Fat contains a higher amount of aromatase than lean tissue. So more fat means more T–>E aromatization. So yes, higher body fat means more estrogen. And the trap is that more estrogen leads to more fat. While it would seem to follow that less fat would lead to needing less AI, that is not a universal truth. It might apply for those who really were carrying a lot of fat who loose a lot of fat. For guys who became flabby as they were loosing muscle with no really net gain of weight, when they loose fat and gain muscle with no significant weight change, they typically do not see a reduction in the needed AI dose. In this case, note that the body weight did not change. If a guy looses 20% of his body weight, it would make sense that he would need less AI. I do advise that the typical starting dose of AI can be scaled up by body weight vs a 160 pound reference. So a 240 pound guy could easily need 1.0 mg/week * 240/160 or 1.5mg/week.
Another factor is that SHBG bound T [SHBG-T] is inert and only bio-available for metabolic processes of elimination by the liver. T–>E reaction rates when on AI are proportional to the amount of non_SHBG-T, which is fT and bio available T [bio-T]. When you start TRT your fT and bio-T levels can increase as you loose fat. Over time higher levels of fT and bio-T reduce SHBG generation rates in the liver, just as lower E levels lower SHBG. This is probably an effect of T interfering with the mechanics of E stimulation higher SHBG rates. So one can consider T to be a competitive inhibitor in this context. As fT increases, SHBG goes down and fT then increases. So we have another self reinforcing swing that can occur.
SHBG does carry sex hormones. E can bind and release to SHBG. T is tightly bound. SHBG carries T to the liver for disposal. You will find statements on the WWW that SHBG carries T around the body to deliver T to tissues. That is absolutely false. If any T is released to tissues from SHBG-T, the amounts are not significant. Bio-T is ft and mostly T that is weakly bound to albumin. It is albumin that transports most of one’s T to tissues in the body. Higher levels of albumin improve bio-T. Some men have lower albumin levels with age. TRT increases protein synthesis and that does typically increase or restore more youthful levels of albumin. While such effects are not hugely significant, understanding the role of albumin is arguably more important than understanding the effects of SHBG.
When bio-T levels increase, that is more pressure on T–>E aromatization rates. The mechanics really do show an increasing need for AI as fT increases. What counter acts this is that increasing fT and bio-T will lead to less fat and less aromatase.
To complete the picture, competitive AI drugs need to be kept in proportion to bio-T levels. If one increases their T dose, AI should be increased in proportion. Where all of this breaks down is when hCG doses are large. T levels in the testes can be up to 80 times higher than serum levels. It is easy to see that typical serum levels of AI drugs are ineffective inside the testes where the T:AI ratios are vastly higher than in the rest of the body. In some cases where hCG doses are too high, E is basically unmanageable.
There seems to be a lot of guys who can report that they have had to increase AI doses over time. The body seems to have an increased T–>E aromatization rate. Some have argued that this is the body trying to compensate for the lower E levels achieved with AI use. But no such mechanism of that sort is understood.
In my case, I did well with 1.0mg/week per 100mg T cyp per week. That requirement could be termed a specific AI demand as it is normalized against the actual dose. My specific AI demand is now 1.46. Specific AI demand would also change with body weight and fat mass changes.
As for increasing one’s AI dose, there are no negative side effects or effects of low estrogen if one targets levels near serum E2=22pg/ml.
More and more research over many years has shown that the prostate is sensitive to E and that E causes prostate enlargement and other adverse changes. Some SERMs can shelter prostate E receptors from the effects of E. AI’s can be used to achieve healthier E levels that will be better for prostate health. These SERM effects are not chemo-preventative. “Chemo” has connotations for selective and controlled poisons used to kill fast dividing cancer cells.
With TRT, if you lower E and SHBG, fT increases and that in turn amplifies the reduction in fT. If one increases T doses to achieve high youthful levels of fT or bio-T, while disregarding TT levels, there can be a disproportionate increase in fT. So at some point the % increases in fT can exceed the % increases in T dosing. One needs to increase AI dosing to match changes in fT or bio-T so an higher specific AI demands makes sense once higher T doses begin to have these fT amplification effects. Some doctors [few] do not even test for TT and only look at bio-T or fT.
GeoBob: There are different tests for fT that do have vastly different ranges and test results. Can you edit your post above to include the fT ranges?