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Effective dose: 20-40 mg / day orally
Average Street-price: $30 for 300 mg (30 tabs of 10)
Available Doses: 10,20,30 and 40 mg tabs
While practically similar compounds in structure, few people ever really consider Clomid and Nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while clomid is generally considered a fertility aid. In bodybuilding circles, from day one, clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.
But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because Nolva is clearly a more powerful anti-estrogen, and the people selling clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.
Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.
This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of Nolva or 100 mg/day of clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.
So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as clomid may actually have a slight negative influence. The reason being that Tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas clomid seems to decrease the responsiveness a bit1.
Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.
Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.
Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case Nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.
Stacking and Use:
If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above.
Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued.
For best results, it is best stacked with HCG (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. HCG use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that HCG itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that HCG possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks.
1 Vermeulen A., Comhaire F., Hormonal effects of an anti-estrogen, tamoxifen, in normal and oligospermic men, Fertil. Ster. 29 (1978) 320-27
2 Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9
HCG / Pregnyl
Pharmaceutical Name: Human Chorionic Gonadotrophin
Effective dose: 1500-7500 IU every 5-6 days
Average Street-price: $4-6 per 5000 IU
Available Doses: 100,125,250,500, 1000, 1500,2000,2500,3000,5000,10000,20000 International Units
Brands & Products:
Amsa Gonadotraphon LH (I) 125,250,1000,2000 or 5000 IU
Biomed Biogonadyl (PL) 500 or 2000 IU
Ferring Choragon (G) 1500 or 5000 IU
Forest Choron 10 (US) 1000 or 10000 IU
Hyrex Chorex (US) 5000 or 10000 IU
Leciva Praedyn (CZ) 1500 or 3000 IU
Leo Physex (DK,NO) 1500 or 3000 IU
Physex Leo (ES) 500,1500 or 5000 IU
Lepori HCG Lepori (ES) 500, 1000 or 2500 IU
Organon Gestyl (BG) 1000 IU
G. Chor. "Endo" (FR) 500,1500 or 5000 IU
Predalon (G) 500 or 5000 IU
Pregnyl (US) 10000 IU
Pregnyl (BG) 100 IU
Pregnyl (A,B,CH,GB,BG,GR,I, NL,PL,S,FI,YU,CZ,NO,HU) 5000 IU
Paines & Byrne Gonadatrophon (GB) 500,1000 or 500 IU
Pharmed HCG (US) 5000 or 10000 IU
Roberts Gonic (US) 1000 IU
Roussel Gonadotropyl-C (MX/FR) 5000 IU
Sanfer Gonakor (MX) 2500 IU
Schering Primogonyl (CH,G,CZ) 250 or 500 IU
Primogonyl (G,CH,YU,CZ) 5000 IU
Serono Profasi (CH,B,MX,S,FI,GB,NO,NL) 10000 IU
Profasi (CH,GB,MX,HU,FR) 500 IU
Profasi (HU,NL,MX) 1000 IU
Profasi (FR) 1500 IU
Profasi (A,B,CH,DK,HU,GB, GR,S,FR,NL,NO,MX) 2000 or 5000 IU
Pregnesin (G,CZ) 250,500,1000,2500 or 5000 IU
Steris HCG (US) 5000 or 10000 IU
Wyeth-Ayerst APL (US, SA) 5000,10000 or 20000 IU
Human chorionic gonadotrophin is a strange hormone. Its only found in the placenta of pregnant women. For women it has fairly little use if any however, but to the male athlete it has one interesting property. It can mimic the action of luteinizing hormone (LH) in the body. LH is a pituitary hormone that is released and signals the manufacture of testosterone in the testicles. The sex hormones in the body work via a negative feedback system, where too much sex hormone (like anabolic androgenic steroids and estrogens) causes a signal to the brain to stop the release of LH. During long duration cycles, if natural test stays suppressed for considerable time, a male user will begin to note an atrophy in his testicles, meaning they will visibly shrink purely out of disuse. By administering an LH-mimicking agent, one can bring back the function of the testicles and let them regain their size. This is the main use of HCG.
