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Gyno Reduction Protocol

pux888

pux888

MuscleHead
Oct 1, 2010
1,256
65
#1
This is a reoccurring topic on every board and here is a great write up on how to deal with it!

Default Gyno reduction protocol
written by C-bino and Nark

I am posting this thread to help answer all of the questions regarding gyno reduction and prevention and reversal, the use of letrozole and other anti-e***8217;s. I will go over everything in very simple easy to understand language. Also we are talking about estrogen gyno here, not progesterone (but using letro will stop progesterone related problems as well since it inhibits all estrogen anyways). Progesterone gyno will be enlargement of your nipple area, the actual aereola, not a lump under it.

Let me make this first point very clear, as I state in my signature this is from my personal experience, so whether you agree with it or not is your own issue. I have helped many people with gyno and it has worked just fine for them as well.

To first understand why you are doing what you are doing I am going to go over a few things and a few definitions:

SERM ***8211; Selective estrogen receptor modulator. These drugs work by binding to the estrogen receptors and flooding them in a sense, making it difficult (but not impossible by any means) for estrogen to bind to the receptors and thus prevent the onset of estrogen related side effects.
Most common forms: Tamoxifen (Nolvadex),Clomiphene (Clomid)
AI ***8211; Aromatise Inhibitor. These drugs work by inhibiting the aromatization of estrogen. This means that in effect AI***8217;s prevent androgens from converting to estrogen, again, making it difficult (but not impossible) for estrogen to reach receptor sites.
Most common forms: Anastrozole (l-dex, a-dex),Exemestane (aromasin),Femera (letrozole). For our purpose of reversing gyno we are interested in Letro.

Letro and your sex drive:
Letrozole will suppress your sex drive. This is another reason why it is so important to act on preventing gyno as soon as possible. Since we all know that Test should be run in every cycle this will cancel out the effect of sex drive suppression.

Running letro to prevent gyno:
If you decide to run estrogen protection while on cycle (and I suggest you do unless you are aware that you do not require it),you can run either a SERM or an AI. Letro will be the most powerful AI you can use, it will inhibit 98+% of estrogen using a dose as low as .25mg and even lower. This is why I suggest you do not use a dose higher than .50mg while on cycle just trying to prevent estrogen related side effects.

You will want to start running the letro approximately 2 weeks before you begin your cycle to allow it to fully stabilize in your blood. I have often heard the argument that letro takes up to 60 days to stabilize, I don***8217;t know if I buy into this for the reason that I have reversed gyno after using letro for only 1 week. Still to be safe I recommend starting it before your cycle as stated above.

If you do decide to run letro there is absolutely no need to run another AI or SERM. Do not make the mistake of thinking more is better. Think of it this way; if letro is preventing the conversion of androgens to estrogen than there is no estrogen, what would the purpose of a SERM be when there is no estrogen to bind to the receptors? Nolva will only take away from the effectiveness of letro.

This brings me to my next point. Do not listen to anyone who tells you to bump up your nolvadex to 60+mg ED if you get gyno. I have no idea where this idea started but I have seen it suggest far too many times recently. Nolvadex will do nothing to reverse your gyno***8230;let me make that clear IT WILL DO NOTHING FOR GYNO. If you are running nolva as your anti-e and start to develop gyno than sure you can bump the dosage a small amount to try to prevent it from progressing further, but letrozole must begin ASAP.

It is very important that you begin taking letrozole immediately, the longer your wait the more risk you take in not being able to reverse it.

How do I know if I have gyno?
If you have developed gyno you will have a lump behind your nipple. It will be fairly hard, and it will be tender to touch.

Running letro to reverse gyno:
I am going to go over the three different scenarios which people could fit into. Remember regardless of what scenario you are in it is important that you begin taking the letro ASAP.

1. Already using an anti-e aside from letro.
2. Already using letro @ a dose of .25mg or .50mg ED.
3. Not running any estrogen protection.

1.
Day 1: .25mg Letro + anti-e*
Day 2: .50mg Letro
Day 3: 1.0mg Letro
Day 4: 1.5mg Letro
Day 5: 2.0mg Letro
Day 6: 2.5mg Letro **

2.
Day 1: .50mg Letro
Day 2: 1.0mg Letro
Day 3: 1.5mg Letro
Day 4: 2.0mg Letro
Day 5: 2.5mg Letro **

3.
Day 1: .50mg Letro
Day 2: 1.0mg Letro
Day 3: 1.5mg Letro
Day 4: 2.0mg Letro
Day 5: 2.5mg Letro **

*Regardless of the anti-e you are using it is important to still use it for the first day you begin letro as the letro will not have taken any effect and you by no means want your body to be without any protection when gyno is already prevalent.

