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Study points to obesity and low Testosterone contribution of neuroinflammation.  No effect of body weight was seen with TRT.  This animal model found similar positive effects of TRT in insulin sensitivity.  Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line.  Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol.  Testosterone's effect on glial survival was positive but not significant.  Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta.   Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.

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.

Awesome review on the current understanding of Testosterone and Diabetes, metabolic syndrome, and CVD.  This article even goes into the literature on androgen receptors.

to be read

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!

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

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.

To be read article on Testosterone and Metabolic Syndrome.

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.

24 week study of 71 women post-hysterectomy finds no increase in cardiovascular biomarkers.  Several problems with this study.  First, there was a large drop out--24%.  Second and most important, the women were pretreated with estrogen prior to Testosterone therapies were initiated.  Other studies have proposed that this protects cardiovascular risk in women on Testosterone.  Previous studies show increasing endogenous Testosterone is associated with increasing cardiovascular disease in women.   This study would be much better if no estradiol was prescribed.  That would give an unbiased view of Testosterone in post-hysterectomy women.  Not much can be taken from this study. If you doctor doesn't know this, find another doctor.  Inherent bias in this study as ties to the manufacturer of the Testosterone was disclosed. This study point to the inherent flaws in so much of the medical literature today.  Most would read the headlines and read no further, but the "further" dispels the headline as flawed.

study of middle aged men (mean age--50) finds no correlation between Testosterone, DHT, and higher Estradiol levels in CVD outcomes, including mortality.  Men who died during the study had lower total Testosterone, free Testosterone, and DHT levels than those that survived during the study.

endogenous, not supplemented, estradiol positively correlated with inflammation, weight, insulin resistance, and increased homocysteine.  Likewise Testosterone positively correlated with increased weight, insulin resistance, yet negatively with HDL and SHBG.  This study looked at post-menopausal women.  The conclusion of this study was that endogenous estradiol and Testosterone are biomarkers for CVD risk.  If they are positively associated with an increased risk, then adding in extra E2 without opposition of Progesterone and Testosterone, then CVD risk is increased.

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.  

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.

New study, SWAN study, finds that bioavailable Testosterone was "significantly positively related" to visceral fat.  As bioavailable Testosterone increases in post-menopausal women, visceral fat increases.  The authors conclude that Testosterone increases visceral fat accumulation.  This increased Testosterone is concluded to be from a decrease in SHBG as a result of falling Estradiol.

Older men, 70-89, Testosterone in the middle range of normal and higher DHT was associated with the lowest death rates.  Estradiol was not found to be associated.  This study only looked at Total levels, free bioavailable levels were not assessed.  This study also highlights the basic thought, that more is not always better as it pertains to Testosterone.  It also highlights the importance of DHT.  Testosterone is a pro hormone.

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.