How many of you guys feel better with your estrogen higher than 20-30?

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KoaNA

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I'm just wondering how many of you feel better on the higher end, like 30-40, 40+, or even higher. And also what your total T and shbg are. I want to run higher levels of test for my trt and also avoid using an AI but I kind of fear the higher estrogen mainly for potential libido and ED sides.

Also I'm curious, wasn't the 20-30 range established with the standard assay, so normal may actually be a little bit lower than that?
 
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Also just to add, the reason I want to use higher levels is I haven't found symptom relief in the 700s for total T and want to try to get it higher and also avoid an AI.
 
I have higher E2 and higher T with no AI. I feel fantastic on year 4 of my protocol.
E2 = 60
TT > 1500
FT > 300
SBHG did not test this year but last year it was 47.
250mg of Tcyp per week.
50mg dheas daily
5mg tadafil daily.
 
I have higher E2 and higher T with no AI. I feel fantastic on year 4 of my protocol.
E2 = 60
TT > 1500
FT > 300
SBHG did not test this year but last year it was 47.
250mg of Tcyp per week.
50mg dheas daily
5mg tadafil daily.
Do you feel like the tadalafil is necessary for your function at these levels?
 
I really haven't tried to eliminate it. Based on the positive results and benefits I continue to take it. I will say if I take the tadafil around 6pm and then take L-arginine an hour before sex, OMG, Amazing.
 
I really haven't tried to eliminate it. Based on the positive results and benefits I continue to take it. I will say if I take the tadafil around 6pm and then take L-arginine an hour before sex, OMG, Amazing.
I've tried compounded Cialis a few times at 3mg but it kind of made me a little tired and stuffy and didn't do all that much for erections. I wonder if more time with it would eliminate the side effects and give some benefit.
 
Personally I've never felt anything from estrogen. Before I started trt, my estrogen was very low. When I increased it, I could not tell. I could tell how much better I felt when I increase my testosterone but I felt nothing from estrogen.
 
Personally I've never felt anything from estrogen. Before I started trt, my estrogen was very low. When I increased it, I could not tell. I could tell how much better I felt when I increase my testosterone but I felt nothing from estrogen.
It seems like some guys are sensitive and some aren't. Maybe the increase in T will be beneficial for me too.
 
I have higher E2 and higher T with no AI. I feel fantastic on year 4 of my protocol.
E2 = 60
TT > 1500
FT > 300
SBHG did not test this year but last year it was 47.
250mg of Tcyp per week.
50mg dheas daily
5mg tadafil daily.


What's your hematocrit like? Mine would be through the roof at these levels.
 
I can feel high or low E, I feel better around 20pg non sensitive, I have also notice morning wood coming back as e goes down.
Having said that I stopped trt now going back to hcg monotherapy to give it a second chance.
On trt I didn’t get consistent results no morning wood, though I have seen it getting better as e goes down. I didn’t give up just trying different thing if hcg monotherapy didn’t work I would try cream or go back to trt injections.
 
E2 in the 20s was meant as a reference for guys with low normal test in the 300-400 range, not on TRT. If your test is 1000 your E2 should match it and be in the 60s probably. Some don't agree with the test to estrogen ratio, but I do. On my last blood draw E2 non sensitive was 72 and total test was 930. I have no symptoms of high E2.
 
E2 in the 20s was meant as a reference for guys with low normal test in the 300-400 range, not on TRT. If your test is 1000 your E2 should match it and be in the 60s probably. Some don't agree with the test to estrogen ratio, but I do. On my last blood draw E2 non sensitive was 72 and total test was 930. I have no symptoms of high E2.
My guess would be that guys with normal 5ar conversion would handle this just fine to balance the high estrogen, but guys with less efficient 5ar might need lower levels of e2. Just a guess.
 
My guess would be that guys with normal 5ar conversion would handle this just fine to balance the high estrogen, but guys with less efficient 5ar might need lower levels of e2. Just a guess.

I don’t think I understand this, mainly because I don’t understand 5ar conversion.

Could you (or someone else) please explain? Is there a way to know whether one is an efficient 5ar converter or not?
 
I don’t think I understand this, mainly because I don’t understand 5ar conversion.

Could you (or someone else) please explain? Is there a way to know whether one is an efficient 5ar converter or not?
The process is analogous to the conversion of testosterone to estradiol with the help of the aromatase enzyme. The efficiency is probably quantified by looking at the T-to-DHT ratio, but I'm not sure about the normal range. My ratio of ~27 probably qualifies as being inefficient.

The point anterlopers was making is bolstered by DHT's role in counterbalancing estradiol. DHT can reduce estradiol's potency through competitive inhibition at receptors, and furthermore DHT has modest aromatase-inhibiting activity of its own.
 
I don’t think I understand this, mainly because I don’t understand 5ar conversion.

Could you (or someone else) please explain? Is there a way to know whether one is an efficient 5ar converter or not?




Regarding 5α-reductase (5AR) conversion:






Testosterone Metabolism
After testicular secretion, a small proportion of testosterone undergoes activation to two bioactive metabolites, estradiol and DHT, whereas the bulk of secreted testosterone undergoes inactivation by hepatic phase I and II metabolism to inactive oxidized and conjugated metabolites for urinary and/or biliary excretion (108).


The amplification pathway converts ~4% of circulating testosterone to the more potent, pure androgen, DHT (50, 52). DHT has higher binding affinity to (109) and 3-10 time greater molar potency in transactivation (110-112) of the androgen receptor relative to testosterone. Testosterone is converted to the most potent natural androgen DHT by the 5a-reductase enzyme that originates from two distinct genes (I and II) (113). Type 1 5a-reductase is expressed in the liver, kidney, skin, and brain, whereas type 2 5a-reductase is characteristically expressed strongly in the prostate but also at lower levels in the skin (hair follicles) and liver (113).

