Estrogen-It's what makes a real man

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Some data have demonstrated that estradiol (E) plays a role in men's SD. Animal data have demonstrated that aromatase knock-out mice have decreased sexual interest, intromission, and ejaculation.17 Once these aromatase knock-out mice were given estradiol, there was a significant improvement in all 3 of these sexual parameters. A study by Finkelstein et al found that it was actually E (not T) deficiency that was primarily accounted for the decline in SD in men.18 This is supported by other data which found on multivariate analysis that the best predictor of SD in men receiving TTh was actually higher E (not T) levels.19 While these data are preliminary, one concern is that many men's health clinics across the country are using large amounts of aromatase inhibitors, which block the conversion of T to E, resulting in low E levels.
 
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Significance and conclusions

The unique experimental design of this study allowed us to examine the effects of E2 on male fat mass in the absence of testosterone. We refute our hypothesis of a direct E2 effect to reduce fat mass but provide suggestive evidence that, contrary to our hypothesis, E2, without testosterone, may increase, rather than decrease total and regional fat mass over 6 months. While preliminary, these findings provide insights into the biological actions of E2 in men, which may be more complex than traditionally assumed. While work by Finkelstein et al., and others, discussed above, has highlighted the importance of E2 in determining fat distribution and accumulation in combination with testosterone replacement, this RCT suggests E2 might be permissive for actions of androgens in preventing fat accumulation but that E2 itself is not solely responsible for these effects. This insight, if confirmed would be relevant for designing optimal hormone replacement regimens for hypogonadal men. Moreover, E2, albeit in higher doses, is currently under investigation as a sole mode of ADT (59). Given that E2 as a sole mode of ADT reduces testosterone to castrate concentrations, a better understanding of the effects of E2 on fat mass and cardiometabolic risk factors has clinical relevance, particularly since cardiovascular events are a common cause of death in men with early prostate cancer.
 


*Circulating testosterone is converted in many peripheral tissues to its two active metabolites, 5α dihydrotestosterone (DHT) and 17β estradiol (E2)

*In many androgen-responsive tissues, a family of steroid 5α reductase enzymes converts testosterone to DHT, and the aromatase enzyme, a product of the CYP19A1 gene, converts it to E2

*Many tissue-specific biologic effects of testosterone are mediated through DHT and E2

*The rates of conversion of testosterone to DHT and E2 vary among people due to polymorphisms of genes that encode the steroid 5α reductases and the aromatase enzyme as well as other host-specific factors that affect the activity of these enzymes

*It is not known how the circulating concentrations of testosterone’s metabolites – DHT and E2 – modulate the effects of testosterone on various outcomes and how their circulating levels rank in their contribution to the observed effects of testosterone treatment on physiologic outcomes
 

Significance and conclusions

The unique experimental design of this study allowed us to examine the effects of E2 on male fat mass in the absence of testosterone. We refute our hypothesis of a direct E2 effect to reduce fat mass but provide suggestive evidence that, contrary to our hypothesis, E2, without testosterone, may increase, rather than decrease total and regional fat mass over 6 months. While preliminary, these findings provide insights into the biological actions of E2 in men, which may be more complex than traditionally assumed. While work by Finkelstein et al., and others, discussed above, has highlighted the importance of E2 in determining fat distribution and accumulation in combination with testosterone replacement, this RCT suggests E2 might be permissive for actions of androgens in preventing fat accumulation but that E2 itself is not solely responsible for these effects. This insight, if confirmed would be relevant for designing optimal hormone replacement regimens for hypogonadal men. Moreover, E2, albeit in higher doses, is currently under investigation as a sole mode of ADT (59). Given that E2 as a sole mode of ADT reduces testosterone to castrate concentrations, a better understanding of the effects of E2 on fat mass and cardiometabolic risk factors has clinical relevance, particularly since cardiovascular events are a common cause of death in men with early prostate cancer.
It would be interesting to see what happens when androgen deprivation is not in the picture, just giving some estradiol to hypogonadal men with low e.
 
Thanks for the info. Started trt as my number were low. Even my doc said how the fk have I managed having such low E2. Since being on trt (3yrs) my E2 has never been high. Always had very low libido. Moody snappy and never happy. I don't not aromatize from trt... I've even taken oral Estridol and still no libido. How can I boost my E2?
 
It would be interesting to see what happens when androgen deprivation is not in the picture, just giving some estradiol to hypogonadal men with low e.

They would simply undergo male -> female conversion to a smaller or larger extent.

High E2 in the presence of low T = gyno, etc

All advocates of running high E2 are doing so within the context of high androgens as well.
 
Libido is more than just about optimal hormones, wellbeing and a healthy mental state are needed for libido.
Yeah I totally agree but it's I can fishes circle having no libido is what's causing my my anxious and low mood.. if my libido was average then everything will be fine
 
 
Yeah I totally agree but it's I can fishes circle having no libido is what's causing my my anxious and low mood..

I have compiled a list of things that affect libido, maybe you can through the process of elimination check these off.

Things that affect libido:

  • Obesity
  • High blood pressure
  • Diabetes
  • Poor sleep
  • Medications
  • Stress/depression
  • Low testosterone
  • Infections
  • High prolactin
  • Low thyroid hormones
  • Alcohol & drugs
  • Surgery
  • Heart disease
  • High cholesterol
 
Libido is more than just about optimal hormones, wellbeing and a healthy mental state are needed for libido

I disagree with this to a large degree except in the most extreme of cases.

As a teenager I never slept and got severely high/drunk pretty much on a nightly basis. My diet was horrible and my mental state all over the place. Regardless, my libido was through the roof and I could masturbate 5 times in a row and have sex 7 times in a row with my girlfriend just afterwards, no exaggeration. In the midst of thinking about throwing myself off a bridge I still had overwhelming sexual thoughts and massive erections just from seeing an attractive girl walk down the street.

Why would it be that suddenly as an adult you need every single lifestyle parameter to be optimized just so you can get it up for 15 minutes? Doesn't make any sense.

I think the idea that your libido is low because there's not enough Potassium in your diet or you're not getting enough sleep, is ridiculous. The impact of those things is minimal relative to that of your baseline brain chemistry
 
As a teenager I never slept and got severely high/drunk pretty much on a nightly basis. My diet was horrible and my mental state all over the place. Regardless, my libido was through the roof and I could masturbate 5 times in a row and have sex 7 times in a row with my girlfriend just afterwards, no exaggeration. In the midst of thinking about throwing myself off a bridge I still had overwhelming sexual thoughts and massive erections just from seeing an attractive girl walk down the street.
 
Most guys here are not teenagers or doing high doses of trenbolone. Using those two examples to discuss libido in men is pretty useless to this discussion.

Poor sleep, medication side effects, stress, relationship issues, etc are issues that men over 40 have to moderate if they want to have good libido. Please don’t dismiss these factors.

There are lots of men with high testosterone and no hormone issues that have come to this site without libido.

 
Anastrozole 1mg/day inhibited Estradiol to the same level independent of the testosterone level! I assumed it would be about 50% inhibition for men. Did I get this correctly from the slides?
 
What I have so far not understood is the relevance of relation of Estradiol to progesterone. There is a term estrogen dominance for women as well as men. In order to keep this ratio balanced with varying T levels the progesterone levels should have adapted?

This study was 16weeks, isn't that the period when starting TRT which is often framed honeymoon phase? Just wondering if the study results would differ at 6 and 12 month period.
 
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