Is elevated E2 the culprit?

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Maruffi35

New Member
Hi everyone, I am very new to this journey of hormone therapy and I am looking for some insight and experiences in regards to the current issues I’m dealing with. I was diagnosed with acromegaly and had a pituitary tumor that was removed in February of this year. The tumor caused damage to my pituitary gland and as a result I developed hypothyroidism as well as secondary hypogonadism. My medication regiment for the past few months has consisted of daily Synthroid 137 mcg, hydrocortisone 20 to 30 mg daily to account for lower cortisol levels, and HCG monotherapy injected twice a week. I also take 5 mg cialis daily. For the first month or so of this treatment plan I felt great and the erectile dysfunction problems I had struggled with previously disappeared and I was able to achieve and maintain quality erections throughout the day. However, over the past two months plus the benefits of raising my testosterone have seemingly disappeared and I am experiencing soft erections and am not able to maintain my erections. I suspected this was potentially due to elevated E2 levels as my E2 levels have always registered as above the normal range since I was 18 and while going through puberty I developed man boobs. I am 23 now and additional bloodwork has confirmed my E2 as elevated. Me and my doctor have experimented with different dosages of HCG in an attempt to find a sweet spot with maintaining a strong testosterone level but also dialing back the E2. When I first started I was injecting 4500 iu twice a week which got my testosterone levels into the 1100s. We then proceeded to dial back the amount of HCG and have continued to do so. On my last lab results, my testosterone level was at 868 and my E2 was at 66. All other bloodwork was normal. I would also like to add that nothing else in my medication regiment or bloodwork has changed or fluctuated since starting treatment. This had led me to believe that my elevated E2 is the culprit causing my issues. I hypothesize that when I first started treatment my testosterone levels were boosted which caused me to feel great but as time passed my E2 caught up and elevated as well and that is what caused the benefits of my increased testosterone to disappear. I would like to hear others opinions and insights on this and also if anyone has experienced something similar in terms of elevated E2 levels canceling out the benefits they experienced from boosted testosterone. Thank you.
 
Defy Medical TRT clinic doctor
On my last lab results, my testosterone level was at 868 and my E2 was at 66. All other bloodwork was normal. I would also like to add that nothing else in my medication regiment or bloodwork has changed or fluctuated since starting treatment. This had led me to believe that my elevated E2 is the culprit causing my issues.
Sometimes when guys start out on the higher end, they do fine for a while, but later on start to see benefits slip away. This happens because of androgen excess and it takes a while for the body to start having issues with it.

This is quite common occurrence on these TRT boards to hear of issues several months down the road and reducing the dosage usually fixes the problem.

Not everyone was built for testosterone on the higher end. Don't get trapped into thinking more testosterone is better, sometimes it is, but sometimes it's as bad as not enough.

If you haven't already, I would try to lower your dosage and see how you feel with hormone levels near midrange.
 
Last edited:
An interesting read, have a look!

Enter the CAG Repeat: The Hidden Player​

Here's where things get interesting. Researchers have discovered that it's not just about how much testosterone you have, but how well your body responds to it. The androgen receptor (AR), which is in charge of controlling this response, can vary greatly between men in terms of sensitivity. The secret? It's all in your genes, specifically the number of CAG repeats in the AR gene. Think of it like a volume knob for testosterone:
  • Fewer CAG repeats = AR turned up to 11, super sensitive to testosterone
  • More CAG repeats = AR with the volume down, less responsive to testosterone
 
Sometimes when guys start out on the higher end, they do fine for a while, but later on start to see benefits slip away. This happens because of androgen excess and it takes a while for the body to start having issues with it.

This is quite common occurrence on these TRT boards to hear of issues several months down the road and reducing the dosage usually fixes the problem.

Not everyone was built for testosterone on the higher end. Don't get trapped into thinking more testosterone is better, sometimes it is, but sometimes it's as bad as not enough.

