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Old 06-13-2009, 09:08 AM
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Default Gyno Prevention and Reversal

GYNO prevention and reversal

again I took this from another site, but I thought it was very informative.

All you need to know about GYNO. written by C-bino and Nark

I am posting this thread to help answer all of the questions regarding gyno prevention and reversal, the use of letrozole and other anti-e’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 – 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 – Aromatise Inhibitor. These drugs work by inhibiting the aromatization of estrogen. This means that in effect AI’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’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…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’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.





TUMORS

Testicular tumors can lead to increased blood estrogen levels by: estrogen overproduction; androgen overproduction with aromatization in the periphery to estrogens; and by ectopic secretion of gonadotropins which stimulate otherwise normal Leydig cells. Tumors causing an overproduction of estrogen represent an unusual but important cause of estrogen excess.

Examples of estrogen-secreting tumors include: Leydig cell tumors, Sertoli cell tumors, granulosa cell tumors and adrenal tumors.
Interstitial cell tumors, or Leydig cell tumors constitute 1%-3% of all testis tumors.

Usually, they occur in men between the ages of 20 and 60, although up to 25% of them occur prepubertally. In prepubertal cases, isosexual precocity, rapid somatic growth, and increased bone age with elevated serum testosterone and urinary 17-ketosteroid levels are the presenting features.

In adults, elevated estrogen levels coupled with a palpable testicular mass and gynecomastia may develop. Though mostly benign, Leydig cell tumors may be malignant and metastasize to lung, liver, and retroperitoneal lymph nodes.

Sertoli cell tumors comprise less than 1% of all testicular tumors and occur at all ages, but one third have occurred in patients less than 13 years, usually in boys under 6 months of age. Although they arise in young boys, they usually do not produce endocrinologic effects in children. Again, the majority is benign, but up to 10% is malignant. Gynecomastia occurs in one third of cases, presumably due to increased estrogen production.

Granulosa cell tumors, which occur very rarely in the testes, can also overproduce estrogen. In fact, only eleven cases have been reported with gynecomastia as a presenting feature in half of them.

Germ cell tumors are the most common cancer in males between the ages of 15 and 35. They are divided into seminomatous and nonseminomatous subtypes and include embryonal carcinoma, yolk sac carcinoma, choriocarcinoma and teratomas. Elevated a fetoprotein (AFP) and b HCG function as reliable markers in some tumors. As a result of the increased b HCG, acting analogously to LH to stimulate the Leydig cell LH receptor, testicular estrogen production is also increased, which, in turn, can cause gynecomastia. Although germ cell tumors generally arise in the testes, they can also originate extra-gonadally, specifically in the mediastinum. These extragonadal tumors also possess the capability of producing b HCG, but they must be differentiated from a multitude of other tumors such as large cell carcinomas of the lung which can synthesize ectopic b HCG.

Some neoplasms that overproduce estrogens also possess aromatase overactivity. Sertoli Cell tumors in boys with Peutz-Jegher syndrome, an autosomal dominant disease characterized by pigmented macules on the lips, gastrointestinal polyposis and hormonally active tumors in males and females, for instance, have repeatedly demonstrated aromatase overactivity, resulting in gynecomastia, rapid growth and advanced bone age as presenting features. Feminizing Sertoli cell tumors with increased aromatase activity can also be seen in the Carney complex, an autosomal dominant disease characterized by cardiac myxomas, cutaneous pigmentation, adrenal nodules and hypercortisolism. Other than sex-cord tumors, fibrolamellar hepatocellular carcinoma has also been shown to possess ectopic aromatase activity, causing severe gynecomastia in a 17-year-old boy. Furthermore, adrenal tumors can secrete excess dehydroepiandrosterone (DHEA), DHEA-sulfate (DHEAS) and androstenedione that can then be aromatized peripherally to estradiol.






