The initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
Aging, liver and kidney problems, and concurrent use of certain medications (such as erythromycin [an antibiotic] and protease inhibitors for HIV) slows the metabolism (breakdown) of sildenafil. Slowed breakdown allows sildenafil to accumulate in the body and potentially may increase the risk of side effects. Therefore, in men over 65 years of age, in men with significant kidney and liver disease, and in men who also are taking medications called protease inhibitors, the doctor will initiate sildenafil at a lower dose (25 mg) to avoid accumulation of sildenafil in the body. A protease inhibitor ritonavir (Norvir) is especially potent in increasing the accumulation of sildenafil, thus men who are taking Norvir should not take sildenafil doses higher than 25 mg and at a frequency of no greater than once in 48 hours. Other medications that may affect the level of sildenafil include erythromycin and ketoconazole.
Sildenafil is available as oral tablets at doses of 25 mg, 50 mg, and 100 mg. Patients should take sildenafil approximately one hour before sexual activity. In some men, the onset of action of the drug may be as early as 11-20 minutes. It's best for men to take sildenafil on an empty stomach for best results since absorption and effectiveness of sildenafil can be diminished if it is taken shortly after a meal, particularly a meal that is high in fat. Sildenafil and the other PDE5 inhibitors don't cause an immediate erection. Sexual stimulation is necessary for these medications to work.
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.
Physicians make a diagnosis of erectile dysfunction in men who complain of troubles having a hard enough erection or a hard erection that does not last long enough. It is important as you talk with your doctor that you be candid in terms of when your troubles started, how bothersome your erectile dysfunction is, how severe it is, and discuss all your medical conditions along with all prescribed and nonprescribed medications that you are taking. Your doctor will ask several questions to determine if your symptoms are suggestive of erectile dysfunction and to assess its severity and possible causes. Your doctor will try to get information to answer the following questions:
Quitting smoking, exercising regularly, losing excess weight, curtailing excessive alcohol consumption, controlling hypertension, and optimizing blood glucose levels in patients with diabetes are not only important for maintaining good health but also may improve or even prevent progression of erectile dysfunction. It is unclear if such lifestyle changes can reverse erectile dysfunction. However, lifestyle improvements may prevent progression of the erectile dysfunction. Some studies suggest that men who have made lifestyle improvements experience increased rates of success with oral medications.
Sexual dysfunction is common in patients with diabetes mellitus. Vascular, neurological and hormonal alterations are involved in this complication. Many studies showed altered endothelium-dependent and neurogenic relaxations in corpus cavernosum from diabetic patients with erectile dysfunction (ED). This finding has been associated with a lack of nitric oxyde (NO) production and a significant increase in NO synthase (NOS) binding sites in penile tissues, induced by diabetes. Advanced glycation endproducts (AGEs) concur to diabetic vascular complications by quenching NO activity and by increasing the expression of mediators of vascular damage such as vascular endothelial growth factor (VEGF), possessing permeabilizing and neoangiogenic effects, and endothelin-1 (ET-1), with vaso-constricting and mitogenic action. Moreover, the differential gene expression for various growth factors in penile tissues may be involved in the pathophysiology of ED associated with diabetes. Neuropathy is also likely to be an important cause of diabetic ED: morphological alterations of autonomic nerve fibers in cavernosal tissue of patients with diabetic ED have been demonstrated. Finally, androgens enhance nNOS gene expression in the penile corpus cavernosum of rats, suggesting that they play a role in maintaining NOS activity. However, sexual dysfunctions in women with diabetes has received less attention in clinical research. Several studies suggest an increased prevalence of deficient vaginal lubrication, making sexual intercourse unpleasant. Sexual dysfunction is associated with lower overall quality of marital relation and more depressive symptoms in diabetic women.
Yet another common erectile dysfunction treatment that can be used in combination with oral drugs is a vacuum pump. This device consists of a plastic cylinder, a pump, a set of constriction bands, and a water-soluble lubricant. The lubricant is applied to the base of the penis to help form an airtight seal. The cylinder is placed over the flaccid penis and held tight against the pelvis. The pump is used to create a vacuum within the cylinder, drawing blood into the penis. Once the penis is engorged with blood, a constriction band is rolled off the cylinder to near the base of the penis. The constriction band is helpful for men with venous leakage, in which blood flows out of the penis as fast as it flows in. However, it should be left on for no more than 30 minutes at a time.
Association between metabolic syndrome (MetS) at baseline and incidence of major adverse cardiovascular events (MACE) during a mean follow-up of 4.3 years. Panel A represents the Kaplan Meier curves for incidence of MACE in a population of 211 men aged 18–52 years having or not MetS at baseline. This group represents the first tertile of age of a sample of patients (n=619) consulting the Sexual Medicine and Andrology Unit of the University of Florence for erectile dysfunction and followed-up for a mean of 4.3 years for the occurrence of MACE. Panel B represents the Cox analyses for the age- and smoking habit-adjusted incidence of MACE associated with the number of MetS components at baseline (glycaemia ≥100 mg/dL, triglycerides ≥150 mg/dL, HDL <40 mg/dL; blood pressure ≥135/80 mmHg, waist circumference >102 cm), according to the tertile of age, in the same population, during the same follow-up. The first, second and third tertile include 211, 199 and 209 patients aged 18–52, 53–60 and 61–88 years, respectively.
When a man becomes sexually excited, muscles in their penis relax. This relaxation allows for increased blood flow through the penile arteries. This blood fills two chambers inside the penis called the corpora cavernosa. As the chambers fill with blood, the penis grows rigid. Erection ends when the muscles contract and the accumulated blood can flow out through the penile veins.
ED is common among patients with cardiovascular diseases (CVD). Sexual problems usually precede the onset of CVD, and should, therefore, be considered as a risk factor for cardiac events. Similarly, patients with preexisting CVD are at increased risk of experiencing ED. Therefore, ED and CVD might be considered as two different clinical manifestations of the same systemic disease.19
Alcohol consumption is a common behavior in social circumstances worldwide. Epidemiological studies have suggested that moderate alcohol consumption reduces cardiovascular morbidity and mortality. The cardiovascular protective effects of alcohol may be attributed to its antioxidant, vasorelaxant, and antithrombotic properties, elevation of high-density lipoprotein or increase of nitric oxide production. Erectile dysfunction (ED) is a harbinger of cardiovascular diseases. Most epidemiological studies have also found that alcohol consumption, like its relationship with coronary artery disease, is related to ED in a J-shaped manner, with moderate consumption conferring the highest protection and higher consumption less benefits. In epidemio-logical studies, it is difficult to distinguish the ethanol effects from those of associated confounding factors. Meanwhile, long-term alcohol users, especially in those with alcohol liver disease, are highly associated with ED. More research is needed to investigate the true effects of alcohol consumption on cardiovascular diseases or ED.
Dr. Anna Murray, of the University of Exeter Medical School, is co-lead author on the study. She said: “Erectile dysfunction affects at least one in five men over 60, yet up until now little has been known about its cause. Our paper echoes recent findings that the cause can be genetic, and it goes further. We found that a genetic predisposition to type 2 diabetes is linked to erectile dysfunction. That may mean that if people can reduce their risk of diabetes through healthier lifestyles, they may also avoid developing erectile dysfunction.”
This initial release of NO causes rapid and short-term increases in penile blood flow and short-term relaxation of the penile smooth muscle, initiating an erection. The resulting expansion of penile blood vessels and smooth-muscle relaxation allows more blood to flow into the penis. This increased blood flow (shear stress) activates the eNOS in penile blood vessels causing sustained NO release, continued relaxation and full erection.