Since it forms testosterone in the body to some extent, it can impart certain performance enhancing properties, but usually these are not major. The side-effects accompanied with HCG use (usually androgenic such as extreme acne), its low rate of effect, the cost compared to more effective steroids and so on will mostly keep athletes from using it for that purpose. Moreover it can be tested for in athletic competitions, so most will stay clear of it. But to the steroid user HCG is an almost essential part of a cycle. Because of its effect on bringing testicle size back it can promote the return of natural testosterone, since the first natural signals can immediately deliver a higher yield of testosterone in the body. And getting natural testosterone back online after a cycle is crucial, especially if you intend to keep most of your hard-earned gains. Without adequate natural endocrine response you will not be able to maintain a mass that was higher than before.
The downside is that HCG too is suppressive of natural testosterone. Because it takes the place of LH. LH is not the first step in the chain of command, instead its manufactured in the pituitary under the response of Gonadotropin releasing hormone (GnRH) which is secreted from the hypothalamus. And since an LH mimicking agent is supplied exogenously, the negative feedback signal to the hypothalamus will still tell it to stop making GnRH, and so no natural LH is produced. This is why the product is always used in conjunction with a potent estrogen receptor antagonist like clomid or Nolvadex. When the androgen level in the body has dropped, these antagonists will lower estrogenic response creating a steroid deficit that signals the Hypothalamus to start making GnRH. When it does, after HCG therapy, testicle size is up again and shortly thereafter natural testosterone manufacture should return to normal. But therefore its crucial that users note that though HCG is essential after long cycles, it shouldn't be used without clomid or Nolvadex AND HCG should be discontinued at least two weeks before coming off Clomid or Nolvadex or else it will suppress natural testosterone itself.
Also important to take into account : using HCG for too long a period of time or in doses that are excessively high, can desensitize the testicles to the effect of LH and would put your right back where you started from. Basically that would mean you spent money to no avail. In terms of side-effects one should expect some androgenic signs such as acne and there is a risk for hair loss or prostate hypertrophy, but in most cases this compound will be used for 3-4 weeks, so these should not manifest themselves to any serious degree. There will also be some estrogen build-up, but since the user HAS to be on clomid or Nolvadex, this should not become apparent either. Next to this, HCG being a fertility drug, one should be aware that increased blood pressure and blood clotting can occur. HCG is clinically used to make women ovulate, or to invoke birth in pregnant women.
Stacking and Use:
You would normally opt to use HCG after you've done a long cycle, usually 8 weeks or more. Note that almost all proper cycles are 8 weeks or more in length, its just that some beginners have a phobia of needles and opt to waste their time with an all oral stack first, in which case the cycle wouldn't be longer than 6-7 weeks. In these cases too HCG can have a use, but most of the time testicular atrophy will not have progressed to such a stage that it is an absolute necessity. In any case, you should run it about 3 weeks, totaling about 4 shots. One every 5-6 days. Start off with one shot of 3000 IU somewhere in the last week of your stack, then another 3000 5 days later, then drop to 1500 5 days later and a last shot of 1500 6 days after that. Sometime after the second or third shot, therapy with Nolvadex or clomid should be commenced and continued for 4-5 weeks. How to do this, I refer you to the Nolva/clomid profile.
In any case, I'll repeat it again, since it is important. HCG IS and always will be an important part of post-cycle recovery, but it should never be run too long or at too high a dose and should always be accompanied by the use of either Clomid or Nolvadex. The use of Clomid or Nolvadex should also be continued at least 2 weeks after HCG is discontinued to avoid the HCG causing problems.
How To Properly Cycle Off Steroids While Keeping Your Gains.
