Diabetes. Erectile Dysfunction is common in people with diabetes. An estimated 10.9 million adult men in the U.S. have diabetes, and 35 to 50 percent of these men are impotent. The process involves premature and unusually severe hardening of the arteries. Peripheral neuropathy, with involvement of the nerves controlling erections, is commonly seen in people with diabetes.
The prevalence of biochemical testosterone deficiency increases with age. This is partly due to decreasing testosterone levels associated with illness or debility but there is also convincing epidemiological data to show that serum free and total testosterone levels also fall with normal aging (Harman et al 2001; Feldman et al 2002). The symptoms of aging include tiredness, lack of energy, reduced strength, frailty, loss of libido, decreased sexual performance depression and mood change. Men with hypogonadism experience similar symptoms. This raises the question of whether some symptoms of aging could be due to relative androgen deficiency. On the other hand, similarities between normal aging and the symptoms of mild androgen deficiency make the clinical diagnosis of hypogonadism in aging men more challenging.
Testosterone begins with cholesterol. In fact, every single sex hormone you make you synthesize from cholesterol – that’s one reason a “heart healthy” low-fat, low-cholesterol diet limits your performance. Fat and cholesterol don’t make you fat. They give your body the building blocks to create abundant testosterone and other sex hormones, which actually makes you lose weight and build muscle, especially if your current testosterone levels are low [1].
Qaseem, A., Snow, V., Denberg, T. D., Casey, D. E., Forciea, M. A., Owens, D. K., & Shekelle, P. (2009). Hormonal testing and pharmacologic treatment of erectile dysfunction: A clinical practice guideline from the American College of Physicians. Annals of internal medicine, 151(9), 639-649. Retrieved from http://annals.org/aim/article/745155/hormonal-testing-pharmacologic-treatment-erectile-dysfunction-clinical-practice-guideline-from 

Having learned a great deal more about erectile dysfunction including its risk factors and causes, you should be equipped to assess your own erectile function. If you have experienced erectile issues or you have some of the risk factors mentioned above, it may be worth making a trip to your doctor’s office. If you choose to seek help, give your doctor as much information as you can about your symptoms including their frequency and severity as well as the onset. With your doctor’s help, you can determine the best course of treatment to restore sexual function.


One of the first steps is to distinguish between physiological and psychological ED. Determining whether involuntary erections are present is important in eliminating the possibility of psychogenic causes for ED.[1] Obtaining full erections occasionally, such as nocturnal penile tumescence when asleep (that is, when the mind and psychological issues, if any, are less present), tends to suggest that the physical structures are functionally working.[19][20] Similarly, performance with manual stimulation, as well as any performance anxiety or acute situational ED, may indicate a psychogenic component to ED.[1]
The dorsal artery provides for engorgement of the glans during erection, whereas the bulbourethral artery supplies the bulb and the corpus spongiosum. The cavernous artery effects tumescence of the corpus cavernosum and thus is principally responsible for erection. The cavernous artery gives off many helicine arteries, which supply the trabecular erectile tissue and the sinusoids. These helicine arteries are contracted and tortuous in the flaccid state and become dilated and straight during erection. [9]
Treatment involves addressing the underlying causes, lifestyle modifications, and addressing psychosocial issues.[1] In many cases, a trial of pharmacological therapy with a PDE5 inhibitor, such as sildenafil, can be attempted. In some cases, treatment can involve inserting prostaglandin pellets into the urethra, injecting smooth muscle relaxants and vasodilators into the penis, a penile prosthesis, a penis pump, or vascular reconstructive surgery.[1][2] It is the most common sexual problem in men.[3]
The dorsal artery provides for engorgement of the glans during erection, whereas the bulbourethral artery supplies the bulb and the corpus spongiosum. The cavernous artery effects tumescence of the corpus cavernosum and thus is principally responsible for erection. The cavernous artery gives off many helicine arteries, which supply the trabecular erectile tissue and the sinusoids. These helicine arteries are contracted and tortuous in the flaccid state and become dilated and straight during erection. [9]
Studies also show a consistent negative correlation of testosterone with blood pressure (Barrett-Connor and Khaw 1988; Khaw and Barrett-Connor 1988; Svartberg, von Muhlen, Schirmer et al 2004). Data specific to the ageing male population suggests that this relationship is particularly powerful for systolic hypertension (Fogari et al 2005). Interventional trials have not found a significant effect of testosterone replacement on blood pressure (Kapoor et al 2006).
Epidemiological data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment. 
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