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What are esters?
When synthetic steroids were first developed they had one major drawback. That drawback was the incredibly fast release and metabolism of the hormone molecule. Scientists developed a technique to add an ester to the 17th-beta hydroxyl group which in essence slows down the release rate of the hormone.
When you inject a steroid that has an attached ester what you're doing is creating a deposit or depot in the tissue you inject in. The ester is a group of mainly hydrogen and carbon atoms that create the acid added at the 17th-beta position of the parent hormone. The shorter the ester the quicker the release the shorter the half life. Conversely the longer the ester the more delayed release and longer half life. Terminal or elimination half life in this context means the amount of time for serum levels to reduce to 1/2 the original concentration after having reached steady state concentration.
While the ester is still attached to the hormone molecule the hormone remains INERT! It has NO biological activity at this time. The ester length determines how fast the ester gets cleaved off the parent hormone and the delay in release rate from depot. The process of metabolizing the ester is called hydrolysis and the more esterified the hormone (the longer the ester) the more liphophillic the molecule becomes or more oil soluble. This solubility is what delays the release. You inject the hormone into the muscle or fat tissue which is composed of a lot water and blood and the oil solubility increases providing a time buffer.
Once the hormone is free from the injection depot it enters systemic circulation. In the blood, esterase enzymes attack the molecule and hydrolyze the ester**. After this has happens the hormone has the normal hydroxyl group restored to the 17-beta position and is now free to bind with an androgen receptor and begin the transcription and signaling process. Again the rate this happens is determined by the half life or ester length. Shorter esters are ones like propionate, acetate, and phenylpropionate while enanthate, cypionate, undecanoate, etc are longer esters. The half life is one of the most important factors to consider when going about deciding upon an injection schedule.
**although most of the molecules get hydrolyzed in general circulation, some happens at the injection site. I believe this is why some ppl believe in site injections as it can leave slightly higher concentrations of hormone and ester acid in localized tissue. This MAY have an impact over the years but certainly nothing in the short term. Another thing to consider is the onset of symptoms and sides. Longer esters take longer to metabolize therefore results usually take a few more weeks to be clearly evident but make no mistake...the hormone is beginning to work as soon as you inject it. Sides may also show up sooner since the hormone is metabolized more quickly bringing about aromatization quicker for instance. Also, some people seem to be particularly sensitive the the propionic acid in test prop for example and get PIP regardless of dose or concentration. If you're one of these you can avoid it by choosing another ester.
One final note on esters, the longer the ester the more the carbon atoms in the acid. More carbon molecules means more weight. The more the ester weighs means the less hormone you'll have per unit of mass since the ester weight is calculated into the hormone weight. Test is test is test is test. This holds true BUT shorter esters invariably have slightly more hormone per mg of powder. This isn't enough to cause significant differences between esters unless you're talking about years and years of use and a ton of volume injected. Don't get caught up the the minutiae, the effectiveness of the steroid molecule is NOT influenced by the ester attached to it.
A chart of ester and hormone weights per 100mg of powder:
How to choose an appropriate dosing protocol based on ester/half-life?
Do you want to pin every day (ED)? Do you only want to pin once a week? Twice a week? Do you want to run a short cycle or long one? These and more are questions you should ask yourself when considering which ester to run, if options are available to you. The reverse is also true, if you're stuck with a certain ester you must adapt your dosing protocol to suit the effectiveness of the ester.
For TRT patients, the general rule of thumb is that stable plasma concentrations are best for an optimal sense of well being. Less fluctuations usually leaves the patient feeling better. This is why many TRT patients who start at once every two week injections oftentimes prefer weekly or bi-weekly injections. The benefit of this is higher trough levels but it does so at the expense of lower peak levels. If running a blast, we are usually more concerned with the peak levels so a less frequent injection frequency is desired bc the less frequent the injection (while remaining within the compound's half-life) the higher the peaks and lower the troughs and the spikes also help with progress.
Consider these general guidelines:
-Shorter esters such as propionate, acetate, phenylpropionate: you can inject 3x/wk, every other day (EOD), or everyday (ED). You'll usually see most of the more experienced guys recommending to go with 3x/wk or EOD at the most frequent. Because results are quicker to show with short esters you'll see their cycles are generally shorter as well. Usually a 6-8wk minimum.
-Longer esters such as enanthate, cypionate, etc: you can inject 3x/wk, 2x/wk, once weekly, or less frequent for the very long esters like undecanoate. Most of the experienced guys you'll see recommending 1-2x/wk injections. The longer esters require more time to build up in serum levels and show clear results so most people recommend no less than 12wks for am enanthate or cypionate run.