NON-TUMOR CAUSES OF ESTROGEN EXCESS:

INCREASED AROMATASE ACTIVITY
Besides tumors, other conditions have been associated with excessive aromatization of testosterone and androgens to estrogen, which results in gynecomastia. For instance, a familial form of gynecomastia has been discovered, in which affected family members have an elevation of extragonadal aromatase activity. More recently, novel gain-of-function mutations in chromosome 15 have been reported to cause gynecomastia, possibly by forming cryptic promoters that lead to over expression of aromatase. As stated, obesity may cause estrogen excess through increased aromatase activity in adipose tissue. Furthermore, hyperthyroidism induces gynecomastia through several mechanisms, including increased aromatase activity.


DISPLACEMENT OF ESTROGENS FROM SHBG
Another cause of gynecomastia from estrogen excess includes steroid displacement from sex-hormone binding globulin (SHBG). SHBG binds androgens more avidly than estrogen. Thus, any condition or drug that can displace steroids from SHBG, will more easily displace estrogen, allowing for higher circulating levels of estrogen. Drugs can cause gynecomastia by numerous mechanisms besides displacement from SHBG.

DECREASED TESTOSTERONE AND ANDROGEN RESISTANCE
Breast development requires the presence of estrogen. Androgens, on the other hand oppose the estrogenic effects. Thus, equilibrium exists between estrogen and androgens in the adult male to prevent growth of breast tissue, whereby either an increase in estrogen or a decrease in androgen can tip the balance toward gynecomastia. Increased estrogen levels will increase glandular proliferation by several mechanisms. These include direct stimulation of glandular tissue and by suppressing LH, therefore decreasing testosterone secretion by the testes and exaggerating the already high estrogen to androgen ratio.

Besides increased estrogen production, decreased testosterone levels can cause an elevation in the estrogen to androgen ratio, producing gynecomastia. Primary hypogonadism, with its reduction in serum testosterone and increased serum LH levels increases testicular estradiol production and is associated with an increased estrogen to androgen ratio. Klinefelter's syndrome, occurring in 1 in 500 males who possess an XXY karyotype and primary testicular failure, features gynecomastia as well, again presumably secondary to decreased testosterone production, compensatory increased LH secretion, overstimulation of the Leydig cells and relative estrogen excess. In addition, any acquired testicular disease resulting in primary hypogonadism such as viral and bacterial orchitis, trauma, or radiation can also promote gynecomastia by the same mechanisms.

Lastly, enzyme deficiencies in the testosterone synthesis pathway from cholesterol also result in ***ressed testosterone levels and hence a relative increase in estrogen. Deficiency of 17-oxosteroid reductase, the enzyme that catalyzes the conversion of androstenedione to testosterone and estrone and estrone to estradiol, for example, will cause elevation in estrone and androstenedione, which is then further aromatized to estradiol.

Secondary hypogonadism, if severe enough, results in low serum testosterone and unopposed estrogen effect from increased conversion of adrenal precursors to estrogens. Thus, patients with Kallmann's syndrome, a form of congenital secondary hypogonadism with anosmia, also develop gynecomastia. In fact, hypogonadism from whatever cause constitutes most cases of gynecomastia.

The androgen resistance syndromes, including complete and partial testicular feminization (e.g. Reifenstein's syndrome) are characterized by gynecomastia and varying degrees of pseudohermaphroditism. Kennedy Syndrome, a neurodegenerative disease, is also associated with decreased effective testosterone due to a defective androgen receptor. The gynecomastia is the combined result of decreased androgen responsiveness at the breast level and increased estrogen levels as a result of elevated androgen precursors of estradiol and estrone. As such, androgens in these diseases are not recognized by the peripheral tissues including the breast and pituitary. Androgen resistance at the pituitary results in elevated serum LH levels and increased circulating testosterone. The increased serum testosterone is then aromatized peripherally, promoting gynecomastia. Thus, gynecomastia is the result of increased estradiol levels that arise due to unopposed androgen unresponsiveness.

OTHER DISEASES
Other disease states have also resulted in gynecomastia.
Men with end stage renal disease may have reduced testosterone, and elevated gonadotropins. This apparent primary testicular failure may then lead to increased breast development.

