low T and elevated E2 result in ED in men. The authors conclude that E2 provides an additive effect on that of low T. Yet, they fail to realize the previous research that high aromatase activity (Testosterone to Estradiol production) causes the low T.
Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
In men with low serum testosterone (for example, <8 or 230 nmol l−1) with obesity, metabolic syndrome and diabetes mellitus, treatment with testosterone is warranted
In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
testosterone replacement has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure in hypogonadal men with the metabolic syndrome as well as type 2 diabetes mellitus
Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
available data clearly show a relationship between obesity, low testosterone levels and ED
Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
Obesity is associated with low total testosterone levels that can be explained at least partially by lower sex hormone-binding globulin (SHBG) in obese men
epidemiological studies have shown a negative correlation between BMI and total testosterone and to a lesser extent with free and bioavailable (biologically active) testosterone levels
Highly active men report better sexual function/performance than less active men, though less active men were not found to have ED or sexual dysfunction.
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!
Interesting study. In this study group, 36% of type II diabetes with ED had low Testosterone. This fits with the estimated 40% of those with Diabetes have low T. What is really interesting about this study is that the degree of improvement with ED by Sildenfafil was dependent on the Testosterone level in the low T group. Meanining that Testosterone therapy in these men would probably be more of a therapy directed at the cause and not Sildenafil. Of course, the Testosterone therapy would benefit glucose regulation as well documented in the literature.