Erectile Dysfunction — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus
Quick Facts
What Is Erectile Dysfunction?
Erectile dysfunction (ED), formerly called impotence, is defined as the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance, present for at least 3 months. It is one of the most common sexual disorders in men, affecting approximately 52% of men aged 40-70 years to some degree. ED has significant psychological, relationship, and quality-of-life consequences. Critically, ED is often an early marker of cardiovascular disease — the penile arteries are smaller than coronary arteries, so they develop atherosclerotic changes and endothelial dysfunction earlier. ED frequently precedes a cardiovascular event (myocardial infarction or stroke) by 2-5 years and should prompt cardiovascular risk factor assessment. Erections depend on intact neurological, vascular, hormonal, and psychological systems — dysfunction in any of these leads to ED. Most cases in older men are organic (vascular/neurological) rather than purely psychogenic.
Causes & Risk Factors
Vascular causes (most common in older men): arteriogenic ED (atherosclerosis and endothelial dysfunction of the penile arteries reduces arterial inflow — the same risk factors as cardiovascular disease: hypertension, diabetes, dyslipidaemia, smoking, obesity); venous leak (failure of the corpora cavernosa smooth muscle to trap blood — impaired veno-occlusive mechanism); endothelial dysfunction (reduced nitric oxide production — the biochemical basis of ED). Neurological causes: diabetic autonomic neuropathy (very common — diabetes is the most common medical cause of ED); pelvic nerve damage from radical prostatectomy for prostate cancer (most common iatrogenic cause), radiation, or pelvic fracture; multiple sclerosis, Parkinson's disease, spinal cord injury. Hormonal causes: testosterone deficiency (primary or secondary hypogonadism — reduced libido and testosterone-dependent components of erection); hyperprolactinaemia (prolactinoma — inhibits GnRH/LH axis); hypothyroidism or hyperthyroidism. Psychological causes: performance anxiety (most common in younger men), depression, relationship problems, PTSD, body dysmorphia — typically present as situational ED (erections preserved during masturbation or on waking). Medication-induced ED: antihypertensives (thiazide diuretics, beta-blockers — but not ACE inhibitors or calcium channel blockers — the antihypertensive drugs of choice in men with ED); antidepressants (SSRIs — anorgasmia and ED; venlafaxine; mirtazapine has less sexual side-effect burden); antipsychotics (prolactin elevation from dopamine blockade); 5-alpha-reductase inhibitors (finasteride, dutasteride for BPH/hair loss — persistent sexual side effects post-discontinuation reported).
Symptoms & Clinical Features
ED presents as: difficulty achieving an erection (even with sexual stimulation), inability to maintain an erection during sexual activity, reduced rigidity of erections, decreased libido (more suggestive of testosterone deficiency), and anxiety or avoidance of sexual situations. The International Index of Erectile Function (IIEF-5 — 5-question validated questionnaire, score 5-25; below 21 suggests ED; below 11 severe ED) quantifies ED severity. Key clinical distinctions: Organic ED — gradual onset, present in all situations (including masturbation and nocturnal erections), no erections on waking, related to identifiable medical conditions. Psychogenic ED — sudden onset often after a psychosexual stressor, situational (erections preserved in some contexts but not others), nocturnal and morning erections preserved, in younger men. Most ED in clinical practice is of mixed organic and psychological aetiology — even primarily organic ED generates performance anxiety that compounds the problem. Testosterone deficiency features: reduced libido (an important distinguishing feature from pure vasculogenic ED), loss of morning erections, reduced body hair, gynaecomastia, reduced testicular volume.
How Erectile Dysfunction Is Diagnosed
History: sexual history (onset, duration, situational vs global, libido, relationship factors); medical history (cardiovascular disease, diabetes, neurological conditions, previous pelvic surgery or radiation); medication review; psychosocial assessment (stress, depression, anxiety, relationship issues); smoking, alcohol, and recreational drug use. Physical examination: BMI and waist circumference; blood pressure; signs of hypogonadism (reduced testicular volume, sparse body hair, gynaecomastia); cardiovascular examination; penile and perineal sensation; prostate examination. Blood tests: fasting glucose or HbA1c (diabetes), fasting lipid profile (dyslipidaemia), testosterone (morning total testosterone — below 12 nmol/L in UK suggests hypogonadism; repeat twice before treatment; add LH and FSH if low to distinguish primary from secondary hypogonadism), prolactin (if low testosterone or suspected pituitary cause), TSH (thyroid disease), FBC and renal function. Nocturnal penile tumescence (NPT) testing: preserved nocturnal erections (RigiScan device worn overnight) suggest psychogenic aetiology rather than organic vascular or neurological cause. Penile Doppler ultrasound: assesses penile arterial blood flow — performed by specialist for evaluation of arteriogenic vs venous leak ED; informs surgical decision making. PSA (prostate-specific antigen) before initiating testosterone therapy. Cardiovascular risk stratification: Framingham or QRISK score for all men with new-onset ED — ED is an independent cardiovascular risk factor.