** You will remain at this dose until gyno symptoms subside. Once you believe your gyno is gone it is important to stay at this dose for another 4-7 days to ensure all traces are gone. I recommend people with a bf% over 15 stay on for a week as it may be harder to judge completely whether the lump is completely gone. Once this period is over it will be important to taper letro down slowly rather than coming off it completely. Regardless of which manner you tapered up your dose you will all taper down in the same fashion.

Day 1: 2.0mg
Day 2: 1.5mg
Day 3: 1.0mg
Day 4: .50mg***
Day 5: .25mg
***You can remain at this dose or go down further to .25mg. It is really up to you at this point. They are both very common maintenance doses as an anti-e while on cycle. Personally I have stayed with .25mg and never had a problem.

Letro and the estrogen rebound:
With your estrogen being completely inhibited there is a definite estrogen rebound as your body tries to re-stabilize the testosterone:estrogen balance. We can prevent this rebound effect by supplementing further with another AI or SERM. So, I suggest that when you are coming to the end of your cycle you will more than likely be using Nolva in your PCT so just make sure that you begin taking nolva the last day you are going to take your letro and then continue on as you would with regular PCT.

This now leads us into the question of reversing gyno while not on cycle. There are a few things to remember here. You have already waited longer than you should have, and your sex drive will be shot. You can use tribulus or another natural test booster to help you in this scenario but I can***8217;t guarantee the effectiveness. Just follow gyno reversal protocols 2 or 3. When coming off again you must taper and begin using nolvadex to prevent any rebound effect that may occur.

How much nolvadex should you use if you are not going into PCT and running this off cycle? I suggest starting at 20mg ED for a week and then lowering it to 10mg for another week and then coming off completely.

I hope this covers most of the issues, still feel free to PM me if you have questions. But make sure you read the entire post first.

Gynecomastia: Etiology, Diagnosis, And Treatment

GYNECOMASTIA: ETIOLOGY, DIAGNOSIS, AND TREATMENT
Chapter 14 - Ronald S. Swerdloff, MD, Jason Ng, MD, and Gladys E. Palomeno, MD,
March 1, 2004

In this thread we will review: the ontogeny and physiology of breast development; factors that influence breast enlargement in the male; the differential diagnosis of gynecomastia; the process of diagnostic investigation; and treatment of gynecomastia.

BREAST DEVELOPMENT
Male breast development occurs in an analogous fashion to female breast development. At puberty in the female breast, complex hormonal interplay occurs resulting in growth and maturation of the adult female breast.
In early fetal life, epithelial cells, derived from the epidermis of the area programmed to later become the areola, proliferate into ducts, which connect to the nipple at the skin's surface. The blind ends of these ducts bud to form alveolar structures in later gestation. With the decline in fetal prolactin, placental estrogen and progesterone at birth, the infantile breast regresses until puberty.

During thelarche, the initial clinical appearance of the breast bud, growth and division of the ducts occur, eventually giving rise to club-shaped terminal end buds, which then form alveolar buds. Approximately a dozen alveolar buds will cluster around a terminal duct, forming the type 1 lobule. Eventually, the type 1 lobule will mature into types 2 and 3 lobules, called ductules, by increasing its number of alveolar buds to as many as 50 in type 2 and 80 in type 3 lobules. The entire differentiation process takes years after the onset of puberty and, if pregnancy is not achieved, may never be completed.

HORMONAL REGULATION OF BREAST DEVELOPMENT
The initiation and progression of breast development involves a coordinated effort of pituitary and ovarian hormones, as well as local mediators (see Figure 1).

Figure 1. Hormones affecting growth and differentiation of breast tissue. (GH= Growth Hormone; ER= Estrogen Receptor; PR= Progesterone Receptor; AR= Androgen Receptor)
Attached Thumbnails
*
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 ***ot 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.

