Erectile Dysfunction — Causes, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Erectile dysfunction (ED) is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual intercourse. It is one of the most common conditions affecting men — estimated to affect 150 million men worldwide, with projections of 322 million by 2025. Prevalence increases significantly with age: approximately 30% of men in their 40s, 40-50% in their 50s, and up to 70% in their 70s, though ED is not an inevitable consequence of ageing. ED is an important marker of overall cardiovascular and metabolic health. It shares the same pathophysiology as atherosclerosis — endothelial dysfunction and reduced nitric oxide bioavailability — and penile arterial disease typically precedes coronary artery disease by 3-5 years. New onset ED in a man without cardiovascular risk factors should prompt cardiovascular risk assessment, as ED can be the first clinical manifestation of systemic atherosclerosis. ED has significant negative impact on quality of life, self-esteem, and intimate relationships.

Organic (physical) causes account for 80-90% of ED in middle-aged and older men: vascular (most common — penile arterial insufficiency from atherosclerosis — risk factors: hypertension, dyslipidaemia, diabetes, smoking, obesity); neurogenic (multiple sclerosis, Parkinson's disease, spinal cord injury, radical prostatectomy — cavernous nerve injury, pelvic fracture, diabetic autonomic neuropathy); endocrine (hypogonadism — low testosterone; hypo/hyperthyroidism; hyperprolactinaemia — pituitary adenoma causing suppressed testosterone; poorly controlled diabetes); drug-induced (very common — antihypertensives: beta-blockers, thiazide diuretics; antidepressants: SSRIs, SNRIs, TCAs; antipsychotics; 5-alpha reductase inhibitors — finasteride, dutasteride; opioids; alcohol and recreational drugs); and anatomical (Peyronie's disease — penile fibrosis and deformity). Psychogenic ED: more common in younger men — performance anxiety, relationship problems, depression, stress, and PTSD; typically presents with sudden onset, situational ED (erections normal in certain situations — masturbation, on waking — but impaired with partner). Mixed etiology is very common — organic cause + psychological overlay. Risk factors: age (strongest predictor); cardiovascular risk factors (diabetes, hypertension, hypercholesterolaemia, smoking — each doubles ED risk); obesity (visceral adiposity reduces testosterone, causes endothelial dysfunction); sedentary lifestyle; alcohol excess; testosterone deficiency.

The primary symptom is difficulty achieving or maintaining an erection for satisfactory intercourse. ED severity assessed by International Index of Erectile Function (IIEF-5) questionnaire (score 1-25: 1-7 severe, 8-11 moderate, 12-16 mild-to-moderate, 17-21 mild, 22-25 no dysfunction). Key clinical distinctions: organic ED typically develops gradually, is present in all situations (with partner and during masturbation), and morning erections are absent or reduced; psychogenic ED is often sudden onset, situational (varies by partner, context, or anxiety level), and morning/nocturnal erections are preserved. Associated symptoms: reduced libido (low testosterone or depression); delayed ejaculation (neurogenic); premature ejaculation (often coexists); penile curvature or pain (Peyronie's disease); loss of secondary sexual characteristics — reduced facial/body hair, reduced testicular volume, gynaecomastia (hypogonadism); lower urinary tract symptoms (LUTS) from benign prostatic hyperplasia (BPH — often coexists). Relationship and psychological impact: partner distress, avoidance of intimacy, depression, and reduced self-confidence are common.

NICE and European Association of Urology (EAU) guidelines recommend a structured assessment. History: onset, duration, situational vs. universal, severity (IIEF-5), morning erections, libido, ejaculation, relationship factors, medications, comorbidities (CVD, diabetes, hypertension), smoking and alcohol. Physical examination: body habitus (obesity); secondary sexual characteristics; penis (Peyronie's plaques — fibrous induration on palpation); testes (size and consistency — small testes suggest hypogonadism); blood pressure. Investigations: fasting glucose or HbA1c (exclude diabetes — 20% of men with new ED have undiagnosed diabetes); fasting lipid profile and total cholesterol (cardiovascular risk assessment); testosterone (total morning testosterone — if low, repeat + LH, FSH, SHBG, prolactin); FBC, TFTs, PSA if clinically indicated. Cardiovascular risk assessment: QRISK3 or Framingham score — all men with ED should have cardiovascular risk quantified; ED is now considered a CAD-equivalent risk marker by some guidelines. Nocturnal penile tumescence testing (RigiScan) or snap gauge: distinguishes psychogenic from organic ED — normal nocturnal erections suggest psychogenic cause. Penile Doppler ultrasound: assesses arterial blood flow (peak systolic velocity above 25-35 cm/s is normal) — used when considering revascularisation or prosthesis. Pituitary MRI: if prolactin elevated or hypogonadism confirmed.

