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PART1
September 06, 2007
September Newsletter Issue 1
Esters: Much more than just half-life…
Esters: Much more than just half-life…
by: Anthony Roberts
Author of: Beyond Steroids , Anabolic Steroids - Ultimate Research Guide Vol. 1, Co-Author of Dr.Jekyll & Mr.Hyde: Body Transformation From Both Sides of the Force
By the end of this article, you’re going to know:
• What an ester is and how it works
• Esters greatly impact much more than just half-life
• Esters influence the degree of a steroid ’s conversion to estrogen
• Esters actually make a given steroid more or less anabolic
• Esters influence peak plasma levels of a given steroid
• Half-life/Active-life charts are all basically incorrect
Bold claims? Keep reading. I’m about to make a case for all of this being true…and by the end, you’re going to agree with me. Let’s go back a bit, first…
When I was in fifth grade I would take my math assignment home every day, and skip to the end of the book for the answers. Math was boring and I had better things to do with my time. And in the end, it was about putting the correct answer in the correct spot, and I really couldn’t see the point of understanding the process. I never understood the argument for being able to do long division…
I wondered if my teachers had ever heard of calculators.
I still spend most of my days looking for answers to questions now, and I still usually only care about the answer. But occasionally, I have an answer, and I need to go back and figure out why that answer is correct.
Let’s go back a bit more now…
An ester is essentially the thing attached to an anabolic steroid to allow it to extend its duration of effects. When you talk about “testosterone cypionate ” or “testosterone enanthate ” you are really talking about testosterone and an ester (cypionate or enanthate , respectively).
Not a single day goes by that I don’t receive an e-mail from somebody on their first cycle asking me about how frequently they should inject something-or-other; whether they need to inject Testosteone Cypionate every 3.5 days, or whether it’s ok to let it go to day 4. They also “know” that testosterone is just testosterone, and besides determining the active life (or half life, or whatever), the ester doesn’t actually change anything about the testosterone itself.
I just don’t have the heart to tell them that everything they think they know about esters…namely that they only influence the half-life and active life…is probably just plain wrong.
I’m going to make a case for different rates of testosterone conversion to estrogen based on different esters…and I’m also going to make a case for different testosterones (depending on ester) actually having differing anabolic potential. I also think this is applicable to virtually all steroids that aromatize and probably to all steroids that are able to convert to DHT or something 5a-Reduced.
Let’s take a look at some anecdotal evidence first, then I’ll give you some studies, and wrap it up with some nice little charts, which will tell you exactly which testosterones do what. First, the problem, as I see it:
Testosterone Propionate bloats me (and everyone else) less than Testosterone Enanthate. But…we often hear (and repeat) that “Testosterone is Testosterone” (especially on the internet, in steroid books, and in all the bodybuilding rags). But if test is test, then why do we see different effects from different esters? We gain more weight, have more water retention, and bloat much more with longer testosterone esters. This also seems to apply to the Nandrolones, as most people find Nandrolone Phenylpropionate (NPP) bloats them less than Nandrolone Decanoate (Deca ). On the other hand, using a long ester with Masteron or Trenbolone doesn’t add any bloating at all.
What the hell is going on here?
By the end of this article you’ll think that testosterone is not just testosterone anymore, and you’ll know why using the propionate ester will bloat you less than the enanthate ester. But don’t just skip to the end…without understanding, the answers are as meaningless as the answers I was turning in to my fifth grade math teacher. Besides, you’ll wanna look smart next time someone asks you “why”, right?
But before I get into why everything you know about esters is probably wrong, let’s take a further look into this stuff and see what we’re missing.
And we’re going to start with the idea (and history) of the ester…
The first anabolic steroid that scientists added an ester to was testosterone. Straight testosterone is absorbed easily during oral administration but is pretty much destroyed by the liver soon after. So the injectable (or “parenternal”) route, for testosterone, was considered far superior, despite the inconvenience of having to inject (unestrified) testosterone every day.
