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Adding Estradiol to Testosterone in rate model significantly increases prostate carcinogenesis in rat model.

no correlation between Testosterone, estradiol, and DHEAS levels and homocysteine in men >40.

Estradiol induces prostatitis in male rat model.

Low total Testosterone, low free Testosterone, and low SHBG associated with increased CRP.  Serum total estradiol and free estradiol trended to a positive association, but did not reach statistical significance.

Estradiol positively associated with RF in men with RA.

Estradiol in men is associated with increased IL-6.  No association was found with CRP or TNF-alpha.

total and bioavailable Estradiol associated with increased hsCRP in men age 40-80.  Bioavailable is calculated with serum calculated free Testosterone and albumin bound Testosterone.

Estradiol found to be associated with increased IL-6 in older men. This after, the adjustments to exclude variables.  Other inflammatory markers were not associated.

Study results suggest that higher Testosterone and lower Estrogen levels provide anti-inflammatory effects in men.  The inflammatory biomarker assessed here was CRP.  Low total and calculated free Testosterone was associated with an increase in CRP.  In contrast, total and free Estrogen was associated with an increase in CRP.  Estradiol increased WBC count and SHBG was inversely related to WBC count in this study.

men with Testosterone levels in the middle quintiles had the lowest risk of death compared to low and high quintile levels.  

To be read article on Testosterone and Metabolic Syndrome.

Higher Testosterone and DHT levels in men was found to be positively associated with FEV1 and FVC; Estradiol was not.  The question here is cause or effect.  

Also interesting is the fact that smokers had higher Testosterone levels compared to non-smokers.

Time that physicians start following the science.  Study using data from the Multi-ethnic Study of Atherosclerosis was used to assess hormones and fatty liver in men and women.  Increasing bioavailable Testosterone levels in women was found to be associated with increasing fatty liver in post-menopausal women.  The opposite was found to be true in men.  Higher Estradiol levels were found to be associated with increased fatty liver in both sexes.  However, the statistical significance was higher with men.  Higher SHBG was associated with lower fatty liver incidence in men.  

Study finds that low free T and low Total T were associated with decline in desire, ED and activity versus none with Estradiol and SHBG in older men.  The difficult issue is the threshold of "low T".  The definition of "low T" is not uniform and varies with age.  Thus baseline evaluations and correlation with symptoms, metabolic dysfunction must be done.

Study finds increased risk of sudden MI in men with low Testosterone and elevated Estradiol.  In converse, increased risk is associated with elevated Estradiol in women.

animal model finds that high fat diet induces ED more through increased Estradiol production than low Testosterone.  Of course the authors focused on the drugs to block E2 once produced, rather then reducing the T to E2 aromatase activity.  This metabolic syndrome model implies that increased aromatase activity will be present.

Study points to association of low Estradiol and spermatogenesis in males in infertile couples.  The authors eluded to the association of low Estradiol with low Testosterone, and BMI which is the likely etiology.  Low BMI will result in low aromatase activity.  For men, the majority of Estradiol production occurs from Testosterone via aromatase activity.  Estradiol likely exists in a "U" shaped pattern of benefit: to low hinders optimal physiologic function and contributes to inflammation and disease in men.

small cohort with low serum Total Testosterone improved T:E2 ratio with clomid.  Clomid restores the HPA through inhibition of the negative feedback of Estradiol on the Hypothalamus and Pituitary in men.  This allows for an increase in gonadotropin production and thus increase in testosterone production.  Aromatase inhibition therapy would likely still prove beneficial in this situation.

from CHAMP study: low serum Testosterone, free Testosterone, Estradiol and Estrone associated with functional decline in elderly men via muscle weakness.

Again, Testosterone and here Estradiol are merely there for libido and sex.  What tunnel vision?!  What about hsCRP?  What about fibrinogen?  What about IL-1beta?  What about TNF-alpha?  These inflammatory cytokines have all been reported to elevate as a result of estrogen production in men.  

And PSA?  No mention of it here.  

This linear, tunnel vision thinking on hormones has got to stop!

The study points out that all clients were using AIs and SERMs irregardless of whether they had elevated estrogens or not.  That is not a well designed study.  One group should have had AI's if elevated estrogens were present and another group should not--this would compare the effects of aromatase activity.  Second, this was simply a retrospective chart review.  Third, a 50% conversion of 34,000 + men is very high when you look at the literature.  Fourth, they point to gynecomastia as a means of negative?  The cardiovascular implications are more significant.  These studies just seem to focus on superficial things.  Fifth, did libido problems exist before?  What were the free levels?  

This falls in the paucity of data (2 studies) that point to excessive lowering of estradiol effecting libido and sexual performance.