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The fact that subq injections do not seem to raise E2 levels more than IM injections (as you originally feared, Dr Crisler), is likely due to the fact that the ester (be it propionate, cypionate, enanthate) is mostly cleaved from the testosterone by esterase enzymes IN THE BLOODSTREAM. This means the testosterone, while sitting in the subq fatty tissue would still mostly have its ester attached. Thus, all of the aromatase sitting around in those adipose cells would be useless for converting the testosterone ester (in other words, the aromatase will convert testosterone (no ester) to estradiol (no ester), but will not convert testosterone cypionate to estradiol cypionate).


Once the testosterone ester is absorbed into the blood and the ester is cleaved off to release testosterone itself, then all is fair game whether it came from an IM source OR a subq source - ie: it may circulate and return to the adipose cells to then be converted to E, but this, in effect, removes the location of injection as a significant variable for affecting E levels. Since ester cleavage occurs primarily in the blood, the actual site of injection should have almost no DIRECT impact on E conversion, but may have an INDIRECT impact by way of differing pharmacodynamics of serum T levels in IM vs subq injections.


Dr Saya


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