Cytadren anti-estrogen profiles

Cytadren

Aminoglutethimide is mainly identified as an inhibitor of adrenocortical steroid synthesis. Its primary function is to block the conversion of cholesterol to pregnenolone, which is required for the biosynthesis of adrenal glucocorticoids, mineral corticoids, estrogens, and androgens. Aminoglutethimide is a nonspecific inhibitor, and also blocks several other steps in steroid synthesis including hydroxylation at C-11, C-18, and C-21, and the aromatization of androgen to estrogens, The drug may be used clinically to treat estrogen dependent breast cancer, and to treat Cushing’s syndrome, which is a condition where the body overproduces the hormone cortical. The effect that Aminoglutethimide can have on cortical and estrogen production is what makes this a drug of interest to athletes and bodybuilders. The drug also works by inhibiting cortical production. While cortical is an essential hormone for life, its levels may also vary greatly within “normal” ranges depending on the individual, their training and dietary status. Aminoglutethimide was FDA approved as an anticonvulsant drug in 1960 under the main trade name of Cytadren. Side effects were common with treatment, however, including drowsiness, dizziness, and partial loss of motor control. In 1966 reports of adrenal insufficiency subsequent to Aminoglutethimide use were reported. The drug was withdrawn from the U.S market as an anticonvulsant that same year due to its recently understood effects on the adrenal gland. The drug is most commonly supplied in tablets of 250mg.

In terms of research conducted in athletes or those looking to use the drug for athletic or cosmetic purposes, there is of course very little as is the case with many drugs used by bodybuilders and strength athletes. For this reason we are left to extrapolate the best methods to use aminoglutethimide from anecdotal information as well as trying to form the available research to fit into our needs. A significant aspect of aminoglutethimide is that along with its ability to inhibit both cortisol and aromatization, it also suppresses the production of adrenal androgens. Obviously this would be a negative for someone that was not using exogenous hormones, but since it is unlikely that athletes or other steroid users would be administering aminoglutethimide without also using anabolic steroids this is likely not to be a concern for most. The cortisol inhibiting effect of aminoglutethimide is short lived in the body due to the body’s ability to adapt to the action of the drug. By lowering the natural production of cortisol the body will begin to produce adrenocorticotropic hormone. The hormone sparks an increase in cortisol production in the body to help normalize its levels causing the action of the drug to become basically moot. It is believed by some that if one staggers their use of the drug to a schedule similar to two days on and then two days off that this may be enough to ward off the body’s response to the lowered cortisol levels while still reaping the benefit of partial suppression. There is little research to indicate that this is true however. It appears that there is a significant risk of hepatoxicity with aminoglutethimide when used over extended periods of time even at relatively moderate dosages. For this reason lengthy use of the drug would not be recommended for most users and even short cycles of it are likely to increase liver values.

Athletes and bodybuilders looking to take Cytadren for the suppression of cortisol usually take the drug in a dosage of 1000mg per day for a period of 2-3 weeks or less. A schedule of 2 days on and 2 days off may be used in an effort to extend the effectiveness of the drug for extended periods of time.

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Teslac testolactone anti-estrogen profiles

Teslac  testolactone

Testolactone is a first generation non selective steroidal aromatase inhibitor, used clinically to treat estrogen dependent breast cancer. Its exact mode of function is unknown, but it is believed to inhibit the aromatase enzyme in a noncompetitive and irreversible manner. If so, this would be an activity that is very similar to that of Lentaron. This might also explain why cessation of the drug does not provide an immediate restoration of normal estrogen production.
Like formestane, it takes several days after ceasing use for the body to replenish its enzyme levels. Testolactone was first approved by the FDA as a prescription drug back in 1970. It was an early anti estrogenic drug, exhibiting a moderately pronounced effect but failing to reach levels of high clinical success. As other more successful medications began to surface for the treatment of breast cancer, testolactone would not see the success that had been planned for it. Currently, the United States is the only country where the product has not been discontinued. Testolactone is most commonly supplied in tablets of 50mg.

Even though the drug no longer being utilized for its originally intended purpose, testolactone still offers several unique advantages for steroid users. First, research has shown that the compound can effectively treat and prevent gynecomastia. This is seemingly accomplished by way of aromatase inhibition as opposed to the estrogen agonist/antagonist mechanism that tamoxifen citrate accomplished this effect with. The second benefit that strength athletes, bodybuilders and other who make use of performance-enhancing drugs could experience by taking testolactone is the ability of the compound to help increase the natural testosterone production of users.

This increase is prompted by several physiological mechanisms. In several studies it has been demonstrated that not only is the level of testosterone increased in users significantly, but that this is likely caused by the ability of the compound to also increase the levels of androstenedione, luteinizing hormone and follicle stimulating hormone in the body. Obviously all of this would suggest that testolactone offers several advantages to those with suppressed natural testosterone production, with male steroid users coming off of anabolic steroids clearly being this group. Returning to the aromatase inhibition action of testolactone, the effects of this drug are similar to those of other aromatase inhibitors.

 That is to say that testolactone can help to minimize aromatization and lowers the levels of circulating estradiol. However the level to which testolactone can accomplish this is somewhat clouded due to contradictory research. For example, one study indicated that administering one gram of testolactone to a group of healthy men for nine days resulted in only a twenty five percent decline in the level of circulating estradiol. However another study found that users taking one gram of the compound over only six days cut their estradiol levels in half. So while it can be concluded that testolactone will lower the level of circulating estradiol, there is no definitive answer as to exactly how effective it truly is. As for controlling aromatization, testolactone has been shown to reduce it by up to ninety five percent in some cases.