If you haven't already, I would try to lower your dosage and see how you feel with hormone levels near midrange.
Thank you for your reply. In my case the benefits for me only lasted a short while, probably a little over a month or so which is why I suspected high estrogen being a problem as I figured the HCG caused it to shoot up. At first I felt great due to the increase in testosterone but as the estrogen raised as well it reached a point where it was negatively affecting me. I am currently experimenting with anastrozole and will see how it affects my levels and my symptoms and go from there. Ultimately I’ve reached the conclusion that hcg monotherapy is probably not a sustainable treatment for me long term if I’m going to need to consistently keep my estrogen in check. But right now I am trying to find out and make sure if the elevated e2 is the problem and I am hoping that the anastrozole will be successful in bringing it down.
 
An interesting read, have a look!

Enter the CAG Repeat: The Hidden Player​

Here's where things get interesting. Researchers have discovered that it's not just about how much testosterone you have, but how well your body responds to it. The androgen receptor (AR), which is in charge of controlling this response, can vary greatly between men in terms of sensitivity. The secret? It's all in your genes, specifically the number of CAG repeats in the AR gene. Think of it like a volume knob for testosterone:
  • Fewer CAG repeats = AR turned up to 11, super sensitive to testosterone
  • More CAG repeats = AR with the volume down, less responsive to testosterone

You might want to give the guy something to chew on here!

Much more to the story!

Again key point here having a CAG repeat length >24 is far from common!


* Based on a total sample of 57,826 males occupying 78 countries, the overall average number of AR CAG repeats was found to be 21.40. National averages ranged from 17.00 to 23.16.

*The same applies to androgen receptor gene CAG repeat lengths >24 in the presence of symptoms and normal testosterone levels may be considered as a state of preclinical TD [93]







You clearly have no clue what you are talking about!

Anyone running around with an absurdly low TT in the 100s with FT in the gutter claiming to feel great let alone thinks its due to having a short CAG repeat length is out to lunch!

Gets even worse thinking such levels would be healthy long-term!

Guess your some special exception though eh?

Unreal!


 
Ultimately I’ve reached the conclusion that hcg monotherapy is probably not a sustainable treatment for me long term if I’m going to need to consistently keep my estrogen in check.
It’s very common for guys to feel good at first on hCG, then feel bad as time goes on. HCG also increases cortisol and other hormones and can create imbalance where there were none before and for some it can fix an imbalance in other hormones.

HCG is perfect for someone with low cortisol, and in many cases, I have recommended it for people with TRT induced low cortisol.

TRT in isolation has better chance of success. There’s also the new oral testosterone options, Jatenzo, Orlando and Kyzatrex twice daily gel capsules.

The oral testosterone options tend to have less side effects than other delivery methods, such as injections, especially with regard to erythrocytosis in all but the minority of patients.
 
It’s very common for guys to feel good at first on hCG, then feel bad as time goes on. HCG also increases cortisol and other hormones and can create imbalance where there were none before and for some it can fix an imbalance in other hormones.

HCG is perfect for someone with low cortisol, and in many cases, I have recommended it for people with TRT induced low cortisol.

TRT in isolation has better chance of success. There’s also the new oral testosterone options, Jatenzo, Orlando and Kyzatrex twice daily gel capsules.

The oral testosterone options tend to have less side effects than other delivery methods, such as injections, especially with regard to erythrocytosis in all but the minority of patients.
Ok thanks and yeah I actually do take a daily dosage of hydrocortisone as well to supplement for my lower cortisol levels. Thank you for your insight, hopefully I can get this figured out and dialed in soon
 
You might want to give the guy something to chew on here!

Much more to the story!

Again key point here having a CAG repeat length >24 is far from common!


* Based on a total sample of 57,826 males occupying 78 countries, the overall average number of AR CAG repeats was found to be 21.40. National averages ranged from 17.00 to 23.16.