ANDROGEN AND AROMATASE

Estrogen effects on the breast may be the result of either circulating estradiol levels or locally produced estrogens. Aromatase P450 catalyzes the conversion of the C19 steroids, androstenedione, testosterone, and 16-a-hydroxyandrostenedione to estrone, estradiol-17b and estriol. As such, an overabundance of substrate or an increase in enzyme activity can increase estrogen concentrations and thus initiate the cascade to breast development in females and males. For example, in the more complete forms of androgen insensitivity syndromes in genetically male (XY) patients, excess androgen aromatizes into estrogen resulting in not only gynecomastia, but also a phenotypic female appearance. Furthermore, the biologic effects of over expression of the aromatase enzyme in female and male mice transgenic for the aromatase gene result in increased breast proliferation. In female transgenetics, over expression of aromatase promotes the induction of hyperplastic and dysplastic changes in breast tissue. Over expression of aromatase in male transgenics caused increased mammary growth and histological changes similar to gynecomastia, an increase in estrogen and progesterone receptors and an increase in downstream growth factors such as TGF-beta and bFGF. Interestingly, treatment with an aromatase inhibitor leads to involution of the mammalian gland phenotype. Thus, although androgens do not stimulate breast development directly, they may do so if they aromatize to estrogen. This occurs in cases of androgen excess or in patients with increased aromatase activity.

PHYSIOLOGIC GYNECOMASTIA

Gynecomastia, breast development in males, can occur normally during three phases of life. The first occurs shortly after birth in both males and females. This is caused by the high levels of estradiol and progesterone produced by the mother during pregnancy, which stimulates newborn breast tissue. It can persist for several weeks after birth and can cause mild breast discharge called "witch's milk".

Puberty marks the second situation in which gynecomastia can occur physiologically. In fact, up to 60% of boys have detectable gynecomastia by age 14. Although it is mostly bilateral, it can occur unilaterally, and usually resolves within 3 years of onset.

Interestingly, in early puberty, the pituitary gland releases gonadotropins in order to stimulate testicular production of testosterone mostly at nighttime. Estrogens, however, rise throughout the entire day. Some studies have shown that a decreased androgen to estrogen ratio exists in boys with pubertal gynecomastia when compared with boys who do not develop gynecomastia. Furthermore, another study showed increased aromatase activity in the skin fibroblasts of boys with gynecomastia. Thus, the mechanism by which pubertal gynecomastia occurs may be due to either decreased production of androgens or increased aromatization of circulating androgens, thus increasing the estrogen to androgen ratio.

The third age range in which gynecomastia is frequently seen is during older age (>60 years). Although the exact mechanisms by which this can occur have not been fully elucidated, evidence suggests that it may result from increased peripheral aromatase activity secondary to the increase in total body fat, coupled with mild hypogonadism associated with aging. For instance, investigators have shown increased urinary estrogen levels in obese individuals, and have demonstrated aromatase expression in adipose tissue. Thus, like the gynecomastia of obesity, the gynecomastia of aging may partly result from increased aromatase activity, causing increased circulating estrogen levels. Moreover, not only does total body fat increase with age, but there may be an increase in aromatase activity in the adipose tissue already present, increasing circulating estrogens even further. Lastly, SHBG increases with age in men. Since SHBG binds estrogen with less affinity than testosterone, the bioavailable estradiol to bioavailable testosterone ratio may increase in the obese older male.

PATHOLOGIC GYNECOMASTIA:

INCREASED ESTROGEN

Since the development of breast tissue in males occurs in an analogous manner to that in females, the same hormones that affect female breast tissue can cause gynecomastia. The testes secrete only 6-10 mg of estradiol and 2.5 mg of estrone per day. Since this only comprises a small fraction of estrogens in circulation (i.e. 15% of estradiol and 5% of estrone),the remainder of estrogen in males is derived from the extraglandular aromatization of testosterone and androstenedione to estradiol and estrone, respectively. Thus, any cause of estrogen excess from overproduction to peripheral aromatization of androgens can initiate the cascade to breast development.
 
captaincaveman

captaincaveman

TID Board Of Directors
Oct 17, 2010
1,143
216
#2
Gyno reversal during PCT?

First - I never had any issues with gyno at all. But at the end of my last cycle, my nipples got itchy and sore.
Had been taking HCG 250iu ew during last 8 weeks of cycle.
Immediately began Letro for two weeks and knocked out all symptoms. (probably too short of time)

Stopped Letro and began my Nolva/Aromasin PCT....on third week and still have small lump (i think) behind one nipple.

Can I pick back up the Letro while taking Nolva/Aromasin? At what dose?

Thanks bro....
-CC-
 
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