Erectile Dysfunction: Causes, Workup, and Evidence-Based Treatment

An erection depends on healthy blood vessels, an intact nervous system, adequate testosterone, and normal psychological arousal. Because it requires so many systems to work together, erectile dysfunction is often the earliest visible sign of cardiovascular disease, diabetes, or hypogonadism — sometimes preceding a cardiac event by three to five years.

Treating ED without investigating why it started is a missed opportunity. Every new case of ED in a man over 40 warrants a metabolic and cardiovascular screen alongside sexual-health treatment.

Vascular disease is the single most common cause in men over 50 — atherosclerosis narrows the small penile arteries just as it does the coronaries. Diabetes, hypertension, and dyslipidemia are the top upstream drivers.

Hormonal causes include hypogonadism, hyperprolactinemia, and thyroid disease. Low testosterone reduces libido and, over time, reduces the responsiveness of erectile tissue to arousal.

Neurogenic causes include diabetic neuropathy, spinal cord injury, and post-surgical nerve damage (particularly after radical prostatectomy). Pharmacologic causes are common and often overlooked: SSRIs, beta-blockers, thiazide diuretics, opioids, and finasteride can all impair erectile function.

Psychogenic ED — driven by anxiety, depression, relationship distress, or performance pressure — is more common in younger men and often coexists with situational patterns (e.g., normal morning erections, difficulty only with a partner).

History alone identifies the likely category in most men. Key questions: onset (sudden vs gradual), presence of morning erections, ability to masturbate to full erection, medication list, cardiovascular risk factors, and mood/relationship context.

Labs: morning total testosterone, fasting glucose or HbA1c, lipid panel, TSH, and — if the story fits — prolactin. Nocturnal penile tumescence testing and penile Doppler ultrasound are reserved for complex or refractory cases.

First-line pharmacologic treatment is a PDE5 inhibitor (sildenafil, tadalafil, vardenafil, avanafil). These work in 60–70% of men across most causes, are safe in men with stable cardiovascular disease (contraindicated with nitrates), and daily low-dose tadalafil is a well-tolerated option for men with frequent activity.

Address the driver: treat hypertension, diabetes, and dyslipidemia; optimize testosterone if labs confirm hypogonadism; consider swapping ED-inducing medications when clinically appropriate. Weight loss, aerobic exercise, and smoking cessation improve erectile function in the same way they improve any vascular endpoint.

Second-line options — intracavernosal injections, vacuum devices, intraurethral alprostadil, and penile implants — are highly effective and appropriate when PDE5 inhibitors fail or are contraindicated. These are urology-led decisions.

Supplements marketed for ED vary widely in evidence. L-citrulline, Panax ginseng, and moderate-quality horny goat weed extracts have some supporting data; most heavily marketed 'male enhancement' pills either contain undisclosed PDE5 inhibitors (a real safety issue) or lack meaningful ingredients. Our reviews focus on transparent, third-party-tested formulas.

Aerobic exercise 40+ minutes 4x/week improves erectile function in randomized trials, comparable to a low-dose PDE5 inhibitor in mild ED. Mediterranean diet, weight loss to a BMI under 30, and smoking cessation each independently improve outcomes.

Poor sleep and sleep apnea are underappreciated drivers — CPAP treatment consistently improves erectile function in men with obstructive sleep apnea, independent of testosterone changes.