^^^again, you must always remember the half life and make sure you're still within it.
Half life of common esters:
Oral Steroid 'esterification'
The issue with taking oral steroids without an 'ester' is that when it's processed by the hepatic system (liver) it gets broken down an deactivated during the first pass effect (or first pass metabolism). This first pass greatly reduces a drug's bioavailability. The solution for oral steroids is methylation.
Most oral steroids are known as C17aa or C17 alpha-alkylated. This means that the hydrogen atom at the 17th alpha position has been replaced with a carbon atom (alkylation/ehtylation/methylation) usually in the form of a methyl group (CH3). This process makes the oral steroid resistant to liver enzymes and therefore retains most or all of its bioavailability. Because the methyl group cannot be metabolized by the body it changes the actions of the steroid as well as creates a new steroid. One of the most considerable changes is the fact that it creates an increased tendency for the parent steroid to produce estrogenic effects due to the 17-alkylation creating a more active/potent form of estrogen (17-methyl estradiol). Not all Orals are like this though as certain ones like Anavar and Tbol were designed not to be aromatizable.
The alkylation process for oral steroids has one major drawback and that's hepatoxicity or damage to the liver. Each compound is toxic to a different degree but don't believe anyone telling you not to be concerned for your liver. There are various reasons for the different levels of toxicity so always keep an eye out for your liver health when performing blood work (AST, ALT, Alkaline Phosphate, Bilirubin, etc). Common supplements or liver protection for on or off cycle are NAC, UDCA, and LIV52. Milk thistle has been shown to benefit liver health but only in mild cases where the elevation in liver enzymes isn't much. Don't use milk thistle as a standalone liver support!
-NAC dosing: off cycle 600mg daily, on injectable cycle 1200-1800mg daily, on orals 1800-2400mg daily (note tren has a reputation to affect liver function more than any other injectable so be careful)
-UDCA dosing: 300-600mg daily, on injectable cycle 600-900mg daily, on orals 900-1200mg daily
-LIV52: 1-2 capsules twice daily
Half-lives of common oral steroids:
References:
1) Anabolics 10th ed.; William Llewellyn
2) http://www.chemguide.co.uk/organicprops/esters/background.html
3) http://chemwiki.ucdavis.edu/Organic_Chemistry/Esters
When synthetic steroids were first developed they had one major drawback. That drawback was the incredibly fast release and metabolism of the hormone molecule. Scientists developed a technique to add an ester to the 17th-beta hydroxyl group which in essence slows down the release rate of the hormone.
When you inject a steroid that has an attached ester what you're doing is creating a deposit or depot in the tissue you inject in. The ester is a group of mainly hydrogen and carbon atoms that create the acid added at the 17th-beta position of the parent hormone. The shorter the ester the quicker the release the shorter the half life. Conversely the longer the ester the more delayed release and longer half life. Terminal or elimination half life in this context means the amount of time for serum levels to reduce to 1/2 the original concentration after having reached steady state concentration.
While the ester is still attached to the hormone molecule the hormone remains INERT! It has NO biological activity at this time. The ester length determines how fast the ester gets cleaved off the parent hormone and the delay in release rate from depot. The process of metabolizing the ester is called hydrolysis and the more esterified the hormone (the longer the ester) the more liphophillic the molecule becomes or more oil soluble. This solubility is what delays the release. You inject the hormone into the muscle or fat tissue which is composed of a lot water and blood and the oil solubility increases providing a time buffer.
Once the hormone is free from the injection depot it enters systemic circulation. In the blood, esterase enzymes attack the molecule and hydrolyze the ester**. After this has happens the hormone has the normal hydroxyl group restored to the 17-beta position and is now free to bind with an androgen receptor and begin the transcription and signaling process. Again the rate this happens is determined by the half life or ester length. Shorter esters are ones like propionate, acetate, and phenylpropionate while enanthate, cypionate, undecanoate, etc are longer esters. The half life is one of the most important factors to consider when going about deciding upon an injection schedule.
**although most of the molecules get hydrolyzed in general circulation, some happens at the injection site. I believe this is why some ppl believe in site injections as it can leave slightly higher concentrations of hormone and ester acid in localized tissue. This MAY have an impact over the years but certainly nothing in the short term. Another thing to consider is the onset of symptoms and sides. Longer esters take longer to metabolize therefore results usually take a few more weeks to be clearly evident but make no mistake...the hormone is beginning to work as soon as you inject it. Sides may also show up sooner since the hormone is metabolized more quickly bringing about aromatization quicker for instance. Also, some people seem to be particularly sensitive the the propionic acid in test prop for example and get PIP regardless of dose or concentration. If you're one of these you can avoid it by choosing another ester.
