Nolva vs. Clomid for PCT

Nolva vs. Clomid for PCT
It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.


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.

The questions you will hear from athletes over and over is if they can get legal steroids clomid and nolvadex, is it possible?well I say yes you just have to look.
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.

References

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

How to Make Anabolic Steroids Orally-Active?

The subject of androgenic / anabolic steroids, and the different ways that have been found to make them orally active, has been tossed around lately on the internet mags. This is an interesting topic to the science minded out there, but beyond that, it also has potential utility to the prohormone supplements. The following is my take on the subject, including scientific references and conjecture on my part.
The problem with natural androgens
Testosterone is the primary androgen in the human, and is the golden standard by which all other steroids are compared. Unfortunately, testosterone has very poor activity when taken orally. This necessitates that testosterone be administered by extra-oral means such by injection, subcutaneous pellet implant, and transdermal gel or patch.
17alpha alkylated steroids
Scientists have developed several synthetic testosterone derivatives that have increased oral bioavailability. The first synthetic alteration that scientists utilized is known as 17 alpha alkylation. 17a alkylation involves the addition of an alkyl group (methyl or ethyl) to the alpha position of the 17 carbon of the steroid backbone. The alkylation at this position prevents the major route of androgen deactivaton – oxidation to a 17-keto steroid - from taking place. This allows a large part of the steroid to avoid liver first pass metabolic degradation. Examples of 17a alkylated steroids are methyltestosterone and Norethandrolone (Nilevar)

While 17a alkylation is a very effective means of rendering steroids orally active, it suffers from a serious drawback. These steroids are all to some extent toxic to the liver. Some are more toxic than others, but they all have been associated with this problem. Jaundice is not completely uncommon with the usage of this stuff, although this condition is generally confined to individuals who are predisposed to liver problems. Several cases of liver cancer have supposedly been linked to 17a alkylated steroids, however, nothing definitive has been established in this regard. On the other hand, it is somewhat common to observe increases in blood test indicators of liver stress such as BSP retention, and intrahepatic cholestasis (a condition where bile clogs up and stops flowing from the liver).
While the dangers of 17a alkylated steroids are not trivial, they still comprise some of the most potent anabolic agents available, and therefore their use continues. Most smart bodybuilders are aware of the potential toxicities of these steroids, and therefore they are judicious with their use of them.
Lipophilic steroid derivatives
After ingestion, most steroids make their way to the intestines where they are absorbed into the portal circulation. The portal circulation carries the steroid directly to the liver, which is the workhouse of destructive metabolism and inactivation of drugs. As a result, if the steroid is not protected in some way, very little will make it through the liver and into the rest of the body where it can do its magic.
In addition to the portal route, there is another route through which substances can be absorbed into the body from the intestine. If a substance is lipophilic (fat like) enough it will be absorbed in the same manner that dietary fat is. Dietary fat is incorportated into chylomicra, which are small fat globules composed of protein and fat. These chylomicra are absorbed into the lymphatic circulation, which by passes the liver. If you make a steroid lipophilic enough by altering its structure, then it too will incorportate into chylomicra and absorb into the lymphatic system. Once in the lymphatic system it can cross over into the general blood circulation, making it there without being subjected to the massive metabolic breakdown in the liver.
Scientists have found that by adding lipophilic side chains to steroids, they will to some extent be absorbed into the lymphatic system. If the side chain is linked on in such a way that it can hydrolyze (break apart) easily after being absorbed, the steroid is essentially rendered orally active. Two side chains that have been utilized to increase the oral bioavailability of steroids through increased lymphatic absorption are long chain alkyl ester groups, such as is seen with testosterone undecanoate (andriol), and enyl ether groups, such as is seen with quinbolone (anabolicum vaster).

The term "orally active" is of course a relative term. Lipophilically modified steroids are more orally active than the free parent steroids, however, they are no where near as active as the 17alpha-alkylated steroids. Testosterone undecanoate (TU) is probably the most commonly known lipophilically modified androgen, and it is not considered a very potent compound (its recommended daily dosage is about 240mg). In fact, one study found the oral administration of testosterone undecanoate led only to an absolute testosterone bioavailability of 6.83 +/- 3.32%. That is very slight, especially considering the fact that in the same study they found the bioavailability of straight testosterone to be 3.56 +/- 2.45% (Eur J Drug Metab Pharmacokinet 1986 Apr-Jun;11(2):145-9). That means TU is just a little less than twice as orally active as free testosterone, which is unimpressive to say the least.
The other problem with lipophilic steroid preparations is the high variability in absorption from one person to another. In other words, one guy might absorb the stuff very well while the other guy might absorb very little. There is also high variation within individuals themselves, depending on their gastrointestinal condition when they take the stuff. In another study, ten post-menopausal women were given 40 mg of TU and their peak blood values were recorded. The values varied widely - more than ten fold (range: 5.8-64.0 nmol/L) - amongst the subjects (J Clin Endocrinol Metab 1998 Nov;83(11): 3920-4).
There is no specific data I can find on the bioavailabilty of enyl ether compounds, but since their mode of action is identical to long chain alkyl ester compounds like TU, it is a fair assumption that they too are not outstandingly high in oral bioavailability, or in consistency of absorption. What I do know is that the one and only enyl ether oral steroid on the market today (quinbolone) is generally regarded by european bodybuilders / athletes as too weak to even bother taking.
Ring A modified steroids
There is one more class of anabolic / androgenic steroids that are orally active. These have unique structural modifications in the steroid A ring. What these modifications do is help preserve the steroids 17beta hydroxyl group, and minimize oxidation to the inactive 17-keto form.
Androgens such as testosterone exist in the body in an equilibrium between their active 17beta hydroxyl form and the inactive 17-keto form.

Normally, the equilibrium lies pretty far to the right (formation of inactive 17 keto steroid), however some steroids have certain modifications made in the A ring that alter this equilibrium by shifting it heavily to the left (towards the formation of active 17beta hydroxyl steroid).
The most common A-ring modifications that shift the 17beta hydroxyl / 17-keto equilibrium to the left are methylation at the 1alpha position, and unsaturation (double bond) in the 1(2) position (Acta Endocr, 41, (1962) 494). Examples of orally active steroids that contain one or more these modifications include methenolone (Primobolan), mesterolone (Proviron), and 1-testosterone.

You probably have heard of mesterolone and methenolone, but it is doubtful you have ever heard of 1-testosterone. 1-testosterone is a very interesting compound, not just because it is orally active but also because it is very anabolic. It has been reported to be over 7 times as anabolic as testosterone in a study funded by the pharmaceutical giant Searle (J Org Chem, 27 (1962) 248). Furthermore, being a 5alpha reduced steroid, it should not aromatize to estrogens.

Nolva vs. Clomid for PCT

Nolva vs. Clomid for PCT
It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.


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.

The questions you will hear from athletes over and over is if they can get legal steroids clomid and nolvadex, is it possible?well I say yes you just have to look.
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.

References

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

How to Make Anabolic Steroids Orally-Active?