Lifestyle modification first — evidence base is strong: aerobic exercise (30 minutes, 4 days/week) improves erectile function by 15-25% (IIEF score improvement) within 6 weeks — equivalent to PDE5 inhibitor response in mild-moderate ED; weight loss (obese men: 10% weight reduction restores erections in 30%); smoking cessation (reverses vascular contribution over years); alcohol reduction; optimise diabetes and hypertension management. Treat underlying causes: optimise diabetes, hypertension, hypercholesterolaemia (statin therapy); consider switching causative drugs (antidepressant-related ED: change to bupropion, mirtazapine, or agomelatine; beta-blocker related: switch to nebivolol — has least ED effect of beta-blockers); testosterone replacement therapy (TRT) for confirmed hypogonadism (total testosterone below 12 nmol/L) — improves erections and libido; manage hyperprolactinaemia (cabergoline). First-line pharmacotherapy — PDE5 inhibitors: sildenafil (Viagra) 25-100 mg taken 60 minutes before sexual activity (most data); tadalafil (Cialis) 10-20 mg (on-demand — lasts 36 hours) or 5 mg daily (daily dosing — allows spontaneity, also treats LUTS from BPH); vardenafil (Levitra) 10-20 mg; avanafil (Spedra) 100-200 mg (fastest onset — 15-30 minutes); all work by inhibiting PDE5 — preventing cGMP breakdown and prolonging nitric oxide-mediated smooth muscle relaxation; contraindicated with nitrates (sildenafil + nitrate = severe hypotension); success rate 60-75% across all etiologies. Second-line therapy: intracavernosal alprostadil injections (Caverject, Viridal — prostaglandin E1 injected into corpus cavernosum; success rate 70-80%; risk of priapism); intraurethral alprostadil (MUSE suppository); vacuum erection device (VED — mechanical pump creating negative pressure; effective and drug-free). Low-intensity extracorporeal shockwave therapy (Li-ESWT): emerging treatment for vasculogenic ED — promotes neovascularisation and endothelial repair; NICE 2023 evidence review suggests efficacy in mild-moderate vasculogenic ED, though long-term data accumulating. Psychological and sex therapy: essential for psychogenic ED; concurrent CBT-based sex therapy significantly improves PDE5 inhibitor outcomes in mixed/psychogenic ED. Surgery: penile prosthesis implant (inflatable or semi-rigid) — for severe refractory ED, post-radical prostatectomy, Peyronie's disease — high patient satisfaction above 90% but irreversible.

Erectile dysfunction (ED) carries significant psychological, relational, and medical complications. Psychologically, untreated ED causes anxiety, depression, reduced self-esteem, shame, and sexual avoidance — affecting an estimated 40-60% of men with ED. Relationship difficulties and partner distress are common, with sexual dysfunction increasing relationship conflict, intimacy avoidance, and relationship breakdown. ED is now recognised as an independent cardiovascular risk marker — the penile arteries (1-2 mm diameter) develop atherosclerosis before the larger coronary arteries (3-4 mm), so ED often precedes coronary artery disease by 3-5 years. Any man with new-onset ED without an obvious cause (psychological, medication-related) requires cardiovascular risk assessment including blood pressure, lipids, HbA1c, and lifestyle risk factors — Princeton III Consensus Guidelines recommend ED as a 'flag' for cardiovascular investigation. In younger men, ED from vasculogenic causes (atherosclerosis, endothelial dysfunction) indicates premature generalised vascular disease. Hypogonadism causing ED leads to the systemic effects of testosterone deficiency including reduced bone density (osteoporosis), loss of muscle mass (sarcopenia), metabolic syndrome, and anaemia if untreated. Men with ED are at increased risk of depression and anxiety disorders — both conditions that further perpetuate the sexual dysfunction through HPA axis effects on testosterone and serotonergic effects on sexual function.

ED is a preventable condition in many cases: maintain healthy weight (BMI 20-25 kg/m²); engage in regular aerobic exercise; avoid tobacco smoking; consume alcohol within recommended limits; eat a Mediterranean-style diet (associated with reduced ED incidence — Esposito RCT, JAMA 2004); maintain glycaemic control (diabetes is the strongest organic risk factor — tight control reduces microvascular and macrovascular complications including ED). ED as a cardiovascular sentinel event: the Princeton Consensus III guidelines recommend cardiovascular risk stratification of all men with ED — low risk (no or mild cardiovascular symptoms, LVF preserved) can initiate sexual activity and PDE5 inhibitors; intermediate risk (e.g. 3+ CVD risk factors, moderate stable angina) — cardiac evaluation before sexual activity; high risk (unstable angina, recent MI, uncontrolled hypertension, severe heart failure) — treat cardiovascular condition first. Hypertensive men: achieve BP below 130/80 mmHg — calcium channel blockers (amlodipine) and ARBs (losartan) have least ED side effects; avoid beta-blockers + thiazides (worst ED profile).

See your GP promptly for any new onset erectile dysfunction — particularly important if: under 50 years old (new ED in younger men has higher risk of underlying organic disease or hypogonadism); no prior cardiovascular diagnosis but has risk factors — new ED requires cardiovascular risk stratification (QRISK3) and may reveal silent coronary artery disease; associated with reduced libido or testicular atrophy — possible hypogonadism; associated with headache, visual field loss, or galactorrhoea — possible pituitary tumour (prolactinoma). Seek emergency care for priapism (prolonged erection lasting more than 4 hours without sexual stimulation) — this is a urological emergency; intracavernosal injection without detumescence requires aspiration and/or injection of phenylephrine to avoid permanent cavernous smooth muscle damage. Do not be embarrassed to seek help — ED is highly treatable and discussing it with your doctor may reveal serious underlying conditions.