The gynecomastia of liver disease, particularly cirrhosis, does not have a clear etiology. Some have speculated that the gynecomastia is the result of estrogen overproduction, possibly secondary to increased extraglandular aromatization of androstenedione, which may have decreased hepatic clearance in cirrhotics. However, testosterone administration to cirrhotics causes a rise in estradiol, but decreases the prevalence of gynecomastia. Therefore, although the association of gynecomastia with liver disease is apparent, current data are conflicting and the mechanism by which this occurs remains unclear.

As previously stated, thyrotoxicosis is associated with gynecomastia. Patients often have elevated estrogen that may result from a stimulatory effect of thyroid hormone on peripheral aromatase. Testosterone may also be increased possibly due to thyroid-hormone-stimulated increase in SHBG, as free testosterone is usually normal. Since SHBG binds testosterone more avidly than estradiol, there is a higher ratio of free estradiol to free testosterone. Thus, with normal testosterone and increased estrogen, there is an elevated estrogen to testosterone ratio. In addition, LH is also increased, which may also stimulate testicular estrogen synthesis.

Gynecomastia can also follow spinal cord disorders. Most patients with spinal cord disorders display ***ressed testosterone levels and, in fact, can develop testicular atrophy with resultant hypogonadism and infertility. Some have speculated that this may result from recurrent urinary tract infections, increased scrotal temperature, and a neuropathic bladder, which ultimately cause acquired primary testicular failure. The exact mechanism, however, remains elusive.

Refeeding gynecomastia refers to breast development in men recovering from a malnourished state. Although most cases regress within seven months, the etiology of this phenomenon has not been fully elucidated.
HIV patients can also develop gynecomastia. There is a high incidence of androgen deficiency due to multifactorial causes, including primary and secondary hypogonadism.




DRUGS
A significant percentage of gynecomastia is caused by medications or exogenous chemicals that result in increased estrogen effect. This may occur by several mechanisms: 1) they possess intrinsic estrogen-like properties, 2) they increase endogenous estrogen production, or 3) they supply an excess of an estrogen precursor (e.g. testosterone or androstenedione) which can be aromatized to estrogen.

Contact with estrogen vaginal creams, for instance, can elevate circulating estrogen levels. These may or may not be detected by standard estrogenic qualitative assays. An estrogen-containing embalming cream has been reported to cause gynecomastia in morticians.

Recreational use of *********, a phytoestrogen, has also been associated with gynecomastia. It has been suggested that digitalis causes gynecomastia due to its ability to bind to estrogen receptors.

The appearance of gynecomastia has been described in body builders and athletes after the administration of aromatizable androgens. The gynecomastia was presumably caused by an excess of circulating estrogens due to the conversion of androgens to estrogen by peripheral aromatase enzymes.

Drugs and chemicals that cause decreased testosterone levels either by causing direct testicular damage, by blocking testosterone synthesis, or by blocking androgen action can produce gynecomastia. For instance, phenothrin, a chemical component in delousing agents, possessing antiandrogenic activity, has been attributed as the cause of an epidemic of gynaecomastia among Haitian refugees in US detention centers in 1981 and 1982.

Chemotherapeutic drugs, such as alkylating agents, cause Leydig cell and germ cell damage, resulting in primary hypogonadism. Flutamide, an anti-androgen used as treatment for prostate cancer, blocks androgen action in peripheral tissues, while cimetidine blocks androgen receptors. Ketoconazole, on the other hand, can inhibit steroidogenic enzymes required for testosterone synthesis. Spironolactone causes gynecomastia by several mechanisms. Like ketoconazole, it can block androgen production by inhibiting enzymes in the testosterone synthetic pathway (i.e. 17a hydroxylase and 17-20-desmolase), but it can also block receptor-binding of testosterone and dihydrotestosterone.

In addition to decreasing testosterone levels and biologic effects, spironolactone also displaces estradiol from SHBG, increasing free estrogen levels.

Ethanol (For you Noobs: the alcohol consumed in beverages )increases the estrogen to androgen ratio and induces gynecomastia by multiple mechanisms as well. Firstly, it is associated with increased SHBG, which decreases free testosterone levels. Secondly, it increases hepatic clearance of testosterone, and thirdly, it has a direct toxic effect on the testes themselves. Unfortunately, besides the drugs stated, a multitude of others cause gynecomastia by unknown mechanisms.

