The lab testing obtained for the evaluation of erectile dysfunction may vary with the information obtained on the health history, physical examination, and recent lab testing. A testosterone level is not necessary in all men; however, a physician will order labs to determine a patient's testosterone level if other signs and symptoms of hypogonadism (low testosterone) such as decreased libido, loss of body hair, muscle loss, breast enlargement, osteoporosis, infertility, and decreased penile/testicular size are present.
Once you have talked to your partner about your issues, you may want to consider taking things one step further with psychosexual therapy. This is a form of therapy in which both you and your partner see a therapist together. The therapist will help you and your partner break out of the cycle of stress and disappointment that has been coloring your sex life and contributing to your ED. Going to a therapist with your partner may also help you work out any relationship issues that have been affecting your sex life so the both of you will be more satisfied.
Erections also require neural input to redirect blood flow into the corpora cavernosae. Psychogenic erections secondary to sexual images or auditory stimuli relay sensual input to the spinal cord at T-11 to L-2. Neural impulses flow to the pelvic vascular bed, redirecting blood flow into the corpora cavernosae. Reflex erections secondary to tactile stimulus to the penis or genital area activate a reflex arc with sacral roots at S2 to S4. Nocturnal erections occur during rapid-eye-movement (REM) sleep and occur 3–4 times nightly. Depressed men rarely experience REM sleep and therefore do not have nocturnal or early-morning erections.

In prescribing sildenafil, a doctor considers the age, general health status, and other medication(s) the patient is taking. The usual starting dose for most men is 50 mg, however, the doctor may increase or decrease the dose depending on side effects and effectiveness. The maximum recommended dose is 100 mg every 24 hours. However, many men will need 100 mg of sildenafil for optimal effectiveness, and some doctors are recommending 100 mg as the starting dose.
As recently as two decades ago, doctors tended to blame erectile dysfunction on psychological problems or, with older men, on the normal aging process. Today, the pendulum of medical opinion has swung away from both notions. While arousal takes longer as a man ages, chronic erectile dysfunction warrants medical attention. Moreover, the difficulty is often not psychological in origin. Today, urologists believe that physical factors underlie the majority of cases of persistent erectile dysfunction in men over age 50.
Some studies have linked bicycling to ED, though more research is needed to confirm the connection. Bicycle seats put pressure on nerves and blood vessels in the pelvic region. If you’re a frequent or long-distance cyclist, consider buying a seat specially designed to reduce pressure on your perineum. Learn more about the effects of cycling on erectile function.

If on one hand, depression and anxiety can lead to ED, drugs commonly used for their treatment can cause ED, as well. Sexual dysfunctions are common side effects of several psychotropic drugs that can disrupt sexual health by several different mechanisms (83). In particular, ED has been reported in subjects using serotonin selective re-uptake inhibitors (SSRI), lithium and benzodiazepines (83). SSRI are associated with a broad spectrum of sexual dysfunctions, but the most commonly reported complaints are delayed ejaculation or anorgasmia and reduced sexual desire (84). Several mechanisms could be advocated including the agonist effect on serotonin receptors type 2 and the increase in PRL levels. ED is a frequent complaint as well (84,85). The relationship between the use of SSRI and ED can be secondary to loss of sexual desire but SSRI, in particular paroxetine, are also able to inhibit cholinergic receptors and nitric oxide synthase (86). In addition, it has been observed that SSRIs might down-regulate hypothalamic-pituitary-testis axis in depressed men (87).
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With coronary artery disease, a buildup of plaque inside the arteries can limit the amount of blood that’s able to flow through them. If the flow of oxygen-rich blood to your heart muscle is reduced or blocked by this hardening of the arteries, the result can be angina (chest pain) or a heart attack.17 Because the arteries that supply blood to the penis are much smaller than the ones that feed the heart, the problem may show up earlier as having difficulty getting an erection.18
A full battery of labs was ordered and returned normal. A PCDU was ordered which revealed normal arterial inflow with velocities greater than >40 cm/sec with increased end diastolic velocities suggestive of venous leak. After pharmacologic erection, he developed a partial erection that resolved within 1 minute. This was consistent with a diagnosis of venous leak impotence. Pharmacologic cavernosography was performed and revealed bilateral crural leakage. He underwent infrapubic bilateral crural ligation of the penis, which cured his ED. The patient returned to clinic 6 months later with recurrent impotence. A pharmacologic cavernosography revealed recurrent venous leak. Additional crural ligation via a perineal approach was performed. Two months later he reported normal penile erections, and the result has lasted for more than 5 years. He continues to follow up annually in clinic.