One final note on esters, the longer the ester the more the carbon atoms in the acid. More carbon molecules means more weight. The more the ester weighs means the less hormone you'll have per unit of mass since the ester weight is calculated into the hormone weight. Test is test is test is test. This holds true BUT shorter esters invariably have slightly more hormone per mg of powder. This isn't enough to cause significant differences between esters unless you're talking about years and years of use and a ton of volume injected. Don't get caught up the the minutiae, the effectiveness of the steroid molecule is NOT influenced by the ester attached to it.
A chart of ester and hormone weights per 100mg of powder:
How to choose an appropriate dosing protocol based on ester/half-life?
Do you want to pin every day (ED)? Do you only want to pin once a week? Twice a week? Do you want to run a short cycle or long one? These and more are questions you should ask yourself when considering which ester to run, if options are available to you. The reverse is also true, if you're stuck with a certain ester you must adapt your dosing protocol to suit the effectiveness of the ester.
For TRT patients, the general rule of thumb is that stable plasma concentrations are best for an optimal sense of well being. Less fluctuations usually leaves the patient feeling better. This is why many TRT patients who start at once every two week injections oftentimes prefer weekly or bi-weekly injections. The benefit of this is higher trough levels but it does so at the expense of lower peak levels. If running a blast, we are usually more concerned with the peak levels so a less frequent injection frequency is desired bc the less frequent the injection (while remaining within the compound's half-life) the higher the peaks and lower the troughs and the spikes also help with progress.
Consider these general guidelines:
-Shorter esters such as propionate, acetate, phenylpropionate: you can inject 3x/wk, every other day (EOD), or everyday (ED). You'll usually see most of the more experienced guys recommending to go with 3x/wk or EOD at the most frequent. Because results are quicker to show with short esters you'll see their cycles are generally shorter as well. Usually a 6-8wk minimum.
-Longer esters such as enanthate, cypionate, etc: you can inject 3x/wk, 2x/wk, once weekly, or less frequent for the very long esters like undecanoate. Most of the experienced guys you'll see recommending 1-2x/wk injections. The longer esters require more time to build up in serum levels and show clear results so most people recommend no less than 12wks for am enanthate or cypionate run.
^^^again, you must always remember the half life and make sure you're still within it.
Half life of common esters:
Oral Steroid 'esterification'
The issue with taking oral steroids without an 'ester' is that when it's processed by the hepatic system (liver) it gets broken down an deactivated during the first pass effect (or first pass metabolism). This first pass greatly reduces a drug's bioavailability. The solution for oral steroids is methylation.
Most oral steroids are known as C17aa or C17 alpha-alkylated. This means that the hydrogen atom at the 17th alpha position has been replaced with a carbon atom (alkylation/ehtylation/methylation) usually in the form of a methyl group (CH3). This process makes the oral steroid resistant to liver enzymes and therefore retains most or all of its bioavailability. Because the methyl group cannot be metabolized by the body it changes the actions of the steroid as well as creates a new steroid. One of the most considerable changes is the fact that it creates an increased tendency for the parent steroid to produce estrogenic effects due to the 17-alkylation creating a more active/potent form of estrogen (17-methyl estradiol). Not all Orals are like this though as certain ones like Anavar and Tbol were designed not to be aromatizable.
The alkylation process for oral steroids has one major drawback and that's hepatoxicity or damage to the liver. Each compound is toxic to a different degree but don't believe anyone telling you not to be concerned for your liver. There are various reasons for the different levels of toxicity so always keep an eye out for your liver health when performing blood work (AST, ALT, Alkaline Phosphate, Bilirubin, etc). Common supplements or liver protection for on or off cycle are NAC, UDCA, and LIV52. Milk thistle has been shown to benefit liver health but only in mild cases where the elevation in liver enzymes isn't much. Don't use milk thistle as a standalone liver support!
-NAC dosing: off cycle 600mg daily, on injectable cycle 1200-1800mg daily, on orals 1800-2400mg daily (note tren has a reputation to affect liver function more than any other injectable so be careful)
-UDCA dosing: 300-600mg daily, on injectable cycle 600-900mg daily, on orals 900-1200mg daily
-LIV52: 1-2 capsules twice daily
Half-lives of common oral steroids:
References:
1) Anabolics 10th ed.; William Llewellyn
2) http://www.chemguide.co.uk/organicprops/esters/background.html
3) http://chemwiki.ucdavis.edu/Organic_Chemistry/Esters
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