While testolactone has been shown to be an effective compound for the treatment and prevention of gynecomastia, the main benefit it can offer users is during post-cycle therapy when they are trying to regain natural testosterone production by the body. The ability to help increase the natural production of testosterone, as well as the precursors to testosterone, would undoubtedly serve a user well when he is attempting to re-start and raise his hormonal production to their regular levels.

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Nolvadex tamoxifen citrate anti-estrogen profiles

Nolvadex tamoxifen citrate

Tamoxifen citrate is a non steroidal anti estrogenic drug, used widely in clinical medicine. It is specifically a selective estrogen receptor modulator of the triphenylethylene family, and posses both estrogen agonist and antagonist properties. As such, it may act as an estrogen in some tissues while acting as an anti-estrogen in others. In breast tissue the drug is a strong anti estrogen and as a result is commonly used in the treatment of estrogen related breast cancer in women. Tamoxifen citrate was first developed in 1962 by the pharmaceutical company ICI. It was made commercially available in the United States not long after, but its initial use was for the treatment of female infertility, a purpose for which the drug does not seem ideally suited for. It was not until 1977 that the FDA approved the drug for use in the United States for the treatment of breast cancer. The drug has been sold by ICI in a number of worldwide markets under the brand name of Nolvadex. The drug is most commonly supplied in tablets containing either 10mg of 20mg of the drug.

In terms of its use in steroid users, tamoxifen citrate can help in two ways. Firstly due to the binding affinity of the compound it is able to help in the prevention of gynecomastia. Tamoxifen will compete with estrogen for the estrogen receptors in certain tissues, including the breast, and if it can bind to the receptor estrogen will not have an opportunity to interact with receptor and therefore gynecomastia should not be able to develop. When using anabolic steroids that can convert to estradiol (estrogen) this protection against gynecomastia can be invaluable. However it should be noted that tamoxifen citrate will not eliminate the estrogen or disallow the conversion to occur. Instead it attempts to counteract the effects of circulating estrogen in the body in those tissues that the drug effects. Therefore there is no evidence that tamoxifen citrate has any effects counteracting estrogenic side effects that are unrelated to the tissues that are not in the breast, liver or bone. Namely there is no real causal connection to any reduction in water retention and acne in users that begin taking tamoxifen citrate as it relates to estrogen. The second, and possibly more beneficial, aspect of tamoxifen citrate for steroid users is its ability to increase the production of luteinizing hormone and follicle stimulating hormone, and therefore increasing testosterone. This ability is why it is often used by steroid users during their post-cycle therapy. There are numerous studies that indicate that tamoxifen citrate can increase the levels of these hormones quite dramatically. Tamoxifen citrate does this by blocking the negative feedback inhibition caused by estrogen at the hypothalamus and pituitary, and this in turn will help to increase the production of these hormones. Unlike clomiphene citrate, tamoxifen citrate has also been shown to increase luteinizing hormone responsiveness to gonadotropin releasing hormone. Clomiphene citrate can lower this responsiveness over time. One of the possible side effects associated with use of tamoxifen citrate is the possible reduction of insulin-like growth factor levels. If these levels are reduced this could suppress the gains an individual can make slightly. However this reduction, if it actually exists, would not be overly significant with gains in muscle mass only being marginally reduced for the most part.

When it comes to dosing for combating gynecomastia that has begun to form, there is very little research. The limited research that does exist does point to the fact that doses of 20-40mgs per day are effective in treating the existing condition. However, anecdotally users have reported sometimes using doses of 60-80mgs per day. For use during post-cycle therapy users have anecdotally indicated that doses ranging between 20 and 40mgs per day are average. These doses have been shown to significantly raise levels of testosterone, luteinizing hormone and follicle stimulating hormone.

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Trenbolone Acetate

Trenbolone Acetate

Trenbolone Acetate represent a powerful mass builder 19-nor steroid. Structurally it is similar to nandrolone; with the difference that is a much stronger androgen and its estrogenic activity is lower than nandrolone one.

 Trenbolone proprieties are much stronger than testosterone once. This steroid is considered to be the drug that binds most tightly to the androgen receptors available these days. Trenbolone help to promote red blood cell production and to increase the rate of glycogen restoration. It was noticed too that this drug increases nitrogen retention in muscle tissue. All of these proprieties are beneficial on muscle gain, hardness and strength. Trenbolone is taken by bodybuilders/athletes not only in bulking cycles but in cutting too. It works well as a fat loss agent. Trenbolone is also appreciated because of its proprieties to increase the level of the extremely anabolic hormone IGF-1 within muscle tissue.

 As many steroids, Trenbolones effects depends of the dose is taken, as higher dose is as pronounced results are. Trenbolone doesn’t have the proprieties to aromatize, that’s mean that such side effects as water retention and gyno will not occur. But bodybuilders/athletes should remember that this drug shut down the body’s natural testosterone production, which can lead to sexual dysfunction.

 Trenbolone acetate represents an injectable steroid that has a short ester attached. Its active life is 2-3 days, although detection time is to 5 months.
 The acetate ester provides quick and high concentration of the hormone which has positive effects to bodybuilders/athletes looking for rapid and quality gains. As we said earlier Trenbolone acetate can be taken both in bulking and cutting cycles. If talking about bulking phase in order to obtain better results bodybuilders/athletes are advised to stack Trenbolone acetate with Methandienone or Oxymetholone. In cutting cycle a good combination will be with Primobolan or Winstrol.