*The same applies to androgen receptor gene CAG repeat lengths >24 in the presence of symptoms and normal testosterone levels may be considered as a state of preclinical TD [93]







You clearly have no clue what you are talking about!

Anyone running around with an absurdly low TT in the 100s with FT in the gutter claiming to feel great let alone thinks its due to having a short CAG repeat length is out to lunch!

Gets even worse thinking such levels would be healthy long-term!

Guess your some special exception though eh?

Unreal!


I’m not a common man and I’m not going play favorites, fu** averages, I prefer to look at people as individuals. You’re not looking at the big picture @madman, what about the endocrine disruption going on in modern society?

Endocrine disruption can create resistance, a secondary influence of how hormones work in the body to AR gene CAG repeats. I imagine endocrine disruption can go the other way. Also, make one more sensitive to hormones.

My sister ran a daycare for over 20 years and she noticed something over the years, she couldn’t feed the same food to everyone, because the children had crazy reactions to all the food, something she hadn’t seen in 10 years earlier.

You have rare cases of toddlers going through puberty because their body was tricked into thinking it was time for puberty. The cause, endocrine disruption.

It seems I need to keep hammering this in your head.

Also, my testosterone value was late afternoon (3:40 pm), I keep mentioning that, and it keeps slipping by you.
 
Last edited:
Hi everyone, I am very new to this journey of hormone therapy and I am looking for some insight and experiences in regards to the current issues I’m dealing with. I was diagnosed with acromegaly and had a pituitary tumor that was removed in February of this year. The tumor caused damage to my pituitary gland and as a result I developed hypothyroidism as well as secondary hypogonadism. My medication regiment for the past few months has consisted of daily Synthroid 137 mcg, hydrocortisone 20 to 30 mg daily to account for lower cortisol levels, and HCG monotherapy injected twice a week. I also take 5 mg cialis daily. For the first month or so of this treatment plan I felt great and the erectile dysfunction problems I had struggled with previously disappeared and I was able to achieve and maintain quality erections throughout the day. However, over the past two months plus the benefits of raising my testosterone have seemingly disappeared and I am experiencing soft erections and am not able to maintain my erections. I suspected this was potentially due to elevated E2 levels as my E2 levels have always registered as above the normal range since I was 18 and while going through puberty I developed man boobs. I am 23 now and additional bloodwork has confirmed my E2 as elevated. Me and my doctor have experimented with different dosages of HCG in an attempt to find a sweet spot with maintaining a strong testosterone level but also dialing back the E2. When I first started I was injecting 4500 iu twice a week which got my testosterone levels into the 1100s. We then proceeded to dial back the amount of HCG and have continued to do so. On my last lab results, my testosterone level was at 868 and my E2 was at 66. All other bloodwork was normal. I would also like to add that nothing else in my medication regiment or bloodwork has changed or fluctuated since starting treatment. This had led me to believe that my elevated E2 is the culprit causing my issues. I hypothesize that when I first started treatment my testosterone levels were boosted which caused me to feel great but as time passed my E2 caught up and elevated as well and that is what caused the benefits of my increased testosterone to disappear. I would like to hear others opinions and insights on this and also if anyone has experienced something similar in terms of elevated E2 levels canceling out the benefits they experienced from boosted testosterone. Thank you.


Was there a reason your doctor wanted to try HCG mono therapy first? I mean, I guess I kind of understand the logic when it comes to maintaining natural production, but 9,000 ius of HCG per week is very hefty dose. That alone will probably cause issues, not the least of which is a good likelihood of burning out receptors resulting in desensitization to the treatment. Imho I’d say the excessive HCG doses are more likely to be an issue than the slightly elevate E2 levels. Have you discussed trt with your doc instead of HCG monotherapy?
 
