Test ester metabolism and SC injections (everything we knew is wrong?)

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FunkOdyssey

Seeker of Wisdom
I remember a long time ago asking the question of whether depositing a testosterone oil depot in fatty tissue surrounded by aromatase could potentially increase E2 production. The universal answer: no, it couldn't possibly, because testosterone can't aromatize until the ester is cleaved off, which only occurs in the liver.

That answer is incorrect.



Many current T replacement therapies formulated as injections and oral preparations are T esters. Ex vivo conversion of these prodrugs to T by non-specific blood esterases after blood collection may result in overestimation of circulating T levels. Thus, in patients administered T esters, the measured T level may not only reflect circulating T but also the ex vivo conversion of the prodrug to the active androgen. This may confound hormone level evaluations as has previously been shown in the measurement of T enanthate (Wang et al., 2008) and T undecanoate (TU) (Lachance et al., 2015). Inaccurate estimation of circulating T levels may lead physicians to make improper dose adjustments in hypogonadal men treated with a T ester such as T enanthate, cypionate, and undecanoate because T levels in blood that are typically collected in plain tubes may yield falsely high T levels due to ex vivo conversion of T esters to T.

Non-specific esterases in liver, tissue, and blood cellular components hydrolyze inactive steroid esters (e.g., androgen prodrugs) into a biologically active form. The use of ester prodrugs for oral administration of androgens allows greater systemic bioavailability and a longer half-life than the active moiety (Behre, 2004). However, when blood samples are collected, the prodrug in the sample can continue to undergo hydrolysis, ex vivo, by non-specific esterases present in the blood (mainly in red and white blood cells) thus leading to overestimation of circulating androgen levels (Williams, 1985).


Now that we've established that blood contains the esterases needed to remove the ester, perhaps the reports that some people have higher E2 on SC injections should not be disregarded as biologically implausible. Maybe it's a real thing for some people, for a real reason. Something like: T ester slowly drips out of the oil depot, the ester is removed, and the first thing it encounters is a sea of aromatase.
 
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I don't know how much this will actually affect results. The size of the error matters. From the methodology of the first study:

TU at a concentration of 160,000 ng/dl and DHTU at a concentration of 74,000 ng/dl were added to freshly collected whole blood containing no additive and mixed.
Huge quantities of esterified testosterone were directly added to the serum in order produce a large error effect in the testing.
 
Actually the forum already knew this was possible a long time ago, which is even stranger to me, because we keep being told this phenomenon of higher E2 on SC cannot be a thing. Great post from @madman that shows how some testosterone is released from the ester while it is still in the fatty tissue:


Screenshot (11535).png


The only thing missing from this diagram is the part where the liberated testosterone in the interstitium meets up with some aromatase enzyme and your E2 goes up.
 
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I don't know how much this will actually affect results. The size of the error matters. From the methodology of the first study:


Huge quantities of esterified testosterone were directly added to the serum in order produce a large error effect in the testing.
I think one of the studies on this testing error problem showed that the preservatives already present in most collection vials helped inhibit the action of these esterases, which if I understood correctly, would mean this is not much of a real world problem. I just found the studies interesting as they show testosterone esters don't need to travel to the liver to have the ester removed.
 
How about the commonly reported lower blood t levels on subq vs some reporting higher.
I do believe there is some estrogenics at play on subq personally, always feel off and anxious eventually.
 
Is there an inference that subq is inferior or more problematic than IM or is it more related to the individual's response to subq regarding conversion to E2? Based on the research of Dr. Swerdloff, et al on subq versus IM test enanthate, the former demonstrated a half life of 10 days. I know that isn't the focus of the topic but I ponder one large subq injection every 10 days. Perhaps in that setting, higher E2 might be beneficial. Yes, my logic might be, or is, flawed. Just playing with hypotheticals.
 
How about the commonly reported lower blood t levels on subq vs some reporting higher.
Perhaps in cases where T is lower with SC the T has been destroyed by the immune system? I was reading this great paper "New Insights Into Drug Absorption From Oil Depots" which talks about how the immune system is recruited to the site of the injection and can cause inflammation there.

Is there an inference that subq is inferior or more problematic than IM or is it more related to the individual's response to subq regarding conversion to E2?
You can draw your own conclusions about whether SC is generally inferior or more problematic based on the sum of anecdotal data. What I'm talking about here is a potential mechanism for the higher E2 that is observed in SOME fraction of people that have compared equal doses of IM and SC injections. If you don't see higher E2 with SC injections, maybe your interstitial fluid doesn't have much esterase, maybe you are injecting into a very thin layer of fat, who knows.

Certainly many people people do not see higher E2 with SC injections. I just wanted to understand: when it does happen, how and why?

SC does have certain advantages with HCT and the slower release pattern is preferred by some people.
 
I revised the SC oil depot absorption diagram to depict what I think is happening here:

SC oil depot revised.jpg

As you can see, mischievous girl heads are being released directly into the bloodstream.
 
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I was reading this great paper "New Insights Into Drug Absorption From Oil Depots" which talks about how the immune system is recruited to the site of the injection and can cause inflammation there.
For me subq oils always eventually resulted in some 'allergic reaction'
 
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