 Effective dose for male bodybuilders/athletes is 50-150mg per day. To get expected results Trenbolone acetate should be administrated every day or every other day. Women are not recommended to use this drug.

Side effects that may occur are hair loss, oily skin, decreased libido, prostate enlargement, temporary impotence, bloating and other.  In order to avoid them it is recommended to take some HCG.

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Femara letrozole anti-estrogen profiles

Femara  letrozole

Letrozole is a non steroidal selective third generation aromatase inhibitor. The structure and activity of this compound are very similar to that of Arimidex, and is prescribed for similar medical reasons. More specifically, United States prescribing guidelines for leptosome recommend it to be used for the treatment of postmenopausal women with estrogen receptor positive or estrogen receptor unknown breast cancer. It is typically used as a second line of treatment after an estrogen receptor antagonist like tamoxifen has failed to elicit a describable response, although it is sometimes initiated as the first course of therapy depending on the circumstances. Male bodybuilders and athletes find value in leptosome for its ability to mitigate the estrogenic side effects associated with the use of aromatically anabolic/androgenic steroids, such as gynecomastia, fat buildup, and visible water retention. The U.S FDA approved leptosome for prescription sale in 1997, where it is sold by the pharmaceutical company Novartis under the brand name of Femara. The company also markets the drug in over 70 nations worldwide. The drug is most commonly supplied in dosages of 2.5mg.

In terms of how this drug can be used to the benefit of bodybuilders and strength athletes, letrozole is primarily used to ward any estrogenic side effects caused by the administration of anabolic steroids. Letrozole has been show to have the capability of reducing the level of estrogen in users' bodies by up to 96-98%. This would seemingly be enough in itself to make the compound a desirable one with which steroid users would be interested in. However letrozole also has been shown to increase the amount of luteinizing hormone, follicle stimulating hormone, and sex hormone binding globulin in users. When you combine these attributes with the fact that it will help protect against gynecomastia, water retention and other estrogenic side effects letrozole obviously can fulfill many users' needs. There are some animal studies that have suggested that letrozole can help to reduce or even eliminate pre-existing gynecomastia as well. Of course there are some limits to this research as it has never been conducted using human subjects but it does demonstrate that there may be a mechanism by which this could occur. Anecdotally some users have reported that they have experienced a reduction in their own pre-existing gynecomastia, but of course these reports have their limits as they were not conducted with the scientific controls in place. Interestingly, it takes approximately 60 days to get a steady blood plasma level of letrozole once administration of the drug begins. This may necessitate that a user begin using the compound prior to beginning their cycle if they wish for the effects to be at full strength once their cycle begins. This may also hinder the ability of the compound to respond quickly if a user begins administration of the drug to counteract some side effects that have appeared quickly.

The maximum dosage that a user would want to use would be 2.5mgs per day. It has been shown in numerous studies that this dosage will eliminate nearly all of the estrogen in the body in nearly all individuals. Any dose that is higher than this would simply be unneeded. Despite the ability to increase the amount of luteinizing hormone, follicle stimulating hormone, and sex hormone binding globulin in users letrozole can be counterproductive if used during post-cycle therapy. This is due to the ability of the compound to drive estrogen levels too low during use. Once the compound is discontinued this can result in a "rebound effect" in estrogen levels with these becoming quite high, something that should be avoided during or after post-cycle therapy. Anastrozole could be seen as an alternative to letrozole in this capacity as it seemingly does not have such a potent effect. The detrimental effect that letrozole has on blood lipid levels is another reason why many will avoid it's use during post-cycle therapy

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Short burst steroid cycles

Short burst steroid cycles

Short burst steroid cycling explained-
One of the best approaches Vie ever used to build muscle tissue is short burst cycling, before i go any further I want to state that short cycling can be implemented to what ever level you are, its not only for the advance Bodybuilder it can be for all stages, its just the amount of gear Mg is adjusted to suit the individual's level. The best part of this thread will be aimed at advanced bodybuilders because of the high dose used with burst cycling but no discussion on dosages will be made on the open board unless it needs to be discussed.

Muscle tissue doesn't grow continuously over long periods of time, weight gain and muscular growth doesn't happen that way. Not in infants, toddlers, teenagers, or even weight trainers. Instead, weight gain seems to come in spurts or surges. It's amazing how you can train hard and eat very well year round yet only seem to make progress in quick little infrequent spurts of growth even with taking all the AAS compounds the body still gets use to what's being taken and builds up tolerance and adapts. If you look back over your cycle history you will notice the growth spurts within the cycles, we don't keep on growing because if we did we would all be 500lbs+. This method can build huge tissue gains in that short growth window if everything is in place.


Pre -Cycle Priming- First you must open the growth window and create a very anabolic environment for muscle tissue to grow, muscle receptors will get very excitable and upgrade to except more glucose which will shift the muscle to fat ratio which in turn will create muscle tissue to build very quickly, when this is coupled with a short burst cycle right after a prime the results can be outstanding, some of you will understand this from rebound cycling after a comp, its very similar except the prime isn't as harsh as the pre-cycle comp diet and the prime is only directed at creating and opening the growth window for the cycle, its a pre-cycle prime.(details of priming is in a separate thread).Hgh protocol should be ran during the prime at low dose and kicked up when cycle starts.


Duration - Short burst cycling usually last for around 30 days, there is no set rule on the length of cycle and normally it can be open ended and stopped when growth slows/stops. You have to listen to the body and adjust, with burst cycling it shouldn't be ran for long periods of time, longer doesn't mean more or better gains. Keep it short and feed the growth window and build the tissue and stop, recover and maintain.

