Steroid 1/2 lifes, absorption and effects in detail.

Mycelium

New member
I've just followed along and focused on esters but how the 1/2 life of AAS is talked about here is way off from drug 1/2 life's I've had other places.

I'll start at injection

I've seen the statements of the AAS being in the injection site. I can't believe that. They are not an implant if suspended in oil. I've seen clinical labs showing test E max out at 24 hours and then follow the 1/2 life curve. The test was absorbed into the the blood stream in 24 hours.

With the testoserone shown to absorb in 24 hours we are to esters and 1/2 life's. I understand them generally but I'm not able to talk about the actual structure. Generally they are like a class of drugs tryptamines in my head. The different esters modify the testosterone actions slightly just like slight variations in the tryptamines slightly different arrangements alter their actions. Some last 5 minutes. Other 2 hours.

To continue with the comparison there are things the body does to the different forms and they bond differently to receptors. Some very short but powerful. Other weaker but lasting much longer. Is there a comparable actions going on with esters? Will a long ester attach as is or do all esters actually get removed to be used as the test alone, and that's why 1/2 life is increased? I don't think so but I've never really searched. Does an ester make the testosterone bond for a different amount of time? Water based test being attach-activate-release and test cyp attaching for 48 hours or something.
 
this is a very articulate question Mycelium, I will talk from my experience when I pin test cyp 200 mg a week, at the point of the injection the ester start working on my blood in about 10 minutes, I feel a rush of warm blood around my body, I assume that's the point of the begining of the long life of the ester, for me after about 48 hrs I would feel a less aggresive mood, I believe that's when the ester starts at 1/2 life a decline curb like you mentioned, for me the right way should be like Todd from Increase my T use to recommend me to pin about every 3 day's, guess what he is right the ester peaks then starts to decline fast in about a time frame 24 to 48 hrs, so a more frequent injection is more of a better approach, yes some docs will say
the long acting ester in test cyp run in the blood for upto 10 days but they don't tell you how bad it declines less than 4 days..
I think I'm answering this very important question the best I can,
 
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The ester is removed freeing the active ingredient..

"2.1. Steroidal Androgens

2.1.1. Testosterone Esters*

Testosterone esters (Figure 8) are often used for clinical management of disease and are usually administered parenterally for prolonged activity. The modification enhances the lipid solubility of the steroid and permits the formation of a local depot after intramuscular injection. However, since the esters are eventually hydrolyzed, testosterone is the actual active species in vivo."

"Similar to testosterone, nandrolone is usually prepared and administered as an ester. Phenpropionate or decanoate esters of nandrolone are administered intramuscularly. Slow hydrolysis of the ester in vivo releases free nandrolone over a prolonged period of time.*"

Chemistry and Structural Biology of Androgen Receptor

Wenqing Gao, Casey E. Bohl, and James T. Dalton


Hydrolosis: chemical*reaction*in which water is used to break down a compound; this is achieved by breaking a covalent bond in the compound by inserting a water molecule across the bond. The opposite of this is a dehydration-condensation*reaction.
 
Mycelium ~ if you want to see Half-Lives in action.

There's a site where you can input your various Compounds ~ Mg per week x up to 20 weeks.
And it will chart the Release of the Hormone, from beginning to end.
You can look at any point in time, and see the Actual Amount of Hormone present.......................... JP
P.S.
Can't give you the link, so you'll have to Type it in.

Steroidcalc dot com
 
I never researched it but had read that different esters caused different amounts of water retention. I always guessed Ibwas a difference in aromiatization or blood levels being different than people expected with build up and with actual amount of test in a mg of its estered form. The test is test. Ester changes things but the test is test and the ester controls the release. Plays into not only watching TT. Test bound to it's ester isn't free T.

Hit Google and what popped up? 'Ology thread already discussing it. Also mentions that the ester has to be removed. Water retention and esters isnt directly related to the ester.

http://www.steroidology.com/forum/a.../674488-different-esters-water-retention.html
 
Long Esters are More Anabolic, by Virtue of the amount of Active Time in the Body.
They will also cause more Water Retention, by the same Mechanism.

