progesterone may be an additional factor acting in association with
the known disturbances of other sex steroids.

High serum progesterone in hyperthyroid men with Graves' disease.
Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
J Clin Endocrinol Metab 1988 Jan 66:1 230-2

Abstract

Interesting but you cannot even begin to compare people with chronic diseases to people who are healthy and use gear. The factors could be brought on by complications related to liver/Grave's disease.

This may hint at a link but it is far from conclusive.

Also we do not know the dosage that was administered or the length of time it was administered.

FOUND BY ULTER

Effects of two classes of progestagens, pregnane and 19-nortestosterone derivatives, on cell growth of human breast tumor cells: II. T47D cell lines.

Schoonen WG, Joosten JW, Kloosterboer HJ

Department of Endocrinology, N.V. Organon, Oss, The Netherlands.

Two classes of progestagens, e.g. pregnane [Org 2058, progesterone (PROG), R5020, medroxyprogesterone acetate (MPA)] and 19-nortestosterone derived progestagens [norethisterone (NE), levonorgestrel (LNG), 3-ketodesogestrel (KDG), gestodene (GES), Org 30659] were studied for their effect on cell growth of two human breast tumor T47D cell lines of different origin, i.e. from ATCC (A) and Sutherland (S) et al. [Sutherland et al., Cancer Res. 48 (1988) 5084-5091]. The effect of estradiol (E2) and progestagens alone as well as the combined effect of E2 (10(-10) M) and progestagens were investigated at several dose levels. Compared with E2-induced growth at 10(-10) M, pregnane and 19-nortestosterone derived progestagens at 10(-6) M alone did enhance cell growth in T47D-A cells up to 25 and 100% respectively, whereas in T47D-S cells they did not influence growth. All these progestagens at 10(-6) M did not affect E2-induced growth in T47D-A cells, whereas in T47D-S cells they completely reduced cell proliferation at doses between 10(-10) and 10(-8) M. The involvement of progestagen (PR) and estrogen (ER) receptors with respect to growth stimulation was studied by using specific antihormones. In T47D-A cells, the antiprogestagens RU 38486 and Org 31710 could not block progestagen-induced growth. Antiestrogens, like 4-hydroxytamoxifen and ICI 164,384, inhibited the 19-nortestosterone derivative-induced cell growth by approx. 50%. Remarkably, both antiprogestagens alone could also inhibit E2-induced growth in T47D-A cells by about 50%. In T47D-S cells, E2-induced cell growth was completely blocked by both antiprogestagens and antiestrogens. Both antiprogestagens in T47D-S cells were equipotent to 4-hydroxytamoxifen and 10-fold more potent than ICI 164,384. In conclusion pregnane and 19-nortestosterone-derived progestagens stimulated cell growth in T47D-A cells at high unphysiological concentrations, whereas they did not affect cell growth in T47D-S cells. The 19-nortestosterone derivative induced growth in T47D-A cells could partially be inhibited by antiestrogens. In T47D-A cells, E2-induced cell growth was not influenced by both classes of progestagens, whereas in T47D-S cells all tested progestagens, antiprogestagens, and antiestrogens inhibited E2-induced cell growth completely. These results with T47D cells as well as those obtained previously with MCF-7 cells show that subclones of cell lines may respond differently to various types of progestagens in the presence and absence of estrogens.

PMID: 8541241, UI: 96132696

------------------

All your study states is that if you have tumors in your breast tissue, then do not take nandrolone because it causes the tumor to expand even if RU486 is used (like you claim works for as an antiprogesterone).

Also this proves my point. "Antiestrogens, like 4-hydroxytamoxifen and ICI 164,384, inhibited the 19-nortestosterone derivative-induced cell growth by approx. 50%."

There has been research done on healthy people using AS (in Europe and mainly Eastern Europe). All I want to see is a study done on a person that does not have potential complications from their chronic disease that would jeopardize the result. That is not much to ask.

Hormonal treatment of advanced breast cancer. A randomized trial of tamoxifen versus nandrolone decanoate.

Abstract

This is how academics deal with each other. They criticize each other's evidence and this eventually leads to more of an understanding of the subject.

BTW- The burden of proof was set squarely on your shoulders and not mine. I claim that progesterone induced gyno by Deca does not exists. You must therefore prove otherwise.

2Thick originally stated (as a fact and not as a thesis to be tested) "Don't worry because Nolvadex will stop the gyno from Deca." Now it seems to me this is the statement to be defended. You have not provided any support for this statement other than your own personal experience.

