Diabetes and Erectile Dysfunction

About 50% of all diabetic men suffer from ED

This usually develops during the course of the disease, but can sometimes be a presenting complaint. The likelihood of ED is related to the quality of Blood Glucose control.

The prevalence of ED is three times higher in diabetic men (28% versus 9.6%), occurs at an earlier age and increases with disease duration, being approximately 15% at age 30 rising to 55% at 60 years [11,12]. The Pathophysiology is multifatorial:

1. Diabetic Neuropathy – Nonsexual nocturnal erections are seen during rapid eye movement sleep in normal men. In diabetics, alterations in potassium efflux across non- junctional ion channels of the corporal smooth muscle may lead to a state of hyper-contraction and lack of erectile response in men. [13] Healthy men experience nocturnal erections several times each night during REM sleep as nature's way of maintaining good penile health for reproductive purposes and intimate relations. When night-time erections do not occur the patient is considered to have organic or physical erectile dysfunction and the penis develops non-use atrophy.
   
   
2. Diabetic Arterial Disease - Penile erection depends upon a greatly increased blood flow into the corpora cavernosa, which is in turn dependent upon perfusion pressure, relaxation of the supplying arterial tree and relaxation of cavernosal smooth muscle. Large vessel atheromatous disease is 40 times more prevalent amongst men with diabetes, occurring at a younger age, and within the penile arterial tree is more commonly associated with ED. [14]
   
   
3. Hyperglycaemia - has both a direct action on smooth muscle cells by increasing the contractile response to noradrenaline and affecting the level of NO synthesis and release mediated by endothelial (reduced eNOS enzyme activity) - and neurogenic means, reducing the level of NO-induced relaxation in corporal tissue. [15-17] A body of evidence exists detailing the various mechanisms by which levels of oxygen free radicals may be elevated in diabetes which quench released NO thereby reducing the vasodilator response. Glucose reacts non-enzymatically with the amino acids of proteins to produce Advanced Glycosalation End Products (AGE's), known to generate Reactive Oxygen Species (ROS). [18] Electron micrographs in diabetic men have shown reduction in smooth muscle content, increased collagen deposition (Peyronie's disease is more common in diabetics) and thickening of the basal lamina compared with controls. [19]