Dosages- The dose for a short burst cycle is a lot more than you would normally use in a standard length cycle, because of the prime and the body being in a very anabolic environment it can take on board a lot more than usual and over loading androgens will fully push the body to grow, it also takes time for the body to adjust to the high level of hormones in relation to sides so before you are experiencing them your off cycle. Over your cycle history you would of tried the heavy dosages and seen the sides come and where its not worth the risk's to muscle gain, this is why its kept to a short period before the body can adjust with sides the cycle is over and growth is completed. Individual dosages are designed off your cycle history, there is no set dose it all depends on what your cycle history looks like, someone who normally uses 500mg per week will be completely different to the guy who uses 1500mgs per week when designing short burst cycles, but both will have the benefit of using high amounts what they normally don't run.

Side effects- If your looking for the best effective way to run hormones without to much negative feedback staying on for long periods of time probably isn't the best option to take. I've had far better blood work back from high burst cycles than when I've ran longer cycles at a lot less dosage. There is minimal impact on the HPTA and recovery is far easier than trying to bring back natural production from a long cycle, there is some elevated aggression because of the high amount of androgens but overall this can be channeled into your workouts. PCT should be painless and within normal boundaries of how you recover. Blood pressure in some can be a problem but not serious but needs to be checked throughout the period so aids can be used to combat the problem if needed. Water retention is low but can be elevated if this system is ran for long periods, but if there is a problem normal AI can be used to help this issue and OTC herbal diuretics. Tren user's within this system get bad BW results due to the harshness of the compound but boy does it produce gains but you have to be prepared to have a hard recovery and sides, kind of defeats the object but again, down to the individual.

Compounds- Because its a short period of time the normal way would to run short ester's, but you can use long ester's within a short cycle, i know what some of you are thinking but it can be done with great results, because of the androgen overload your simply frontloading long ester's to an amount were it is effective straight from the start, the only problem is you have to drop them out 14 days before the end and swap them with fast ester's so everything is clear for PCT, i know what some are saying sounds pointless but its not, to the BB's who prefer long ester and they respond better to them, remember its designed of your cycle history so if your better with long esters go with them until 14 days from the end and swap to fast ester's, the daily injection and the amount of tissue the body can produce in a short period is amazing, if anyone wants to discuss long ester's with this theory i will but at this moment in time I will stop before I complicate things more. Short ester's and fast acting compounds are used and the exact compounds depends on what your trying to achieve but normally its Test based or what you respond best to, 2 /3 compounds are ran at a time but no need to run loads, keep them limited less is better, I've even known guys used 1 compound with stunning results. HGH is increased to a high amount when cycle starts just like all the compounds. I did a study once with some BB's and the dosages range a lot with all different HGH protocol's which is interesting reading but i can go into that at a later date.

Maintenance - Due to the HPTA being shut down or suppressed for a short period of time its far better to get it to respond when the cycle is over, remember being shut down for weeks on end cause's serious issues about recovery and maintenance, shorter shut downs produces easier recovery no matter how much you have pushed in the body, which in turn results in better maintenance which equals keeping more gains. Once you have shut down your HPTA its down and its the period of shutdown what cause's damage, would you rather shut down your HPTA for 14 weeks or 30 days?? or continually shutting down and recovering isn't the other best approach either, depends on the person's goals and what he wants to achieve with Bodybuilding, some of my friends who are at a high level use short burst cycling coupled with bridge's because of what they have to compete with on stage and get ready for photo shoots nearly all the time. Recovering from a standard or long cycle it cost muscle tissue while trying to recovery even with all the peptide's chemicals this day and age we still lose tissue, with this theory losing tissue is limited.

Diet - After the prime as been implemented correctly, the cycle should be started and this day should line up with the first high carb day after the low day carbs within the prime, calories from then on should be increased to over maintenance, different opinions here to how much, again down to knowing your body and how it responds, many who increase too fast will create huge water retention due to the increase of carbs, some don't and over load can be implemented, if your one of these guys who has water retention when carbs are increased after being depleted then over maintenance should be ran for 1 week ish then, overload should be used, if your not and you don't carry the water from the carbs increase calories well over maintenance and go with growth, also depends on how much of a prime as been ran!! feed the dramatic growth what can occur if you have done the procedure correctly. Over eat, over feed, overload on the first day of the cycle straight after the prime from low carb phase. One last thing and i hope many understand this- diet is 24hr dedication while running the theory.

Training - Train to how you grow, best advice here is heavy intense workouts to total failure, HIT style or what ever works for you, you have the answers on how you grow. Intense is the key, stimulation of the whole body to grow, don't waste this time, remember to train how I am recommending is impossible for 10-12 weeks, its to hard and wouldn't last 4 weeks, before a turn around is needed and lay up from the heavy training session, so with this in mind you can mentally focus on this because its only for around 30 days long. I've used many ways myself but the best for me with this style of cycling was heavy drop sets to failure plus forced, swapped to pre-exhausted drop sets to failure the following next total body workout, then swapped again. Workouts are short but seriously intense but you have the food/chemicals and energy to support this for this short period so don't waste it, I've seen huge amounts of tissue build from this, myself I created 10lbs of clean tissue in a very short period of time after PCT and maintenance. Everybody's different to how much they build and comes down to if you have primed correctly, designed the perfect stack for you, placed the correct amount of mg's in the blood every day and how well you train to build fresh tissue.