2Thick later says:
"Point me towards a scientific article that claims that deca induces progesterone, I will gladly read it."
E2 and I did this, not just one article, but a plethora of studies which overwhelmingly support the progestenic properties of nandrolone in females, rabbits, mice and MEN. The fact that 2Thick rejects the cumulative conclusion of many decades of research on this topic just means he's being pig-headed, not scientific. Now if 2Thick had at least hedged some of his statements as Dr. Juice does by saying that deca MAY interact with other receptors and other systems in the body which Nolvadex might have an effect on, as well as being progestenic, then there could have been room for an interesting discussion of recent research. If you ever have to write a grant to beg for funding for a research project you will someday understand that how you ask your question is THE most important part of the scientific process.

For instance

Abstract

...........CONCLUSIONS: Our results revealed that
tamoxifen can increase progesterone receptors and decrease estrogen receptors in
endometrial cancer. The effect was most pronounced in tumors with favorable
clinicopathologic parameters. We conclude that tamoxifen therapy can induce
progesterone receptor synthesis even in tumors with low initial progesterone receptor
levels, making such tumors potentially responsive to additional hormonal therapy with
progesterone.

Are you still arguing?

You claim that all of these studies back you up. I can always find something wrong with the study, and sometimes I can find things in your own studies that prove YOU wrong. For every study that you bring up I can find another one that claims the exact opposite.

If you knew anything about science, then you would know that criticism is the heart of the scientific process.

Secondly, most anti-estrogen and anti-androgen drugs work by BINDING to one receptor or another. Nolvadex binds to ER. It just doesn't do anything that estrogen does. I'm assuming that Deca, when it binds to PR, probably does not do much of anyhing either. Deca also converts to DHN(dihydronandrolone), and binds to DHT receptors. However, it's androgenic effect is very weak.

Ya dig?

They also obviously haven't taught you the concept of concensus yet. That's where, for instance, even though 20 years of damning research showed clearly that smolking causes lung cancer, the tobacco companies would always find flaws in the research and say you have no proof. But the concensus was that smoking DOES cause lung cancer. The moral is, if you want to be an ass you can always shred what someone else says or does. That does not make you right and the other person wrong.

quote:

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Originally posted by MS:
Wow, a whole year of micro and biochem. What are you, a first year med student with a grudge against the world?

All I said was that you need to finish at least one year of micro and bio-chem to understand these concepts more clearly. What I have done was never mentioned. Don't assume things because you can make yourself look very foolish.

They also obviously haven't taught you the concept of concensus yet.

For your information it is not called consensus. It is called empirical research. If you would have taken any classes in Research Methods, then you would know that empirical data can be flawed (or biased).

---

Take it easy bro's.....let the ego's subside. At this point nobody will back down even if they're wrong.

Where is it???

quote:

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isn't this thread about a poor bro who's got breasts. . .lets not lose r way here

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I know I said I would have research on the site by a certain day but I haven't had the time. I have deadlines to meet in real life. That is why I have not been around. I only contribute to help out the board and the members. It's not ego trip for me. This is the Internet and I don't give a shit what people think of me (relatively speaking).

When I have real-life work to do (that will determine my future) then I must place it on the top of my list.

quote:

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Originally posted by MS:
But when ther is an overwhelmingly amount of empirical research to support a scientific idea, scientists in general agree to a concensus stance on the issue, such as "smoking causes cancer".

Listen my good friend. You showed me faulty data and I pointed it out. I see that there is a link between nandrolone and progesterone. That is a moot point. You have failed to show a conclusive link between nandrolone and progesterone-induced gyno.

Why haven't you come up with any research to support your claim that deca is not progesetenic yet?

I admit I am tardy with my evidence but I have research to complete very soon. It is ultimately more important than this "pissing contest".

By the way, my claim is that Deca does not cause progesterone induced gyno.

Seems you keep dodging the whole issue with your word games and attacks on my research background.

I did not insult you my friend. You were insulting me, remember?

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I see that this thread is leading nowhere so I will quote a famous philosopher, "...and that's all I got to say about that"

I will not respond anymore.

You guys don't seem to understand that all you can do is give safe advice and hope for the best.

I have been using for 15 years and I can say that I did not see me or my buddies get gyno from a cycle even with deca since we started using nolvadex.

Lets give a big "Hurrah!!" for hooch...