Shor Esters will reach Peak Blood Plasma Levels sooner, but aren't as Anabolic.
They also cause Less Water Retention, because they leave your System quicker........................ JP
 
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I'll need a reference for that. I've posted clinical graphs showing a 24 hour time for blood levels to peak. Just because it's absorbed doesn't mean it interacting with receptors as the reference above says. The testosterone doesnt sit in the oil in the injection site and it doesn't bond to receptors until the ester is removed. It circulates the bkdy getting the ester busted off. The 1/2 life is how long it takes our body to chew the ester off the test. The very molecule itself is time release. Withing minutes it's entering the blood stream and being to get stripped. Longer esters build up over longer curves but at a steady dose every days a certain amount is free test, stripped of its esters. Not released by the body but separating the ester from the testosterone. Then the bodies process are effected or use it.



I experienced first hand the delayed onset of esters. My AI anastazole kicked in before the test cypionate. My gyno disappeared and came back as the total blood levels increase and the amount if that being separated from its ester. Based on gyno estered testosterone did not aromatize.
 
Mycelium, not sure what Reference you need.
I gave you the Site to Run Graphs on different Compounds.
So you can see Exactly how they Release.
You can follow the Timeline and see how much Hormone is present.

As far as how Esters work, it's Half-Life dependent.

As for Test, I explained it, it the post above yours.

As for how any Individual will react to Estrogen is dependent on that Specific Person.
Some Guys are more Prone to Gyno than others............................ JP
P.S.
Don't understand your last Sentence.
All Testosterone will Aromatise to varying degrees.


Post Edit:
Comparative Pharmacokinetics of Testosterone Esters.
You can find this on (Link. Springer. com)

This will give you a Reference.
 
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I understand blood levels and 1/2 life, I'm past that. 1/2 life IS NOT active life. At least not when androgen receptors are the discussion. According to the reference I posted estered AAS are not active on androgen receptors until separated.. The anabolic/androgenic results we want do take time to "kick in". If a compound has a 1/2 life of 10 days and we inject 100 mg we have 50mg released/aromatized over 5 days and 50mg still bound to it's ester floating in our blood.

Reading more things I found:

"Serum levels of E2 increased 1.7 times on day 1 after administration but returned to its pre-ART value by day 14 after administration." in "Hormone profiles after intramuscular injection of testosterone enanthate in patients with hypogonadism.".

With estrogen increasing and the article showing only unbound androgens bind to receptors are we seeing we have aromiatization of estered test increase before we get the results we want? Test binding to receptors. Or is the test that's being released being gobbled up by aromatase?

"Serum levels of SHBG did not change throughout the observation period."

This isn't found in the one below. SHBG changes but so does dose and ester. Leading to more issues with exactly how esters work in our body.

Looking in "A pharmacokinetic study of injectable testosterone undecanoate in hypogonadal men." They inject 500mg or 1000mg of test every 3 months.

"Pharmacokinetic analysis showed a terminal elimination half-life of 18.3+/-2.3 and 23.7+/-2.7 days"

Then there is "The mean serum levels of estradiol were normalized following the injections, and prolactin levels were normal throughout the study.*" even tho there is a huge spike in it at the 1 week measurement they fell withing normal ranges shortly. It basically follows blood levels/TT/estered T.

They also show very little difference in blood levels between 500/1000mg at 1 week after 1st injection. That surprised me. It really makes absolutely no sense how doubling the dosage changed peak test very little. A couple pmol.

I lost the page but a dose of orally active test was given and they measured it via radioactive markers and the majority was quickly bound, cleared or aromatize. The test released by the ester may be the same way. Higher blood levels will result in higher levels being released from their ester bond and increased reactions.

If estered androgens can aromatize, be converted, or bind to something before they get released from their bond I dont know.

If I'm not getting my thought pattern or something out I will try to word things better. I'm also keeping only freed testosterone acts on androgen receptors.

