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).
Before taking any medication for erectile dysfunction, including over-the-counter supplements and herbal remedies, get your doctor's OK. Medications for erectile dysfunction do not work in all men and might be less effective in certain conditions, such as after prostate surgery or if you have diabetes. Some medications might also be dangerous if you:

Not only can guilt affect your ability to perform sexually, but so can low self-esteem. The correlation between erectile dysfunction and low self-esteem seems obvious from one direction – an inability to perform in the bedroom can cause you to feel bad about yourself. But how does low self-esteem cause ED? Self-esteem is defined as, “confidence in one’s own worth or abilities.”
Patients should continue testosterone therapy only if there is improvement in the symptoms of hypogonadism and should be monitored regularly. You will need periodic blood tests for testosterone levels and blood tests to monitor your blood count and PSA. Testosterone therapy has health risks, and thus doctors should closely monitor its use. Testosterone therapy can worsen sleep apnea and congestive heart failure.

Rates of erectile dysfunction have significantly increased over the last 15 years, especially in men younger than 40. In 2002, a review of 23 studies from Europe, the United States, Asia and Australia found that the rate of erectile dysfunction in that age group was two per cent. More recent studies suggest that erectile dysfunction is becoming more prevalent in younger men, with as many as 15 per cent of men in that age group battling it.


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Then you have to be able to make the right diagnosis. What is the basis for their erectile dysfunction? Is it psychogenic? Is it some sort of neurological or blood vessel or hormonal issue? So you have to make a diagnosis. You have to be able to make an assessment. And then only after those things are done, then you start to think about medications.
Care for these patients, who in many cases are emotional, demanding, and time consuming, may evoke feelings of frustration and anticipatory anxiety in the time-strapped urologist. Early in the encounter, the urologist must understand the patient’s psychosocial environment and establish a rapport and meaningful alliance with the patient and his family, if present (13). It is important to ensure that the doctor-patient interaction is informative and task oriented for greater patient buy-in and compliance with treatment (13,14). Affirm to the patient that regardless of the short time allotted for the visit that the doctor-patient relationship will endure even after the visit. This may be accomplished through a scheduled follow-up telephone call, electronic message, follow-up clinic visit, or a written letter. It may also be beneficial to refer the patient to a sex therapist or counselor though many young men will reject the idea that there is a psychosocial element to their ED and may refuse to consider therapy.
For patients who have ED related to hypertonic cavernous smooth muscle and excessive sympathetic discharge, we recommend a trial of a low-dose alpha adrenergic blocker, such as terazosin 1 mg PO at bedtime nightly. We typically increase the dosage as needed every 2–3 weeks for 3–5 months until the patient experiences improvement of the erection or we determine that treatment is ineffective. We explain the potential side effects of orthostasis, dizziness, and retrograde ejaculation in detail. We also take great care and time in explaining to the patient, and his family/partner if present, the pathophysiologic mechanism of their erectile dysfunction and the biological basis of the treatment plan. This detailed discussion helps to engage the patient in the treatment plan and provides encouragement regarding the potential for response to treatment and recovery. During these encounters, we utilize teaching tools, such as diagrams, drawings, printed handouts, and other visual aids to ensure that the discussion is patient-focused and patient-friendly. Patient education is critical to exploring treatment options and developing confidence in our ability to treat the ED, and their own ability to overcome and eventually resolve the problem of ED.

For many young men, performance anxiety plays a large role in erectile dysfunction. Other factors include money and work problems, as well as relationship issues and even issues about sexual orientation. Undiagnosed depression and post-traumatic stress disorder can cause erectile dysfunction--especially if the PTSD is related to a past sexual experience.


Erectile dysfunction is more common than most people think. About 40% of men will notice some degree of problem by age 40. The aging of the penis can begin as early as the late 20s but becomes severe enough to notice typically starting in the 40s. As men get older, their odds of getting erectile dysfunction increases by about 10% per decade, and the severity of the problem also increases.
A sexually competent male must have a series of events occur and multiple mechanisms intact for normal erectile function. He must 1) have desire for his sexual partner (libido), 2) be able to divert blood from the iliac artery into the corpora cavernosae to achieve penile tumescence and rigidity (erection) adequate for penetration, 3) discharge sperm and prostatic/seminal fluid through his urethra (ejaculation), and 4) experience a sense of pleasure (orgasm). A man is considered to have ED if he cannot achieve or sustain an erection of sufficient rigidity for sexual intercourse. Most men, at one time or another during their life, experience periodic or isolated sexual failures. However, the term “impotent” is reserved for those men who experience erectile failure during attempted intercourse more than 75% of the time.

The most common inflatable prosthesis is the three-piece penile prosthesis. It is composed of paired cylinders, which doctors surgically insert inside the penis. Patients can expand the cylinders using pressurized fluid (see figure 3). Tubes connect the cylinders to a fluid reservoir and pump, which doctors also surgically implant. The reservoir is usually in the pelvis. A doctor places the pump in the scrotum. By pressing on the pump, sterile fluid transfers from the reservoir into the cylinders in the penis. An erection is produced primarily by expansion of the width of the penis, however, one model can increase in length a small amount also. Lock-out valves in the tubing prevent the fluid from leaving the cylinder until a release valve is pressed. By pressing the relief valve and gently squeezing the penis, the fluid within the cylinders transfers back into the reservoir.

If not properly controlled, both type 1 and type 2 diabetes can cause complications due to high blood sugar levels. Over time, these high levels can cause irreversible nerve damage and narrow your blood vessels. While nerve damage may affect the sensitivity of your penis, blood vessel damage can affect the blood flow to your penis and make it more difficult for you to get an erection.
If the patient complains of loss of sensation on his penile shaft or glans, it is useful to perform hot and cold perception testing and/or additional vibratory sensory testing with biothesiometer. These are tests that can be performed quickly during the office visit and provide useful information about the function of the dorsal nerve of the penis (Table 3).

The bad news: Men with diabetes are three times more likely to report having problems with sex than non-diabetic men. The most common sexual problem is Erectile Dysfunction, or ED, sometimes called impotence. Even worse, because ED is such a private issue, many men feel embarrassed to discuss the problem with their doctor, or even their partner, so the problem is never addressed.
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