By: Jonathan Deprospo
The biggest pit fall many people encounter when using a cycle of steroids is the course of action taken once the cycle is complete. Many people will start a cycle without fully researching the topic of steroid cycling for bodybuilders, and the intricate details seem to get left behind.
Bodybuilders and weight lifting enthusiasts in gyms around the world will hop on a cycle of steroids without even knowing what the word Anti-estrogen means (although more and more people are starting to see the merit of using these drugs) and when the side effects hit, all the blame goes to the drugs that they took and not the fact that they poorly planed their cycle.
Every cycle you embark on should be properly planed for the goals that you wish to achieve, and you should also have the necessary drugs for post cycle and also during cycle for estrogen control.
This will make a difference like night and day compared to using steroids without any auxiliary drugs.
What Are Your Goals?
Employing an anti-estrogen during your cycle to control estrogen related water retention, and gynecomastia is a must, and I feel people shouldn't embark on a course of anabolic/androgenic steroids without using a drug for this purpose.
When finishing your cycle an anti-estrogen should continue to be used during your recovery phase because of the fact that your testosterone levels will be very low at this point, and you will have an elevated level of estrogen hormone in your system.
By using an anti-estrogen during this time, you will be able to keep your estrogen levels to a minimum so you will avoid post cycle side effects such as water retention, gynecomastia, depression, sickness, and acne.
At the same time you must employ a drug to help raise your testosterone levels to a normal level as quickly as possible. By using a drug for this purpose you will be able to retain the majority of your gains made on your cycle when the cycle is complete, and avoid the loss of gains from coming off AAS.
In this article I will outline the different drugs used for the two purposes mentioned above. The first is Anti-Estrogens rated from the most effective, to the least effective. I will then discuss the two drugs used to raise testosterone levels back to normal. And finally I will outline a few different post cycle protocols that will help you minimize side effects from your cycle, and also help you to keep your gains made while on ASS while avoiding the dreaded "post cycle crash."
(from most effective to least effective)
Arimidex or Femara
Arimidex is an anti-aromatize drug used while on anabolic/androgenic steroids to help prevent water retention (edema) and Gynecomastia (bitch tits) build up that is a common side effect of using drugs such as synthetic testosterone and androgenic drugs. Arimidex's mechanism of action is by blocking the aromatize enzyme, which will block the production of the hormone estrogen.
This drug is also used for the weeks after your cycle while on a post cycle therapy regimen for the same purpose for using it while on the AAS. Arimidex has a half-life of 3 days, so many will administer it everyday (ED) to every other day (EOD). If it is being used everyday most bodybuilders will use .25mg to 1mg, and if used EOD .5mg to 1mg is the recommended dose. This will vary if you are using other anti-estrogens while using the Arimidex, and also the amount you are willing to use due to the cost of the drug.
Femara has very similar characteristics as Arimidex, but some believe that it is more effective at estrogen control. Most users report no water retention what so ever while using this drug, and in some studies it is shown to slightly raise IGF-1 levels, unlike a drug like Nolvadex, which has been shown to decrease them slightly. The normal dose for Femara is 2.5mg ED to every third day during cycle and also during post cycle recovery periods.
Novadex is usually employed during cycles of Anabolic/Androgenic steroid cycles due to the fact that the hormone estrogen will become elevated from the conversion of testosterone to estrogen. When this problem arises many male bodybuilders will use Nolvadex to combat feminization symptoms such as gynecomastia, increased fat deposition, and also high levels of water retention.
For the most part though, Nolvadex is used to prevent gynecomastia build up. This is because Nolvadex acts on the estrogen receptors of the effected body tissue, so in turn it will prevent the bonding on the estrogen hormone to the receptor on the tissue.
Unlike Arimidex and Femara, Nolvadex does not act as an anti-aromatize drug, but rather acts as an estrogen antagonist. This drug will not prevent the conversion of testosterone to estrogen. It will only fight it at the receptor level. This right here goes to show why drugs like Arimidex and Femara are far more superior drugs to use during a cycle than Nolvadex.
