halfwit
I like turtles.
Okay, for starters: I found something out I didn't know. Conversion of testosterone to DHEA and estrogen is responsible by the cytochrome process! In fact aromatase IS a CYP enzyme known as CYP19A1.
Source
I have to agree with Dre in that the bloat and other sides like that which used to be attributed to ester are usually based on poor estrogen management. Just like deca dick and other nasties that we all hear about when starting in this game, it's a lack of an Aromatase inhibitor (AI) or dopamine agonist that contributes to these and the spread of misinformation. This is easily proved by seeing how successful 19-nor runs or long ester cycles have fantastic gains with minimal sides and a panel showing a good optimal E2 value on mid-cycle bloods.
Now to the function and role of CYP3A4; unfortunately I am finding the need to quote wikipedia for this part:
That partly explains how the hormones are delivered to receptors and the role of the enzymes, but doesn't truly explain how this conversion to enable cytoplasmic transfer occurs. To try to find how this occurs, I had to do a bit more digging, and found a pretty wordy explanation, but it is a little hard to follow:
I realize that this isn't a clear-cut explanation, but apparently this is an area of human biology that still does elude modern science. I know it doesn't answer your question regarding possible ester issues, but if there was one; I'd wager that it is largely to do with not only a potential esterase problem, but possibly a cytochrome problem - causing you to excrete (hyper-excretion) the hormone before it is put to use. Here is some good reading on esterase for some leisurely reading in case you're interested.
The only thing that bothers me is if you had a total test blood panel run and it showed you at supraphysiological levels of testosterone, you shouldn't have a problem at all as that means you've cleaved the ester, and it hasn't been excreted entirely. I'd honestly get a look (as Megatron mentioned) your SHBG and Free Testosterone to get a bigger picture here.
Hope this helps.
I have to agree with Dre in that the bloat and other sides like that which used to be attributed to ester are usually based on poor estrogen management. Just like deca dick and other nasties that we all hear about when starting in this game, it's a lack of an Aromatase inhibitor (AI) or dopamine agonist that contributes to these and the spread of misinformation. This is easily proved by seeing how successful 19-nor runs or long ester cycles have fantastic gains with minimal sides and a panel showing a good optimal E2 value on mid-cycle bloods.
Now to the function and role of CYP3A4; unfortunately I am finding the need to quote wikipedia for this part:
SourceWikipedia said:Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5***945;-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5-alpha reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[126] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
That partly explains how the hormones are delivered to receptors and the role of the enzymes, but doesn't truly explain how this conversion to enable cytoplasmic transfer occurs. To try to find how this occurs, I had to do a bit more digging, and found a pretty wordy explanation, but it is a little hard to follow:
SourceMolecular Function: quinine 3-monooxygenase activity; oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen; albendazole monooxygenase activity; taurochenodeoxycholate 6alpha-hydroxylase activity; oxidoreductase activity; oxygen binding; steroid binding; testosterone 6-beta-hydroxylase activity; vitamin D3 25-hydroxylase activity; enzyme binding; electron carrier activity; iron ion binding; heme binding; steroid hydroxylase activity; monooxygenase activity.
I realize that this isn't a clear-cut explanation, but apparently this is an area of human biology that still does elude modern science. I know it doesn't answer your question regarding possible ester issues, but if there was one; I'd wager that it is largely to do with not only a potential esterase problem, but possibly a cytochrome problem - causing you to excrete (hyper-excretion) the hormone before it is put to use. Here is some good reading on esterase for some leisurely reading in case you're interested.
The only thing that bothers me is if you had a total test blood panel run and it showed you at supraphysiological levels of testosterone, you shouldn't have a problem at all as that means you've cleaved the ester, and it hasn't been excreted entirely. I'd honestly get a look (as Megatron mentioned) your SHBG and Free Testosterone to get a bigger picture here.
Hope this helps.