When i was first learnt this method my whole body changed to a serious level, I never went back to the normal way of cycling, it suited me so much and the growth was amazing. Borreson sat me down and explained in detail how this can happen and to this day things have moved forward so much from Paul's day but i always remember him saying "please try it you will be amazed" he was right and it could for you. Look at Dorian what he did straight after a show....he was back in the gym the day after while the other were on vacation, he was using the growth window to create a very anabolic environment for tissue to grow and he used it, that's why in some years he produced some serious muscle tissue gains what has been seen since due to his method and style, many top pro's used this system but its tweaked to suit their individual's needs.

Please note, I am not saying do short burst cycles with little time off and then back on short burst cycle, no I haven't gone into that side of things, all i am doing is explaining the whole theory behind short burst cycling with first hand experience from myself and many bodybuilder's.

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Faslodex anti-estrogen profiles

Faslodex

Fulvestrant is a highly selective estrogen receptor antagonist. It exerts its action in the body not by targeting the production of estrogen, but by preventing it from exerting activity on the body. It does this by binding available estrogen receptors in a competitive manner, making them unavailable for circulating estrogens. This mode of action is very similar to Nolvadex and Clomid, although unlike these two agent fulvestrant does not have mixed agonist/antagonist properties. It is a pure estrogen receptor antagonist. This agent also stands out as the first inject able estrogen antagonist to catch the attention of the athletic and bodybuilding world. Although not widely used here, when applied it may be effective drug for mitigating the side effects of excess estrogen caused by anabolic/androgenic steroid use such as gynecomastia, fat buildup, and increased water retention. Fulvestrant was developed by the pharmaceutical company AstraZeneca. It was approved as a prescription drug in the U.S in 2002, and is sold under the brand name of Faslodex. The drug is indicated for the treatment of estrogen receptor positive breast cancer with disease progression following traditional anti estrogen treatment with drugs such as nolvadex. The company has since expanded its market for Faslodex to include over a dozen countries worldwide.

Fulvestrant is very potent as an anti estrogen, significantly more so than earlier medications like nolvadex and clomid. Although it targets estrogen at its receptor and not its production, it can still produce an environment of low estrogencity on par with strong aromatase inhibition. One study, for example shows fulvestrant to be as effective in Arimidex in treating breast cancer patients who have already failed with first line endocrine treatments. Another shows the drug prevents tumor cell turnover and growth significantly more effectively than tamoxifen citrate. Studies investigating the physiological response to fulvestrant note that the drug actually down regulates estrogen receptor concentrations. Furthermore, it also tends to down regulate progesterone receptor concentrations. Fulvestrant does not cross the blood brain barrier, and for this reason is believed to produce fewer neurological side effects such as hot flashes, mood alterations, and low energy. The most common side effects associated with the drug include gastrointestinal disturbances such as nausea, vomiting, constipation, abdominal pain, and diarrhea. Other common adverse effects include headache, back pain, hot flashes, and sore throat. Less common side effects include rash, loss of strength, urinary-tract infections, venous thromboembolism, liver enzyme elevations, vaginal bleeding, muscle pain, and low white blood cell count. Injection side reactions may also occur. Anti estrogens can harm the development of unborn fetuses and should not be taken by pregnant women. The drug is most commonly supplied in pre-filled syringes containing 50mg/ ml.

Fulvestrant is FDA approved for the treatment of hormone receptor positive metastatic breast cancer in postmenopausal women with disease progression following anti estrogen therapy. The recommended dose is 250mg administered intramuscularly per month as a single 5ml injection or two 2.5ml injections. When used off label to mitigate the estrogenic side effects of anabolic/androgenic steroid use, male athletes and bodybuilders may find a similar dose as is used for medical reasons to be effective for their needs.

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Anabolic steroids Tips on keeping gains

Anabolic steroids Tips on keeping gains

Keeping the gains from steroid use
 Some tips for coming off a cycle for the moderate user to hold on to the new found muscle -
 These tips are for the moderate user and not for the high dose or long term AAS user, these basic methods will help maintain a degree of muscularity while in the off period. If all procedures are carried out during cycle you would of maximize gains and will be carrying new muscle tissue, then you need to focus on the off period and put yourself in an optimal position to keeping your new found gains once the cycle is stopped.

 One of the areas of focus is the HPTA (Hypothalamus-pituitary-testicular axis), Recovering the HPTA is vital to maintaining gains, typically on a 10 week standard AAS cycle will almost certainly cause full suppression despite any strategies we might undertake. This is why shorter cycles are becoming increasingly more popular because with these type of cycles there is a significant chance you will have testicular function straight after or very shortly after the cycle as stopped.
 Once the cycle as stopped we must preserve our gains and if steps haven't been taken during cycle we must now take some steps to reduce estrogen binding in the hypothalamus. clomid is preferred choice in this area but aromatise inhibitor will also be as effective or better still both. The only way to fully recover your HPTA is to completely come off cycle, with this day and age of PCT compounds to recover with, the job will be easy.Problems occur if you stay on cycle to long or keep taking low suppression drugs to bridge cycles together, all this will have an effect on your HPTA and long term health of it. Recover and maintain the new found gains and stay as healthy as possible, remember suppression and shutdown are linked they both effect your HPTA.

