TRUTH ABOUT ESTERS REVEALED FOR THE FIRST TIME!
iSteroids.com EXCLUSIVE!
September Newsletter Issue 1
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Esters: Much more than just half-life…
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. 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 = subdermal 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)
Figure 2:
Testosterone , estrified
It is the slow release of the hydrophobic testosterone ester from its
oily depot in the muscle that accounts for its extended duration. The
longer the side chain, the greater the hydrophobicity of the ester and
the greater the duration of action. Thus testosterone enanthate with
its longer side chain has a longer duration of action than testosterone
propionate. The more carbons an ester has, typically, the longer it
will take to release the parent hormone into the bloodstream. Esters
have even been used to make steroids orally available (notably with
Primobolan tabs and Testosterone capsules- Methenolone Acetate and
Testosterone Undecanoate respectively).
However, testosterone undecanoate capsules are not nearly as effective
as testosterone injections, based on both real world as well as
clinical evidence, Primobolan tabs don’t stack up well against the
injectable version, and and Trenbolone is roughly 100x more anabolic
when you inject it instead of taking it orally:
Figure 3:
Comparison of the relative anabolic potency of oral (po) vs. injectable
(sc) dosing of Trenbolone on LABC muscle. (Toxicol. Sci., Dec 2002; 70:
202 - 211.)
Whether taken orally or injected, an esterfied steroid molecule is
temporarily deactivated. In an injection, the ester chain temporarily
blocks the 17-ß position, making binding to the androgen receptor is
impossible. When the compound enters the bloodstream, esterase enzymes
cleave off (hydrolyze) the ester, thus restoring the functional
hydroxyl (OH) group at the 17-ß position, enabling the drug to attach
to the androgen receptor and exert its effects.
Figure 4: Orally Active steroids
So now that we’ve taken a look at some different oral and injectable
steroids, and their structures, you can see exactly what I’m talking
about with the idea of adding an ester (in the parenternal box) versus
the box showing the oral. You can see the long faty acid chain at the
end, which we already know delays release of the hormone.
But that’s not all the ester does…
In 1954, a researcher named Reifstein and his colleagues compared an
injection of Testosterone Propionate with Testosterone Enanthate, and
they found that the injection of testosterone
propionate resulted in nitrogen retention of 1.02g/day with a
total measurable anabolic activity of 12 days, while the Enanthate
version resulted in nitrogen retention of 1.76g/day and had a total
measurable anabolic activity of 33 days. (1). Therefore, a 200mg shot
of Testosterone (long ester) is going to have a greater overall
anabolic effect than a 200mg shot of a short ester. That’s actually
kind of common sense, isn’t it?
So does that mean that the ester effects the anabolic ability of the
actual steroid. Well, yes, that would seem to be the case. If a steroid
hangs out in your body for a longer amount of time, and helps you
retain more nitrogen, then its overall anabolic effect would be
greater. Granted, they’re studying a single injection- but with a
typical injection schedule of testosterone propionate, as compared to
testosterone enanthate, most people gain more weight from the enanthate
version. Think about it; experience tells us that with an every other
day injection schedule of 100mgs of testosterone propionate versus
400mgs/week of testosterone enanthate, most people gain more weight
from the enanthate. Yet, the actual amount of injected (pure)
testosterone is virtually the same, even when you subtract the weight
of the ester.
Here’s my position, S-P-E-L-L-E-D out for you:
Testosterone, depending on the ester, will give you different effects
in a variety of areas.
Yeah, I’m saying the ester will have it’s own effect on how the
testosterone is metabolized and used by your body. And that will give
you different effects, depending on the ester you choose.
Testosterone
I thought testosterone is testosterone? Isn’t that what they say on the
internet? If you hear it on a steroid forum, isn’t it true? Well,
research dating as far back as 1954 says no. In fact, (primate)
research as recent as this decade seems to say the same thing. Alright,
I can hear the pubmed-scientists and keyboard-cowboys all over the
internet shouting in protest right now. I know that primate studies
aren’t perfect, but they’re offering us a clue as to why we all gain
more weight on the longer esters versus the shorter esters. And in this
case, they offer us a perfect- even elegant – explanation.