DHT circulates at ~10% of blood testosterone concentrations, due to spillover from the prostate (122-123) and nonprostatic sources (124).


Screenshot (741).png






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Dihydrotestosterone has anti-estrogenic properties as it competes with other substrates for binding to the aromatase enzyme.

Mesterolone is a modified form of dihydrotestosterone and is believed to have anti-estrogenic properties.






William Llewellyn's ANABOLICS

Andractim® (dihydrotestosterone)

Description: Andractim is a prescription steroid preparation that contains the potent androgenic steroid dihydrotestosterone. This product comes in the form of a transdermal gel, typically containing 2.5% dihydrotestosterone by weight in an 80 gram tube. As with Androgel, roughly 10% of the active steroid will make it into circulation with each application.This would equate to 80 doses of 25 mg, with each dose delivering approximately 2.5 mg of steroid to the body. Dihydrotestosterone itself is the most active androgen in the human body, displaying an ability to bind and activate the androgen receptor at least three or four times greater than that of its parent steroid testosterone. This trait, however, is not accompanied by equally powerful anabolic tendencies. In the case of dihydrotestosterone, we have a steroid that is almost purely androgenic, with only minimal muscle-building (anabolic)action.

Dihydrotestosterone is a weak muscle builder because it is extremely open to alteration by the 3-alpha-hydroxysteroid-dehydrogenase enzyme, responsible for breaking down active steroids like DHT into their inactive metabolites. 3a-HSD is present in high quantities in muscle tissue, running interference between the outer cell membrane and the androgen receptors that all steroid hormones are trying to reach. In humans, little DHT ends up actually reaching this receptor. Testosterone is very resistant to this enzyme, however, which allows it to be a much more effective muscle-building agent. 3a-HSD steroid deactivation in muscle tissue causes the same problem with Proviron (1-methyl-dihydrotestosterone). DHT and Proviron both have very effective uses in areas such as fat loss, hardening, increasing CNS activity,and pure strength gains, but they do not perform well as anabolic agents.


Dihydrotestosterone is not aromatized by the body, and is not measurably estrogenic. An anti-estrogen is not necessary when using this steroid, as gynecomastia and water retention should not be concerns even among sensitive individuals. DHT also has inherent anti- estrogenic properties, competing with other substrates for binding to the aromatase enzyme. Percutaneous dihydrotestosterone may be an effective option for the treatment of gynecomastia. Studies have reported a good level of success when treating certain forms of this disorder with Andractim, the drug affecting the ratio of androgenic to estrogenic action in the breast area enough that a notable regression of mammary tissue has been achieved in many cases.




Proviron (Mesterolone)

Mesterolone is actually believed to act as an anti-aromatase in the body, preventing or slowing the conversion of steroids into estrogen. The result is somewhat comparable to Arimidex®, although less profound. The anti-estrogenic properties of mesterolone are not unique, and a number of other steroids have demonstrated similar activity. Dihydrotestosterone and Masteron (2-methyl-dihydrotestosterone), for example, have been successfully used as therapies for gynecomastia and breast cancer due to their strong androgenic and potentially anti-estrogenic effect.
 
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DHT and Proviron (Mesterolone) both have very effective uses in areas such as fat loss, hardening, increasing CNS activity,and pure strength gains, but they do not perform well as anabolic agents.


AAS that are derived from dihydrotestosterone that posses such properties stated above such as oxandrolone (Anavar), drostanolone propionate (Masteron), stanozolol (Winstrol).....come to mind and with the added benefit that they are effective as anabolic agents when taken using the proper dose as oppose to DHT or Proviron!
 
@madman as always great information. I had little water retention from Tcyp and felt a bit emotional. So I added half a tablet or 12.5mg Proviron to my protocol as an anti-estrogenic. This had its effect after 2-3 days. After 80 days I am on a break from it but have aches in my hands, knuckles as in my knees after sitting for a long time. This feels to me that my estradiol/DHT ratio needs to rebalance in the upcoming week. Next I will try some 5mg Drostanolone Propionate to my daily SubQ injections or add a click of cream to the nutsack to up my DHT levels.
 
I don’t think I understand this, mainly because I don’t understand 5ar conversion.

Could you (or someone else) please explain? Is there a way to know whether one is an efficient 5ar converter or not?
The guys in this thread did a much better job of explaining it than I ever could. But my thought was that as long as DHT levels (from 5ar conversion of T) rose in proportion, it would balance out higher e2 levels because it competes w estrogen and has a mild anti aromatase effect. A lot of guys on trt seem to not have great 5ar conversion levels, which could be why some do great even with higher estrogen and some guys don't.
 
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The guys in this thread did a much better job of explaining it than I ever could. But my thought was that as long as DHT levels (from 5ar conversion of T) rose in proportion, it would balance out higher e2 levels because it competes w estrogen and has a mild anti aromatase effect. A lot of guys on trt seem to not have great 5ar conversion levels, which could be why some do great even with higher estrogen and some guys don't.
This figure, which I recently posted in another thread, may be of interest. It shows how E2 and DHT rise with the dose of injected testosterone.
Untitled 20.jpeg

The important features are the saturation effects—less conversion as testosterone increases—due to the finite supple of enzymes, and the observation that E2 conversion is more efficient in older men, while DHT conversion stays about the same.
 
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