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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.

new study finds that men >65 with low libido and Testosterone levels < 275 increase sexual function with Testosterone therapy.  Only libido was improved; no benefit to erectile function was noted--note that is likely due to depleted NO.  Given time that should improve with he increase in NO synthase and thus NO.  I have a fault with on elf the comments on this study: they point out that increased free Testosterone and estradiol levels were associated with improved sexual activity.  This lacks an understanding of the physiology.  In men with low T > 65, the majority are dealing with inflammation and excess weight; all of which increase aromatase activity and thus estradiol activity.  This does not indicate that an increase in estradiol activity is associated with improved libido in men.  How can elevated estrogen levels lead to low T and then increase levels are associated with improved libido?  This is merely a reflection of the body's dysfunctional physiology.  This observation of increased estradiol by no means shows cause and effect.  Scientists need to due a better job in vetting what they write!

This study confirms what we know about Testosterone, but this study finds that Estradiol aids libido and fat loss.  The conclusion on Estradiol I believe to be extremely premature.  First, it flies in the face of all the accumulative data on estradiol, second, what normal physiology is being replicated with goserelin???  Goserelin has been shown to decrease Prolactin which can effect libido also.  What about the potential there?  The men included in the study were described as "healthy".  So, you are taking "healthy" normal funcitoning men, throwing in a monkey wrench and looking at the effects of your monkey wrench.  Sorry, not physiologic.  In all my practice, I have seen one man with low Estradiol levels.  There is no reference to the hormone levels in the men preceding the suppression with goserelin.  This is a study that lacks application.

Interesting study.  Adipose production of Estradiol in both men and women not reflected in serum Estradiol.  Serum Estradiol is just transport hormones.  This same finding has been shown in prostate aromatase activity.  

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.

testosterone and Estradiol effect IGF-1 levels.  This small study looked at 8 men and 8 postmenopausal women.  Findings:  low testosterone and high estradiol decrease IGF-1 availability.   Estradiol in postmenopausal women will result in a decrease in IGF-1 through an elevation of IGFBP-1.  In men, testosterone replacement stimulates increased HGH secretion and resultant IGF-1 secretion

This is the perfect study to compare synthetic, unnatural hormones with bioidentical hormones.  Premarin was compared with bioidentical estradiol.  Premarin reduced the endothelial NO synthase transcription and activity by 30-50% compared to Estradiol.   Thus, premarin results in a lower NO production and thus greater endothelial dysfunction compared to Estradiol.

Men with metabolic syndrome found to be associated with higher Estradiol levels.  Thus, Estradiol in "older men", >65 in this study, is associated with metabolic syndrome.

In this animal study, estradiol is added to Testosterone to increase prostate carcinogenesis.  Previous rat studies have shown that adding estradiol to Testosterone, which occurs naturally, increases prostate cancer risk.  

Estradiol found to be associate, though weakly, with IL-6 in men.  This provides a link between estradiol production in men and inflammation.

Estradiol found to be associated with Metabolic syndrome in men. This was independent of other confounding variables.  Most men, the excess estradiol comes from increased aromatase activity on testosterone.

Men with BPH found to have higher levels of stromal Estradiol and Estrone.  This is associated with aging.  This elevation was not found in the prostate epithelium.  No correlation with Testosterone and the stroma and epithelium were found.  So, the point is that what is happening in the prostate appears to be related to increased aromatase activity in the prostate.  Which this has been shown to be evident in the lateral lobes of the prostate in other studies.  But DHT?  The numbers here are slightly elevated.  BUt the balance of DHT to Estradiol may be more important than the individual levels.  This study was done in humans.

Older men have Estradiol levels that are 3 x that of a post-menopausal women.  The bioavailable levels of Testosterone and Estradiol showed the greatest precipitous decline.

Study finds association between elevated Estradiol in young men and obesity.  No correlation was found with Testosterone.  This fits other research that points to early increased Estradiol production and late decrease in low T.  The men in this study were "young".  Testing was done in saliva.

Great confusion exists in the medical profession about Testosterone and PSA and the health of the prostate. The conversion of Estrogen, whether E2 or E1, and other variables are responsible for increases in PSA while on Testosterone therapy. This study points out that Estradiol in men stimulates cell line growth of prostate cancer. In contrast, Epitestosterone, an androgen metabolite, has antiandrogen, inhibits this estrogen activity. Epitestosterone exists in an inverse relationship to Estradiol and IGF-1.

Study of 500 men with CHF and reduced LVEF found that estradiol has a "U" shaped relationship to prognosis.  A low and high estradiol levels are associated with increased poor prognosis.  Other biomarkers in these 2 groups were different, suggesting different physiologic mechanisms.

Estradiol increased thyroid papillary and follicular cancer cells via both ER alpha and ER beta in this study.  What is also interesting is that estradiol did not increase PR expression.

This is an important study.  Study found that Estradiol increased the transcription of pyruvate kinase M (PKM2)production in endometrial stromal cells.  This increase in PKM2 shifted metabolism to a aerobic glycolysis pattern similar to the Warburg effect described in cancer.  Additionally, increased PKM2 via Estradiol increased ER alpha transcription and functioned as a ER alpha coactivator.

review of estrogen metabolites and breast cancer risk in premenopausal women.