Drugs that induce gynecomastia by known mechanisms:

Estrogen-like, or binds to estrogen receptor:

Estrogen vaginal cream
Estrogen-containing embalming cream
Delousing powder
Digitalis
Clomiphene (Clomid bros...Clomid )
*********

Stimulate estrogen synthesis:

Gonadotropins
Growth Hormone (Dammit... )

Supply aromatizable estrogen precursors:

Exogenous androgen (This should read aromatisable exogenous androgens ~Nark)
Androgen precursors (ie androstenedione and DHEA)

Direct Testicular Damage:

Busulfan
Nitrosurea
Vincristine
Ethanol (Yes you boozers.. the alchy DOES DAMAGE!)

Block testosterone synthesis:

Ketoconazole
Spironolactone
Metronidazole
Etomidate

Block androgen action:

Flutamide
Bicalutamide
Finasteride (yup...)
Cyproterone
Zanoterone
Cimetidine
Ranitidine
Spironolactone (repeat offender)

Displace estrogen from SHBG:

Spironolactone (repeat offender)
Ethanol (the booze does it again )




Drugs that cause gynecomastia by uncertain mechanisms:

Cardiac and antihypertensive medications:
• Calcium channel blockers (verapamil, nifedipine, diltiazem)
• ACE Inhibitors (captopril, enalapril
• b blockers
• Amiodarone
• Methyldopa
• Reserpine
• Nitrates
Psychoactive drugs:
• Neuroleptics
• Diazepam
• Neuroleptics
• Diazepam
• Phenytoin
• Tricyclic anti***ressants
• Haloperidol
Drugs for infectious diseases:
• Indinavir
• Isoniazid
• Ethionamide
• Griseofulvin
Drugs of Abuse:
• amphetamines
Other:
• Theophylline
• Omeprazole
• Auranofin
• Diethylpropion
• Domperidone
• Penicillamine
• Sulindac
• Heparin



MALE BREAST CANCER
Male breast cancer is rare and comprises only 0.2 percent of all male cancers. Although uncommon, it has been associated with gynecomastia and necessitates inclusion in the differential diagnosis. Other risks include Klinefelter's syndrome, exogenous estrogen exposure, family history, and testicular disorders. It is unclear if these are specific risks for breast cancer are linked to the stimulatory process responsible for gynecomastia. New evidence suggests obesity and consumption of red meat may also raise the risk for the development of male breast cancer.

PATIENT EVALUATION:

HISTORY AND PHYSICAL EXAMINATION
At presentation, all patients require a thorough history and physical exam. Particular attention should be given to medications, drug and alcohol abuse, as well as other chemical exposures. Symptoms of underlying systemic illness, such as hyperthyroidism, liver disease, or renal failure should be sought. Furthermore, the clinician must recall neoplasm as a possible etiology and should establish the duration and timing of breast development. Obviously, rapid breast growth that has occurred recently is more concerning than chronic gynecomastia.

Additionally, the clinician should inquire about fertility, erectile dysfunction and libido to rule out hypogonadism, either primary or secondary, as a potential cause.

In our experience, the breast examination is best performed with the patient supine and with the examiner palpating from the periphery to the areola. The glandular mass should be measured in diameter. Gynecomastia is diagnosed by finding subareolar breast tissue of 2 cm in diameter or greater. Malignancy is suspected if an immobile firm mass is found on physical examination. Skin dimpling, nipple retraction or discharge, and axillary lymphadenopathy further support malignancy as a possible diagnosis.

A thorough testicular exam is essential. Bilaterally small testes imply testicular failure, while asymmetric testes or a testicular mass suggest the possibility of neoplasm. Visual field impairment may suggest pituitary disease. Physical findings of underlying systemic conditions such as thyrotoxicosis, HIV disease, liver, or kidney failure should also be assessed.