Treatment Options
Address cardiovascular risk factors and modifiable causes first: smoking cessation, weight loss, increased exercise, optimise blood pressure and lipid control, reduce alcohol — these alone may improve ED significantly. PDE5 inhibitors (phosphodiesterase type 5 inhibitors — first-line pharmacotherapy): sildenafil (Viagra — 50 mg taken 30-60 minutes before sex; also available OTC from pharmacists and supermarkets since 2018 at low dose; efficacy approximately 70%); tadalafil (Cialis — 10-20 mg on-demand or 2.5-5 mg daily for spontaneous activity — the preferred choice for men who want less-planned sexual activity); vardenafil (Levitra); avanafil (Spedra — fastest onset). All PDE5 inhibitors are contraindicated with nitrates (GTN sprays, isosorbide dinitrate) — risk of fatal hypotension. Common side effects: headache, flushing, nasal congestion, visual disturbance (sildenafil — temporary blue tinge to vision). Testosterone replacement therapy (TRT): for confirmed hypogonadism (testosterone below 12 nmol/L on two occasions with symptoms) — testosterone gels (Testogel, Testavan), injections (Sustanon, Nebido), or implants; improves libido and may improve PDE5 inhibitor response. Vacuum erection devices (VEDs): cylindrical pump draws blood into the penis; constriction ring maintains erection; effective but less spontaneous; particularly useful for men unable to use PDE5 inhibitors. Intracavernosal alprostadil injections (Caverject, Viridal): prostaglandin E1 injected directly into the corpora cavernosa before sex; highly effective (80-90%); used when PDE5 inhibitors fail or are contraindicated; requires patient training. Intraurethral alprostadil (MUSE — medicated urethral system for erections): pellet inserted into the urethra; less effective than injections. Penile implants (inflatable or semirigid prostheses): surgical implantation for severe, treatment-refractory ED; high patient satisfaction (95%); permanent and irreversible. Psychosexual therapy: essential for psychogenic ED or as adjunct to medical treatment for organic ED — CBT, sensate focus exercises, couples therapy.
Complications of Erectile Dysfunction
Untreated erectile dysfunction causes a range of psychological, relational, and physical complications. Psychological impact: ED causes significant anxiety, depression, loss of self-esteem, and shame — depression is both a cause and consequence of ED in a bidirectional relationship. Performance anxiety from a first episode of ED can trigger a self-perpetuating cycle of anticipatory anxiety that worsens subsequent attempts. Relationship strain: ED frequently causes relationship conflict, partner distress, reduced intimacy, and in some cases relationship breakdown; partners of men with ED often report guilt, feeling unattractive, or rejection. Cardiovascular disease: as ED is a sentinel marker of systemic vascular disease and endothelial dysfunction, men with untreated ED who are not assessed and treated for underlying cardiovascular risk factors are at substantially elevated risk of myocardial infarction, stroke, and peripheral artery disease; studies show men with ED have a 44-65% increased risk of cardiovascular events. Quality of life: untreated ED causes avoidance of sexual activity, loss of intimacy, and reduced overall sense of wellbeing and life satisfaction. Reproductive impact: severe ED precludes natural conception, requiring assisted reproductive techniques or adoption. Medication side effects from prolonged PDE5 inhibitor use are generally mild and reversible.
Prevention & Cardiovascular Risk Reduction
ED in men over 40 should prompt a full cardiovascular risk assessment — it is a marker of systemic vascular disease. Addressing cardiovascular risk factors reduces ED risk: stop smoking (smoking is the single most important modifiable risk factor for vasculogenic ED — nicotine causes acute vasoconstriction and chronic endothelial damage); maintain healthy weight (obesity is strongly associated with ED — weight loss of 15% improves ED significantly); regular aerobic exercise (150 minutes weekly — improves endothelial function and erectile function, comparable to PDE5 inhibitor therapy in studies of obese men with ED); control blood pressure and blood glucose (hypertension and diabetes are major vascular risk factors); limit alcohol (moderate consumption may not impair, but excessive alcohol causes direct neurological and hormonal damage to sexual function). Avoid recreational drugs (cocaine, opioids, cannabis, anabolic steroids — all cause or worsen ED through different mechanisms). Review medications causing ED with your doctor — switching antihypertensive from beta-blocker to ACE inhibitor or calcium channel blocker may improve ED substantially.
When to See a Doctor
Consult your GP for persistent erectile difficulties lasting more than 3 months, or any sudden change in erectile function. Do not be embarrassed — ED is extremely common, has effective treatments, and may indicate underlying health conditions (cardiovascular disease, diabetes, testosterone deficiency) requiring attention in their own right. See your GP urgently if ED is accompanied by: chest pain or shortness of breath (possible cardiovascular disease), reduced libido with tiredness and weight gain (possible hypothyroidism or hypogonadism), severe depression, or penile pain or curvature that has changed (possible Peyronie's disease). ED developing after pelvic surgery or radiation for prostate cancer is expected and should be discussed with your urologist — penile rehabilitation programmes (early use of PDE5 inhibitors post-surgery) may help preserve long-term erectile function. If PDE5 inhibitors (sildenafil, tadalafil) are not effective, ask for specialist urology or andrology referral.
Frequently Asked Questions
References
- EAU Guidelines on Male Sexual Dysfunction — European Association of Urology, 2023
- NICE Clinical Guideline CG171 — Erectile Dysfunction, 2013 (updated 2019)
- Feldman HA et al. — Impotence and Its Medical and Psychosocial Correlates: Results of the Massachusetts Male Aging Study, Journal of Urology, 1994
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Last updated: 2026-07-06
Important: This information is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider for diagnosis and treatment.
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