The subject of androgenic / anabolic steroids, and the different ways that have been found to make them orally active, has been tossed around lately on the internet mags. This is an interesting topic to the science minded out there, but beyond that, it also has potential utility to the prohormone supplements. The following is my take on the subject, including scientific references and conjecture on my part.
The problem with natural androgens
Testosterone is the primary androgen in the human, and is the golden standard by which all other steroids are compared. Unfortunately, testosterone has very poor activity when taken orally. This necessitates that testosterone be administered by extra-oral means such by injection, subcutaneous pellet implant, and transdermal gel or patch.
17alpha alkylated steroids
Scientists have developed several synthetic testosterone derivatives that have increased oral bioavailability. The first synthetic alteration that scientists utilized is known as 17 alpha alkylation. 17a alkylation involves the addition of an alkyl group (methyl or ethyl) to the alpha position of the 17 carbon of the steroid backbone. The alkylation at this position prevents the major route of androgen deactivaton – oxidation to a 17-keto steroid - from taking place. This allows a large part of the steroid to avoid liver first pass metabolic degradation. Examples of 17a alkylated steroids are methyltestosterone and Norethandrolone (Nilevar)

While 17a alkylation is a very effective means of rendering steroids orally active, it suffers from a serious drawback. These steroids are all to some extent toxic to the liver. Some are more toxic than others, but they all have been associated with this problem. Jaundice is not completely uncommon with the usage of this stuff, although this condition is generally confined to individuals who are predisposed to liver problems. Several cases of liver cancer have supposedly been linked to 17a alkylated steroids, however, nothing definitive has been established in this regard. On the other hand, it is somewhat common to observe increases in blood test indicators of liver stress such as BSP retention, and intrahepatic cholestasis (a condition where bile clogs up and stops flowing from the liver).
While the dangers of 17a alkylated steroids are not trivial, they still comprise some of the most potent anabolic agents available, and therefore their use continues. Most smart bodybuilders are aware of the potential toxicities of these steroids, and therefore they are judicious with their use of them.
Lipophilic steroid derivatives
After ingestion, most steroids make their way to the intestines where they are absorbed into the portal circulation. The portal circulation carries the steroid directly to the liver, which is the workhouse of destructive metabolism and inactivation of drugs. As a result, if the steroid is not protected in some way, very little will make it through the liver and into the rest of the body where it can do its magic.
In addition to the portal route, there is another route through which substances can be absorbed into the body from the intestine. If a substance is lipophilic (fat like) enough it will be absorbed in the same manner that dietary fat is. Dietary fat is incorportated into chylomicra, which are small fat globules composed of protein and fat. These chylomicra are absorbed into the lymphatic circulation, which by passes the liver. If you make a steroid lipophilic enough by altering its structure, then it too will incorportate into chylomicra and absorb into the lymphatic system. Once in the lymphatic system it can cross over into the general blood circulation, making it there without being subjected to the massive metabolic breakdown in the liver.
Scientists have found that by adding lipophilic side chains to steroids, they will to some extent be absorbed into the lymphatic system. If the side chain is linked on in such a way that it can hydrolyze (break apart) easily after being absorbed, the steroid is essentially rendered orally active. Two side chains that have been utilized to increase the oral bioavailability of steroids through increased lymphatic absorption are long chain alkyl ester groups, such as is seen with testosterone undecanoate (andriol), and enyl ether groups, such as is seen with quinbolone (anabolicum vaster).

The term "orally active" is of course a relative term. Lipophilically modified steroids are more orally active than the free parent steroids, however, they are no where near as active as the 17alpha-alkylated steroids. Testosterone undecanoate (TU) is probably the most commonly known lipophilically modified androgen, and it is not considered a very potent compound (its recommended daily dosage is about 240mg). In fact, one study found the oral administration of testosterone undecanoate led only to an absolute testosterone bioavailability of 6.83 +/- 3.32%. That is very slight, especially considering the fact that in the same study they found the bioavailability of straight testosterone to be 3.56 +/- 2.45% (Eur J Drug Metab Pharmacokinet 1986 Apr-Jun;11(2):145-9). That means TU is just a little less than twice as orally active as free testosterone, which is unimpressive to say the least.
The other problem with lipophilic steroid preparations is the high variability in absorption from one person to another. In other words, one guy might absorb the stuff very well while the other guy might absorb very little. There is also high variation within individuals themselves, depending on their gastrointestinal condition when they take the stuff. In another study, ten post-menopausal women were given 40 mg of TU and their peak blood values were recorded. The values varied widely - more than ten fold (range: 5.8-64.0 nmol/L) - amongst the subjects (J Clin Endocrinol Metab 1998 Nov;83(11): 3920-4).
There is no specific data I can find on the bioavailabilty of enyl ether compounds, but since their mode of action is identical to long chain alkyl ester compounds like TU, it is a fair assumption that they too are not outstandingly high in oral bioavailability, or in consistency of absorption. What I do know is that the one and only enyl ether oral steroid on the market today (quinbolone) is generally regarded by european bodybuilders / athletes as too weak to even bother taking.
Ring A modified steroids
There is one more class of anabolic / androgenic steroids that are orally active. These have unique structural modifications in the steroid A ring. What these modifications do is help preserve the steroids 17beta hydroxyl group, and minimize oxidation to the inactive 17-keto form.
Androgens such as testosterone exist in the body in an equilibrium between their active 17beta hydroxyl form and the inactive 17-keto form.

Normally, the equilibrium lies pretty far to the right (formation of inactive 17 keto steroid), however some steroids have certain modifications made in the A ring that alter this equilibrium by shifting it heavily to the left (towards the formation of active 17beta hydroxyl steroid).
The most common A-ring modifications that shift the 17beta hydroxyl / 17-keto equilibrium to the left are methylation at the 1alpha position, and unsaturation (double bond) in the 1(2) position (Acta Endocr, 41, (1962) 494). Examples of orally active steroids that contain one or more these modifications include methenolone (Primobolan), mesterolone (Proviron), and 1-testosterone.

You probably have heard of mesterolone and methenolone, but it is doubtful you have ever heard of 1-testosterone. 1-testosterone is a very interesting compound, not just because it is orally active but also because it is very anabolic. It has been reported to be over 7 times as anabolic as testosterone in a study funded by the pharmaceutical giant Searle (J Org Chem, 27 (1962) 248). Furthermore, being a 5alpha reduced steroid, it should not aromatize to estrogens.