Nolvadex is a very effective drug to use when discontinuing your steroid cycle due to the fact that it will help reduce the side effects from the elevated levels of estrogen in your body. When you come of steroids the relationship between the levels of testosterone compared to estrogen become "out of whack" so to speak.
Since you have discontinued the steroids your testosterone levels will become severely reduced, which in turn will raise your estrogen levels to become the dominant hormone in your system. This is a very good time to use a drug such as Nolvadex to combat this problem.
Doses of Nolvadex should range from 20mg.-40mg. Per day. If you are using it post cycle without a drug such as Arimidex I would suggest using 40mg. ED to EOD. If you are using it during your cycle for gynecomastia prevention 20mg. ED should suffice. Prices of this drug are usually fairly reasonable compared to Arimidex or Femara, but I still feel Nolvadex doesn't compare to drugs such as Arimidex or Femara.
Proviron is a strange drug due to the fact that it has many different uses in the bodybuilding world. In this article the main feature I will discuss is its effective properties as an anti-estrogen during a steroid cycle.
Proviron is used during a cycle of steroids because it acts as an anti-estrogen in that due to the drug's unique structure it has a higher affinity to the aromatize enzyme than testosterone, but at the same time it does not convert to estrogen.
This in turn means that if you administer Proviron with testosterone, Proviron will bind to the aromatize enzyme very strongly, which will not allow the testosterone to convert to estrogen and bind with the receptor. This will prevent the usual estrogen build up seen with testosterone like compounds.
Due to Proviron's mechanism of action, using steroids and employing Proviron will prevent the estrogenic side effects and water retention seen while using some of the more androgenic steroids. It has also been noted that Proviron will increase levels of testosterone during a cycle. The mechanism of action for this effect is difficult to explain, but it allows for more of the synthetic testosterone employed during your cycle to be used more efficiently, and not be converted to the hormone estrogen.
Proviron is seen to be effective at dosages from 25mg all the way up to 150mg. For the reasons discussed in this article 25mg to 50mg ED is sufficient for its purpose. Another aspect worth mentioning is that Proviron should not be used post cycle. Proviron should only be used during a cycle because it is an androgen, and when coming of Proviron you could experience some negative effects with your body's natural testosterone levels.
The cost of this drug is very reasonable, so it could be a good addition to your next cycle to prevent estrogen build up.
Clomid is using in the bodybuilding community as a testosterone stimulant. This drug is used when you end a cycle of steroids to help bring your natural levels of testosterone back up to normal. Clomid's mechanism of action occurs through the hypothalamohypophysial testicular axis (HPTA).
Clomid is used to stimulate the hypophysis to release more gonadotropin so that a faster and higher release of FSH (follicle stimulating hormone) and LH (luteinizing hormone) occurs. By doing this, the result is an elevated endogenous (body's own) testosterone level. Needless to say this is a very important aspect when coming off a cycle of steroids and should always be employed to bring your testosterone levels back up to normal.
Clomid is usually used once you finish a cycle of steroids, and it is employed for the 2-3 weeks following it. The recommended dose of Clomid is 50mg to 100mg ED, although some will opt to do a high front load (200mg+) on the first day and continue to taper down as the days go on.
HCG is a unique drug used by male bodybuilders because of the fact that it can mimic the hormone LH (luteninizing hormone) in the body. LH is the hormone that is responsible for making testosterone in the testicles. Bodybuilders use HCG during long cycles due to the fact that after sometime on testosterone mimicking hormones the testicles will stop producing testosterone due to the use of a synthetic testosterone-mimicking drug.
HCG has significant applications to the steroid using bodybuilder due to the fact that it can help bring testosterone levels back to normal levels. This is where many will opt to employ HCG for the last 3-4 weeks of a steroid cycle.
A very important fact to note is that while using HCG you must use a drug such as Nolvadex or Clomid, and one of these (preferably both) should be used for the 2-3 weeks after using HCG, or you could end up where you started with low testosterone levels once again.
