How does high estrogen cause poor erections and low libido?

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jonfranks

New Member
Are there any scientific/medical explanations as to how and why high estrogen will cause weak erections or "up and down" erections and/or a poor libido?

Also of note, why can PDE5 medications ( Cialis, Viagra ) mask or override high e2 and allow for a decent erection? Does high e2 do something to your body in which it cannot produce NO or smooth the penis muscles for blood flow? Its interesting to note that 95% of the time if you crash your e2 a PDE5 will not help you at all.

Note: when people say "hey I have high e2 symptoms" what they are really saying is "hey I have poor T:e2 ratio for a man". Same for low e2.
 
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Defy Medical TRT clinic doctor
Theres some bit about E in the penis affecting penile tissue though this get's little discussion. This is different than just libido, the difference between wanting to have sex and the ability to have sex.
 

HealthMan

Member
Estrogen induces nitric oxide production so that might explain the erection part (although some men complain about ED issues when estradiol is too high)
 

jonfranks

New Member
OK so to edit the question - a better way to phrase it would be why does a poor testosterone to estrogen ratio cause libido and ED? When guys say "my e2 is high and I have high e2 symptoms" its not just the e2 number in a void. Its a high e2 in the context of their testosterone levels.

For very simplified example ( assume all other health markers are good ).. if a guy has a TT of 720 and an E2 23 he will have a normal libido and erection. If that e2 number went to 40 then he might have ED and say hey I got high e2 symptoms.
 

broker

Active Member
High estrogen will effect a natural guy more so in that the high E will lower testosterone production due to the feedback loop. That wouldnt apply to men using T replacement.
Another theory is that excess estrogen attatches to the androgen receptor preventing T from binding. I have heard this a few times. Anyone care to expound?
 

YBWV

Member
OK so to edit the question - a better way to phrase it would be why does a poor testosterone to estrogen ratio cause libido and ED? When guys say "my e2 is high and I have high e2 symptoms" its not just the e2 number in a void. Its a high e2 in the context of their testosterone levels.

For very simplified example ( assume all other health markers are good ).. if a guy has a TT of 720 and an E2 23 he will have a normal libido and erection. If that e2 number went to 40 then he might have ED and say hey I got high e2 symptoms.

It's not the T to E2 that is the issue in this context it is the DHT:E2.

In the case of your example of a guy with TT of 720 and E2 at 23 he could be doing ok, from a hormonal perspective, if he had DHT in the 60's which would seem around average for 5-ar conversion.

Problem is that, as with most things, the conversion rate isn't linear so with treatments that raise the total levels of the sex hormones the balance can get thrown off.

If the same guy had E2 of 40 (unlikely with TT of 720 but common at higher levels) then he would need DHT of around 120 to 160 which is 50 or 100% over the top of range and would scare many doctors.

It's worth remembering that with DHT circulating Serum levels are not an accurate reflection of action at receptors or in target tissue. So, more than ever, subjective improvements in symptoms is what counts rather than levels and ranges.

DHT gets ridiculously demonised because it can exacerbate and accelerate the balding process in susceptible individuals.

Yet the fact remains that guys need adequate DHT in their Brain and in their Balls for good sexual function.
 

broker

Active Member
YBWV
Can you explain the dht / estrogen theory with regards to my personal blood work?
When my total T is 700’s, my estradiol is about 26 but my dht is almost 110.
This is from 100 mgs of T per week when i was using,
 

YBWV

Member
If the 100mg was all from injected T then 110 with a total in the 700s would seem slightly high but not if some was from transdermals. Reasons for higher than average conversion could include exposure to endocrine disruptors, other pharmaceutical/drug use, synthetic steroids, having higher than usual 5-ar activity - being a preferential converter - probably loads more.

From the way you pose your question I assume that you had problems at those levels. The serum levels of DHT, more so than the other sex hormones, are not an accurate measure of activity in peripheral tissue. (Many TRT providers don't measure Serum DHT even for patients presenting with sexual dysfunction). Horton's 1992 study showed DHT to be a Paracrine hormone - formed and acting in target tissue - if that is the case then I assume an individual could have excessive DHT in some tissue and insufficiency elsewhere.