Dan Duchaine - Interview with Hardcore Muscle

Dan Duchaine - Interview with Hardcore Muscle
HM: IGF-1 … Dan you seem to be standing back on this one. Colgan thinks it will bring on the age of the superfreak, while you have only spoken of its use in fat reduction. We know GH never panned out as incredible as everyone wanted it to. Do you want to make sure it is the real deal before you give it your stamp of approval? We keep hearing every imaginable scenario ranging from "the stuff is fantastic" to "didn't do anything for me." Do you have any opinions on how it is best used? It was reported to work a lot better with HGH in a study. Do you have any theories on how or what compounds (steroids, anticatabolics, insulin mimickers) could be used in a synergistic protocol for best results with IGF?
Dan: Well Colgan really calls it all the time, doesn't he? (laughs) Because he's always wrong - when Twinlabs changes their mind. Vanadyl sulfate is toxic but now that Twin is selling it, it's not toxic any more! But anyway, enough about Colgan. You know the thing is … I've never seen any real IGF-1. All the stuff I've seen pictures of and read about is the lab cell culture which is doctored not to bind on the carrier proteins. So it would probably be wonderful. You sent me a couple of reports and I read some others and if you look at the amounts they were using, it was quite high actually. Because of a four hour half-life they were using it twice a day, at a calculated dosage of 18mg a day. That's a very high amount. And these bodybuilders are taking 50 micrograms. And I find it hard to believe that 50 micrograms might do anything considering … God knows what they might have stacked on top of that. Maybe I'm wrong, but I think IGF will be terrific once it gets cheap enough to use. And you really want it to bind on the carrier proteins. You want it to last for the 4 hours. The cell culture stuff has a half life of 20 minutes, you don't want that. It's as short as growth hormone … you have to use the high amounts. Eventually someone will offer it either out of Russia or Australia. Of course you know, there were some side effects such as jaw pain and weird funky stuff. And it does work well with GH synergistically. They're just the opposite of each other. IGF-1 would lower your blood sugar and GH does the opposite. Together it stabilizes it. So the worst thing you could do is to use IGF-1 and insulin at the same time, you would conk out. I think it has a lot of potential. The only problem with all that stuff … if you remember back to the geriatrics using GH, when they stopped using GH, within a few weeks all the benefits ceased. At least when you stop steroids, it takes a year or more for all those gains to completely disappear. And I'm afraid for the high expense of IGF-1, that when you go off it, I wonder how long it will last.
HM: Yeah, a couple people told us they used it, and they said how awesome it worked and they weren't using anything else.
Dan: Over the phone…?
HM: Yeah.
Dan: Oh, yeah you know how that goes - "I'm 190 and ripped" and you see them in real life and it's a fat piece of shit. (We are all laughing hard.) It's like on the Internet, everybody is big and strong and ripped - on the computer and you meet them in real life and they are little dorks!
HM: (Laughing) Hypothetically, if you were going to use IGF-1, would you use it with…?
Dan: Oh yeah, steroids, GH, you would want to use it all for a synergistic effect. But definitely with growth hormone, all the studies say it's not only additive … put it this way … if you could get a ½ pound gain from IGF-1, and a ½ pound gain from growth hormone - if you put them together you wouldn't get just one pound, you would get much more, they are synergistic with the two added together … so yeah, go for it.
HM: Anything on the amounts of growth hormone?
Dan: Frankly, I think, nobody has used enough growth hormone because of the cost. The only guy I know of, the rumors were that (top WBF guy) was using like 12 IU's of GH a day. Every day. I don't know if that's true but that is pretty close to what someone should be using, for best results I would think. In the PDR, it's pretty cut and dry in what you should be using. The Genetech is not as efficient as the Lilly. It's microgram per kilogram - you can figure it out. It seems that a lot of bodybuilders are going low in dosage. In the early 80's it was worse, the recommended dosage was 2 IU's a week at $90 bucks a pop - like 2 IU's would even do anything. And people were wondering why it didn't work…
HM: Yeah, you might as well pound down some arginine. (joke)
Dan: I know the stunted growth children were taking it 3 times a week, but I don't know why only 3 times a week. Why not every day? It seems logical to me that it should be everyday. It's just like IGF-1 is supposed to be twice a day. And GH is even shorter acting so who knows.
HM: Maybe 4 times a day might do some good??!!
Dan: Yeah.
HM: Do you still feel Nolvadex can be put to good use - even though studies show it to decrease serum blood IGF levels in the body by 25%? Many have theorized that it lessens the muscle gains on a steroid cycle - do you agree?
Dan: Everyone said that even though they liked to use Nolvadex during dieting, they always found that during the off-season … they grew better without it. That was interesting. It might be the IGF-1. We somehow thought it was tied to estrogen but I don't know why. It depends. Past a certain age … like I'm 43 … if you measured my growth hormone and IGF-1 at middle age it is not very large. Would reducing it 25% make a major difference when it is so low to begin with? Probably not. It depends. As you get older, estrogen is more important to avoid for a lot of reasons, you know … prostate cancer, this and that. But when you're young, you could probably avoid Nolvadex. You know so many people have spent so much money on Nolvadex to combat gyno that they could have easily gotten the surgery for the same amount of money and cured the problem. Half of the people who go through puberty usually get some kind of gyno. They don't necessarily remember it, but it happens. And if you had gyno as an adolescent, you are going to get it if you use steroids - unless you totally avoid all the things that would cause it. And I don't know if Nolvadex will help those kind of people. I don't know if it is a real preventative. Close to two bucks a tab - get the surgery.
HM: How do you feel about Clomid's use as a prevention of gyno - overrated? Could a 2 on / 2 off program of Clomid be something in which gyno could be prevented in your opinion?
Dan: You know Teslac is an ideal antiestrogen but we could never find it out of the country, and we looked too. Clomid … inexpensive in Mexico but very expensive here. Everyone has done quite well with it for raising testosterone if you are young enough with 2 tabs a day. As far as an … they never approved it as an antiestrogen because it was more toxic than Nolvadex. Most people who use Clomid, they are not using it all year long. The problem is everyone's using so much testosterone - not a little but a lot! Back in the 80's we thought there was some kind of precision to anabolic use but now it is not quality but quantity…
HM: Have you had a chance to look at the other growth factors (EGF, fibroblast growth factor, nerve growth factor, TGF, etc.)… If so, do you feel any or all of these are interesting on a muscle-building standpoint?
Dan: Oh sure! There has been some research that the epidermal growth factor has been effective … but all the G.F.'s have been marketed at such a high price that people are unable to use high dosages. But who knows what's going to happen when prices come down and people are on some higher dosages. At the higher dosages, who knows what will be the outcome.
HM: Have you heard or have any insight on the new fat hormone drug in development?
Dan: Leptin … a few years ago we were talking about brown fat and having the beta 3 receptors and I believe they figured out that leptin is one of the naturally occurring beta 3 agonists in the body. The interesting thing about beta 3 receptors is that there's not many in the body, you got many more beta 2 receptors in the muscle. The beta 3's are only in small areas. However the nice thing about leptin is you don't need a lot and unlike clenbuterol, you don't down regulate the receptors. So for bodybuilding, it might be pretty good. However, for most of the obese people who think they are going to need it, some research has shown that they (obese) have genetically damaged beta 3 receptors that don't accept it. And many obese people have very high leptin levels already. The body is trying to compensate so it's not going to help them much. But it will be good for athletes because - clenbuterol is good but it only lasts 2-3 weeks at a time unless you jack up the dosage sky-high. As I mentioned on an audiotape a while ago, there is another thermogenic compound that I'll probably introduce at the end of the year. Even though I promised January 1. It is much more thermogenic than clenbuterol and doesn't even involve those receptors at all. It is much better and cheaper. More dangerous though because if you take too much you don't get sick … you die! Because you raise your body temp over 105 degrees and your cooked brain turns into poached eggs. So I have been hesitant introducing it or writing about it without some safeguards.