Another important aspect to note is that HCG should not be used for more than a 3-4 week period and it should also not be used at very high doses, because this could desensitize the testicles to LH, and could leave you back in a bad position.
Typically HCG is used for the 3-4 weeks towards the end of a long cycle of steroids to raise natural testosterone levels in the testicles. HCG should be administered every 5 days to every 3 days (if you opt to use it more frequently doses should be adjusted accordingly) with the first shot in the last week of your cycle.
If you opt to go every five days the first two shots should be around 3000 IU, then the second two should be 1500 IU. It would be very wise to use Nolvadex during this time, and Clomid should be using following the HCG for 2-3 weeks along with the Nolvadex.
Post Cycle Recovery Design
Moderate length Cycle
For a moderate length steroid cycle (6-8 weeks) your post cycle recovery plan should last for two to three weeks due to the length of you're "on" time. Every post cycle regimen should include an Anti-estrogen drug (Femara, Arimidex, or Nolvadex) and Clomid, a drug like HCG is not necessary for a cycle of this length.
Since I recommend an anti-estrogen throughout your cycle you should already be using one to begin with, if you want during the post cycle time you can increase the dose of this slightly for a better effect. Once the steroids have cleared from your system (depends on the esters used, but you should try to get everything cleared around the same day) Clomid therapy will begin.
Now, there are many different ways of using Clomid during Post cycle recovery, and I will outline three that I feel are very effective, and do not result in significant differences in recovery between the three.
The first is the frontload theory (this is used if you have been using moderately high doses during your cycle), which starts the first day with 200mg+ on day one, down to 150mg, to 100mg for the rest of the first week, then down to 50mg for the next two weeks.
The second starts with 50mg ED the first week, 100mg ED the second, back down to 50mg ED for the third (this is for a lighter dose cycle).
The last is to use 100mg ED for two weeks post cycle. All of these work very well in there own right, and you will have to find out which one works best for your body type and also the drugs you used during the cycle.
(4 months or more)
For a long cycle of 12 weeks or more your post cycle recovery plan should first start out with HCG. Your HCG therapy should begin during the last week of your cycle before you come off. Also, needless to say during this time you should be using an anti-estrogen to combat estrogenic side effects. HCG should be administered in four shots starting the last week of your cycle continued on to the two weeks following.
So your post cycle HCG should look like this: 3000 IU on day one, another 3000 IU 5 days later, 1500 IU 5 days later, and following up with another 1500 IU 5-7 days after that, equaling out to three weeks total.
After finishing the HCG therapy Clomid should be administered along with the anti-estrogen for two to three weeks after the HCG making your post cycle therapy a total of four to five weeks. For the Clomid therapy I believe that 100mg ED for the two to three weeks should be sufficient, although if you want you could use one of the protocols listed in the moderate length cycle section.
This article gives a very complete overview of how to construct a very effective post cycle regimen. Many people skip out on anti-estrogens due to cost and also availability, and then complain later about the steroids causing side effects such as water retention, loss of sex drive, gyno, and acne.
No cycle should start with out having the proper anti-estrogens on hand, and you should also have you post cycle drugs before you start your cycle in case for some reason you can't get them once you come off.
This happens to many people and then they are kicking themselves in the rear when the side effects hit. I hoped I provided valuable information with this article that can help people have more effective cycles while minimizing any of the side effects that are sometimes very common with steroid use.
A tutaj nieco inne podejscie:
By: Par Deus
O.K. You have been on an awesome 4-month cycle of Sustanon and Dianabol. Youâ€™ve gained a massive 20 lbs, and are extremely pleased with your results. You canâ€™t stop looking in the mirror. But there is a problem now starting to eat away at you. You are going to run out of steroids very soon (you know you need a break anyway), and your testicles are the size of raisins.
