Possible that I am not gyno prone at all?

[Atomini]

So, i'm on my 6th week of my 10 week Test E cycle at 300mg/week. Started off frontloading 1,000mg the first week and then 500mg the second week, and finally down to 300mg every week after that. Now, after the first week I started thinking i'm going to experiment with my body's tolerance to estrogen related sides, so here's what I did:

The first week I took 12.5mg aromasin (Exemestane) every day. Kept down all estrogen-related sides, though my forearms started to hurt slightly, felt like there were shin splints in my forearms (I assume this is the joint-hurting due to lower estrogen).

The second week I dropped the dose down to 5mg of aromasin every day. Still kept down estrogen-related sides. Forearms still hurt, though less.

The third week I dropped it down to 5mg of aromasin every OTHER day now. Ever so slight bloat started to show. Forearms stopped hurting from here on in.

The fourth week I dropped it down to 5mg of aromasin once every THREE days now (and have been doing this ever since the 4th week). Still have a slight bloat but not much, and no other estrogen-related sides.

Now, is it safe to consider the fact that estrogen levels have risen enough to cause gyno in most people, but it's not happening to me because i'm not gyno prone? Should I drop the Aromasin COMPLETELY (until PCT of course) because it's a waste at this point? Or because 5mg of aromasin in the bloodstream every 3 days is still enough to prevent gyno and that I should still see if it happens with zero aromasin? However, i'm convinced at this point i'm probably not gyno prone at all.

... unless of course the first week of aromasin reduced levels of the aromatase enzyme enough to prevent estrogen conversion at this point that gyno won't show up. Though, I highly doubt that because as I stated above, I started getting some bloat after I drastically reduced the dose and frequency of the aromasin. What do you all think?

[Atomini]

bump

[scull]

IMOP you should of went with dex---your AI is to harsh[at that low a dose of TE] it may hinder your gains ,your AI has been reported to block AR.Im on a similar cycle at 375mg TE and using 1/2 mg of dex EOD,and its working great

[Booz]

it is possible mate...........
i have frontoaded with a hell of a lot more than what you have stated and never have used any form of anti's watsoever,been using gear on and off for a good few years and have never had a problem at all.................

[sonnygll]

I agree with Scull on the a-dex.

I think I share your problem. I started out taking a-dex on my frontloaded test E cycle, I frontloaded a gram the first week and then 500 per week after that. I inject twice a week. I was taking .25mg a-dex. I didn't get the joint pain, but I got sexual issues. I stopped using it the end of week 4. I'm at the end of week 9 now. I think I might have a slight bit of water retention, but it is so little that I can't tell for sure. No nipple problems. All I know is my dick works again.

I think some people, like myself are sensitive to AI's. Low estrogen is likely the main part of it. High progesterone could be an issue too since it's ratio to estrogen is important. So people with this probably may likely have issues with things like deca and tren . We might might need quite a high dose of caber to prevent sexual problems, gyno and lactation.

I am going to take a-dex during the first week of PCT. That's it. I would recommend you drop aromasin . Then get some a-dex, and take just .25mg per day for the first 7 days of PCT, which is what I am going to do.

I got no response to a question similar to yours. So I think our problem is pretty rare.

[Atomini]

IMOP you should of went with dex---your AI is to harsh[at that low a dose of TE] it may hinder your gains ,your AI has been reported to block AR.Im on a similar cycle at 375mg TE and using 1/2 mg of dex EOD,and its working great

1. I have not had any sexual dysfunction issues at all during this cycle.

2. I have gained 25 lbs. since the start of this cycle.

So no, my gains are not being hindered and I never used a full 25mg dose. Where is this evidence about Aromasin blocking AR? Is this actual fact you're telling me, or a bunch of conjecture? In any case, my gains have not been affected and this is straying far from the main topic.

[Merc..]

Keep in mind gyno needs estrogen , progesterone , plus other mediators like ( GH and igf-1 ) to form..


Merc.

[Merc..]

ESTROGEN, GH AND IGF-1, PROGESTERONE, & PROLACTIN

Estrogen and progesterone act in an integrative fashion to stimulate normal adult female breast development. Estrogen, acting through its ER a receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development. This is demonstrated by experiments in ER a knockout mice which display grossly impaired ductal development, whereas the PR knockout mice possess significant ductal development, but lack alveolar differentiation.

Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones. Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1, as confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development. The GH effects on ductal growth are mediated through stimulation of IGF-1. This is demonstrated by studies of estrogen and GH administration to IGF-1 knockout rats that showed significantly decreased mammary development when compared to age-matched IGF-1- intact controls. Combined estrogen and IGF-1 treatment in these IGF-1 knockout rats restored mammary growth. In addition, Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development. Furthermore, other data indicates that estrogen promotes GH secretion and increased GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.
Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones. For example, prolonged treatment of dogs with progestogens such as depot medroxyprogesterone acetate or with proligestone caused increased GH and IGF-1 levels, suggesting that progesterone may also have an effect on GH secretion. In addition, clinical studies have correlated maximal cell proliferation to specific phases in the female menstrual cycle. For example, maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL [3.1nmol}), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase. Furthermore, immunohistochemical studies of ER and PR showed that the highest percentage of proliferating cells, found almost exclusively in the type 1 lobules, contained the highest percentage of ER and PR positive cells. Similarly, there is immunocytological presence of ER, PR, and androgen receptors (AR) in gynecomastia and male breast carcinoma. ER, PR and AR expression was observed in 100% (30/30) of gynecomastia cases. Given these data and the fact that PR knockout mice lack alveolar development in breast tissue, it appears as if progesterone, analogous to estrogen, may increase GH secretion and act through its receptor on mammary tissue to enhance breast development, specifically alveolar differentiation (28, 18).
Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. . Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.

[rock75]

IMOP you should of went with dex---your AI is to harsh[at that low a dose of TE] it may hinder your gains ,your AI has been reported to block AR.Im on a similar cycle at 375mg TE and using 1/2 mg of dex EOD,and its working great

please stop spreading the misconception that AI's "hinder" gains - as I mentioned before the real issue that would hinder his gains would be poor diet and lack of rest

[Seattle Junk]

I would personally switch to armidex over aromasin . You don't want to blunt your estrogen too much or that will affect your gains. For some reason armidex works great for me and it seems other people like it here too.

Never think you are not prone to any side affect. It could just take awhile for the glands to develop gyno over time? Once it starts you can't stop it. You can only control it with AIs or get surgery. I've never had gyno but I always take an AI with androgens for prevention. I can't stand excessive bloating but that is mostly controlled by diet anyway. It's ok to get a little bloating as that creates a perfect environment for growth.

[scull]

1. I have not had any sexual dysfunction issues at all during this cycle.

2. I have gained 25 lbs. since the start of this cycle.

So no, my gains are not being hindered and I never used a full 25mg dose. Where is this evidence about Aromasin blocking AR? Is this actual fact you're telling me, or a bunch of conjecture? In any case, my gains have not been affected and this is straying far from the main topic.

Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.

[Seattle Junk]

please stop spreading the misconception that AI's "hinder" gains - as I mentioned before the real issue that would hinder his gains would be poor diet and lack of rest

You must have some estrogen for maximum growth, that is the truth.

[buffgator]

I believe that ai's can hinder gains. Also I cycled for 5 years before my first encounter with gyno.

[Seattle Junk]

I believe that ai's can hinder gains. Also I cycled for 5 years before my first encounter with gyno.

Case and point....

[scull]

Is there any truth to the statment that if your not gyno prone and your older, say over 30 that you will never get gyno no matter what you do?--Or put it this way has anyone whos over 30 ever gotten gyno for the first time?

[Merc..]

I believe that ai's can hinder gains. Also I cycled for 5 years before my first encounter with gyno.

Higher levels of estrogen are linked to a rise in GH and IGF-1 ..

Tests effects on GH and IGF are dependent on aromatization to estrogen..

Estrogen plays a huge role in building muscle..








Merc.

[buffgator]

It was rock that said it merc, not me.

[Merc..]

It was rock that said it merc, not me.

I was just saying...



Merc.

[buffgator]

oh..got ya. Ill take you back of my ignore list now

[Merc..]

oh..got ya. Ill take you back of my ignore list now

hehehhehe

[Seattle Junk]

Is there any truth to the statment that if your not gyno prone and your older, say over 30 that you will never get gyno no matter what you do?--Or put it this way has anyone whos over 30 ever gotten gyno for the first time?

No, you can develop gyno at any age. It has to do with the receptors in the mammary glands. Your glands may have been resistant to estrogen for many years. Then all of a sudden the receptors could bind to the free estrogen and enlarge. It's kind of like somebody knocking at your door once in awhile and you don't know who it is so you don't answer it. Then that person keeps knocking more and more and now with a few of her (estrogen) friends helpiing day and night. Eventually you are going to open the door to shut them up.

[Merc..]

Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.

Thats study is for ATD .. Do you have one for adex or letro showing the same thing?? Just curious .. I was researching this before but I cant find the links to the studies I had saved on my CPU..

[Atomini]

Great info there Merc, thanks.

And Scull, did your dosages increase over those years you were cycling?