Was there a reason your doctor wanted to try HCG mono therapy first? I mean, I guess I kind of understand the logic when it comes to maintaining natural production, but 9,000 ius of HCG per week is very hefty dose. That alone will probably cause issues, not the least of which is a good likelihood of burning out receptors resulting in desensitization to the treatment. Imho I’d say the excessive HCG doses are more likely to be an issue than the slightly elevate E2 levels. Have you discussed trt with your doc instead of HCG monotherapy?
Yes, my doctor is an endocrinologist who I started seeing originally for my acromegaly. He tested me and sent me for surgery and now since then we have been trying to get my hormone levels balanced as a result of damage done to my pituitary by the tumor. He examined my testes and ran bloodwork on my LH and FSH to confirm that I have secondary hypogonadism and can produce my own testosterone with proper stimulation. Based on my age and concerns of fertility he recommended starting with hcg monotherapy and he has seen success with it in other patients before. When we first started I was on the full dosage of 5000 iu twice a week which got my testosterone up to the 1100s and I felt great for the first month or two of treatment. He wanted me to dial back the dosage and I did to 4500 iu twice a week and I still felt the same until suddenly it all seemed to level off. The big indicator to me was a steady drop in erection quality. I know people go through a honeymoon phase with testosterone that levels off but I was noticing I was no longer getting fully engorged and over time my erections continued to get softer and weaker to the point now where I have not had a full erection in a month. We’ve continued to dial back the dosage but it’s not seeming to help and my e2 is still elevated. The reason I believe the problem could be e2 is because I have always had higher estrogen levels even before treatment and I know hcg causes more aromatization. Also, nothing else changed in my regiment from the time that I started to the time that I started experiencing the issues I’m facing now. The only thing that made sense to me was my e2 steadily rising until it reached a problematic level. I’m at a point now where daily cialis is no longer working. It did not work for me prior to treatment either which led me to believe my erectile issues were hormonal based. As of right now, I have started on anastrozole to see if it helps. How I see it is it either helps lower my estrogen causing symptom relief, it helps lower my estrogen but doesn’t cause symptom relief, or it doesn’t effectively work to lower my estrogen at all. Either way like you said I plan to consult with my doctor about more standard trt treatments as this protocol will not be sustainable for me long term if I have to continually keep dialing in my estrogen. But right now I’m viewing this as an experiment to see if lowering my e2 improves my symptoms which would then give me a clear idea of what my problem is.
 
Also, nothing else changed in my regiment from the time that I started to the time that I started experiencing the issues I’m facing now.
It could be the way LH receptors are being stimulated that is causing issues. Naturally, LH receptors are stimulated in a pulsatile fashion and hCG creates more constant stimulation.

Below is ten male patients naturally stimulated LH responses. There are lots of small but very brief spikes of the LH hormone. Since stimulation of LH receptors influences other hormones, this near constant state of stimulation can create imbalance, or balance where there is imbalance in other hormones.

Screenshot (16320) 1.png
 
I’m not a common man and I’m not going play favorites, fu** averages, I prefer to look at people as individuals. You’re not looking at the big picture @madman, what about the endocrine disruption going on in modern society?

Endocrine disruption can create resistance, a secondary influence of how hormones work in the body to AR gene CAG repeats. I imagine endocrine disruption can go the other way. Also, make one more sensitive to hormones.

My sister ran a daycare for over 20 years and she noticed something over the years, she couldn’t feed the same food to everyone, because the children had crazy reactions to all the food, something she hadn’t seen in 10 years earlier.

You have rare cases of toddlers going through puberty because their body was tricked into thinking it was time for puberty. The cause, endocrine disruption.

It seems I need to keep hammering this in your head.

Also, my testosterone value was late afternoon (3:40 pm), I keep mentioning that, and it keeps slipping by you.

what about the endocrine disruption going on in modern society?

Endocrine disruption can create resistance, a secondary influence of how hormones work in the body to AR gene CAG repeats. I imagine endocrine disruption can go the other way. Also, make one more sensitive to hormones.



Again as I have stated numerous times on the forum when it comes to AR DDS (distribution, density, sensitivity/polymorphisms) especially polymorphism of the AR/CAG repeat length (short/long) you need to tread lightly when speaking on such!

