Yep you read it right, all the bro-science that's pushed around forums about 'test being test' and 'ester only affects the half-life of the drug' is bullshit. Don't worry, I have my citations to back up these bold, but true claims. I've been getting a lot of PMs to get more information on the subject, as I've been dropping hints around the forums on my new thoughts and findings; so, I figured it's best to make a post so everyone can read this. We're going to talk about esters. This is something I've been researching about for the last 2 months or so, after using different esters of compounds and noticing different effects, both positive and negative. The common belief among the huge majorly of us is that “Testosterone is Testosterone”, the ester attached to the parent hormone just affects the half life. Well, after much research, I've found that this is just not the case. Different esters will greatly influence many different aspects of the drug's actions including:
1) Conversion to estrogen
2) Nitrogen retention/anabolic nature
3) Peak plasma levels of the drug
4) Level of HPTA suppression
5) And a few other things
How esters work
I'm sure most of you understand what an ester is, but here's a more in-depth explanation. Steroids are 4 ring structures with 19 carbon atoms. Here's a picture of what the Testosterone molecule looks like.
The easiest way to explain an ester is a time release mechanism. The ester prolongs the half-life of the drug. So pure testosterone, or, 'test no ester' is in and out of the system very quickly (less then a few hours). So multiple daily injections would be necessary for stable blood levels. This would obviously be very inconvenient and also very painful, so scientists decided to add a side chain or “ester” to extend the active life of the steroid. As a result, injection frequencies can be cut down. If you look at the picture above, you will see how the molecule is numbered. Notice the OH or hydroxyl group at the 17th position. That's necessary for the steroid to bind to the androgen receptor. This is where they add the ester. With this side chain or “ester” blocking the 17th carbon in the beta position, the steroid is temporally inactive. However, as soon as it gets into the blood stream, esterase enzymes come and hydrolyze the ester, or in other words remove the ester, which restores the hydroxyl group making the steroid active. Lastly, the longer the ester, the less water soluble it is and more fat soluble. Something that is more fat soluble is going to take longer be released from the deposit or “depot” the injection creates.
Long esters are more anabolic and will cause more muscle gain
Now that you have a better understanding of how esters work, we can talk about their actions and how “test is not test." First, we'll talk about how longer esters are more anabolic, and will cause more muscle gain than shorter esters. In 1954, a scientist named Reifstein and his team conducted a study comparing Testosterone Enanthate with Testosterone Propionate. The results of these studies were that Test Enanthate resulted in total nitrogen retention of 1.76g/day vs Propionate only 1.02g/day. They also found that the duration of anabolic activity was 33 days with test e and 12 days with prop.(1) These were with the same doses 200mgs of each. Overall, the longer ester retains more nitrogen (muscle gain) per day then shorts, and remains active in the body for much longer. It doesn't take a rocket scientist to know that if something causes higher levels of nitrogen retention, and hangs around in your body longer, it's going to be more anabolic. Real life experience tells us the same. Think of a prop kicker, of 150mgs every other day, or just a prop cycle. I've done 6 week kickers while waiting for 500mgs a week of test e to kick in, and the results of the Propionate are not even close to the same as the long esters. Despite the same dosage AND 150mgs of prop, every other day (525mgs total per week) actually contains more pure test then 500mgs of test Enanthate due to the ester weights,.
Plasma levels, suppression, and Estrogen
Scientists did a study on 3 different testosterone esters, short, medium and long esters. Their study showed that the short esters caused the greatest peak plasma levels of testosterone, next highest was the medium and lowest peak was the longest esters. However, they found that the long esters caused the greatest suppression on the gonadal axis and metabolic functions.(2) They even upped the short ester dose by 2-3 times and were still not able to replicate the suppression and metabolic effects of the long esters. This greater suppression is also due to the fact that longer esters convert more readily to estrogen, which will cause greater suppression which is what I’m going to get to next.