[scull]

Thats study is for ATD .. Do you have one for adex or letro showing the same thing?? Just curious .. I was researching this before but I cant find the links to the studies I had saved on my CPU..

adex and letro are different .ATD is whats call a suicidal AI the others are not and they dont block AR like ATD

[Merc..]

adex and letro are different .ATD is whats call a suicidal AI the others are not and they dont block AR like ATD

I was going to say I thought the studies I saw showed it didnt ( type 2 AI's )have that effect on the AR , but like I said I couldnt find them on my cpu so asked you to post if you had any that showed it does ..

Adex and letro are type 2 AI's and aromasin is a type 1 AI ..


Merc.

[scull]

Great info there Merc, thanks.

And Scull, did your dosages increase over those years you were cycling?

Well I started with orals only for a long time till they really didnt work anymore.Then IGF.LR3 for a while .So Im lucky for waiting to use INJ -TE in that a low dose 375mg works good right now

[scull]

I was going to say I thought the studies I saw showed it didnt ( type 2 AI's )have that effect on the AR , but like I said I couldnt find them on my cpu so asked you to post if you had any that showed it does ..

Adex and letro are type 2 AI's and aromasin is a type 1 AI ..


Merc.

Ive never seen any studies that show that dex or letro block AR like ATD does ,but I guess Ill take your word for it

[Merc..]

Ive never seen any studies that show that dex or letro block AR like ATD does ,but I guess Ill take your word for it

NO NO re read my post..

I said I saw studies showing the type 2 AI's, letro and adex, does not have that effect like ATD !!

[Atomini]

Am I missing something? What is ATD??

[Merc..]

Am I missing something? What is ATD??

Its an OTC AI ..


http://www.bodyconcept.com/family/2299/display.html




Merc.

[Kratos]

attention to detail

[Merc..]

attention to detail

LOL

Merc.

[scull]

Am I missing something? What is ATD??

AROMASIN is the parent compound of ATD

[scull]

Hey how many years you have to be a member ,to not be called a new member I joined in "06"

[Merc..]

Hey how many years you have to be a member ,to not be called a new member I joined in "06"

Its related to the amount of post you have not how long you been here..

You gotta post up more ..

Come hangout with us more often lol...



Merc.

[Ashop]

So, i'm on my 6th week of my 10 week Test E cycle at 300mg/week. Started off frontloading 1,000mg the first week and then 500mg the second week, and finally down to 300mg every week after that. Now, after the first week I started thinking i'm going to experiment with my body's tolerance to estrogen related sides, so here's what I did:

The first week I took 12.5mg aromasin (Exemestane) every day. Kept down all estrogen-related sides, though my forearms started to hurt slightly, felt like there were shin splints in my forearms (I assume this is the joint-hurting due to lower estrogen).

The second week I dropped the dose down to 5mg of aromasin every day. Still kept down estrogen-related sides. Forearms still hurt, though less.

The third week I dropped it down to 5mg of aromasin every OTHER day now. Ever so slight bloat started to show. Forearms stopped hurting from here on in.

The fourth week I dropped it down to 5mg of aromasin once every THREE days now (and have been doing this ever since the 4th week). Still have a slight bloat but not much, and no other estrogen-related sides.

Now, is it safe to consider the fact that estrogen levels have risen enough to cause gyno in most people, but it's not happening to me because i'm not gyno prone? Should I drop the Aromasin COMPLETELY (until PCT of course) because it's a waste at this point? Or because 5mg of aromasin in the bloodstream every 3 days is still enough to prevent gyno and that I should still see if it happens with zero aromasin? However, i'm convinced at this point i'm probably not gyno prone at all.

... unless of course the first week of aromasin reduced levels of the aromatase enzyme enough to prevent estrogen conversion at this point that gyno won't show up. Though, I highly doubt that because as I stated above, I started getting some bloat after I drastically reduced the dose and frequency of the aromasin. What do you all think?

in my early years I could do massive cycles and no estrogen sides only great gains,,,now as Ive gotten older,,,I must use an AI in most my heavy cycles.

[Kratos]

use an ai regardless. If you look at clinical studies any chemical that is close to resembling estrogenic action either weak or strong sends the testicular cancer rate into the stratosphere. I am a fan of not letting estrogen levels get too high.

[scull]

use an ai regardless. If you look at clinical studies any chemical that is close to resembling estrogenic action either weak or strong sends the testicular cancer rate into the stratosphere. I am a fan of not letting estrogen levels get too high.

So what is your AI of choice?

[Kratos]

So what is your AI of choice?

arimidex for cost reasons on cycle

aromasin for pct

letro when running tren

[bigtwin]

i do beleive its possible