Until that point, testosterone was the only game in town for androgen therapy. Then in 1953, 19-nortestosterone was discovered. And furthermore, it was discovered that an oral dose of 60mgs/kg/day of 19-nortestosterone was needed for the same results as 7mgs/kg/day of the injectable (non-estered) version. So an oral, in this case (19-nortestosterone with no alkylation or methylation) requires a dose of about 8.5x the same drug given by injection (without ester), to elicit the same results (Anabolic Steroids and Sports). I think this is about right. If you were to down a bottle of testosterone suspension you’d likely need to be drinking a bottle a day to see any kind of decent results. On the other hand, you’d only need 100mgs a day if you were injecting it. E
Therefore, we don’t see unaltered (non-estered) testosterone available as an oral formula. The best (oral) solution is to use 17- alkylated derivatives of testosterone (such as methyltestosterone ), which are considerably more resistant to destruction in the liver; although, the potential for hepatotoxicity is much higher with this modification. So there is a way to take testosterone (or any steroid) and make it orally useful. But, of course, there is a way to make injecting them more convenient also, and that is to add an ester.
Adding an ester delays the amount of time that it takes for the steroid to leave the body, although peak concentrations are realized (with both long as well as short esters) within a day or two at most.
Figure 1:
Different testosterone preparations and the years they became available for clinical use: 1940 = su**ermal testosterone pellet implants, 1954 =intramuscular testosterone enanthate, 1977 = oral testosterone undecanoate, 1992 = scrotal testosterone patch, 1995 and 1998 = transdermal testosterone patches, 2002 = transdermal testosterone gels, 2004 = buccal testosterone and intramuscular testosterone undecanoate Adapted from: Human Reproduction Update Advance Access originally published online on August 5, 2004 Human Reproduction Update 2004 10(5):409-419; doi:10.1093/humupd/dmh035
================================================== ====
The esterification of the testosterone molecule at the 17-ß-hydroxy position makes the molecule hydrophobic (hydro means water, and phobic means “scared of”…just like any other phobia) and extends its duration of action. This means you don’t need daily injections of testosterone suspension, but rather, you can choose to utilize an estrified version. Although there were implants available previously (ouch!), testosterone propionate and enanthate were the first ones to widely be used clinically. You can see the 17th position on this diagram (where it says “17” of course)
September 06, 2007
September Newsletter Issue 1
Esters: Much more than just half-life…
Esters: Much more than just half-life…
by: Anthony Roberts
Author of: Beyond Steroids , Anabolic Steroids - Ultimate Research Guide Vol. 1, Co-Author of Dr.Jekyll & Mr.Hyde: Body Transformation From Both Sides of the Force
By the end of this article, you’re going to know:
• What an ester is and how it works
• Esters greatly impact much more than just half-life
• Esters influence the degree of a steroid ’s conversion to estrogen
• Esters actually make a given steroid more or less anabolic
• Esters influence peak plasma levels of a given steroid
• Half-life/Active-life charts are all basically incorrect
Bold claims? Keep reading. I’m about to make a case for all of this being true…and by the end, you’re going to agree with me. Let’s go back a bit, first…
When I was in fifth grade I would take my math assignment home every day, and skip to the end of the book for the answers. Math was boring and I had better things to do with my time. And in the end, it was about putting the correct answer in the correct spot, and I really couldn’t see the point of understanding the process. I never understood the argument for being able to do long division…
I wondered if my teachers had ever heard of calculators.
I still spend most of my days looking for answers to questions now, and I still usually only care about the answer. But occasionally, I have an answer, and I need to go back and figure out why that answer is correct.
Let’s go back a bit more now…
An ester is essentially the thing attached to an anabolic steroid to allow it to extend its duration of effects. When you talk about “testosterone cypionate ” or “testosterone enanthate ” you are really talking about testosterone and an ester (cypionate or enanthate , respectively).
Not a single day goes by that I don’t receive an e-mail from somebody on their first cycle asking me about how frequently they should inject something-or-other; whether they need to inject Testosteone Cypionate every 3.5 days, or whether it’s ok to let it go to day 4. They also “know” that testosterone is just testosterone, and besides determining the active life (or half life, or whatever), the ester doesn’t actually change anything about the testosterone itself.
I just don’t have the heart to tell them that everything they think they know about esters…namely that they only influence the half-life and active life…is probably just plain wrong.
