Ageing is one of the most important unmodifiable risk factors for the development of metabolic disorders and CV diseases. Accordingly, the common algorithms for the estimation of risk of forthcoming diabetes or CV events include age as a factor of the equations (24-29). The weight attributed to age for estimating the risk in these equations is often so significant that younger men are automatically considered at low risk, irrespective of the other possible risk factors. However, even in younger subjects, overlooking the contribution of cardio-metabolic factors to pathogenesis of ED is a mistake that can lead to the loss of the opportunity of early recognition of patients who deserve a change in life-style or a pharmacological correction of risk factors. ED, besides being considered one of the clinical manifestations of metabolic and cardiovascular diseases (CVD), is regarded as an early marker of CV events (17). In fact, according to Montorsi’s hypothesis (30), impairment of penile artery blood flow occurs before that of coronary or carotid arteries, whose diameter is greater and needs longer time to acquire a clinically relevant damage. The clinical consequence of this pathological event is that ED often manifests earlier than myocardial infarction or stroke. In particular, it has been demonstrated that ED occurs on average three years before the first major adverse CV event (MACE) (31). Quite surprisingly, although CV risk increases with ageing, the role of ED as a harbinger of forthcoming MACE becomes progressively less evident. Data derived from almost 2,500 community-dwelling men aged 40–79 years, involved in the Olmsted County study show that ED is associated with an almost 50-fold higher risk of incident heart diseases in men aged 40–49 years, whereas the difference in risk between ED and non-ED men progressively declines in older men (32). The different CV risk associated with ED in different age bands has been confirmed by the meta-analysis of the available longitudinal studies (33). These observations suggest that, in younger men, the role of ED as a marker of CV risk is even more dramatic than in older ones and as a consequence, investigating the presence of metabolic or CV conditions in younger ED patients is pivotal for identifying men in whom an early life-style modification may avoid serious CV consequences. Even more than erection during sexual intercourse, erection during masturbation is considered a physiologic function that mirrors metabolic and CV health. In fact, erections during masturbation are far less affected by relational and psychological components than sex-related ones (34). In a population of subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, more than 2,500 men reported autoeroticism in the previous 3 months. Among these men, the impairment of erection during masturbation was associated with family and personal history of CVD (35), as well as with impaired response to the test with the intracavernous injection (ICI) of prostaglandin E1, which suggests an arteriogenic damage of penile arteries and predicts forthcoming MACE (36). For a subset of these men (n=862), information on the occurrence of MACE during a mean follow-up of 4.3 years was available and those who reported impaired erections during masturbation had a significantly higher incidence of MACE (35). However, when considering separately younger and older men, this association was confirmed only in younger ones, and it was still significant after excluding men reporting severe ED during masturbation (35). This suggests that the impairment of erection during masturbation is a symptom not completely overlapping with sex-related ED and that it can provide different and supplementary information, in particular when assessed in younger and apparently healthy men. Similarly to what is observed for erection during masturbation, acceleration of blood in penile arteries, as measured by the colour Doppler ultrasound in flaccid conditions, is associated with an adverse CV profile in men consulting for ED. A reduction in flaccid acceleration, which can be used by clinicians to objectively verify the arteriogenic origin of ED and to characterize the extent of a self-reported symptom, has been also associated with a future risk of CV events, with the association being significant in younger but not in older men (37).
Aging: There are two reasons why older men are more likely to experience erectile dysfunction than younger men. First, older men are more likely to develop diseases (such as heart attacks, angina, cardiovascular disease, strokes, diabetes mellitus, and high blood pressure) that are associated with erectile dysfunction. Second, the aging process alone can cause erectile dysfunction in some men by causing changes in the muscle and tissue within the penis.
These commonly prescribed medications affect sexual function in different ways depending on the specific type of drug and how it works. “Central regulation of erections relies on dopamine and serotonin, so any impact on these processes can worsen erectile function,” says Trost. He notes that Wellbutrin (buproprion) and Remeron (mirtazipine) are the antidepressants that likely have the least impact on erectile function.

The various PDE5 inhibitors for the treatment of ED share several common side effects, including headache, flushing, nasal congestion, nausea, dyspepsia (stomach discomfort), and diarrhea. Differences exist in side effects of the different PDE5 inhibitors, and thus it is important to be familiar with the prescribing information of the PDE5 inhibitor you are prescribed.

Circulatory problems: An erection occurs when the penis fills with blood and a valve at the base of the penis traps it. Diabetes, high blood pressure, cholesterol, clots, and atherosclerosis (hardening of the arteries) can all interfere with this process. Such circulatory problems are the number one cause of erectile dysfunction. Frequently, erectile dysfunction is the first noticeable symptom of cardiovascular disease.

Without pharmaceuticals, we'd die a lot sooner, feel a lot worse and spend more time in hospitals than in our homes. But drugs aren't perfect. And many classes of drugs—especially beta-blockers and the SSRI class of antidepressants—list erectile dysfunction as one of the major side effects. (How's that for a trade-off? Take a drug to improve your mood, but risk cutting off your sexual interest and capabilities at the same time.)

This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the person's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
One reason erectile dysfunction becomes more common with age is that older men are more likely to be on some kind of medication. In fact, an estimated 25% of all ED is a side effect of drugs, according to the Harvard Special Health Report Erectile Dysfunction: How medication, lifestyle changes, and other therapies can help you conquer this vexing problem.
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The contents of your medicine cabinet could affect your performance in the bedroom. A long list of common drugs can cause ED, including certain blood pressure drugs, pain medications, and antidepressants. But do not stop taking any medicines without talking to your doctor first. Street drugs like amphetamines, cocaine, and marijuana can cause sexual problems in men, too.