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.
Lifestyle changes: One of the first things a young man can do to potentially improve or eliminate ED is make positive choices that will also have an impact on the rest of his life. Some changes a man can consider include increasing exercise, eating a heart-healthy diet, quitting smoking, and drinking alcohol only in moderation. Where a man has relationship problems, seeking counseling may also be helpful.
With all of that said, it should be clear that we lack evidence from nationally representative sex surveys to support claims about a massive increase in erectile difficulties among young men. It may be that reports of mild problems are increasing in this group (we need more data to know), but even if this is true, the data don’t suggest anything along the lines of, say, a 1000% increase.
Low intracavernosal nitric oxide synthase levels are found in people with diabetes, smokers, and men with testosterone deficiency. Interference with oxygen delivery or nitric oxide synthesis can prevent intracavernosal blood pressure from rising to a level sufficient to impede emissary vein outflow, leading to an inability to acquire or sustain rigid erection. Examples include decreased blood flow and inadequate intracavernosal oxygen levels when atherosclerosis involves the hypogastric artery or other feeder vessels and conditions, such as diabetes, that are associated with suboptimal nitric oxide synthase activity.
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.
Regardless of age, if a man is obese and sedentary, with poor dietary habits, he is at greater risk of developing diseases that can lead to erectile dysfunction. These include heart disease, hypertension and type 2 diabetes. Some forms of congenital heart disease may remain hidden and only cause problems in adulthood. Men of any age noticing a marked change in sexual function should contact their physicians to rule out the possibility of a more serious condition.
Surgery to repair arteries (penile arterial reconstructive surgery) can reduce impotence caused by obstructions that block the flow of blood to the penis. The best candidates for such surgery are young men with discrete blockage of an artery because of a physical injury to the pubic area or a fracture of the pelvis. The procedure is less successful in older men with widespread blockage of arteries.
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.
For obvious reasons, ED can be a sensitive subject, one that until relatively recently men were more likely to try to hide than to deal with. Fortunately, a deeper understanding of the variety of causes of erectile dysfunction has led to medications, therapies, and other treatments that can be more individualized and more likely to be effective—and more open discussion about addressing the concern.
Many different health conditions can affect the nerves, muscles, or blood flow that is needed to have an erection. Diabetes, high blood pressure, hardening of the arteries, spinal cord injuries, and multiple sclerosis can contribute to ED. Surgery to treat prostate or bladder problems can also affect the nerves and blood vessels that control an erection.

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.
Cardiovascular diseases account for nearly half of all cases of erectile dysfunction in men older than 50 years. Cardiovascular causes include those that affect arteries and veins. Damage to arteries that bring blood flow into the penis may occur from hardening of the arteries (atherosclerosis) or trauma to the pelvis/perineum (for example, pelvic fracture, long-distance bicycle riding).
Sexual dysfunction appears to be common among male subjects with alcohol dependence. Seventy-two per cent of the subjects with alcohol dependence complained of one or more problems with sexual functioning. This is similar to what has been reported in earlier studies.[10,16] Multiple co-existing dysfunctions seemed to be the norm in the sample studied. The most common condition reported in our study was premature ejaculation followed closely by low sexual desire and erectile dysfunction.
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Taking one of these tablets will not automatically produce an erection. Sexual stimulation is needed first to cause the release of nitric oxide from your penile nerves. These medications amplify that signal, allowing some men to function normally. Oral erectile dysfunction medications are not aphrodisiacs, will not cause excitement and are not needed in men who get normal erections.
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.
Nerve or spinal cord damage: Damage to the spinal cord and nerves in the pelvis can cause erectile dysfunction. Nerve damage can be due to disease, trauma, or surgical procedures. Examples include injury to the spinal cord from automobile accidents, injury to the pelvic nerves from prostate surgery for cancer (prostatectomy), and some surgeries for colorectal cancer, radiation to the prostate, surgery for benign prostatic enlargement, multiple sclerosis (a neurological disease with the potential to cause widespread damage to nerves), and long-term diabetes mellitus.
As blood flows into the penis, the corpora cavernosa swell, and this swelling compresses the veins (blood vessels that drain the blood out of the penis) against the tunica albuginea. Compression of the veins prevents blood from leaving the penis. This creates a hard erection. When the amount of cGMP decreases by the action of a chemical called phosphodiesterase type 5 (PDE5), the muscles in the penis tighten, and the blood flow into the penis decreases. With less blood coming into the penis, the veins are not compressed, allowing blood to drain out of the penis, and the erection goes down.
Venous leak occurs when veins are unable to keep enough blood in the penis for a suitable erection.  As noted above, a firm erection results when blood flows into the penis.  Veins normally constrict to keep the blood inside until the man ejaculates.  A venous leak prevents blood from staying in the penis.  Instead, blood leaks back into the body and the erection fails to stay rigid.
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