HM: To be blatantly honest with you, Dan, we have seen you come full circle on your diet theories. In your first book you recommended eating a lot and often. Now it seems you are approaching a nutrient density theory on diet. Low calories - high nutrients. Correct us if we are wrong. Even though nutrient density looks good on paper and looks like it will build the muscle desired, how come the guys (natural and unnatural) who really push the calories, really seem to be the ones putting on the greatest amount of muscle (and of course, extra bodyfat too)? i.e. … Yates, Sombaty versus Ray, Wheeler, etc. … Do you feel there is any possibility that the body can speed up with a more efficient anabolic effect with abundant calories - just as the metabolism slows down somewhat at deprivation of food? Couldn't the body adapt somewhat to a tremendous muscle building overload effect with food if a huge amount of demand (brutal workouts) is there?
Dan: Well … I don't think Yates and Sombaty get that fat actually. I must admit when I started out I wasn't the smartest guy in the world back then. I just had a knack with the words back in the early 80's. And I'm sure we were wrong on a lot of things. The thing is … there are a few individuals that can get up to 15-20% bodyfat, put on a lot of muscle and then be able to take it off. I have no problem getting that fat in off-season if they can prove to me they can get in shape. Obviously, like Rory Leidermeyer, he never got it right - he always fucked up. And most people who get that fat (15-20%) have trouble getting back down and even if they do, their vascularity and skin taughtness suffers.
HM: Do you feel it is a compromise though, not taking in enough food, with trying to maximize muscle mass?
Dan: You should always eat as much food as you can, but I think some people should spend the thirty bucks on calipers and keep the threshold of bodyfat at 12% or lower. Fifteen percent of bodyfat with a guy with a lot of muscle … he looks pretty fat. That's a bodybuilder who really is a powerlifter with a gut. Twelve percent isn't too sloppy and you can come down and up in bodyweight with some ease. But there are some people that can pull it off, but rarely have seen anyone going into a contest not fuck up on the way down.
HM: If you could pull it off, and eat a lot more food in the off-season, do you feel that you could gain more mass like that?
Dan: Sure, sure, but the secret is to keep it when you diet it off. First of let me say this. People lie. Vic Richards does not eat 15,000 calories. The guy pretty much can't count, he's so stupid. The guy wouldn't be able to count up the boxes with a calculator if the boxes were in front of him so I doubt 15,000. Very few people can hit 7,000. Strydom hit 7,000 but he had a lot of support to do that. People think if you eat so many calories you must be hotter. That's not true. An inch of fat all around the body will keep the heat in. If you have thin skin you are radiating heat out into the room so you can get away with taking in more calories.
HM: But let's say you have two twins. One of the twins says I'm going to get as big as I can while the other twin wants to build muscle but keep lean. Do you think that the guy who is taking in the gross amount of calories to build big time muscle (when they measure him in a water tank) will have a lot more muscle than the twin who tried to keep his bodyfat to a minimum?
Dan: Yes. Yes, but when they both come down to 6% bodyfat it will be very close because of the dieting. I think the high calorie guy will have a slight advantage in muscle mass but what is his skin and vascularity going to be like? But I must tell you, most bodybuilders I know eat more than 3,000 unless they lie around all day. Even I eat close to 3,000 but I … well I ride my bike quite a bit now. Most of those pros, of course, hold water but a lot of that fat is held under their abdominal wall in their viscera. That's not increase size of the gut from GH but a combination of high carbs, high insulin and high testosterone. All that fat in there is very sensitive to androgens especially DHT.
HM: Do you think they can ever get rid of that? The visceral fat?
Dan: They would lose a lot of muscle. Visceral fat is like the last fat to come off the body. Back in the old days when they weren't using a lot of androgens, you didn't have that. But now with everyone using so much testosterone, that gut is all over the place now. Pros, amateurs … you know.
HM: Wouldn't clenbuterol be at its most useful in these high density / calorie diets? Have you ever experimented with a clen / volume food intake protocol?
Dan: That's kind of like pointless, because many of these top pros use clen all year round unless they run out of it. And they are using 10-15 tablets a day. The problem is that it works 2 weeks and that's it. If you cycle it 2 weeks on and then three weeks off then … yeah it could work well. You could be precise about it but you'll never do it. (Dan was speaking of the thermometer method each morning as he has described in past articles.) It's so nice to eat so much shit on clen that people just don't get off it.
***
HM: You have spoken of a high fat diet. Is this different somewhat than DiPasquales'? If so, what are your basic recommendations?
Dan: First off, high fat diets have been around for quite awhile. I mean before Zumpano, there was the Atkins diet which was mostly low carbs all the time, which is not the healthiest thing in the world. Especially for athletes because it is too catabolic, over time. Both DiPasquales' and mine are based on the 7 day (5 on, 2 off) plan. I'm a little more precise. He doesn't care to get into ketosis, blood sugar, ketones in the urine and I do. Ketones are fractured fats and they are not as efficient as regular fats so you need more grams for the energy. Of course, it is a nice diet that he has done because it is just a rip-off of our stuff from the early 80's.
HM: He seems really vague about it.
Dan: The problem is I used that diet for a long time in the early 80's and most of the guys in prison were on it. You have to really do it yourself. He doesn't seem to have a lot of people on a one-to-one basis to really get the feedback. I doubt he has done it himself for a prolonged amount of time. He's armchair about it. People rebel against it and don't want to follow it. But you have to expect that.
HM: On your 33/33/33 diet are there any important do's and don'ts? Do you feel that the above diet is more beneficial dieting or can it be used ideally for muscle building too?
Dan: About 25% of the people in the U.S. wouldn't need that diet. They have really great insulin sensitivity. These people process carbs well and don't give a shit about aerobics and that would be fine. There are another 25% that are quite lousy at processing carbs like myself. And then there are about 50% that are somewhere in the middle. There is no such thing as an essential carbohydrate. There are essential amino acids, essential minerals / vitamins. There are essential fatty acids. There is no such thing as essential carbs. Protein can be turned into fat. Protein can turn into glucose. Past a certain point on many people, much of the protein and carbs that you eat are turned into fat right in the body - right in the liver and you have no control over it - and it is only one kind of fat. Saturated fat. Saturated fat really lowers insulin sensitivity. So if you just accept that your body is going to have some kind of fat in there, it is better to control it yourself than let the body do it.
***
HM: I have heard of some people still trying to crush up those Anadrol tablets and inject them.
Dan: Yeah, I remember one 50 mg shot injected seemed to feel like 3 orals. Hey, have you guys seen some of these guys with the instant calves? I talked to Nadler about that because some of these guys are way too poor for implants. I asked, could you do collagen there and he said, "Yeah, but it's 250 dollars a cc." But you can easily inject saline water in the muscle and it will swell up for a few days. You could do that for calves for a contest and it's a lot cheaper than Esiclene. It would swell up much better.
HM: Some people get nerve damage from …
Dan: Well, Nadler showed me step-by-step instructions on how to put silicone in your calves. Just long small amounts in your calves, not large amounts, and your muscle will encapsulate it. And you can keep building it up and building it up. You could do biceps too.
HM: How do you put the silicone in though?
Dan: A needle, but of course it is not legal to do it in this country. But you could easily do it in Tijuana.
HM: Could be dangerous with the silicone though - like it is with breast implants.
Dan: That's a little different; you're only using small amounts. When they originally did silicone in the 70's before they put it in the sac, they put a massive amount in the gland. But if you used a small amount and let the body encapsulate it, you could do it. I would do it.
HM: Will it move with the muscle though?
Dan: Yes it will. That's the nice thing about it. Nadler can't do it in this country but I could ask him - if he went to Tijuana, would he do it there? You would have to go back and forth because you couldn't do it all at once.
HM: Could someone do it themselves?
Dan: (Dan got a good chuckle out of that one.) I could probably do it. I have no fear of needles. I'll ask him.

Primobolan® Tablets (methenolone acetate)

Primobolan® Tablets (methenolone acetate)


Quick overview:

Active Life: 4-6 hours
Drug Class: Anabolic/Androgenic Steroid (Oral)
Average Dose: Men 50-150 mg/day......Women 50-75 mg/day
Acne: Rare
Water Retention: No
High Blood Pressure: Rare
Liver Toxic: Very low and only in very high dosages
Aromatization: None
DHT Conversion: No
Decrease HPTA function: Low
Comments: Moderately Anabolic/Low Androgenic

This section refers to the oral Primobolan® preparation, which contains the drug methenolone acetate. It is very similar in action to the injectable Primobolan® Depot (methenolone enanthate), but obviously here the drug is designed for oral administration. At one time Schering was in fact also manufacturing an injectable methenolone acetate (Primobolan® acetate, out of manufacture since 1993), which proved to be very useful for pre-contest cutting purposes. This steroid is now gravely missed, as it was once a favorite among European competitors. Although we still have the acetate in oral form, it is a close, but not equal substitute (injection is a much more efficient form of delivery for this steroid).

Methenolone regardless of the ester is a very mild anabolic steroid. The androgenic activity of this compound is considerably low, as are its anabolic properties. One should not expect to achieve great gains in muscle mass with this drug. Instead, Primobolan® is utilized when the athlete has a specific need for a mild anabolic agent, most notably in cutting phases of training. It is also a drug of choice when side effects are a concern. A welcome factor is that Primobolan® is not c17 alpha alkylated as most oral steroid are. Due to the absence of such an alteration, this compound is one of the few commercially produced oral steroids that is not notably stressful to the liver. While liver enzymes values have been affected by this drug in some rare instances, actual damage due to use of this substance is not a documented problem. Unfortunately the 1 alkylation and 17-beta esterification of Primobolan® do not protect the compound very well during first pass however, so much of your initial dose will not make circulation. This is obviously why we need such high daily dose with the oral version of Primobolan®.

