Erectile dysfunction (ED) is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance. The key word is persistent, occasional difficulty does not constitute ED. Clinical ED affects an estimated 30 million men in the United States according to NIH estimates, and its prevalence increases with age: roughly 40% of men at age 40, rising to 70% by age 70, report some degree of erectile difficulty.

ED is not an inevitable part of aging, and in many cases it signals underlying cardiovascular or metabolic disease. Treating ED effectively often requires identifying and addressing the root cause rather than relying solely on symptomatic treatment.

How Erections Work

An erection is a vascular event. Sexual arousal triggers the release of nitric oxide in the smooth muscle of the corpus cavernosum, the spongy tissue along the length of the penis. Nitric oxide activates an enzyme that produces cyclic GMP, which relaxes smooth muscle cells in the penile arteries. Blood flows in, pressure builds, and the corpora cavernosa compress the veins draining the penis, maintaining the erection.

Any disruption in this chain, inadequate nitric oxide production, arterial disease reducing blood flow, venous leak allowing blood to escape, neurological damage impeding signaling, or hormonal deficiency affecting arousal, can cause or contribute to ED.

Vascular Causes

The most common cause of ED in men over 40 is vascular disease. The penile arteries are small-diameter vessels, approximately 1-2 mm, and are among the first vascular beds to show atherosclerotic changes. ED caused by endothelial dysfunction often precedes cardiac symptoms by several years.

A meta-analysis published in the Journal of Sexual Medicine found that ED was associated with a 44% increase in the relative risk of major cardiovascular events. Clinicians now treat new-onset ED in a middle-aged man without an obvious psychological cause as a potential early marker of cardiovascular disease, warranting lipid, blood pressure, and glucose evaluation.

Major vascular risk factors for ED:

  • Hypertension (damages endothelium and reduces nitric oxide availability)
  • Dyslipidemia (promotes atherosclerosis in penile arteries)
  • Type 2 diabetes (damages both vasculature and penile nerves)
  • Smoking (acute vasoconstriction and long-term endothelial damage)
  • Obesity

Neurological Causes

Normal erections require intact neurological signaling from the brain, spinal cord, and peripheral nerves to the penis. Conditions that damage these pathways cause neurogenic ED:

  • Type 2 diabetes produces peripheral neuropathy that can affect penile sensation and autonomic signaling
  • Pelvic surgery, particularly radical prostatectomy for prostate cancer, frequently damages the cavernous nerves that run adjacent to the prostate
  • Multiple sclerosis
  • Parkinson’s disease
  • Spinal cord injury

Neurogenic ED typically does not respond as well to PDE5 inhibitors (sildenafil, tadalafil) as vascular ED, because the drug mechanism depends on nitric oxide release that requires functional neural input.

Hormonal Causes

Testosterone contributes to erectile function through multiple mechanisms including nitric oxide synthesis in penile tissue and central arousal effects. Low testosterone does not reliably cause ED on its own, but it reduces the motivation for sexual activity and impairs the quality of erections. In men with both low testosterone and ED, treating low testosterone first sometimes resolves the ED without requiring PDE5 inhibitor treatment.

High prolactin, from a pituitary tumor or certain medications, suppresses testosterone and independently impairs erectile function. A prolactin measurement should be included in the workup for ED if testosterone is also low.

Psychological Causes

Psychological ED, where the physical mechanism is intact but anxiety, depression, relationship conflict, or performance anxiety prevents erection, is more common in younger men without vascular risk factors. It often presents as situation-specific ED (works with one partner or with self-stimulation but not in another context).

Psychological and physical ED commonly coexist. A man with mild vascular ED develops performance anxiety, which further impairs erectile response, a self-reinforcing cycle. Treatment may need to address both components simultaneously.

Treatment Options and Evidence Strength

PDE5 inhibitors (sildenafil, tadalafil, vardenafil, avanafil): The first-line pharmacological treatment. They inhibit the enzyme that breaks down cyclic GMP, prolonging the vasodilatory effect. Head-to-head trials show all four are effective, with tadalafil offering a longer duration of action (up to 36 hours versus 4-6 for sildenafil). For a detailed comparison, see Sildenafil vs. Tadalafil: How the Two PDE5 Inhibitors Compare.

Lifestyle modification: Weight loss, exercise, smoking cessation, and blood pressure control improve erectile function through improved vascular health. These are not just supplementary, in men with ED due to metabolic risk factors, lifestyle change can restore function without medication.

Testosterone replacement: Appropriate only in men with confirmed low testosterone. TRT plus a PDE5 inhibitor often outperforms either alone in hypogonadal men with ED.

Penile injections, vacuum erection devices, penile prosthesis: Second- and third-line options for men who do not respond to or cannot tolerate PDE5 inhibitors. Penile prosthesis (implant) has satisfaction rates above 90% in appropriately selected patients but is irreversible.

Psychotherapy and sex therapy: Effective for psychological ED and for addressing the anxiety component of mixed ED. Often most effective when combined with pharmacological treatment initially.