Measuring and monitoring our own individual DHT levels, along with those of the other sex hormones, can help us over time to gauge what we need to do to improve hormonal function.
 

broker

Active Member
Well, i do have some prostate enlargement at 51 years old.
I do notice my hair thinned a tad but now that im off, it seems better.
It was all injectable. I can tell you when my T levels were higher from 125 mgs per week, my dht went to 150 ! my estrogen never gets high though.
I always wondered about taking very small dosage of finasteride and getting DHT to lets say the 40-50 range, not crashing dht, while Using T injections would be a thought? Opinion?
 
Suppression of an Androgen like DHT thru the use of Finasteride is akin to chemically neuturing a guy. That's a little overstated but in general you won't find this forum to be accepting of Finasteride/et al..., You should google "post finasteride syndrome".

To that end genetics has far more to do with MPB and Prostate issues than DHT.
 

YBWV

Member
Well, i do have some prostate enlargement at 51 years old.
I do notice my hair thinned a tad but now that im off, it seems better.
It was all injectable. I can tell you when my T levels were higher from 125 mgs per week, my dht went to 150 ! my estrogen never gets high though.
I always wondered about taking very small dosage of finasteride and getting DHT to lets say the 40-50 range, not crashing dht, while Using T injections would be a thought? Opinion?

I get you. You seem to have your sensitivity to the androgens well measured. If avoiding/slowing further hair loss is the priority then I guess keeping androgens at a lower but sufficient level would work.
It doesn't take high levels though - women get androgenic alopetia too.

The potential use of finasteride and balancing act with DHT & T sounds an unlikely prospect in my view. I go out of my way to avoid even mild endocrine disruptors and finasteride sounds like some potentially nasty stuff. I don't know that there is a 'very small dosage' with that?
 

broker

Active Member
Im not talking about crashing DHT, i am talking about using a very small amount of finasteride in conjunction with T just to bring DHT to a mid normal level from a very high level when using T. Example, if i use T and my dht goes to 100, a small amount of finasteride to bring dht to 50 ? Does that make sense?
 
Im not talking about crashing DHT, i am talking about using a very small amount of finasteride in conjunction with T just to bring DHT to a mid normal level from a very high level when using T. Example, if i use T and my dht goes to 100, a small amount of finasteride to bring dht to 50 ? Does that make sense?

No it doesn't.
If you want to use Finasteride and/or suppress DHT its unlikely this forum is going to help you do it.
 

rafapark

Member
Estrogen induces nitric oxide production so that might explain the erection part (although some men complain about ED issues when estradiol is too high)
Most people blame high E2 for many things without really knowning was is causing the problem, including erections. As Nelson noted there is not a single study linking higb E2 to poor erections.
 

YBWV

Member
Im not talking about crashing DHT, i am talking about using a very small amount of finasteride in conjunction with T just to bring DHT to a mid normal level from a very high level when using T. Example, if i use T and my dht goes to 100, a small amount of finasteride to bring dht to 50 ? Does that make sense?

The theory makes some sense to me - Finasteride is a 5-ARi - but the reduction of the DHT:T ratio by attempting to balance your hormones from the top down with Finasteride seems a horrible proposition. Finasteride is potentially any man's Kryptonite.

Have you considered/tried hCG? With your apparent tendency to convert preferentially to DHT and lowish aromatase conversion (opposite to many guys) it could have possibilities either as mono-therapy or adjunctive with T at a lower dose than taken previously.

Your experience is the opposite of mine in that I've always looked to increase DHT, yet the solution is perhaps the same: the balancing of the 2 metabolites E2 and DHT.
 

broker

Active Member
My concern with long term hcg is the possibility of decentisization which is not proven but speculated. Further, i took hcg at 1000 iu per week( 500 iu 2x per week) for 6 weeks and coincidentaly got eppididimytis and a swolen prostate. I dont know what the actual cause was. The fact that hcg directly effects the testes leads me to be concerned.
My theory on finasteride is using it to prevent dht from skyrocketing. A very small amount that keeps it ( maintains) within a normal range. The problem with my theory is if you can actually control dht with finasteride or just taking any amount of finasteride is enough to kill it. I suspect no because its available in 5mgs and 1mg which means the effects are dose dependant. I was thinking of taking .5mgs 3x per week and then getting tested for dht levels. Thats only 1.5 mgs per week.
a cautionary thought is if the actual drug can somehow permanantly damage the 5ar enzyme or somehow damage the androgen receptor itself, i just dont know.
Whats interesting is arimidex does exactly the same thing with estrogen as finasteride does to dht and yet no one ever has permanant issues with estrogen production after arimidex use.
I realize they are two different drugs but they both prevent conversion at the respective enzymes. Just some food for thought.
 
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