Primobolan® will also not aromatize, so estrogen related side effects are of no concern. This is very useful when leading up to a bodybuilding contest, as subcutaneous water retention (due to estrogen) can seriously lessen the look of hardness and definition to the muscles. Non-aromatizing steroids are therefore indispensable to the competitor, helping to bring about a tight, solid build the weeks leading up to a show. And of course without excess estrogen there is little chance of the athlete developing gynecomastia. Likewise there should never be a need for anti-estrogen use with this steroid. Primobolan® is also said to have a low impact on endogenous testosterone production. Although this may well be true in small clinical doses, it will not hold true for the bodybuilder. For example, in one study more than half of the patients receiving only 30-45 mg noted a suppression of gonadotropin levels of 15% to 65% a. This is a dose far less than most bodybuilders would use, and no doubt increasing it would only lead to worse suppression. One would therefore still need a testosterone stimulating drug like HCG or Clomid®/Nolvadex® when concluding a low-dose Primobolan® cycle, unless a deliberately small dose were being used.

It is also important to note that although the androgenic component of Primobolan® is low, side effects are still possible. One may therefore notice oily skin, acne and facial/body hair growth during treatment. Men with a predisposition for hair loss may also find it exacerbates this condition, and wish to avoid this item (nandrolone injectables are a much better choice). While always possible, side effects rarely reach a point where they interfere with the progress of cycle. Primobolan® is clearly one of the milder and safer oral steroids in production. Female athletes, older or more sensitive individuals and steroid beginners will no doubt find this a comfortable steroid to experiment with.

The dosage for men is somewhere in the range of 75-150mg daily. This can obviously be tedious (and costly) if one can only obtain the 5mg tablets from Mexico and S. America. A mild anabolic such as Primobolan® is often used in conjunction with other steroids for optimal effect, so some users find a slightly lower dose effective when stacking. During a dieting or cutting phase, thought to be its primary application, a non-aromatizing androgen like Halotestin® or trenbolone can be added for example. Such combinations would enhance the physique without water retention, and help bring out a harder and more defined look of muscularity. Non-aromatizing androgen/anabolic stacks like this are in fact very popular among competing bodybuilders. This compound is also occasionally used with more potent androgens during bulking phases of training. The addition of testosterone, Dianabol or Anadrol 50® would prove effective for instance, although the gains are likely to be accompanied by some level of smoothness due to the added estrogenic component.

Among women, Primobolan® is one of the most popular steroids in use. At a dosage of 50-75mg daily, virilization symptoms are extremely uncommon. One would of course not expect a tremendous amount of muscle mass with this drug, and instead should expect a slow and steady (quality) increase. Some women choose to further add-in other anabolics such as Winstrol® or oxandrolone, in an effort to increase the muscle building effectiveness of a cycle. While both of these compounds are quite tolerable to women, one must be sure not to use too high an accumulated dosage. Troublesome androgenic side effects are always a possibility with steroid use, even with very mild substances. Taken at too high a dosage, these weak anabolics can become a formidable danger to femininity. It would therefore be the best advice not to use the normal dosage range of both, but instead start with a much lower dosage of each steroid to compensate for the other. On the black market Primobolan® orals are popular, but still much less commonly found than the injectable. This is due to the higher cost effectiveness of the injectable, which uses the same active compound but with 100% bioavailability due to the form of administration.

Aromasin

Anabolic Steroids Profile Aromasin Exemestane Aromasin (Exemestane) is a steroidal suicide aromatase inhibitor, which means that it lowers estrogen production in the body by blocking the aromatase enzyme, the enzyme responsible for estrogen synthesization. (1)(2)(3) This stuff was developed to fight breast cancer in post-menopausal women, who need a particularly aggressive therapy, and for whom first line defenses such as SERMS (Tamoxifen) have not worked. This should be our first clue in inferring that this stuff is pretty strong, or at least stronger than some of the other compounds which are used to fight breast cancer. Aromasin and Side Effects Aromasin averages an 85% rate of estrogen suppression (4), so it´s clearly a very effective agent for bodybuilders and other athletes wanting to avoid estrogen related side effects such as gyno, acne, or water-retention brought on by aromatizing steroids. Specifically, Exemestane dose this by selectively inhibiting aromatase activity in a time-dependent and irreversible manner (hence the "suicidal" portion of it´s name, I guess).(7) As with most of the compounds in this class, it also causes a reasonable rise in testosterone levels (6), and as you may have guessed, this rise in testosterone means that Exemestane can also cause androgenic sides(8)(9)(10). As you can see from the chart below, exemestane is very effective at both lowering estrogen (estradiol) and raising testosterone: FIG. 1. Estrogen and androgen plasma levels after 10 d of daily exemestane (25 or 50 mg) in healthy young males (mean ± SD; n = 9-11). To convert to Systeme International units: estradiol, picomoles per liter (x3.671); estrone, picomoles per liter (x3.699); androstenedione, nanomoles per liter (*0.003492); and testosterone, nanomoles per liter (x0.03467). (13) So we can see that 25mgs is a very effective dose from that chart, right? As an added benefit, exemestane not only increases testosterone and lowers estrogen, but it also increases IGF levels (11).Additionally Worth noting is that Aromasin may possibly be less harsh on blood lipids (14)than some of the other (similar) compounds we use in the world of bodybuilding or athletics (other AI´s). It also has, at best no effect on IGF, and at worst could lower (13) it. AI´s are very tricky with regards to inconsistencies in IGF levels. Unfortunately, you need to take Exemestane for a week to reach steady blood plasma levels of it, and exemestane has a ½ life of 27 hours (12.). The ability of exemestane to lower estrogen levels by the aforementioned 85% makes it a very nice choice for use in any cycle where aromatizing steroids are used. In addition, since it´s not too harsh at all on blood lipid profiles, it´s a very good choice for longer cycles. It´s ability to raise both testosterone levels also seem to suggest that it would be a very nice addition to a Post-Cycle-Therapy (PCT).

HCG (Human Chorionic Gonadotropin)

HCG (Human Chorionic Gonadotropin)


Quick overview:


Active Life: 64 hours
Drug Class: Leutenizing Hormone (LH) - Gonadotropin
Average Dose: debatable
Acne: Yes
Water Retention: Yes
High Blood Pressure: Yes
Liver Toxic: No
Aromatization: No, but it will raise testosterone levels and increased aromatization may occur.

Chorionic gonadotropin is a hormone found in the female body during the early months of pregnancy (it is produced in the placenta). It is in fact the pregnancy indicator looked at by the over the counter pregnancy test kits, as due to its origin it is not found in the body at any other time. Blood levels of this hormone will become noticeable as early as seven days after ovulation. The level will rise evenly, reaching a peak at approximately two to three months into gestation. After this point, the hormone level will drop gradually until the point of birth. As a prescription drug, HCG offers us some interesting benefits. In the United States, we have the two popular brands, Pregnyl, made by Organon, and Profasi, made by Serono. These are FDA approved for the treatment of undescended testicles in young boys, hypogonadism (underproduction of testosterone) and as a fertility drug used to aid in inducing ovulation in women. When prepared as a medical item, this hormone comes from a human origin. Although there is often a fear of biological origin products, there is little research to be found regarding pathogen or sterility problems with HCG. The problems seen with human origin growth hormone are certainly not to be repeated with HCG, as this compound is obtained in a much different way.