Why do we need an explanation for this? Well, because for literally
decades we’ve been using short esters for cutting cycles and long
esters for bulking cycles, and for all that time we’ve also been
claiming that “testosterone is testosterone” regardless of ester. If we
actually believed that last “fact”, we’d just be using the longest
esters all the time, because they’re more cost effective per bottle.
But we don’t; and we see different effects on water retention, gyno,
weight gain, and other parameters, depending on the ester lengths.
Here’s what scientists found out when they examined different ester
lengths:
Testosterone ester length can (and does) influence suppression of the
gonadal axis, effects on anabolic parameters, and lipid metabolism.
Furthermore, they reassure us that their results are most likely
transferable to human males. Further-furthermore (I made that up),
their research indicates that esters influence conversion to estrogen.
(2) And when you think about what
experience tells us, doesn’t that agree with the real world? Don’t
people get gyno more frequently, more water retention, and higher
bodyweight gains with longer esters? When is the last time you saw
someone using a short ester and still need an anti-estrogen? And more
estrogen also means more hypothalamic-pituitary-testicular axis
suppression, because of the body’s negative feedback loop.
Haven’t we always known that long esters suppress you more than short
ones? It’s not just the time they are in the body, but also the amount
that they convert to estrogen. Do the math if you don’t believe me…it
can’t just be the extra couple days that long esters are active in the
body. It’s the estrogen conversion.
Thus - the amount you suppress your natural hormonal system, the
potential anabolic effect, and the effects on lipids, are all
influenced by the ester length. Esters are not just something that
delays the release of the hormone into the body…their length plays a
crucial role in what degree the steroid actually performs certain
functions.
I know it goes against everything that is typically said about esters,
but think about it…don’t we use different testosterone esters (in the
real world) for different things….long esters for bulking and short
esters for cutting? I’m presenting new information
Alright…let me tell you about a study now. Scientists (real ones, with
lab coats and everything) examined 3 different testosterone
preperations with different ester lengths. What they found was that the
shortest ester provided the highest peak levels of testosterone,
followed by the medium length ester, and the lowest peak level was
found with the longest ester. Even a two- to threefold higher dose of
the shortest acting ester studied did not fully achieve the effects of
longer esters concerning gonadal and metabolic functions. (2) Did I
mention that the amount of pure testosterone (minus the ester) was the
same in all injections? So what does that tell us?
The ester influences far more than just the release time and active
life of the parent hormone.
Estradiol levels were significantly higher with the longest ester.
Yes…Using longer estered testosterone will cause a higher rise in
estrogen. And, although the same total amount of testosterone was
injected in all groups, the group using the longest acting version
gained the most weight.
Also of interest in this study is that even though testosterone was
used for 28 weeks in a row, the shortest ester allowed the most rapid
return of natural hormonal levels. Sperm count also remained highest
with the shortest ester, and lipid profiles were worse with the longer
acting testosterone. And once again, even though this was only a
primate study, the authors believe these results are transferable to
human males…and bodybuilders who have used different esters for
different goals will confirm this as well.
The identifiable pattern of exposure and degree of aromatization and
estrogen, rather than overall exposure to testosterone, determined the
differing effects of the different esters. Longer esters cause a higher
rise in estrogen (even when the total dose of testosterone is
identical). That’s why we all get more water retention on testosterone
enanthate, while testosterone propionate doesn’t cause much if any.
This is the explanation that we have been waiting for…because I know
that even when people say “test is test” they don’t really believe it-
or we’d be seeing short ester bulking cycles and long-ester cutting
cycles.
Oh…and if this weren’t the case, then why is it that people almost
always talk about using an anti-estrogen with long estered testosterone
and not usually with the short estered variety?