The water retention with different esters can be from some pathway of hydrolosis. Actual water riding alo mg breaking down longer esters. Maybe it's the esters themselves floating around.

I can't do it now and not sure if my doctor would ever allow it but people on TRT, stabilized doses/labs and dialed in could switch esters but maintain the actual testosterone dose as small, uncontrolled tests. Say when I'm at 2 years on TRT switch to test undecanote. Get labs at 1 week, 1 month, 3 months and 6 months. Only variable change being the ester it's self. Going from cyp to undec and I puff up would show physical differences and labs could show levels. Or go the other way and go to a shorter ester and I dry out. Same actual testosterone dose, AI dose and HCG dose.

It's hard to compare 125mg test e to 500&1000mg test undecanoate. If they did 125mg wk by 8 weeks there would be the same total of 1000mg but that doesn't measure actual testosterone.
 
Back to my nipple soreness going away. Both of those showed increases in estrogen. One in a day with test e and the other at 1 week with test undec. My nipple soreness faded and didn't return well after those measured increases. There was also no AI mentioned in those. There was no gyno reported in the undec groups even when estrogen was above range at first. The study shows E elevated 3-4 weeks post injection which matches TT being elevated but that's also when the most T is being released.
 
Back to my nipple soreness going away. Both of those showed increases in estrogen. One in a day with test e and the other at 1 week with test undec. My nipple soreness faded and didn't return well after those measured increases. There was also no AI mentioned in those. There was no gyno reported in the undec groups even when estrogen was above range at first. The study shows E elevated 3-4 weeks post injection which matches TT being elevated but that's also when the most T is being released.

The one thing that you have to realize, is that everyone, even those Tested Subjects.
Reacted within a +/- variance, No 2 People will have the same Results.
Either in Total Test or Estradiol.

This is why with any Cycle, it's important to keep a Daily Journal.
And Log all your Dosages, from Compounds to AI's.
And any Side Effects that you notice.
This way when you do Bloodwork, you can see what effect the Doses have on your Particular Physiology................. JP
 
I've paid more attention to how I feel since starting TRT. I've started watching everything more.

I have been thinking about what I'm thinking about if that makes sense. I'm at hydrolosis and how the removed ester is handled. The released T is just T so I'll look at the easiest difference and that's the esters and their path out of the body.
 
I'd be interested in what you find out, from a health perspective. Some esters don't sound that great for you, take phenypropionate - that phenyl group looks a lot like ethyl benzene which is not good for you at all.
 
I've paid more attention to how I feel since starting TRT. I've started watching everything more.

I have been thinking about what I'm thinking about if that makes sense. I'm at hydrolosis and how the removed ester is handled. The released T is just T so I'll look at the easiest difference and that's the esters and their path out of the body.

Not to make things more Confusing for you.

I remember reading some Clinical Study quite a few years ago.
They were looking at the effect of Different Injection Sites and Release of the Hormone.

They looked at Quads vs Delts vs Glutes vs Triceps.
And which one released Sooner as compared to the other Injection Sites
The Minutia on some of this data will make your Head Swim.

This is why I always keep a Daily Journal.
Cause at the end of the Day.
The only thing of Importance, is how your Body reacts to the particular Compounds.................. JP
P.S.
I have rarely seen where they take into consideration.
If the subject is on any Prescription Meds, or has any Genetic Pre-Existing Conditions.
 
It as a well written article but didn't have references. The idea the injected compounds stays in the site was explained as the esters are not very water soluble. Makes self in the statement. Blood measurements shoe absorption withing. Smarter of hours. The test is already suspended in an oil/fat. I think there is merit that some amoint of the compound stays in tje injection site I've seen no evidence it is slowly released and that is the 1/2 life.

I find myself scanning a lot of information for what I want. DNA transcription, intracellular communications and other things. I try to book mark them sonic I'm ever at that level I can reread them.

I found a study on test E and nandrolone deconate in liver cells.