 Nutrition - is another area which we must focus on to help maintain the new found gains, after a cycle androgen levels are going to be lower than normal even with the above strategies. We have to maximize the anabolic hormones as much as possible while our system is recovering. Overeating has been shown in numerous studies to maximize these factors. Over maintenance calories are needed to promote the anabolic edge, sure some fat gain will occur but this will almost totally retain the new found muscle from the cycle. As testosterone returns to normal and recovery is nearly over the calories can be lowered to maintenance or below depending on your goals. Never start dieting in the recovery stage.

 Training - If you have been training intensely during the on period you can help to maintain the new found gains with a slight alteration in the way your training. In some cases further gains have been seen in the recovery part of cycling, this is normally with short cycles and very intense training. If you implement more rest days and make sure your C.N.S get fully recovered further gains can be seen. Keep the training sessions down to around 30 mins and incorporate longer rest days in-between. Long workouts lower testosterone to cortisol ratio, so don't go for long workouts no matter how strong or fit you may feel, short and fast will help with recovery without further stress on your system.

 Still concentrate on the basic heavy movements this and still focus on HIT type of training, also take more attention on the eccentric part of the lift because this causes most of the muscle fiber damage, after warm up do about 2 sets per bodypart and dropset them, which should consist of eccentric reps start with maximum followed by 90% Max, then 80%max, making sure you take a good 5-6 seconds for the eccentric portion of the reps on all dropsets. There are many other ways of training to help recovery but this method does have great benefits by making the workout shorter and the muscle being hit in a different way. Further gains can be achieved if careful planning is done of your training sessions.

 Supplements- Its hard to advice what supplements will help and work for you in recover and maintenance so i wont go to much into this section. clearly a quality protein powder and a good creatine in the off period does help drastically also high levels of BCAA's and glutamine all aid recovery, past experience will help to pick which other supps may help and agree with your body.
 The more advance you become the more advanced procedure need to be carried out.
 marcus

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Fareston toremifene citrate anti-estrogen-profiles

Fareston toremifene citrate

Toremifene citrate is an anti-estrogenic drug, specifically classified as a selective estrogen receptor modulator (SERM) with mixed agonist and antagonist properties. It is a non steroidal triphenylethylene derivative, similar in structure to both the drugs nolvadex and clomid. Toremifen citrate is used for the treatment of breast cancer in postmenopausal women with the estrogen receptor positive or estrogenic receptor unknown tumors. It works by attaching to the estrogen receptor in various tissues in a competitive manner, blocking endogenous estrogen from exerting biological activity. Toremifene citrate was first approved by the FDA as a prescription drug in 1997. It is sold in the U.S under the Fareston brand name, which is made by the pharmaceutical company Gtx Inc. Fareston is also available in over 25 other countries worldwide. Fareston is most commonly supplied in tablets of 88.4mg, which are labeled and equate to 60mg of toremifene base.

The difficulty in using toremifene citrate is the lack of research conducted using human subjects, and specifically male subjects. While it is possible to apply most of what is known about the other selective estrogen receptor modulators to toremifene citrate, independent research conducted with the drug itself is invaluable and therefore a risk is taken when using the drug because of the lack of information. Unfortunately toremifene citrate is possibly the least researched selective estrogen receptor modulator, with the possible exception of raloxifene. 

Despite the lack of human-based research available, in terms of its use in steroid users, toremifene citrate can help in two ways. Firstly due to the binding affinity of the compound it is able to help in the prevention of gynocomastia. Toremifene citrate will compete with estrogen for the estrogen receptors in certain tissues, including the breast, and if it can bind to the receptor estrogen will not have an opportunity to interact with receptor and therefore gynocomastia should not be able to develop. When using anabolic steroids that can convert to estradiol (estrogen) this protection against gynocomastia can be invaluable. However it should be noted that toremifene citrate will not eliminate the estrogen or disallow the conversion to occur. Instead it attempts to counteract the effects of circulating estrogen in the body in those tissues that the drug effects.

 Therefore there is no evidence that toremifene citrate has any effects counteracting estrogenic side effects that are unrelated to the tissues not affected by the drug. Namely there is no real causal connection to any reduction in water retention and acne in users that begin taking toremifene citrate as it relates to estrogen.The second, and possibly more beneficial, aspect of toremifene citrate for steroid users is its ability to increase the production of luteinizing hormone and follicle stimulating hormone, and therefore increasing testosterone. This ability is why it is often used by steroid users during their post-cycle therapy. Toremifene citrate would accomplish this by blocking the negative feedback inhibition caused by estrogen at the hypothalamus and pituitary, and this in turn will help to increase the production of these hormones.

Currently there is no available research that directly links toremifene citrate to being able to raise testosterone levels in male users, however due to the nearly identical mechanisms that both tamoxifen and toremifene citrate use and the reactions that they produce in the body, it would be easy to extrapolate that both drugs should have similar effects in this respect as well. Anecdotally users have reported good results with toremifene citrate and say that they are at least comparable that those of tamoxifen citrate.

Athletes and bodybuilders will usually take around 60-100 mg per day of toremifene per day which is equal to roughly 20-40mg per day of the drug nolvadex.