While HCG offers the female no performance enhancing ability, it does prove very useful to the male steroid user. The obvious use of course being to stimulate the production of endogenous testosterone. The activity of HCG in the male body is due to its ability to mimic LH (luteinizing hormone), a pituitary hormone that stimulates the Leydig's cells in the testes to manufacture testosterone. Restoring endogenous testosterone production is a special concern at the end of each steroid cycle, a time when a subnormal androgen level (due to steroid induced suppression) could be very costly. The main concern is the action of cortisol, which in many ways is balanced out by the effect of androgens. Cortisol sends the opposite message to the muscles than testosterone, or to breakdown protein in the cell. Left unchecked (by an extremely low testosterone level) in the body, cortisol can quickly strip much of your new muscle mass away.

The main focus with HCG is to restore the normal ability of the testes to respond to endogenous luteinizing hormone. After a long period of inactivity, this ability may have been seriously reduced. In such a state testosterone levels may not reach a normal point, even though the release of endogenous LH has been resumed. Many who have suffered severe testicular shrinkage may be able to relate, as it is often some time before normal testicle size and feelings of virility are restored if ancillary drugs had not been used. The excessive stimulation brought forth by administration of HCG can likewise cause the testicles to rapidly return to their normal size and level of activity. We are not simply looking for it to fix the problem however, as the resulting high testosterone level can itself trigger negative feedback inhibition at the hypothalamus. Estrogen production is also heightened with the use of HCG, due to its ability to increase aromatase activity in the Leydig's cells. This is due to the main action of HCG, namely the increase of cycIicAMP (a secondary messenger that regulates cellular activity). When stimulated by HCG, the ability of the testes to aromatize androgens could potentially be heightened several times greater than normal. This also may inhibit testosterone production, so we therefore use HCG only as a quick shock to the testes.

The usual protocol is to inject 1500-3000 I.U. every 4th or 5th day, for a duration usually no longer than 2 or 3 weeks. If used for too long or at too high a dose, the drug may actually function to desensitize the Leydig's cells to luteinizing hormone, further hindering a return to homeostasis. Timing the initial dose is also very crucial. If your were coming off a cycle of Sustanon for example, testosterone levels in your blood will likely stay elevated for at least 3 to 4 weeks after your last injection. Taking HCG on the day of your last shot would therefore be useless. Instead one would want to calculate the last week in which androgen levels are likely to be above normal, and begin ancillary drug therapy at this point. In this case HCG would be started around the third or fourth week. Likewise, after ending a cycle of Dianabol (an oral) your blood levels will be sub normal after the third day. Here you may want to begin HCG therapy a few days before your last intake of tablets, giving it a few days to take effect. One would also want to give some thought to the level of suppression that the cycle might have brought about. After an 8 week cycle of Equipoise for example, 1500-2500 I.U. would likely be a sufficient initial dosage. The lower amount of hormonal suppression one associates with this drug would probably not require much more. On the other hand, 750-1000mg of Sustanon per week might incline the user to inject a much larger HCG dose, perhaps as much as 5000 I.U. for the opening application. It may thereafter also be a good idea to reduce the dosage on subsequent shots, so as to step down the intake of HCG during the two or three weeks of intake.

As discussed above, HCG acts only to mimic the action of LH. It is likewise not the perfect hormone to combat testosterone suppression, and for this reason it is used most often in conjunction with estrogen antagonists such as Clomid, Nolvadex or cyclofenil. These drugs have a different effect on the regulating system, namely inhibiting estrogen-induced suppression at the hypothalamus. This of course also helps to restore the release of testosterone, although through a much different mechanism than HCG. A combination of both drugs appears to be very synergistic, HCG providing an immediate effect on the testes (shocking them out of inactivity) while the anti-estrogen helps later to block inhibition on the hypothalamus and resume the normal release of gonadotropins from the pituitary. The typical procedure involves giving the Clomid/Nolvadex dose from the start with HCG, but continuing it alone for a few weeks once HCG has been discontinued. This practice should effectively raise testosterone levels, which will hopefully remain stable once Clomid/Nolvadex have been discontinued. While unfortunately there is no way to retain all of the muscle gains produced by anabolic steroids, using ancillaries to restore a balanced hormonal state is the best way to minimize the loss felt with ending a cycle.

Nolva vs. Clomid for PCT

Nolva vs. Clomid for PCT
It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.


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.

The questions you will hear from athletes over and over is if they can get legal steroids clomid and nolvadex, is it possible?well I say yes you just have to look.
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.

References

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 (Human Chorionic Gonadotropin)

HCG (Human Chorionic Gonadotropin)


Quick overview:


Active Life: 64 hours
Drug Class: Leutenizing Hormone (LH) - Gonadotropin
Average Dose: debatable
Acne: Yes
Water Retention: Yes
High Blood Pressure: Yes
Liver Toxic: No
Aromatization: No, but it will raise testosterone levels and increased aromatization may occur.

Chorionic gonadotropin is a hormone found in the female body during the early months of pregnancy (it is produced in the placenta). It is in fact the pregnancy indicator looked at by the over the counter pregnancy test kits, as due to its origin it is not found in the body at any other time. Blood levels of this hormone will become noticeable as early as seven days after ovulation. The level will rise evenly, reaching a peak at approximately two to three months into gestation. After this point, the hormone level will drop gradually until the point of birth. As a prescription drug, HCG offers us some interesting benefits. In the United States, we have the two popular brands, Pregnyl, made by Organon, and Profasi, made by Serono. These are FDA approved for the treatment of undescended testicles in young boys, hypogonadism (underproduction of testosterone) and as a fertility drug used to aid in inducing ovulation in women. When prepared as a medical item, this hormone comes from a human origin. Although there is often a fear of biological origin products, there is little research to be found regarding pathogen or sterility problems with HCG. The problems seen with human origin growth hormone are certainly not to be repeated with HCG, as this compound is obtained in a much different way.

While HCG offers the female no performance enhancing ability, it does prove very useful to the male steroid user. The obvious use of course being to stimulate the production of endogenous testosterone. The activity of HCG in the male body is due to its ability to mimic LH (luteinizing hormone), a pituitary hormone that stimulates the Leydig's cells in the testes to manufacture testosterone. Restoring endogenous testosterone production is a special concern at the end of each steroid cycle, a time when a subnormal androgen level (due to steroid induced suppression) could be very costly. The main concern is the action of cortisol, which in many ways is balanced out by the effect of androgens. Cortisol sends the opposite message to the muscles than testosterone, or to breakdown protein in the cell. Left unchecked (by an extremely low testosterone level) in the body, cortisol can quickly strip much of your new muscle mass away.

The main focus with HCG is to restore the normal ability of the testes to respond to endogenous luteinizing hormone. After a long period of inactivity, this ability may have been seriously reduced. In such a state testosterone levels may not reach a normal point, even though the release of endogenous LH has been resumed. Many who have suffered severe testicular shrinkage may be able to relate, as it is often some time before normal testicle size and feelings of virility are restored if ancillary drugs had not been used. The excessive stimulation brought forth by administration of HCG can likewise cause the testicles to rapidly return to their normal size and level of activity. We are not simply looking for it to fix the problem however, as the resulting high testosterone level can itself trigger negative feedback inhibition at the hypothalamus. Estrogen production is also heightened with the use of HCG, due to its ability to increase aromatase activity in the Leydig's cells. This is due to the main action of HCG, namely the increase of cycIicAMP (a secondary messenger that regulates cellular activity). When stimulated by HCG, the ability of the testes to aromatize androgens could potentially be heightened several times greater than normal. This also may inhibit testosterone production, so we therefore use HCG only as a quick shock to the testes.