LABORATORY EVALUATION
All patients who present with gynecomastia should have serum testosterone, estradiol, LH and b HCG measured. Further testing should be tailored according to the history, physical examination and the results of these initial tests. An elevated b HCG or a markedly elevated serum estradiol suggests neoplasm and a testicular ultrasound is warranted to identify a testicular tumor, keeping in mind, however, that other non-testicular tumors can also secrete b HCG. A low testosterone level, with an elevated LH and normal to high estrogen level indicates primary hypogonadism. If the history suggests Klinefelter's Syndrome, then a karyotype should be performed for definitive diagnosis. Low testosterone, low LH and normal estradiol levels imply secondary hypogonadism, and hypothalamic or pituitary causes should be sought. If testosterone, LH and estradiol levels are all elevated, then the diagnosis of androgen resistance should be entertained. Liver, kidney and thyroid function should be assessed if the physical examination suggests liver failure, kidney failure, or hyperthyroidism, respectively. Furthermore, if examination of breast tissue suggests malignancy, a biopsy should be performed. This is of particular importance in patients with Klinefelter's syndrome, who have an increased risk of breast cancer.



TREATMENT
Treatment of the underlying endocrinologic or systemic disease that has caused gynecomastia is mandatory. Testicular tumors, such as Leydig cell, Sertoli cell or granulosa cell tumors should be surgically removed. In addition to surgery, germ cell tumors are further managed with chemotherapy involving cisplatin, bleomycin and either vinblastine or etoposide.

Should underlying thyrotoxicosis, renal or hepatic failure be discovered, appropriate therapy should be initiated. Medications that cause gynecomastia should also be discontinued whenever possible based on their role in management of the underlying condition. Of course, if a breast biopsy indicates malignancy, then mastectomy should be performed.
If no pathologic abnormality is detected, then appropriate treatment is close observation. A careful breast exam should be done initially every 3 months until the gynecomastia regresses or stabilizes, after which a breast exam can be performed yearly. It is important to remember that some cases of gynecomastia, especially that which occurs in pubertal boys, can resolve spontaneously. (Mine didn't )





MEDICAL TREATMENT
If the gynecomastia is severe, does not resolve, and does not have a treatable underlying cause, some medical therapies may be attempted.

There are 3 classes of medical treatment for gynecomastia: androgens (testosterone, dihydrotestosterone, danazol), anti-estrogens (clomiphene citrate, tamoxifen) and aromatase inhibitors such as testolactone.

Testosterone treatment of hypogonadal men with gynecomastia often fails to produce breast regression once gynecomastia is established. Unfortunately, testosterone treatment may actually produce the side effect of gynecomastia by being aromatized to estradiol. Thus, although testosterone is used to treat hypogonadism, its use to specifically counteract gynecomastia is limited.

Dihydrotestosterone, a non-aromatizable androgen, has been used in patients with prolonged pubertal gynecomastia with good response rates. Since dihydrotestosterone is given either intramuscularly or percutaneously, this may restrict its usefulness.

Danazol, a weak androgen that inhibits gonadotropin secretion, resulting in decreased serum testosterone levels, has been studied in a prospective placebo-controlled trial, whereby gynecomastia resolved in 23 percent of the patients, as opposed to 12 percent of the patients on placebo. Unfortunately, undesirable side effects including edema, acne, and cramps have limited its use.

Investigators have reported a 64 percent response rate with 100 mg/day of clomiphene citrate, a weak estrogen and moderate antiestrogen. Lower doses of clomiphene have shown varied results, indicating that higher doses may need to be administered, if clomiphene is to be attempted.

Tamoxifen, also an antiestrogen, has been studied in 2 randomized, double-blind studies in which a statistically significant regression in breast size was achieved, although complete regression was not documented.

One study compared tamoxifen with danazol in the treatment of gynecomastia. Although patients taking tamoxifen had a greater response with complete resolution in 78 percent of patients treated with tamoxifen, as compared to only a 40 percent response in the danazol-treated group, the relapse rate was higher for the tamoxifen group.

Although complete breast regression may not be achieved and a chance of recurrence exists with therapy, tamoxifen, due to relatively lower side effect profile, may be a more reasonable choice when compared to the other therapies. If used, tamoxifen should be given at a dose of 10 mg twice a day for at least 3 months.

An aromatase inhibitor, testolactone, has also been studied in an uncontrolled trial with promising effects. Further studies must be performed on this drug before any recommendations can be established on its usefulness in the treatment of gynecomastia.