Have I mentioned that testosterone’s effect on Growth Hormone and IGF-I
(two very anabolic hormones) are also dependant on aromatization to
estrogen? Again, this is why we gain more muscle with the long estered
tests. (3, 4, 5). This means that you actually
get far more anabolism from the longer estered testosterones, because
the increased conversion to estrogen will provide a greater elevation
in your GH and IGF-1 levels. And many other positive effects of
testosterone are actually dependent on it’s conversion to estrogen as
well. (6, 7, 8)
But does this apply across the board, to esterfied
(aromatizable/DHT-convertible) hormones other than testosterone?
It probably does…in fact I’m pretty much positive that it does. Let’s
take a look at the 19-nortestosterone derived family of anabolics,
specifically Nandrolone.
When comparing different preparations of Nandrolone, many of these
similar properties were found when a long ester (decanoate) was
compared with a short one (Phenylpropionate).Peak plasma levels are
higher with the shorter esters, suppression is greater with longer
esters, and so on. (9,10) Of course, with
Nandrolone (compared with testosterone) the degree of suppression is
pretty harsh regardless of the actual ester used…but still, you can see
more lengthy suppression with the longer ester. And another study also
shows a higher anabolic effect when longer nandrolone esters are
compared with short ones (11,12). Basically,
what I’m saying here is that we’re seeing the same thing with different
Nandrolone esters as we saw with testosterone esters; more
imnportantly, the scientific research confirms what we know to be true
in our own cycles, and also
gives support for my explanation as to why this is happening.
It’s the ester length! And it sure as hell isn’t just affecting the
half-life! Well….it’s likely that the release of the parent hormone is
subject to different aromatization levels based on it’s release
time…but still, the end result is that the ester is greatly influencing
the actual effects because of this.
Unfortunately, in this study, only one injection was used…but again, we
know that people who’ve used Nandrolone Phenylpropionate get less
bloating then when they’ve used Nandrolone Decanoate.
Let’s go back to the other two drugs I mentioned earlier, namely the
long estered versions of Trenbolone and Masteron. It doesn’t matter
what ester you use with them, because neither of them convert to
estrogen at all. In fact, since one is already derived from DHT, and
the other isn’t subject to 5a-reduction, neither “convert” to DHT at
all.
Dihydrotestosterone
In order for a hormone to become the dihydro version, is must be
5alpha-reduced (or already exist as such).
Does ester length also influence 5a-Reduction? I suspect it may. But in
this case, I would imagine that the long esters convert less readily to
DHT (though I guess I could be wrong).
If I’m right, then it would seem to give us another explanation of why
we gain less weight on short esters…DHT is a potent androgen, but a
disappointing anabolic, due to deactivation by the 3-alpha
Hydroxysteroid Dehydrogenase enzyme. Increased conversion to DHT in
short esters inversely correlated with a decreased conversion to
estrogen would provide us with a neat, bow-wrapped, conclusion to all
of this. I tend to think that the fact that ester length doesn’t have
any real effect on 1. non-aromatizing androgens which also 2. can’t be
further 5a-reduced – gives us strong inductive evidence to believe that
there is more DHT conversion with short esters. Unfortunately, the
research doesn’t give me 100% reassurance on the DHT-thing (however,
the estrogen thing regarding esters is set-in-stone- gospel now, as far
as I’m concerned). There is, however, some strong evidence in medical
journals to support my thoughts on this (13, 14, 15, 16).
I’m speculating that short esters convert to more
(not-really-very-anabolic) DHT, and that would also give us a clue as
to why stuff like testosterone propionate is better at getting us a
nice hard physique than testosterone enanthate. It fits…I just can’t be
100% sure on it. But I hope you joined me in that logical leap…because
it sure gives us a safe landing on the other side, doesn’t it? I think
this modulation and difference depending on ester in DHT levels is much
more modest than those we see with estrogen levels (depending on
ester).
To sum everything up in a nice neat package:
• Longer esters are more anabolic than shorter ones
• Shorter esters cause less water retention
• Longer esters cause more gonadal suppression
• Shorter esters cause a higher peak plasma level
• Most of this is only applicable to steroids that are estrified,
aromatizable, and able to convert to DHT
I think I’ve made a pretty reasonable case for esters influencing far
more than just active-life or half-life…and I think we’re about to see
a new paradigm in the use of esters for different reasons.
Best Steroids
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