Well I wouldn't say that I understand this well enough to really have any strong opinions/theories that I would call my own. Just brainstorming really.
Again this is likely oversimplified and may reflect my lack of understanding - I'm just trying to learn here. But I the way I see it is this:
If ND has a greater binding affinity to androgen receptors than T, and therefore a lot of the exogenous T ends up essentially "locked out", and therefore far more of it converts to E2 than it would in the absence of ND...why inject more proportionately more T when using ND? Wouldn't we want to use "just enough" T to keep our FT values wherever we like them to be (upper 20s to mid 30s for me, for example)?
I recall another forum member noting that when he introduced ND his E2 shot up to 90. And I recall another knowledgeable forum member saying something to the effect of when ND is added to a T protocol, it may not have a large effect on TT but that one should expect FT numbers to increase.
So I guess my thoughts are: if using ND, wouldn't a more sensible approach be to adjust the T dose so that FT is in the patients desired range, rather than relying on ratios like 1.5:1 T to ND which may result in higher FT levels than desired and more conversion to E2?