Your body is producing less testosterone than a 9-year-old girl, and you are scrambling to figure out what to do to avoid a nasty post-cycle crash that could potentially strip away some of your hard-earned muscle. The opinions on how to restore endogenous testosterone production post-cycle seem to be different everywhere you look.
What option is best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right post-cycle program can be quite confusing. In this article I would therefore like to discuss the role of anti-estrogens and HCG during this delicate window of time, while detailing an effective strategy for their use.
The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your bodyâ€™s natural production of testosterone. Too much testosterone and the furnace will shut off. Not enough, and the heat is turned up, to put it very simply. For the purposes of our discussion here we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response.
LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed.
Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.
Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks.
Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement started.
This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH.
Post-Cycle LH Levels
Post Cycle Testosterone Levels
Figure I. LH and Testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively). Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are already rebounding. From weeks 5 to 10 testosterone levels are at or very near baseline, to spite the substantial LH levels by this point. No significant increase in testosterone is noted until after the 10-week mark.
The Role Of Anti-Estrogens
It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher.
Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens.
Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.
So we now see, contrary to the dominating opinion of the times, that anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH.
Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources.
We want it to reach a level far above what our body, even when supported by anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while anti-estrogens are relegated to a supportive role at best.
Finalizing The Program
An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2), which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regularHCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly.
Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone.
This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of Clomid would typically be added (my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)).
Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.
Sample Post-cycle Plan:
Week 3: 5000IU HCG total + 20mg Nolvadex daily
Week 4: 5000IU HCG total + 20mg Nolvadex daily
Week 5: 2500IU HCG total + 20mg Nolvadex daily
Week 6: 20mg Nolvadex daily
Week 7: 20mg Nolvadex daily
Week 8: 20mg Nolvadex daily
I hope this article provided a well-needed new look at the mechanisms involved in post-cycle testosterone recovery. Indeed I believe it should debunk a commonly held belief these days, as we seen now that those advocating the sole use of Clomid post cycle are sorely missing the mark. The problem goes much deeper than just getting LH levels back.
In fact, we see that LH doesnâ€™t even need much help kicking back into gear, and a drug like Clomid will do very little to help this anyway in the absence of significant estrogen levels anyway. HCG is a drug with undeniable usefulness during the post-cycle window, and many bodybuilders have been much too quick to abandon it. It is truly fundamental to an effective recovery program, and would not consider any dose or combination of anti-estrogens or aromatase inhibitors capable of doing the job without it.
Nolvadex vs Clomid by WW (troche amatorskie podejście ale IMO b.sluszne):
I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.
Clomid and Nolvadex
I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.
Pituitary Sensitivity to GnRH
Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.
But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.
The Estrogen Clomid
The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".
Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.
To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.
Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.
Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.
Administration of the antiestrogen tamoxifen for one month to 12 patients with idiopathic oligozoospermia significantly increased the mean basal testosterone (T) level and the responses of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to constant luteinizing hormone releasing hormone (LHRH) infusion but did not significantly influence the mean oestradiol (E2) levels or the E2 over testosterone ratio. Mean sperm concentration and total sperm output increased by about 70% after a mean treatment period of 5.5 /- 0.4 months. No statistically significant difference was found between the two subgroups of patients treated with either the lower (5 or 10 mg once daily) or higher dose of tamoxifen (10 mg twice daily) with respect to basal or LHRH stimulated gonadotropin and testosterone response or the E2/T ratio and the effect on sperm density and total sperm output. In both subgroups the sperm motility and morphology remained unchanged. In conclusion higher doses of tamoxifen in this study prove not to be superior to lower doses in improving mean sperm density and total sperm output. The relative small percentage of patients achieving normalisation of only these sperm parameters pleads for further search for more effective selection of patients and other more effective treatment modalities in patients with idiopathic oligozoospermia.
Zreszta to nie jest tez nic nowego bo przy leczeniu oligospermi endokrynolodzy uzywali hcg i clomidu badz innego selektywnego antyestro od dlugiego czasu.
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