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This study found that lower TT and E1 associated with more "poor health" as defined by questionnaire.  The conclusion might lead one to think that Estrogen therapy is need in men.  Eightly percent of estrogen production in men occurs from Testosterone.  If Testosterone declines, then estrogen production will likewise decline.  A simple fact that the authors did not comment on.  Also, E1 binds with high affinity to ER alpha, which is pro-inflammatory and pro-proliferative: neither of which is a positive health benefit.   This appears to point more to a broad HPA suppression as an association to the "poor health".

High Estrone (E1) associated with increased prostate cancer risk.  This occurs through high aromatase activity.

Study looked at inflammatory markers in RA.  The authors point to high aromatase activity, low androgens, and elevated estrone in synovial fluid as an indicator of a link between aromatase activity and inflammation production through E1 production.  The authors also point to the 16 alpha metabolite pathway as pro-inflammatory as well.  One very interesting point made by the authors is that vitamin D down regulates aromatase activity.  In addition to NK-kappaB inhibition, this may be another mechanism by which vitamin D reduces inflammation.

This study proves the problems rampant in science today.  This study looked at older men with mobility limitations: safe to say, not optimal health.  They give 10 grams of testosterone daily to these men.  Physiologic doses are 5-10 mg.  And they are surprise that there is an increase in side effects, here in this study CVD.  They did look at cytokines, I'll give them that; but they did not look at aromatase activity and E2, E1 levels which have been shown to be the driving forces behind these inflammatory cytokines in men.  Testosterone has in fact been shown to downregulate these inflammatory cytokines.  Poor study.  No conclusion can be taken from this study.

Estrogens appear to have an immune stimulatory effect in the presence of inflammatory cytokines.  The estrogens appear to increase inflammation through activation of NFkappaB.  But of course, not all estrogens are equal.  This article is primarily referencing E2.  I would expect E1 due to its preference for ER alpha, but not E3, due to its ER beta preference.

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.

Obesity in young girls increases Estradiol production compared to thin young girls.  Obesity increased  the Estrogen metabolite 16lpha-OH-E1  and this positively correlated with IL-6. 

Study shows that estradiol decreases ER beta in the prostate. ER beta is anti-inflammatory, inhibits growth, and promotes cell death: all of which would decrease risk of prostate growth and/or cancer.   We know that men increase estrogen production through increased aromatase activity, which according to this study, will decrease ER beta and the prostate associated benefits.

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.

Study finds that lower SHBG, higher Estradiol, Estrone, Testosterone levels, and free androgen index is associated with increased CRP in "healthy" postmenopausal women.

intro to incretins

to be read

great review on Gc-MAF in cancer.  An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.