The usual protocol is to inject 1500-3000 I.U. every 4th or 5th day, for a duration usually no longer than 2 or 3 weeks. If used for too long or at too high a dose, the drug may actually function to desensitize the Leydig's cells to luteinizing hormone, further hindering a return to homeostasis. Timing the initial dose is also very crucial. If your were coming off a cycle of Sustanon for example, testosterone levels in your blood will likely stay elevated for at least 3 to 4 weeks after your last injection. Taking HCG on the day of your last shot would therefore be useless. Instead one would want to calculate the last week in which androgen levels are likely to be above normal, and begin ancillary drug therapy at this point. In this case HCG would be started around the third or fourth week. Likewise, after ending a cycle of Dianabol (an oral) your blood levels will be sub normal after the third day. Here you may want to begin HCG therapy a few days before your last intake of tablets, giving it a few days to take effect. One would also want to give some thought to the level of suppression that the cycle might have brought about. After an 8 week cycle of Equipoise for example, 1500-2500 I.U. would likely be a sufficient initial dosage. The lower amount of hormonal suppression one associates with this drug would probably not require much more. On the other hand, 750-1000mg of Sustanon per week might incline the user to inject a much larger HCG dose, perhaps as much as 5000 I.U. for the opening application. It may thereafter also be a good idea to reduce the dosage on subsequent shots, so as to step down the intake of HCG during the two or three weeks of intake.

As discussed above, HCG acts only to mimic the action of LH. It is likewise not the perfect hormone to combat testosterone suppression, and for this reason it is used most often in conjunction with estrogen antagonists such as Clomid, Nolvadex or cyclofenil. These drugs have a different effect on the regulating system, namely inhibiting estrogen-induced suppression at the hypothalamus. This of course also helps to restore the release of testosterone, although through a much different mechanism than HCG. A combination of both drugs appears to be very synergistic, HCG providing an immediate effect on the testes (shocking them out of inactivity) while the anti-estrogen helps later to block inhibition on the hypothalamus and resume the normal release of gonadotropins from the pituitary. The typical procedure involves giving the Clomid/Nolvadex dose from the start with HCG, but continuing it alone for a few weeks once HCG has been discontinued. This practice should effectively raise testosterone levels, which will hopefully remain stable once Clomid/Nolvadex have been discontinued. While unfortunately there is no way to retain all of the muscle gains produced by anabolic steroids, using ancillaries to restore a balanced hormonal state is the best way to minimize the loss felt with ending a cycle.

Guide to rHGH use

Guide to rHGH use

Disclaimer (warning): This information is for entertainment value only. I am not a medical doctor , therefore, I am not qualified to offer any medical advice nor advise you on how to take any substances. What follow is my experience and knowledge of HGH.
According to studies in the New England Journal of Medicine GH use will:
- Shed Bodyfat- Increase Muscle Tone- Boost your Energy, Strength, and Endurance- Reduce Wrinkles - Create Tighter, Smoother Skin- Help you Sleep Better- Improve Sex Drive and Performance- Improve Immune and Heart Function, Bone Density, Healing Time and Cholesterol, Improve Brain Function, Memory and Mental Focus
Wow! Sure sounds like a wonder drug to me! Yeah right, anyway here is some real world information for bodybuilders. Somatropin (rHGH) is produced by the pituitary gland and is responsible in adolescence for growth of tissues, protein deposition, and the breakdown of sub-q fat stores. As we age, growth hormone levels decrease but still remain active in the body, releasing in cycles during the day. Synthetic growth hormone used exogenously by bodybuilders is a 191 chain sequence of amino acids that replicates the bodies natural production of growth hormone.
Growth hormone has been in use by bodybuilders since the early 1980’s, though at this time, HGH was being extracted from the pituitary glands of cadavers and had enormous side effects, most prominently Creutzfeldt Jacob disease. This is a rare and fatal brain disease, it need not be discussed here since it is not possible in synthetic forms of HGH, but if you want more info just run a search in google. rHGH stimulates growth in most body tissues which is due to an increase in cell number rather than cell size. This includes muscle tissue as well as internal organs, hence the dreaded GH gut.
Use of growth hormone by bodybuilders will cause increased muscle size, localized and overall bodyfat loss, increased protein synthesis, increased glucose output by the liver, increased insulin resistance and lowered thyroid output. Stored fats will be used as a primary fuel source, thus the body fat loss.
So is rHGH the wonder drug everyone lusts after? It certainly is beneficial but not for everyone. You must be willing to take risks to achieve maximum benefits from its use, as well as substantial financial investment. Do it right the first time or don’t do it at all! You will achieve faster and greater growth from cycles of steroids than with GH, though once you reach a plateau, not many products work better.
Ok, so now you have decided that this is the drug for you and you are ready to try it, so what next? Well here are some general guidelines to follow for maximal results from GH use:
Daily injections are a must to maintain stable blood levels as GH has a very short life span in the body. It will peak almost immediately after injection and will clear the body with a half-life of only 20-30 minutes. It is best injected first thing in the morning upon rising to raise levels that are very low from sleeping, and immediately after training. I do not recommend injecting before bed as many bodybuilders do, since that is the time of day that your body will release naturally high levels of growth hormone, and exogenous use will only block that release. If you take it in the morning when levels are low, after training when levels are depleted and then let your body release while sleeping, you are getting one extra release for free! GH is best taken long term, short cycles do not maximize the benefits of muscle cell increase, only fat loss. Here is how I take my GH for maximum benefits:
6iu ed injected sub-q, preferably in the stomach (IM for certain brands)3iu injected upon rising, 3iu injected immediately post-workout10iu insulin taken 30 minutes after HGH injection25mcg cytomel eduse of androgens such as testosterone
The timing of GH and insulin injections is critical. If insulin is injected before the GH, your pancreas will stop release of insulin monitoring due to the exogenous source. GH when injected will mobilize stored glycogen release which will turn into glucose for energy. This will cause a rapid rise in blood sugar levels that will not shut down or stop rising due to the feedback loop being momentarily cut off. You will go hyperglycemic and end up in the hospital. You must first inject your GH, then the insulin; this will cause a rise in glucose release by the GH and will be controlled and shuttled into muscle tissue for repair by the later injection of insulin.Use of cytomel or some type of T3 hormone is critical since GH use will severely lower thyroid levels. Small exogenous sources are necessary to maintain normal levels and 25 mcg ed is sufficient. This will also aid in body fat loss by maintaining proper thyroid functioning.Use of androgens is also necessary due to the promotion of anabolism by increasing muscle size that benefits the new cell number increase by the GH. Remember GH will not directly cause muscle cell size increase, just the number of cells, therefore, androgens are necessary to increase size. Testosterone or trenbolone are both highly androgenic and perfect for out stack.
One myth that needs to be cleared up: high doses of GH use and the 5 on 2 off program. First, if you find that you are not achieving results off of 4-6iu ed, than something else is the problem, not your dose. The use of high doses if primarily cause by heat damage to the protein chain causing denatured proteins. This will decrease the effect and you must use higher doses to achieve the same effect. Other reasons for high dose use are; fake gh, not using insulin, cytomel or test, poor diet, improper timing schedule and the 5 on 2 off. This program was recommended by dealers as a way to move product by offering a lower cost cycle. No doctor in the world would recommend this protocol, Peak blood concentrations are reached in 2-6 hours after injection, and therefore, multiple daily injections are necessary to achieve stable release schedule and results. If you take your last injection Friday afternoon, and then not again till Monday morning, then you have negated all effects offered by the 6 hour concentration. Yes, you will achieve results using a 5 on 2 off program, but not as well as if you inject ed. It’s your money; I can only tell you how to optimize use.
Side effects of GH use include; carpal tunnel syndrome, tingling in the extremities, numbness in the hands and feet, increased organ growth, decreased insulin reception, acromegaly but only in extreme dose use, and decreased thyroid output causing fat accumulation. If you find that you are experiencing any of the above side effects, lower your dose immediately. This is especially important with carpal tunnel. If you feel like your wrists are hurting then lower the dose until pain subsides. You do not want to have that surgery, trust me.
GH is a fantastic product, beneficial for many reasons. Most people will experience thinning of the skin, increased vascularity, fat loss, permanent increases in muscle size due to the cell number increase, and overall feelings of wellness. You will probably need less sleep and feel supercharged all day long. I highly recommend HGH use, but only when you have the money to do it right. 4-6 month cycles are optimal, year round if you are over age 35.

