Just the abstract, but Testosterone to estrogen production through aromatase activity plays role in prostate cancer. This is due to the lack of correlation in androgens and prostate cancer in the androgen hypothesis. Estrogen receptors alpha/beta balance equally play a role.
Life extesnsions rebuttal to recent JAMA study. There was several significant flaws in that study and thus limited evidence can be gained by that study. In fact, I find no useful clinical information from that study.
In the rebuttal, there are flaws. The reference the low serum T after treatment and correctly discuss aromatase activity. But they fail the mention that the less than optimal serum T is likely the result of the high aromatase activity in these men. Age, stress, and weight are primary causes of increases estrogen production in these men. These would be why likely high estrogen production occurred and less than optimal serum T resulted. And, increased E2 will cause an increase in CRP which can precipitate CVD events.
Study finds that increasing body fat and associated insulin resistance in women with PCOS is associated with an increase in CRP. These women with PCOS are hyperandrogenic. It makes absolutely no sense to give these women more Testosterone.
Study finds that Testosterone provided a small anti-inflammatory effect in post-menopausal women and men, whereas Estrogen increased macrophage cytokine production in post-menopausal women with elevated LDL. Now, this study did not differentiate PCOS versus non-PCOS, nor did it look at the effects of adiposity in these hormonal effects in women. Both of which, will effect the outcome.
Study confirms aromatase activity in the prostate itself. Systemic Testosterone and Estradiol evaluation (ie blood) will not necessarily reflect endogenous prostate aromatase activity.
The genesis of cancer is complex. To simply say that cancer is genetic is both niave and uninformed. This study displays the complexity of the timing of hormones and cancer genesis. This rat study found that Estradiol added to Testosterone increased "markedly". Estrogen plays a role in the genesis of prostate disease. However, this varies among individuals. The response of prostate cancer to estradiol appears to change according to the progression of the cancer.
As these authors call it--late onset hypogonadism (what is with all these names), Testosterone therapy provides no increased risk of prostate cancer or elevated PSA when followed for 5 years.
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.
Study finds that Testosterone is associated with reduced CRP. This association was especially evident in the higher weights. No association was seen with E2 in this study.
Post menopause women with PCOS have high CVD. PCOS is essentially metabolic syndrome separated by age. Both PCOS and MetS in women is associated with an increase in Testosterone levels.