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Atherosclerosis The most common recognized cause of ED is atherosclerosis. Atherosclerosis is known to be associated with such cardiovascular diagnoses as hypertension and dyslipidemia, which produce oxidative stress and damage to the endothelial cells.

The underlying pathophysiology seems to stem from endothelial cell dysfunction, which would be a common factor between general cardiovascular disease and ED. Failed vasodilation seen in ED is a direct effect of the inability of smooth muscle cells lining the arterioles to relax. Atherosclerosis has been found to be associated with up to 40% of cases of ED in men over age 50.

Cholesterol One group looked at cavernous biopsies of rabbits after three months of a cholesterol-rich diet versus controls. The control group showed normal muscle cells on biopsy while the high cholesterol group showed muscle cell degeneration. This tangible evidence of direct effect of high cholesterol diet on cavernous muscle cells suggests that abnormalities in lipid metabolism has a direct effect on cavernous smooth muscle cell degeneration, thus contributing to ED.

Hypercholesterolemia is a known direct risk factor for cardiovascular disease. Erectile dysfunction in association with hypercholesterolemia was documented in a group of healthy men with no known cardiac risk factors.

These otherwise healthy men with ED were found to have abnormal cholesterol levels at a rate of 60%. In addition, over 90% of these men with abnormal cholesterol levels were also noted to have penile arterial disease on Doppler ultrasound.

Saltzman et al. evaluated men with ED in which their only known risk factor was hypercholesterolemia. They were able to meet their treatment goals of total cholesterol less than 200 mg/dl and LDL less than 120 mg/dl. They found that ED improved in men with hypercholesterolemia when treated with a statin drug.

The resulting decreased cholesterol levels improved ED while also decreasing overall cardiovascular risk. Primary care physicians may theoretically have more success with patient compliance of statin drugs for current improved sexual function than for future cardiovascular risk. Of note, there is also contradicting evidence, based on literature review, that statins and fibrates may actually cause or worsen ED.

Should this be the case, it would be very difficult to determine the effect of cholesterol on ED, as in order to treat a known risk factor of ED, we may be in effect worsening ED with the use of medication.