First off CAG repeat testing is not widely available let alone many would never up the cost for such!

Top it off that AR density is difficult to measure let alone there would be no way for the average joe to even test it!

Yes EDCs can easily wreak havoc on the endocrine system but we are talking about CAG repeat lengths here you know the shit you keep parroting on here without painting the full picture.

Post #3 says it all!

Again key point here having a CAG repeat length >24 is far from common!

* Based on a total sample of 57,826 males occupying 78 countries, the overall average number of AR CAG repeats was found to be 21.40. National averages ranged from 17.00 to 23.16.

*The same applies to androgen receptor gene CAG repeat lengths >24 in the presence of symptoms and normal testosterone levels may be considered as a state of preclinical TD [93









Also, my testosterone value was late afternoon (3:40 pm), I keep mentioning that, and it keeps slipping by you.



No shit sherlock!

Going to make a shit lick a difference when your TT is absurdly low or better yet FT is in the gutter or did you forget that there is only a 20-25% difference in peak--->trough.

Do I need to keep hammering that in your dome too?

Your reply from a previous thread:

Context is crucial. I'm natural at 104 ng/dL, Free T in the 2.89 ng/dL, both well below range in the late afternoon and I feel amazing and look and feel better than when I was at 592 ng/dL when on TRT/Jatenzo.

Take your f**king TT/FT and throw the 20-25% difference in peak--->trough in there LMFAO!

Top it all off that your FT was calculated and would most likely be slightly lower if it was tested using an accurate assay you know the gold standard Equilibrium Dialysis that I have preached on here for years!

Beyond me why you would even waste your time testing in the late afternoon let alone not even use the proper testing method for FT!

Again give people something to f**king chew on here!

Now getting back to AR DDS (distribution, density, sensitivity/polymorphisms) let alone resistance due to EDCs even if you have a short CAG repeat length having an absurdly low TT or more importantly FT in the gutter is not going to cut it!

Your FT is ridiculously low!

You would be flagged as hypogonadal with those absurdly low levels.

Sure as hell never bounced back to your baseline!

Again there is no way in hell you were running around with a TT 100-200s and absurdly low FT in your prime even if you had low SHBG to boot!

No way anyone is going to derive any benefits let alone feel stellar running around with FT in the gutter!

Pure nonsense!

Nothing healthy about this here long-term.

Look into taking up a new hobby as you should not be dishing advice out on here!

Take your side kick that lost all his CRED or better yet officially became a member of the dime a dozen club and go spew your nonsense over on bumNATION, mind you last I heard they wanted to give you the boot!
 
Your protocol is shit. Its high even for fertility. Try 300-500iu everyday and you will feel fine. Hcg need inject daily or everyotherday.
 
First off CAG repeat testing is not widely available let alone many would never up the cost for such!
Then why are you mentioning average AR gene CAG repeat values?

Seems to me, the data and the pool of people tested for CAG repeats is relatively very small.
 
Beyond Testosterone Book by Nelson Vergel
Then why are you mentioning average AR gene CAG repeat values?

Seems to me, the data and the pool of people tested for CAG repeats is relatively very small.

The point being stressed here is having a CAG repeat length >24 is far from common!

Population averages!

*In humans, the AR gene comes in many forms, called alleles. The best-studied alleles are those involving a CAG repeat sequence that encodes a polyglutamine tract near the amino end of the androgen receptor. This CAG repeat has different lengths for different people. In humans, the number of AR CAG repeats ranges from as few as 9 to as many as 36, but population averages are typically between 17 and 24 (Chamberlain et al., 1994; Hsiao et al., 1999; Irvine et al., 2000; La Spada et al., 1991).

* The same applies to androgen receptor gene CAG repeat lengths >24 in the presence of symptoms and normal testosterone levels may be considered as a state of preclinical TD [93]
 
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