You don’t know this Period.
Some men don’t respond well to higher E2 levels. Some do.
Just stop.
I hate these blanket bullshit “i know it all” statements.
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Dont get so angry. Cortisol is a bigger threat to you. Take it easy man. No need to flip tables on the internet
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This is a long one stick with me…
I see two mechanisms for the e2 and ED relationship.
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High e2 affecting the brain and not signalling adequate NO production.
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High e2 affecting the dick veins that carry the blood to an erection and the veins that allows the blood to exit the erection.
To address point 2 only- it’s been proven in the papers listed above that higher e2 is correlated with reduced arterial wall stiffness. This means that for a given pressure, a less stiff arterial wall will distend more than a stiffer one.
To define stiffness in terms of materials science where in this case the material is human tissue which exhibits viscoelastic characteristics(stretches under tension over time)- stiffness is defined as the ability of a material to resist deformation when subjected to a given force.
To describe an erection in some physical sense. There is an inlet, volume chamber and an outlet.
Blood flows in through the inlet, the larger the diameter of the inlet the easier the blood will flow. This is good for erection obviously and is the essence of PDE5 inhibitors.
The pressure in the chamber I.e the penis, will increase and expand until final volume is reached only if the rate of flow at the inlet is greater than the rate of flow at the outlet.
I would like to focus on the rate of flow at the outlet.
If oestrogen can change the material strength of the exit vein tissue, might it become too weak too control the flow out of the penis? If so, this could easily lead to an increased outlet flow rate and an inversely proportional decrease in erection pressure inside the chamber.
I am attempting to present food for thought and merely a hypothesis as to why some people do well with higher e2 numbers and some don’t. Giving the above, it’s quite clear that our veins and arteries will all have different material properties namely stiffness. A primary cause of ED in older guys is a plaque build up in arteries which makes them stiffer. It might simply be a case of TRT and an increase e2 helps guys achieve erection if they have stiffer arteries to begin with. This also ties in with properly managed TRT that yields adequate e2 levels is a good thing for the cardiovascular system as a whole as stiff arteries is not good. Pulse pressure can be an indicator of arterial stiffness.
Younger guys for example or anyone who’s arteries are below a certain stiffness might have issues. The increase in e2 might make their outlet vein too ductile and unable restrict flow to adequately maintain and erection.
Like I said just a hypothesis, you can find papers on everything I’ve discussed individually but I’ve not seen anything investigating the bio mechanical relationship with e2 and dorsal vein stiffness directly.
If you think the hypothesis is utter nonsense please do let me know….
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My biggest problem with this dude is he tries to play this “I’m neutral game and there are both sides to the story”, but he himself is completely biased and refuses to acknowledge that these boards swing way more in favor of the militant anti AI + E2 loving crowd than not. Heck the “pro AI” mostly consists of dudes who say THEY need to control THEIR E2 to make TRT work, they don’t preach that everyone else should do what they do, like the E2 lovers such as himself.
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The thread title is incomplete, so many other hormones push, pull things in other directions to create balance and there’s so many thing we know about hormones and so many things we don’t.
I think a lot of men, once on TRT, their bodies don’t just aromatize the way a natty’s would. The ratios with T:E don’t come out right.
Too much E, and erections may fail… but then again, you want higher test to feel the effects of testosterone. But with it, comes higher E.
SO a little ai tinkering may be necessary.
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