""Most androgenic drugs are available as esters for a prolonged depot action. However, the enzymes involved in the hydrolysis of the esters have not been identified. There is one study indicating that PDE7B may be involved in the activation of testosterone enanthate. The aims are to identify the cellular compartments where the hydrolysis of testosterone enanthate and nandrolone decanoate occurs, and to investigate the involvement of PDE7B in the activation. We also determined if testosterone and nandrolone affect the expression of the PDE7B gene. The hydrolysis studies were performed in isolated human liver cytosolic and microsomal preparations with and without specific PDE7B inhibitor. The gene expression was studied in human hepatoma cells (HepG2) exposed to testosterone and nandrolone. We show that PDE7B serves as a catalyst of the hydrolysis of testosterone enanthate and nandrolone decanoate in liver cytosol. The gene expression of PDE7B was significantly induced 3- and 5- fold after 2 h exposure to 1 ***956;M testosterone enanthate and nandrolone decanoate, respectively. These results show that PDE7B is involved in the activation of esterified nandrolone and testosterone and that the gene expression of PDE7B is induced by supra-physiological concentrations of androgenic drugs."

PDE7B is involved in nandrolone decanoate hydrolysis in liver cytosol and its transcription is up-regulated by androgens in HepG2




The actual article is way over my head. The abstract is deeper than I'm at but it's about the process I'm focusing on. I just hold my breath, scan and look for the details and keywords I know.
 
Mycelium, you need to go back over that Study, as it was done In-Vitro (meaning in a Test Tube/Culture Dish).

Go down to the Materials and Methods Section.
It says, "Five Human Livers were obtained from our Liver Bank".

You will Never get the same Results on In-Vitro Studies, as you will with an In-Vivo Study.
In-Vivo means inside the Human Body.
These are the Studies you need to be looking at.
There's a Big Difference between the Test Tube, and a Human Body..................... JP
P.S.
And at least 1 of those Livers was Diseased with Hepatitis.
HepG2 Cells are Human Liver Carcinoma Cells (Cancer).
 
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Yeah the scientific conflict. Once all variables are standardized and the test goes on it's not "reality" anymore. Reality is variables.

I haven't done any more searching today but I'm pretty sure there is more to it than the study tested or showed. I got gyno from a medication that supposedly cant/doesn't cause it. Proved by mammogram and ultra sound. I'm an uncontrolled study of one. I don't prove it causes gyno. I just prove it causes gyno in me. Along the lines of studies for FDA approval. The real test begins when the new drug is released on the population.
 
I never take any study at face value. Most are just correlations and partial causation. Human wise anyway. We are a complex system only mentally seperated from everything else. I believe nothing really deeply. The more I've learned the more questions I end up with. 1 answers leads to 4 "whys" and eventually there is no information or a macro-hypothesis that can never be tested. If somehow I became a billionaire I'd run some real steroid experiments. I was scrolling the references on that article and seen this.

Pope H. G., Jr., Katz D. L. (1994).Psychiatric and medical effects of anabolic-androgenic steroid use. A controlled study of 160 athletes.*Arch. Gen. Psychiatry51, 375***8211;382 10.1001/archpsyc.1994.03950050035004


Garbage really. Based on the huge amount of misinformation corrected on this forum alone I can imagine the studied AAS users had a wide variety of proper/improper use, poor lifestyle and improper pct and off time. The abstract sounds like they gave them a questionnaire and labs. Gyno, short balls, mood swings and depression sounds like issues. Please post stats, dosages, labs and cycle history haha
 
That's the other thing with most of the Studies on AAS.
From Inception, the study was put together looking for certain Parameters.
And once a Study is Slanted from the Beginning, you can make all types of Inaccurate Assumptions based on Poor Data Collection.

As in that study above, there's No Correlation between Dead and Diseased Livers.
And Healthy Alive Livers.
That has been Proven time and again, where Tests on Cadavers didn't yield the same results as Live Patients............... JP
P.S.
The best you can hope for, is to keep Detailed Records on your Personal Experiences.

I saw another Study with Trained Athletes doing AAS.
But it also said that they doing Narcotics on a regular basis.
WTF would you hope to prove in that study.
Its Flawed before it even begins.
 
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