Newer aromatase inhibitors such as anastrozole and letrozole may have therapeutic potential but no study has been published to confirm its efficacy in treatment of gynecomastia.



SURGICAL TREATMENT
When medical therapy is ineffective, particularly in cases of longstanding gynecomastia, or when the gynecomastia interferes with the patient's activities of daily living, or when there is suspicion of malignancy of breast, then surgical therapy is appropriate. This includes removal of glandular tissue coupled with liposuction, if needed. In our experience, uses of delicate cosmetic surgical techniques are warranted to prevent unsightly scarring.


PREVENTION OF GYNECOMASTIA IN MEN WITH PROSTATE CANCER
Because androgen ***rivation is one of the commonly used treatment modalities for advanced prostate cancer, its possible role in the development of gynecomastia is of particular concern to clinicians. Low dose prophylactic irradiation has been variably reported to reduce the rate of gynecomastia in men receiving estrogens or antiandrogens for advanced prostate cancer
.
SUMMARY
In summary, gynecomastia is a relatively common disorder. The causes of its development range vastly from benign physiologic processes to rare neoplasms. Thus, in order to properly diagnose the etiology of the gynecomastia, the clinician must understand the hormonal factors involved in breast development. Parallel to female breast development, estrogen, along with GH and IGF-1 is required for breast growth in males. Since a balance exists between estrogen and androgens in males, any disease state or medication that can increase circulating estrogen or decrease circulating androgen, causing an elevation in the estrogen to androgen ratio, can induce gynecomastia.

Due to the diversity of possibly etiologies, including neoplasm, performing a careful history and physical is imperative. Once gynecomastia has been diagnosed, treatment of the underlying cause is warranted. If no underlying cause is discovered, then close observation is appropriate. If the gynecomastia is severe, however, medical therapy can be attempted and if ineffective, glandular tissue can be removed surgically.
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Old 10-20-2010, 08:39 AM
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Thanks for this WW! Hopefully, guys will refer to this first b4 going wild w/ gyno questions.

Gr8 thread!
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I agree!
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Old 10-20-2010, 08:42 AM
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does anyone know how to post a new thread on this web site?
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Old 12-12-2011, 05:24 AM
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Great Post!!
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Old 01-03-2012, 11:28 PM
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how after this procedure is the sex drive shot for?

can this procedure cause permanent damage to the sex drive?
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Old 01-03-2012, 11:51 PM
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how after this procedure is the sex drive shot for?

can this procedure cause permanent damage to the sex drive?
mine bounced back fast. I did this procedure twice.
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Old 01-04-2012, 06:46 PM
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Wet works - Letro has been banned in India. The last PCT/ ancillaries order I placed with ADC, I couldn't order Letro. Is there a place that someone could suggest to order tabs? I don't like the liquid stuff as you never know what you are getting (under/ over dosed).

Thanks.
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Old 01-04-2012, 09:01 PM
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Wet works - Letro has been banned in India. The last PCT/ ancillaries order I placed with ADC, I couldn't order Letro. Is there a place that someone could suggest to order tabs? I don't like the liquid stuff as you never know what you are getting (under/ over dosed).

Thanks.
I used the liquid stuff both times. I don't know on Pharma stuff.
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Old 01-15-2012, 12:18 PM
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i started to follow this procedure, i am now on day 11 and only have about a 19 day supply of liquid letro left.

here's the situation:

- i dont feel like my gyno has reduced enough in 11 days to assume that it will be gone after 19 days from now

- i take letro every 24 hours but after about 10 hours of my dose, i start to feel itchy nip, as if the rebound effect is happening 10 hours after every single dose

my question:

should i run a small amount of nolva at the same time to prevent that daily 10 hour-after itchiness?

should i buy more letro before i run out of the one i have and continue to run it for longer and if so, how long should i run it for?

or would it be a better idea to finish the 19 days that i have following it up with the nolva, of course, and then a few weeks later, run another cycle of letro?
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Old 01-16-2012, 03:01 AM
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Quote:
Originally Posted by orthe View Post
i started to follow this procedure, i am now on day 11 and only have about a 19 day supply of liquid letro left.