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Anabolic Steroid Detection Times and Half life

Anabolic Steroid Detection Times and Half life

Anabolic Steroid Detection Times

Anavar ............................................3 weeks
Anadrol........................................... ..2 months
Andriol........................................... ...1 week
Boldenone Undecyclenate...................4-5 months
Clen.............................................. ...4-5 Days
DBol ................................................5-6 weeks
Deca ................................................18 months
Ephedrin ...........................................4-5 Days
Halo.............................................. ....2 months
Methamphetamin ...............................6-10 Days
Nandrolon Phenylprop ........................12 months
Nilevar........................................... ....5-6 weeks
Parabolan......................................... ..4-5 weeks
Proviron.......................................... ...5 weeks
Primo Depot.......................................4-5 weeks
Sustanon ...........................................3 months
Spiropent......................................... ...4-5 days
Test cyp .............................................3 months
Test enat ............................................3 months
Test Prop.............................................2 -3 weeks
Trenbolon Acet ....................................4-5 weeks
Equipoise......................................... ....4-5months
Winny oral...........................................3 weeks .
Winny inj.............................................2 months

Factors which influence the detection times
Metabolism
Fluid intake
Tolerance to the drug
Frequency of intake
Duration of intake
Body fat
Potency of drug
Dosage


Half lives

Oral steroids Drug Active half-life

Anadrol / Anapolan50 (oxymetholone) 8 to 9 hours
Anavar (oxandrolone) 9 hours
Dianabol (methandrostenolone, methandienone) 4.5
Methyltestosterone 4 days
Winstrol (stanozolol
tablets or depot taken orally) 9 hours
Halotestin (Fluoxymesterone) 9.5 hours
Turinabol (Tbol) 16 hours


Depot steroids Drug Active half-life

Deca-durabolin (Nandrolone decanate) 15 days
Equipoise 14 days
Finaject (trenbolone acetate) 3 days
Primobolan (methenolone enanthate) 10.5 days
Sustanon or Omnadren 15 to 18 days
Testosterone Cypionate 12 days
Testosterone Enanthate 10.5 days
Testosterone Propionate 4.5 days
Testosterone Suspension 1 day
Winstrol (stanozolol) 1 day

Steroid esters Drug Active half-life

Formate 1.5 days
Acetate 3 days
Propionate 4.5 days
Phenylpropionate 4.5 days
Butyrate 6 days
Valerate 7.5 days
Hexanoate 9 days
Caproate 9 days
Isocaproate 9 days
Heptanoate 10.5 days
Enanthate 10.5 days
Octanoate 12 days
Cypionate 12 days
Nonanoate 13.5 days
Decanoate 15 days
Undecanoate 16.5 days

Ancillaries Drug Active half-life

Arimidex 3 days
Clenbuterol 1.5 days
Clomid 5 days
Cytadren 6 hours
Ephedrine 6 hours
T3 10 hours
Nolvadex 5-7 days

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raloxifene anti-estrogen profiles

raloxifene

Raloxifene hydrochloride is a second generation selective estrogen receptor modulator (SERM) of the benzothiophene family. This drug is similar in its effects to the drug tamoxifen (nolvadex), exhibiting estrogen receptor antagonist properties in some tissues while acting as an estrogen receptor agonist in others. The main point of variation between the two drugs is their tissue selectivity. While raloxifene hydrochloride is a strong anti-estrogen in breat and uterine tissues, it appears to be estrogenic in bone. This allows it to protect bone density, mimicking the effects of endogenous estradiol. This is quite different than nolvadex, which is anti estrogenic in both breast and bone. In a role that novel for an anti-estrogen, raloxifene was approved by the FDA for the prevention and treatment of osteoporosis in post menopausal women. It is also being investigated for several other potential uses, including the treatment and prevention of cardiovascular disease. Raloxifene was developed by Eli Lilly & Company, and the FDA approved for U.S sale in 1997. Its first indictated use was as that of an osteoporosis treatment, owing to its ability to increase bone density. In 2007, the FDA expanded the indicated uses for the drug to include reducing the risk of invasive breast cancer in two populations. Today, the drug is a fairly popular drug in clinical medicine, and is approved for sale in over 50 countries. The most common brand name is Evista and dominates the global market.

There is some evidence that raloxifene hydrochloride may actually be more effective for the treatment of gynecomastia than is the drug nolvadex. In one study it was shown that while both tamoxifen citrate and raloxifene hydrochloride had relatively similar rates of success in reducing the size of gynecomastia in pubertal males, raloxifene hydrochloride had a higher rate of effectively reducing the size to noticeably significant smaller levels. Obviously when one is faced with the option of choosing which compound to use when a treatment for gynecomastia is needed this should indicate that raloxifene hydrochloride may indeed be the more effective choice. A second benefit of raloxifene hydrochloride is that it seemingly has the ability to lower low-density lipoprotein and total cholesterol levels in users. The drug is able to accomplish this by way of its agonist actions on lipid metabolism. However it appears that these effects may be marginal at best and may not be all that significant in terms of the health of the user. However in a minority of studies there is some evidence that improvements in cholesterol levels can be quite significant and should improve the health of the user. It appears that more research needs to be conducted in this area before any proclamations can be made about the effect of this drug on the cardiovascular health of users. Combine this with the fact that anabolic steroid use will have a significant impact on cholesterol levels and any attempt at reaching a conclusion about this issue for bodybuilders and strength athletes is even further away. For now the use of this drug for cholesterol lowering effects is questionable. A far less contentious issue is the ability of raloxifene hydrochloride to raise the levels of follicle stimulating hormone, luteinizing hormone and testosterone levels in male users. Like tamoxifen citrate, clomiphine citrate and toremifene citrate raloxifene hydrochloride has been demonstrated to help raise the levels of these hormones when they are suppressed. The research regarding the ability of raloxifene hydrochloride to raise testosterone levels in males is limited when compared to both clomiphine citrate and tamoxifen citrate so it is difficult to compare their effects in this regard.

When used by athletes and bodybuilders to mitigate the side effects of anabolic/androgenic steroids, the most common dosage is 30-60mg per day during the course of the steroid cycle.