A 25-year-old male presents with a past medical history of mild traumatic brain injury, remote bilateral orchitis, depression, anxiety, and PTSD from childhood bullying. He presents with his mother. His chief complaint is ED that began at 19 years old. He reports that it is "hard to obtain an erection, takes a lot of work to get almost nothing out of it" and “extreme loss of sensation in specific areas” on his penis. He feels that this might be related to “over masturbation without lubricant” 1–3 times per day and reports that he is “addicted to masturbation”, using it as a coping mechanism to manage his PTSD. He reports strong, sustainable erections with tadalafil 5 mg and recovery of sensation when he uses marijuana. He has read extensively on the internet and self-treats with topical vitamin creams, self-administered laser treatment to the penis, pulsed electromagnetic therapy, and hyperbaric oxygen treatment for ED for the past 6 months. He reports no change with any of these treatments. He reports reduced libido and has recently started treatment with HCG and testosterone gel for testosterone of 198 without any change in his symptoms with T of 450. His free T is normal. He lives at home, is unemployed, and is sedentary. He takes Wellbutrin. His physical examination is normal. His CBC, CMP, pituitary, and thyroid functions are normal. Prior to the visit, his mother called the clinic to inform personnel that her son was very sensitive, potentially suicidal, and emotionally disturbed by this problem. He has seen two other urologists already for his erectile dysfunction and been displeased with the outcome of his visits.
Unconventional CV risk factors, such as impaired erections during masturbation and reduced flaccid acceleration, are interesting parameters to implement in Sexual Medicine context, because they can help fill the gap of information on CV risk, left by the conventional risk factors (the so-called residual risk) (38). However, it should be recognized that not all the healthcare professionals who deal with the complaint of ED (i.e., general practitioners, diabetologists, cardiologists, sport physicians, nurses, etc.) have the facilities or competence for the specific assessment of these parameters. In contexts different than Sexual Medicine and Andrology, the assessment of conventional risk factors is certainly more convenient. Metabolic syndrome (MetS) represents a cluster of metabolic derangements easily and commonly evaluated in several different medical contexts. In a population of more than 600 subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for ED, the presence of MetS was associated with an increased incidence of MACE during 4.3 years of follow-up in younger (first tertile of age: 18–52 years) (Figure 3, Panel A and B) but not in middle aged and older men (second and third tertiles of age: 53–60 and 61–88 years, respectively) (Figure 3, Panel B). Similar to MetS, the algorithms for estimating the risk of developing MACE are easily computed and they take into account factors largely available in a clinical setting. In Europe, the most commonly used algorithm is the SCORE, which takes into account age, smoking habits, systolic blood pressure and total cholesterol (26). These parameters are introduced in a calculation tool that returns the 10-year risk of developing the first MACE. The same estimated risk rate can obviously be derived from different combinations and extent of the single risk factors and, as aforementioned, age has a heavy weight in the amount of risk, even when the other parameters are normal. For overcoming this overestimation, the concept of vascular age, based on the predicted CV risk, has been introduced. Vascular age of a subjects with a specific CV risk profile corresponds to the chronological age of a subjects who has the same estimated risk but only due to chronological age, because of the absence of the other modifiable risk factors (i.e., a non-smoker, normotensive and normocholesterolemic subject) (39,40). Vascular age carries the advantage of easily and directly communicating the concept of high relative risk to patients, in particular to younger ones, who are by definition at low absolute risk (“Your CV risk is the same of a man that is 15 years older than you”). Based on this interesting and useful concept of vascular age, we recently studied the clinical consequences of having a high discrepancy between the estimated vascular and the actual chronological age in our population of men consulting for ED. In our sample, a greater difference between vascular and chronological age was associated with higher glucose and triglyceride levels as well as with impaired penile colour Doppler ultrasound parameters, suggesting a CV impairment (41). When evaluating the subset of men for whom information on incident MACE during a mean follow-up of 4.3 years was available, a greater difference between vascular and chronological age was associated with the incidence of MACE in younger, but not in older men (42).
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
To understand what happens in ED, it's helpful to know some anatomical basics. When aroused by either sensory or mental stimuli, the brain sends a signal through the nerves to the penis, causing the muscles there to relax. This opens up space for blood to flow in and engorge the penis. A membrane within the penis traps blood inside to help maintain the erection, which subsides when the penile muscles contract, forcing blood back into the rest of the body. Any number of things can go wrong in this process, leading to erectile dysfunction.
In rare cases, the drug Viagra ® can cause blue-green shading to vision that lasts for a short time. In rare cases, the drug Cialis® can cause or increase back pain or aching muscles in the back. In most cases, the side effects are linked to PDE5 inhibitor effects on other tissues in the body, meaning they are working to increase blood flow to your penis and at the same time impacting other vascular tissues in your body. These are not ‘allergic reactions'.
Men with diabetes tend to develop erectile dysfunction 10 to 15 years earlier than men without diabetes. As men with diabetes age, erectile dysfunction becomes even more common. Above the age of 50, the likelihood of having difficulty with an erection occurs in approximately 50% to 60% of men with diabetes. Above age 70, there is about a 95% likelihood of having some difficulty with erectile dysfunction.
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