here's the situation:

- i dont feel like my gyno has reduced enough in 11 days to assume that it will be gone after 19 days from now

- i take letro every 24 hours but after about 10 hours of my dose, i start to feel itchy nip, as if the rebound effect is happening 10 hours after every single dose

my question:

should i run a small amount of nolva at the same time to prevent that daily 10 hour-after itchiness?

should i buy more letro before i run out of the one i have and continue to run it for longer and if so, how long should i run it for?

or would it be a better idea to finish the 19 days that i have following it up with the nolva, of course, and then a few weeks later, run another cycle of letro?
I ran it until my joints hurt so bad I stopped. it was shorter than the protacol above. my gyno wasn't completely gone when I stopped, but it did keep going down. if your joints are not crippling you than run it like above. my .02
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Old 01-16-2012, 03:03 AM
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Lots of good info from WW. thank god i dont have to read( i did skim thru it) it as i have no probs with ANY sides, ima lucky basatard

Wetworks is the man
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Old 01-17-2012, 12:04 AM
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I ran it until my joints hurt so bad I stopped. it was shorter than the protacol above. my gyno wasn't completely gone when I stopped, but it did keep going down. if your joints are not crippling you than run it like above. my .02
so basically, i can potentially be on letro for months, this is most likely something thats not gonna go away in just a few weeks.
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Old 01-17-2012, 01:29 AM
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so basically, i can potentially be on letro for months, this is most likely something thats not gonna go away in just a few weeks.
I had to stop my Letro, cause my joints hurt so bad. I never made it thru the whole cycle as above. my gyno went away both times. I had bad gyno too. I finally figured out what was causing it, so I never got it again. I don't run anti-e's. I use to be like Powerman and could do anything without issues. mixing Tren and Deca did me in. I plan on mixing them again one of these days
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Old 01-17-2012, 02:00 AM
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According to alot of talk on Letro, it actually doesn't haven an instantaneous effect on the reduction of gyno due to running a balanced course in your blood levels. With that being said dont expect to see anything major unless your megadosing because your afraid shitless that your new acquired boobies will never go away. I got gyno really bad one time and because I had never had it before with everything else I used, I never kept Boob-away pills on hand, so about a good 4 weeks deep into gyno I finally got letro but I started taking it for the first week at a relatively lower dose. 1/4 of the actual 2.5mg tab for the first 7 days, than 1/2 for the next 7 days and than a full tab for the next 7. Well on day 17, out of nowhere, I wake up and realized "Holy fuck, my nips shrunk to shit over night". Literally. I was surprised that they had shrunk in size by half over night. Well I continued to take a full tab daily for another week and a half until my gyno had completely subsided and than I immediately hopped onto a Nolva cycle to prevent rebound. The point is, yes you are freaked out, yes your titties are sore and yes want to eat the whole bottle of Letro. Again, this information is all based on my individual experience, but I personally do not prefer to megadose on Letro as to the latter of a gradual increase. I've done it once and have experienced major libido death as well as emotional up's and downs. The closet thing I can compare it to is alcohol. You drink a whole shit ton and than it hits you like a sack of shit all at once, or you can gradually consume until you find that sweetspot that works for you. MAJOR POINT HERE >>> Most fellas I know experience libido death with Letro, I HIGHLY, HIGHLY, HIGHLY recommend looking into PT-141 anytime you use a heavy anti-e cycle or start your PCT. Dont ask me why, just thank me later after you do it. Your wife/gf can use it to

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Old 02-29-2012, 01:57 AM
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Default gyno