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Aromasin (Exemestane) anti-estrogen profiles

Aromasin (Exemestane)

6-Methylenandrosta-1,4-diene-3,17-dione; 10,13-Dimethyl-6-methylidene-7,8,9,10,11,12,13,14,15,16-decahydrocyclopenta[a]phenanthrene-
Molecular Formula C20H24O2
Molecular Weight 296.40
CAS Registry Number 107868-30-4
Melting point 155.13 ºC

Exemestane is a steroidal suicide aromatase inhibitor. It is very similar in structure and action to formestane, although it is significantly more potent in comparison. As a class of drugs, aromatase inhibitors offer an anti estrogenic effect by blocking the enzyme responsible for synthesizing estrogens. Exemestane is approved by the FDA for the treatment of breast cancer in women, specifically in post menopausal patients whose cancer has progressed following therapy with tamoxifen (nolvadex). Male bodybuilders and athletes often use the drug for non approved purposes, namely to counter the estrogenic side effects associated with the use of aromatizable anabolic/androgenic steroids. This may include gynecomastia, fat buildup, and water retention. Exemestane is one of the most potent aromatase inhibitors presently available. The most commonly cited date reports a lowering of estrogen around 85% on average in clinical studies with women. Exemestane was developed by Pharmacia & Upjohn, which gained FDA approval for sale of the drug in late 1999. They introduced it under the Aromasin brand name in early 2000. Although the drug proved to be effective in doses as low as 2.5mg per day in some patients, the company developed it in a standard and near universally effective dosage of 25mg per tablet. The company has since introduced the drug to many other nations under the same trade name of Aromasin.

Aromasin, as it is most commonly called, is a very potent AI which works by blocking the aromatase enzyme in the body. This drug was originally developed to help fight breast cancer in women by reducing estrogen which some believe to aid in cancer cell growth. While not quite as strong as Letrozole, aromasin is considerably stronger than Anastrozole. Studies done with this substance typically show around an 85% reduction in estrogen levels in the body. This can be very useful to bodybuilders who are using aromatizing compounds such as testosterone. Typically, one will begin the use of aromasin the same day they begin their cycle. It is also important to note that Aromasin has shown to be very effective at increasing testosterone and IGF levels in the body. Because of this, this drug is also very useful during PCT regime when one is trying to restore natural testosterone levels in order to avoid a post cycle "crash". It is important to keep doses of aromasin reasonable, as too much estrogen suppression can result in hindered muscle gains and loss of sex drive. One 25mg tablet a day should be sufficient for effectively keeping estrogen related sides out of the picture, or for effectively raising natural testosterone levels during PCT.

Exemestane reaches peak plasma concentrations within 2 hours following the oral administration of a 25 mg dose. The active life of the drug is between 24 and 30 hours. This is significant since it is quite shorter than for the non-steroidal inhibitors. A single oral dose of 25 milligrams of exemestane causes a relatively long-lasting reduction in plasma and urinary estrogen levels, with maximal suppression occurring approximately 2 to 3 days after dosing and persists for about 4 to 5 days.It has been shown that 25 milligrams of exemestane is basically just as effective as 50 milligrams at suppressing estrogen, raising testosterone levels, and levels of IGF. It is therefore unnecessary to go higher in doses than 25 milligrams per day. Due to the active life of the compound exemestane should be administered roughly once every twenty-four hours. Users often start the drug on the first or second week of steroid use and continue to take it throughout the cycle and for a few weeks afterwards in order to prevent any type of estrogen rebound.

Anastrozole anti-estrogen profiles

Anastrozole

Tetramethyl-5-(1H-1,2,4-triazol-1ylmethyl) 1,3-benzenediacetionitrile
Molecular Formula C17H19N5
Molecular Weight 293.37
CAS Registry Number 120511-73-1
Melting point
81-82 ºC

Although Arimidex does increase testosterone levels slightly in the body, it is more often used in conjunction with other steroids to lower estrogen in the body. Many anabolic steroids will convert, or aromatize, in the body into estrogen, which causes many of the unwanted side effects like bloating and acne. Arimidex is one of the best compounds to lower the aromatizing effect of steroids.


There are some concerns with using an aromatase inhibitor such as this during prolonged steroid treatment however. While it will effectively reduce estrogenic side effects, it will also block the beneficial properties of estrogen from becoming apparent (namely its effect on cholesterol values).
Studies have clearly shown that when an aromatase inhibitor is used in conjunction with a steroid such as testosterone, suppression of HDL (good) cholesterol becomes much more pronounced. Apparently estrogen plays a role in minimizing the negative impact of steroid use.
Since the estrogen receptor antagonist Nolvadex is shown not to display an anti-estrogenic effect on cholesterol values, it is certainly the preferred from of estrogen maintenance for those concerned with cardiovascular health.


Arimidex has another principle drawback, namely the great price of this drug. Tablets can easily sell for $10 each, becoming quite costly with regular use. Clearly the price of an ancillary drug can be much greater than the steroids themselves, a situation destined not to be popular with recreational bodybuilders. Competitors on the other hand are likely to welcome this item. It can ward off the side effects of strong androgen therapy much better than Nolvadex and/or Proviron, making heavy cycles much more comfortable. As the number of countries manufacturing this drug increases, we may be able to look forward to a reduction in price.

Privately compounded versions of “liquid Arimidex” have also been formulated “for research purposes” are also available. Generic tabs are also available and these two forms represent a very cost-effective alternative for buying the brand name drug.

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