I’m going to make a case for different rates of testosterone conversion to estrogen based on different esters…and I’m also going to make a case for different testosterones (depending on ester) actually having differing anabolic potential. I also think this is applicable to virtually all steroids that aromatize and probably to all steroids that are able to convert to DHT or something 5a-Reduced.
Let’s take a look at some anecdotal evidence first, then I’ll give you some studies, and wrap it up with some nice little charts, which will tell you exactly which testosterones do what. First, the problem, as I see it:
Testosterone Propionate bloats me (and everyone else) less than Testosterone Enanthate. But…we often hear (and repeat) that “Testosterone is Testosterone” (especially on the internet, in steroid books, and in all the bodybuilding rags). But if test is test, then why do we see different effects from different esters? We gain more weight, have more water retention, and bloat much more with longer testosterone esters. This also seems to apply to the Nandrolones, as most people find Nandrolone Phenylpropionate (NPP) bloats them less than Nandrolone Decanoate (Deca ). On the other hand, using a long ester with Masteron or Trenbolone doesn’t add any bloating at all.
What the hell is going on here?
By the end of this article you’ll think that testosterone is not just testosterone anymore, and you’ll know why using the propionate ester will bloat you less than the enanthate ester. But don’t just skip to the end…without understanding, the answers are as meaningless as the answers I was turning in to my fifth grade math teacher. Besides, you’ll wanna look smart next time someone asks you “why”, right?
But before I get into why everything you know about esters is probably wrong, let’s take a further look into this stuff and see what we’re missing.
And we’re going to start with the idea (and history) of the ester…
The first anabolic steroid that scientists added an ester to was testosterone. Straight testosterone is absorbed easily during oral administration but is pretty much destroyed by the liver soon after. So the injectable (or “parenternal”) route, for testosterone, was considered far superior, despite the inconvenience of having to inject (unestrified) testosterone every day.
Until that point, testosterone was the only game in town for androgen therapy. Then in 1953, 19-nortestosterone was discovered. And furthermore, it was discovered that an oral dose of 60mgs/kg/day of 19-nortestosterone was needed for the same results as 7mgs/kg/day of the injectable (non-estered) version. So an oral, in this case (19-nortestosterone with no alkylation or methylation) requires a dose of about 8.5x the same drug given by injection (without ester), to elicit the same results (Anabolic Steroids and Sports). I think this is about right. If you were to down a bottle of testosterone suspension you’d likely need to be drinking a bottle a day to see any kind of decent results. On the other hand, you’d only need 100mgs a day if you were injecting it. E
Therefore, we don’t see unaltered (non-estered) testosterone available as an oral formula. The best (oral) solution is to use 17- alkylated derivatives of testosterone (such as methyltestosterone ), which are considerably more resistant to destruction in the liver; although, the potential for hepatotoxicity is much higher with this modification. So there is a way to take testosterone (or any steroid) and make it orally useful. But, of course, there is a way to make injecting them more convenient also, and that is to add an ester.
Adding an ester delays the amount of time that it takes for the steroid to leave the body, although peak concentrations are realized (with both long as well as short esters) within a day or two at most.
Figure 1:
Different testosterone preparations and the years they became available for clinical use: 1940 = su**ermal testosterone pellet implants, 1954 =intramuscular testosterone enanthate, 1977 = oral testosterone undecanoate, 1992 = scrotal testosterone patch, 1995 and 1998 = transdermal testosterone patches, 2002 = transdermal testosterone gels, 2004 = buccal testosterone and intramuscular testosterone undecanoate Adapted from: Human Reproduction Update Advance Access originally published online on August 5, 2004 Human Reproduction Update 2004 10(5):409-419; doi:10.1093/humupd/dmh035
================================================== ====
The esterification of the testosterone molecule at the 17-ß-hydroxy position makes the molecule hydrophobic (hydro means water, and phobic means “scared of”…just like any other phobia) and extends its duration of action. This means you don’t need daily injections of testosterone suspension, but rather, you can choose to utilize an estrified version. Although there were implants available previously (ouch!), testosterone propionate and enanthate were the first ones to widely be used clinically. You can see the 17th position on this diagram (where it says “17” of course)