I'm sure a lot of you have noticed bloat is greater with long esters. Despite the fact the same people say 'test is test,' we don't typically use short esters for bulks and long esters for cuts. We use shorts for cuts and contest preps because they don't convert to estrogen to the same degree as longs do, in turn causing less water retention. Going back to the study, (2) estradiol levels were much higher with the group using long esters despite identical doses of the drug. In short, long esters cause a higher rise in estrogen. The study with the 3 different testosterone esters was done over a 28 week period. The shortest esters allowed for the quickest return of natural levels of hormones. Sperm count also remained the highest with the short esters. Concluding that short esters are less suppressible than long esters. Part of the reason why long esters are so much more suppressive is due to the rise in estrogen they cause. I'm not going to explain the negative feedback system of the HPTA here in depth, but basically the mechanism that tells the HPTA to cease testosterone production is estrogen biding in the hypothalamus. The feedback system thinks ok estrogen is binding which is converted from testosterone so this reflects adequate levels of testosterone. So the HPTA shuts down.
Estrogen and IGF-1 and GH
I’m sure many of you know that using testosterone increases Growth hormone (GH) and Insulin like growth factor-1 (IGF-1) levels to a degree. But did you know that the increase in these hormones are due on estrogen aromatization? (3)(4) Going back, we know that long esters cause greater increases in estrogen, and estrogen increases GH and igf-1. So using long esters will result in greater muscle gain due to the factors I presented earlier, and also the increase in GH and IGF-1 levels that are much higher when using long esters. And as we all know HGH and IGF-1 are two very anabolic hormones. So higher levels of these hormones means more gains in size and strength.
So what about hormones/steroids other than Testosterone?
So now I've talked about how esters affect the effects of testosterone. Is it the same for all steroids with esters? Well, I've found some medical studies done on the different nandrolone esters. These studies had the exact same findings as the testosterone esters. The short ester Nandrolone Phenylpropionate (NPP) had greater peak plasma levels then its long estered counterpart. And suppression was greater with the long estered nandrolone deconate (deca-durabolin), and the anabolic effect was greater with the long ester (deca). Most people who have ran both Deca and NPP can say NPP causes less water retention. And the people I've talked to still say Deca is superior for muscle gain despite the same parent hormone, just different ester lengths. So its seems this the ester length and its effects on the drugs behavior remains true among many different hormones.
Summary
-Longer esters cause higher levels of estrogen
- Longer esters cause more water retention
- Longer esters cause more suppression of the HPTA
- Longer esters cause higher levels of nitrogen retention (muscle gain)in other words are more anabolic
-Shorter esters cause higher peak plasma levels
More research on how this applies to other esterfied steroids. But from the short amount of reading I did do, it seems this applies to steroids that can aromatize, and can convert to Dihydrotestosterone. So the only ones that don't apply to this is Trenbolone, as it doesn't convert to DHT or estrogen, an Masteron as its already in DHT form. However, further research is needed, and that may be presented in my next post.
1. Reifenstein, et. al. Studies comparing the effects of certain testosterone esters in man.J Am Geriatr Soc. 1954 May;2(5):293-8.. PMID: 13162731
2. Journal of Andrology, Vol. 24, No. 5, September/October 2003 Copyright © American Society of Andrology Pharmacokinetics and Degree of Aromatization Rather Than Total Dose of Different Preparations Determine the Effects of Testosterone: A Nonhuman Primate Study in Macaca fascicularisGERHARD F. WEINBAUER*, CARL-JOACHIM PARTSCH, MICHAEL ZITZMANN, STEFAN SCHLATT AND EBERHARD NIESCHLAG
3. [Veldhuis JD, Metzger DL, Martha Jr PM, Mauras N, Kerrigan JR, Keenan B, Rogol AD, Pincus SM 1997 Estrogen and testosterone, but not a nonaromatizable androgen, direct network integration of the hypothalamo-somatotrope (growth hormone)-insulin-like growth factor I axis in the human: evidence from pubertal pathophysiology and sex-steroid hormone replacement. J Clin Endocrinol Metab 82:3414–3420
4. Keenan BS, Richards GE, Ponder SW, Dallas JS, Nagamani M, Smith ER 1993 Androgen-stimulated pubertal growth: the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty. J Clin Endocrinol Metab 76:996–1001
5. Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects of Ester, Injection Site and Injection VolumeCharles F. Minto, Christopher Howe, Susan Wishart, Ann J. Conway, and David J. HandelsmanJ. Pharmacol. Exp. Ther., Apr 1997; 281: 93.
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