There is no doubt that ED is associated with age, but it must be remembered that a wide range of medical problems and their treatment, which could possibly impair erectile function, are inevitably present or are increasingly being used with advancing age. The current cadre of men aged 60 years and beyond is more accepting of the idea that impotence is a natural consequence of the ageing process. Clearly such attitudes will change. Baby boomers, the people who have lived through the so-called sexual revolution, will probably be more demanding of treatment than were the generations that preceded them.

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ED is one of the most common complications of diabetes, its prevalence ranging from 35% to 75% of diabetic men.

Damage to small blood vessels is the main etiology and, therefore, ED often occurs in association with diabetic retinopathy. Diabetic peripheral autonomic neuropathy is a further contributory factor. ED may develop as a result of the progressive loss of small unmyelinated so-called C fibres secondary to diabetes. Saenz de Tejada et al has reported that diabetes is associated with loss of nitric oxide synthatase(NOS) from NANC nerve endings and endothelial cells in the corpora. This may explain the common association of ED with diabetes.

In a study of the clinical features of diabetic patients both with and without ED, the duration of diabetes mellitus was found to be significantly longer in those with ED. In addition, the proportion of patients receiving insulin treatment was considerably higher in the group with ED (61% versus 9%) proving that the overall probability of impotence is higher in treated diabetics.

The prevalence of ED amongst diabetic patients is also age related. Changes in the cavernous artery and cavernous erectile tissue have been reported in patients with diabetes. Diabetic men and older men were found to have a high incidence of fibrotic lesions in the cavernous artery, with intimal proliferation, calcification, and luminal stenosis.

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Heart disease and its associated risk factors, hypertension and low serum high-density lipoprotein, had significant correlation with impotence in the MMAS (Massachusetts Male Ageing Study) samples.

In the MMAS sample, though minimal impotence was unchanged, two different patterns were noticed in moderate and complete impotence with respect to cigarette smoking. In the non-smoking group, both moderate and complete impotence doubled, whereas in the smoking group, moderate impotence decreased slightly and complete impotence increased six times. This data may imply that patients with heart disease and moderate impotence could have complete impotence if they were smokers.

Treated heart disease is associated with 78% overall impotence in non-smokers and 94.3% in smokers, thereby making heart disease an important risk factor for erectile dysfunction. Impairments in the hemodynamics of erection have been demonstrated in patients with myocardial infarction, coronary bypass surgery, cerebrovascular accidents and peripheral vascular disease. This can be correlated with the study by Oaks and Moyer, who reported that 8 to 10% of all untreated hypertensive patients were impotent at diagnosis of hypertension. Greenstein et al report a significant correlation between the number of coronary vessels occluded on angiography and erectile dysfunction Assessment of plasma fibrinogen concentrations revealed higher levels of this coagulation factor in men with ED.

Approximately one-third of men beyond middle age have a diastolic blood pressure (DBP) > 90 mmHg. Hypertension causes damage to small blood vessels and this may adversely affect intracorporeal vasodilatory mechanisms. Moreover, many of the agents used to control hypertension, especially -blockers and diuretics, are associated with the development of ED. It has been postulated that, because high intracorporeal pressures are required to produce penile rigidity, the reduction of blood pressure by any agent is likely to increase the incidence of ED. However, -blockers, perhaps through the induction of intracorporeal vasodilation, appear to enhance erection, while still lowering both systolic blood pressure (SBP) and diastolic blood pressure (DBP).

Billups and Friedrich, suggest that erectile dysfunction may be one of the earliest indications of vascular disease. The logical conclusion from their work is that a vascular screening evaluation should become a part of the diagnostic evaluation for all men presenting with erectile dysfunction. Most erectile dysfunction experts suggest that the screening vascular evaluation should include a fasting lipid panel, a hemoglobin level and an electrocardiogram.

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Cigarette smoking has been shown to be an independent risk factor for vasculogenic impotence. This is because of its deleterious effects on blood vessels and its action leading to an increase of platelet stickiness.

The MMAS (Massachusetts Male Ageing Study) demonstrated the contribution of smoking to the probability of ED development. The association of ED with certain risk factors, such as heart disease and hypertension, was amplified in current cigarette smokers. In subjects with treated heart disease, the age-adjusted probability of complete ED was 56% for current smokers compared with 21% for current non-smokers.

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Impaired erectile function is frequent in men with chronic renal failure, and the prevalence of ED has been reported to be as high as 45% in this setting. The pathophysiology of ED in patients with renal failure is not clear. Hypogonadism due to dysfunctioning Leydig cells, hyperprolactinemia, hyperpara-thyroidism, anemia, protein malnutrition, zinc deficiency, hypertension and use of antihypertensive drugs have all been implicated.

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The role of some drug classes such as estrogens (used in the treatment of prostatic cancer), antihypertensives, and cardiac-active drugs in causation of ED is well documented. Newer classes of antihypertensive agents are less frequently associated with sexual dysfunction than diuretics or -blockers. However, nearly every first-line antihypertensive drug has been reported to cause some degree of erectile dysfunction.

ED has been reported in patients with most psychotherapeutic drugs that produce central nervous system sedation or depression, and the mechanism has been attributed to an elevation of serum prolactin concentrations, sedative effects, an anticholinergic effect, decreased dopaminergic activity, or central effects on the limbic system.

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Available data reveals that a high proportion of alcoholics showed signs of sexual deviation. Alcohol increases libido, inhibits sexual physiological responses and adversely affects reproductive processes in both men and women.

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Reactive or endogenous depression is strongly associated with ED: nearly 90% of severely depressed men report complete impotence. Treatment with antidepressants may sometimes improve the situation, although both monoamine oxidase inhibitors and tricyclic antidepressants may in themselves cause ED. Selective serotonin reuptake inhibitors, such as fluoxetine may not only cause ED, but may also retard ejaculation.

Psychological explanations for impotence, which are common in popular conceptions and in case histories, have a specific physiological basis. While psychogenic stimuli normally facilitate erection, cerebral signals can produce impotence equally well by inhibiting reflex activation of the parasympathetic dilator nerves that enhance inflow of blood to the penis.

In MMAS (Massachusetts Male Ageing Study) the psychological factors strongly associated with impotence included depression, low levels of dominance and anger.

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Pelvic surgery, particularly radical prostatectomy, cystoprostatectomy and abdomino perineal resection (APR) are all strongly associated with subsequent ED.

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