Lifestyle and Metabolic Effects on Erectile, Vascular Health
Lifestyle and Metabolic Effects on Erectile, Vascular Health
Obesity is associated with increased pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. Obese individuals require more calories to maintain their weight and the burning of that extra fuel generates more reactive oxygen species. Men with ED with and without obesity have higher levels of C-reactive protein compared to men with normal erectile function. Tumor necrosis factor-α, interleukin-6, C-reactive protein and reactive oxygen species all cause insulin resistance. Insulin is an integral stimulator of vascular NO and thereby increased skeletal muscle glucose disposal. Insulin resistance therefore reduces vascular NO, causing increased circulating glucose, and hyperglycemia itself impairs insulin action and also increases the formation of advanced glycation end products, which increase reactive oxygen species and further impair NO production. Antioxidants increase NO and insulin sensitivity; for example, ingestion of cocoa has been shown to increase insulin sensitivity in various animal and human studies, and a potent polyphenolic antioxidant in green tea increases endothelial NO and insulin sensitivity in vitro and in vivo. In 110 obese men without diabetes, hypertension or dyslipidemia, ED was strongly correlated with waist/hip ratio and was significantly improved with weight loss and increased activity, which lowered glucose, insulin, waist/hip ratio, blood pressure and triglycerides, and increased endothelial NO production. In obese men, increased insulin sensitivity, induced by diet and vigorous activity and reflected by reduced circulating insulin, was very strongly correlated with increased NO production (r=0.83).
Weight Loss
Obesity is associated with increased pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. Obese individuals require more calories to maintain their weight and the burning of that extra fuel generates more reactive oxygen species. Men with ED with and without obesity have higher levels of C-reactive protein compared to men with normal erectile function. Tumor necrosis factor-α, interleukin-6, C-reactive protein and reactive oxygen species all cause insulin resistance. Insulin is an integral stimulator of vascular NO and thereby increased skeletal muscle glucose disposal. Insulin resistance therefore reduces vascular NO, causing increased circulating glucose, and hyperglycemia itself impairs insulin action and also increases the formation of advanced glycation end products, which increase reactive oxygen species and further impair NO production. Antioxidants increase NO and insulin sensitivity; for example, ingestion of cocoa has been shown to increase insulin sensitivity in various animal and human studies, and a potent polyphenolic antioxidant in green tea increases endothelial NO and insulin sensitivity in vitro and in vivo. In 110 obese men without diabetes, hypertension or dyslipidemia, ED was strongly correlated with waist/hip ratio and was significantly improved with weight loss and increased activity, which lowered glucose, insulin, waist/hip ratio, blood pressure and triglycerides, and increased endothelial NO production. In obese men, increased insulin sensitivity, induced by diet and vigorous activity and reflected by reduced circulating insulin, was very strongly correlated with increased NO production (r=0.83).