Sustanon 250

Sustanon 250
(testosterone)
This product was developed by Organon as an ideal HRT (Hormone Replacement Therapy) solution, and it was thought at the time that the different esters would be able to provide a constant release of Testosterone over a months time. Sustanon is a blend of different estered testosterones (4 of them): testosterone propionate - 30 mg, testosterone phenylpropionate - 60 mg, testosterone isocaproate - 60mg, and testosterone decanoate -100 mg.

This drug was highly sought after as a "superior" version of testosterone in the late 80´s and through the mid 90´s. No doubt this is partly due to the very nice write-up Dan Duchaine gave it in his newsletters. However, lets keep in mind that this drug was designed for convenience, not athletics or bodybuilding. The advantage to this drug, according to the manufacturer, is that it can be injected once a month, and the different esters would provide different timed releases over that month, and the patient would therefore only need to visit the doctor once a month for his shot. For athletes or bodybuilders (who routinely use between half a gram and a gram of testosterone per week), this product is really no better than any other form of injectable testosterone.

Lately, it seems that this product has fallen out of favor with Steroid.com members, as many feel that the inclusion of the Propionate and phenylpropionate estered forms of testosterone in this blend would necessitate shooting every other day. This stems from the fact that testosterone propionate would be shot every other day at least, and testosterone phenylpropionate would generally be shot every third day.

Sustanon will do exactly what other forms of testosterone will do:

Testosterone will cause both muscle growth as well as fat loss. It sends a message to muscle cells to store more contractile protein (called actin and myosin), thus making your muscles grow. It also protects your muscles from catabolic (muscle wasting) glucocorticoid hormones(1). Thus it is often said that testosterone is not only anabolic, but it is strongly catabolic. Not only does it cause an increase in size of the muscle fibres (hyperfascia) but it also can change the appearance and the actual number of muscle fibres (Hyperplasia)(2). Testosterone has the ability to increase erythropoiesis (red blood cell production) in your kidneys(4), and a higher Red Blood Cell (RBC) count may improve endurance by producing more highly oxygenated blood. More RBCs can also improve recovery from strenuous physical activity. Agression levels often rise dramatically with the use of any exogenous testosterone (3). Testosterone improves muscle contraction by increasing the number of motor neutrons in muscle(5) and improves neuromuscular transmission(6). It also promotes glycogen synthesis(7)

And, since Sustanon is simply a form of (well actually 4 forms of) testosterone, we also know that administration of this compound will produce a dose respondant curve. (10)A what? Yeah...basically a "dose respondant curve" is the fancy way of saying "the more you take, the bigger you get..."

This is true of Sustanon as well as for every form of testosterone, up to a point.

Unfortunately, Sustanon will also do all of the bad things that any form of testosterone is known for:

It will convert to the female hormone estrogen (via a mechanism known as aromatization) by the (you guessed it) aromatize enzyme. Excessive estrogen can lead to unwanted side effects, such as acne, the growth of breast tissue (gynecomastia), fat gain and reduced fat breakdown, loss of sex drive, testicular shrinkage and water retention. Water retention can increase blood pressure weakening blood vessels over time. Unfortunately, this isn´t all it does& it can also interact with the 5 alpha-reductase enzyme. This interaction converts the testosterone to Dihydro-testosterone (DHT), a more androgenic form of the parent hormone. DHT has a high binding affinity to the tissues of the scalp resulting in hair loss in loss in users who suffer from male pattern baldness. DHT can affect the prostate as well, making it larger. This swelling can cause the gland to press against the bladder causing urinary problems. Drugs called 5alpha-reductase inhibitors can prevent these symptoms without blocking testosterone´s anabolic effects.(8) Higher dosages of test can also negatively impact cholesterol, lowering HDL(9). Testosterone is probably the safest steroid around, but it can´t be taken lightly, and Sustanon is no different.

The principal drawback to Sustanon is it´s cost. It can cost between $5 an ampule and $12 an ampule. Compared with Omnadren, Testoviron, or even Sten (other testosterone products featuring various blends of Testosterone), the cost makes it prohibitive. An equal amount of an of the aforementioned products can be had for less than half the average cost of an amp of Sustanon. Sustanon, therefore, is no better or worse than any other form of testosterone... if the price is right.

17b-hydroxy-4-androsten-3-one
Testosterone base + 4 different esters
Propionate, Phenylpropionate, Isocaproate, Decanoate
Formula (base): C27 H40 O3
Molecular Weight (base): 288.429
Molecular Weight, Esters:
Propionate: 362.5082
Phenylpropionate: 438.6058
Isocaproate: 404.5886
Decanoate: 460.6958
Formula (base): C19 H28 O2
Melting Point (base): 155
Manufacturer: Organon
Effective Dose (Men): 500-2000mg/ week
Effective Dose (Women): Not recommended
Active life: Up to 3 weeks
Detection Time: 3+ months
Anabolic/Androgenic ratio:100/100


References:

Human Anatomy and Physiology, 6th Edition, John W. Hole jr.
J Appl Physiol 94: 2273-2281, 2003. First published February 14, 2003; doi:10.1152
Journal of Applied Physiology, Vol 77, Issue 1 23-29,
EFFECTS OF RECOMBINANT GROWTH HORMONE ON VISCERAL FAT ACCUMULATION: PILOT STUDY IN HIV-INFECTED ADOLESCENTS. J Clin Endocrinol Metab. 2005 Apr 19; [Epub ahead of print]
Measures of submaximal aerobic performance evaluate and predict functional response to growth hormone (HGH) treatment in HGH-deficient adults. J Clin Endocrinol Metab. 1999 Dec;84(12):4570-7.
Hormonal responses to consecutive days of heavy-resistance exercise with or without nutritional supplementation. J Appl Physiol, Oct 1998; 85: 1544 - 1555.
Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol, Oct 1990; 69: 1442-1450
High dose growth hormone exerts an anabolic effect at rest and during exercise in endurance-trained athletes.J Clin Endocrinol Metab. 2003 Nov;88(11):5221-6.
Christ ER, Cummings MH, Westwood NB, Sawyer BM, Pearson TC, Sonksen PH, Russell-Jones DL. The importance of growth hormone in the regulation of erythropoiesis, red cell mass, and plasma volume in adults with growth hormone deficiency., J Clin Endocrinol Metab 1997 Sep;82(9):2985-90
The Journal of Clinical Endocrinology & Metabolism Vol. 87, No.8 3573-3577
Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E601-7.
Testosterone blunts feedback inhibition of growth hormone secretion by experimentally elevated insulin-like growth factor-I concentrations.J Clin Endocrinol Metab. 2005 Mar;90(3):1613-7. Epub 2004 Dec 7.
Comparison of the Metabolic Effects of Raloxifene and Oral Estrogen in Postmenopausal and Growth Hormone-Deficient Women.J Clin Endocrinol Metab. 2005 Apr 26; [Epub ahead of print]
Serum insulin-like growth factor I levels in growth hormone-deficient adults: influence of sex steroids.Horm Res. 2004;62 Suppl 1:73-6.
Growth hormone enhances effects of endurance training on oxidative muscle metabolism in elderly women. Am J Physiol Endocrinol Metab, Nov 2000; 279: 989 - 996.
J Gerontol A Biol Sci Med Sci 1998 May;53(3):M183-7