I’m afraid that is not my position nms.
Most bodybuilders that stack steroids simply do not know what they are doing/what the endocrine effects are and I don’t think that trying to split bodybuilders into two sub groups and re-naming the more ignorant of the bodybuilders is unhelpful.
Yes some bodybuilders have a basic understanding of the concepts of endocrinology, yes some of them know quite detailed information regarding pharmacology, but only a very, very limited number understand the wider implications of their actions or take on board professional help in managing their drug use.
The vast majority of men/bodybuilders in gyms from the US/Europe and further afield have very limited/inadequate understanding of the potential problems that their drug taking can cause.
Many bodybuilders don’t develop gynecomastia and for those men it is a case of them knowing enough limited information to avoid this condition, plus kind genetics (poor genetics can cause gynecomastia in the most carefully crafted protocols).
Gynecomastia is just one issue, because it is so apparent and undesirable it is one that has received a lot of attention.
However there are many other problems that can stem from increasing hormones to supra physiological levels.
There are a disproportionate amount of bodybuilders that turn up in fertility clinics sometimes many years after there use, a disproportionate number also who end up with hypogonadism due to steroid induced pituitary failure or testicular failure.
Whilst testosterone is actually beneficial to the heart at optimal levels, protects the heart via improved vascular action, try and find a single cardiologist that believes that supraphysiological levels are anything but harmful.
You would struggle to find one who is respected in his field.
The heart is a muscle and has androgen receptors just like normal muscles and very high testosterone used over time can increase the thickness of the left ventricle which can lead to cardiomyopathy.
High blood pressure increases the chance of heart attack and stroke, abnormal cholesterol levels, can increase the chance of heart attack and blood vessel disease.
Damage to the liver and even liver cancer can occur in those with underlying liver disease something that is often asymptomatic. This is a particular problem with steroids that are methelated, but is also an issue with all those that require a first pass on the liver.
Then there is the potential for steroid induced polycythemia and the consideration of the requirement of PSA checks to ensure there is no underlying prostate disease.
I could go on and on and on.
The fact of the matter is genetics and chance play as much a part of how a bodybuilder gets through such potential problems as their ability to control the issues involved.
Do you seriously think for one second that a top bodybuilder knows what the long term consequences are for the use of something like rebound xt?
Because supplements like this have never undergone long term controlled double blind placebo based studies in significant numbers, the fact is information of this nature simply doesn’t exist. It doesn’t exist for rebound xt and it doesn’t exist for many synthetically altered steroids and various medications for controlling estrogen.
In fact even the likes of Tamoxifen and Arimidex have obtained their license following their use in aforementioned trials only in the setting of breast cancer in women. So in terms of safety and dosage in men, even with something so well developed as the above there are still potential issues.
Now am I saying that all of these things are going to have terrible side-effects that will be seen 10 year from now?
No, but I am saying that we do not know the extent to any long term consequences for many stacked or singularly used substances. So the fact is NO ONE not even an endocrinologist using such medications could know for a fact what the long term problems maybe!!
Furhtermore with regard to stacking you get into a human version of kaos theory because you have the potential for drug interactions, for which no large database of information exists.
Just to show that I am not being over the top I will detail the use of one synthetically altered version of testosterone.
Methltestosterone;
The medical literature makes it very clear that the liver toxicity from methylated steroids is significant. Cases of benign and malignant tumors, and more commonly peliosis hepatitis (formation of blood filled cysts in the liver), related to use of these compounds has been widely reported.
Methltestosterone is still sold in the US but has been banned in many countries across the world due to its hepatotoxicity. That still did not stop some bodybuilders wanting an oral steroid from dying from its use.
In terms of using anti estrogens or aromatase inhibitors, there is the potential for throwing thyroid function out, how many bodybuilders check there thyroid when using such meds?
I could go on and on and on…..
P.S
Moobius, you haven't got a clue and your refusal to reveal any details regarding your own situation shows how worried you are about your ability to defend your own actions 
What is your Profession Hypo? You are very well versed!!
I actually think its fair to split bodybuilders up from common steroid users. Theres your 30 year olds using supplements with the help of their doctors, dieticians etc, and then there's your 16 year olds, throwing 500+mgs of test a week into their body, closing off their growth plates, and causing all sorts of other issues. As for long term effects, ALL BODYBUILDERS, are aware of these. They are aware of the effects on their, heart, liver, they are aware that "cutting" drugs have adverse thyroid effects etc, they are aware that IGF-1 and Insulin are a dangerous combination, that cause organs to grow out of preportion, but its THEIR choice.. They do know enough, to know what they are doing... Its the younger ones that I hate seeing, they are balding by the time they are 20.. Im only 22 and I am a natural bodybuilder, all though I have used pro hormones, which had adverse side effects, such as weakening collagen sysnthesis, and leading to a ruptured medial and lateral tendon.. Its small things like these that uneducated people do not know, and I learned the hard way. Below was written by a bodybuilder.
"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
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.
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.
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.
__________________
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 marijuana, 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
Sorry for the size of the post.. but it goes on and on for more information
Topic: 6-OXO to Battle Estrogen & Gyn (Read 16458 times)
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