Group items tagged

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.

A cross-sectional study of 1,458 men over a 13 years found an increase risk of diabetes incidence with elevated Estradiol and Estrone levels.  The greatest association was found with Estrone.  This should come as no surprise to anybody as type II diabetes is clearly associated with increasing weight and this is the source of 80% of estrogen production in men.

The point of this study post is not the focus on the sex change, but that estrogen dosing in men is associated with increased CVD. This is known from the other literature.

Declining Testosterone, calculated free Testosterone, Estradiol, and Estrone levels appear to be associated with muscle mass/strength decline in elderly men.  This points to a global decrease in HPA function rather than an individual, specific hormone deficiency.

High Estradiol is reproducible finding in men with Diabetes.  Link to MI not able to be determined.

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.

Presentation of a familial incidence of male gynecomastia and hypogonadotropic hypogonadism via peripheral aromatase activity.

First, Testosterone pellets are not the way to go.  Historically, these will go the way of all the implantable contraceptive devices.  However, the conclusion of this study is good and confirms the benefit of anastrazole to inhibit aromatase activity and help to maintain Testosterone levels.

Study finds a link between Estradiol, venous insufficiency, and ED in men.  The signaling is through VEGF and NO.

This article points to the impact of T:E2 on ED in men.  A declining T:E2 increases ED in older men.  

Fascinating difference in the sexes.  High estradiol is found to be associated with depression in men and high Testosterone is found to be associated with depression in women.  The exact mechanism or strength of association is unstated.