I got gyno from some sust and its been about 8 months and I've used every avenue to get some letro. My doc won't do it, my other sources don't have it, I've already bought two batches of bunk liquid letro off the net ..... I'm worried that too much time has passed if I can't get it soon... any other ideas or maybe a different approach to go at my doc with?
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Old 02-29-2012, 07:09 AM
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Go to a different doctor. Find one that keeps his hipocratic oath.
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Old 02-29-2012, 08:30 AM
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Wow, thank you for all the useful information WW. Well worth reading.
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Old 02-29-2012, 04:37 PM
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I had to stop my Letro, cause my joints hurt so bad. I never made it thru the whole cycle as above. my gyno went away both times. I had bad gyno too. I finally figured out what was causing it, so I never got it again. I don't run anti-e's. I use to be like Powerman and could do anything without issues. mixing Tren and Deca did me in. I plan on mixing them again one of these days
WW... Just curious..;what do you mean The Tren and Deca did you in? In a good way or bad way?
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Old 02-29-2012, 06:43 PM
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WW... Just curious..;what do you mean The Tren and Deca did you in? In a good way or bad way?
I'm interpreting as a mixing of the 19-Nors as a double whammy. The proverbial straw that caused gyno when in the past he had no issues with either on their own. Probably had some killer gains though while on.
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Old 02-29-2012, 09:36 PM
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Quote:
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I'm interpreting as a mixing of the 19-Nors as a double whammy. The proverbial straw that caused gyno when in the past he had no issues with either on their own. Probably had some killer gains though while on.
Gotcha! Damn, that sucks. I bet it was fun while it lasted. I feel the Pain though. I have yet to experience running a cycle without any Anti e's. In fact, this is my second cycle and so far for both cycles, I have had to run AI's almost right from the beginning due to gyno issues. It totally blows!!! I feel like I am completely missing the full effect of the gear. I may have to just stop running longer esters. Which I really don't want to do.

In my next cycle (3rd Cycle) I am going to try real hard to use compounds that don't convert or as much anyway. I was going to use test prop and EQ but now I'm thinking of test prop and mast or if I can afford it, primo and/or both along with proviron. I still have a hard time considering proviron as an anti-e since it is an androgen. I also like the fact that I can pair it up with nolva and use it in high doses. I would love to run Test prop/Mast/and NPP but I already have too many problems with estrogen related gyno and am still learning to control it. I don't want to run into a problem with progesterone either.
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Old 02-29-2012, 11:45 PM
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Gotcha! Damn, that sucks. I bet it was fun while it lasted. I feel the Pain though. I have yet to experience running a cycle without any Anti e's. In fact, this is my second cycle and so far for both cycles, I have had to run AI's almost right from the beginning due to gyno issues. It totally blows!!! I feel like I am completely missing the full effect of the gear. I may have to just stop running longer esters. Which I really don't want to do.

In my next cycle (3rd Cycle) I am going to try real hard to use compounds that don't convert or as much anyway. I was going to use test prop and EQ but now I'm thinking of test prop and mast or if I can afford it, primo and/or both along with proviron. I still have a hard time considering proviron as an anti-e since it is an androgen. I also like the fact that I can pair it up with nolva and use it in high doses. I would love to run Test prop/Mast/and NPP but I already have too many problems with estrogen related gyno and am still learning to control it. I don't want to run into a problem with progesterone either.

Bump Prime

I never had any issues until I mixed Tren and Deca in my two cycles. they were awesome, but the gyno made me cut them short. DHT's like Mast, Primo, Winni, are all anti-e's Anavar and proviron are weaker anti-e's.

I think you would lover running Prop, Mast, and NPP. it worked great for me and gives you a nice look. add a DHT and it should help with estrogen. I'll run a DHT over an anti-e any day. my .02
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Old 03-01-2012, 04:20 PM
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Bump Prime

I never had any issues until I mixed Tren and Deca in my two cycles. they were awesome, but the gyno made me cut them short. DHT's like Mast, Primo, Winni, are all anti-e's Anavar and proviron are weaker anti-e's.

I think you would lover running Prop, Mast, and NPP. it worked great for me and gives you a nice look. add a DHT and it should help with estrogen. I'll run a DHT over an anti-e any day. my .02
Now you got the balls rollin in my head WW. LOL! How long would you suggest running that combo for anyway? 10-12 weeks?
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Old 03-01-2012, 11:00 PM
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Now you got the balls rollin in my head WW. LOL! How long would you suggest running that combo for anyway? 10-12 weeks?
how long is up to you.
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Old 04-29-2012, 04:50 AM
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i got aromasin for pct do you think that would be fine to use if i develop gyno on cycle or should i get letro?
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