Erectile Dysfunction — Symptoms, Causes & Treatment | MyMedicPlus

Erectile dysfunction (ED) — also called impotence — is the persistent inability to achieve or maintain a penile erection of sufficient rigidity and duration for satisfactory sexual performance. This definition, derived from the NIH Consensus Panel (1993), distinguishes ED from transient difficulty (which affects most men occasionally) by its persistence and impact on sexual satisfaction. ED affects an estimated 30–50 million men in the United States alone and 150–322 million men globally — with population-based studies consistently showing that moderate to severe ED affects approximately 20% of men over 40, rising to 50% of men over 50 and above 70% of men over 70. The Massachusetts Male Aging Study (MMAS) reported a total ED prevalence of 52% in men aged 40–70 years. Critically, ED is not merely a quality-of-life condition — it is an independent cardiovascular risk marker. Penile erection depends on an intact nitric oxide-cGMP signalling cascade causing cavernosal smooth muscle relaxation and arterial inflow. Any process impairing endothelial function, nitric oxide synthesis, autonomic innervation, or smooth muscle integrity can cause ED. Endothelial dysfunction — the same pathophysiological substrate underlying coronary artery disease, peripheral vascular disease, and stroke — is the principal mechanism of organic ED. Men with new ED have a 2 to 5-fold increased risk of a major cardiovascular event (MI or stroke) within 10 years — ED may precede clinical cardiovascular disease by 3–5 years and represents a 'window of opportunity' for cardiovascular risk factor intervention.

Organic (non-psychogenic) causes account for 70–80% of ED presentations: Vascular disease is the most common organic cause — atherosclerosis of the cavernous or pudendal arteries reduces penile arterial inflow; any risk factor for cardiovascular disease (hypertension, hyperlipidaemia, diabetes, smoking, obesity, metabolic syndrome) substantially elevates ED risk. Penile arterial insufficiency is detectable by penile Doppler ultrasound (peak systolic velocity below 25 cm/s indicates arterial disease). Venous leakage (corporo-venous occlusive dysfunction) impairs maintenance of erection despite adequate arterial inflow — the veins fail to constrict sufficiently during erection. Diabetic ED: both type 1 and type 2 diabetes cause ED through autonomic neuropathy (impairing parasympathetic innervation necessary for erection), endothelial dysfunction, and microvascular disease — ED prevalence in diabetes is 40–60% at 10 years and 55–75% at 20 years. Neurological: Parkinson's disease, multiple sclerosis, spinal cord injury or disease, cauda equina syndrome, and radical prostatectomy (bilateral nerve-sparing technique reduces ED risk by 50–70% versus non-nerve-sparing). Hormonal: hypogonadism (low total testosterone below 12 nmol/L or free testosterone below 0.225 nmol/L) — causes reduced libido and ED; hyperprolactinaemia (often from pituitary adenoma); hypothyroidism and hyperthyroidism. Medications: antidepressants (SSRIs — paroxetine, fluoxetine cause ED and delayed ejaculation in 30–40%; mirtazapine has lowest sexual side effect profile); antihypertensives (beta-blockers — atenolol; thiazide diuretics; alpha-blockers paradoxically can treat ED); antipsychotics; anti-androgens (for prostate cancer); opioids; 5-alpha reductase inhibitors (finasteride, dutasteride — cause persistent sexual dysfunction in 1–2%). Psychogenic causes (20–30%): performance anxiety (often secondary to organic ED); depression (bidirectional relationship — ED causes depression and vice versa); relationship difficulties; PTSD; sexual abuse history.

The primary symptom is consistent difficulty achieving or maintaining an erection firm enough for satisfactory sexual intercourse. ED severity is formally quantified using the International Index of Erectile Function (IIEF-5) questionnaire — five questions scored 1–5; total score 22–25 = no ED; 17–21 = mild; 12–16 = mild-moderate; 8–11 = moderate; 5–7 = severe ED. Additional symptoms and clinical features: Reduced sexual drive (libido): low testosterone is the most common hormonal cause of both reduced libido and ED — distinguishing loss of libido (hormonal) from preserved libido with erection failure (usually vascular or neurogenic) is diagnostically important. Ejaculatory dysfunction: premature ejaculation (most common male sexual dysfunction — affects 20–30%) or delayed ejaculation (less common; associated with SSRIs, autonomic neuropathy, and ageing) may coexist with ED. Morning erections (nocturnal penile tumescence — NPT): presence of spontaneous morning erections suggests intact vascular and neurological pathways and points toward psychogenic aetiology; absent morning erections suggest organic ED. Penile curvature or painful erections (Peyronie's disease — fibrous plaque within the tunica albuginea — affects 1–9% of men, causing acquired penile curvature during erection and pain; it is associated with ED in 50% of cases). Relationship and psychological distress: avoidance of intimacy, partner distress, reduced self-esteem, depression, and anxiety are secondary consequences of untreated ED affecting quality of life in both partners.

A structured clinical approach identifies the aetiology and guides treatment. Clinical history: duration, onset (sudden vs gradual — gradual onset suggests vascular, sudden suggests psychogenic or medication-induced), severity (IIEF-5 score), situational (with partner vs masturbation — situational suggests psychogenic), morning erection presence, libido, pain (Peyronie's), urinary symptoms (LUTS), medications, smoking and alcohol history, and relationship status. Physical examination: secondary sexual characteristics and testicular size/consistency (hypogonadism — small soft testes below 15 mL); blood pressure (hypertension); BMI and waist circumference (metabolic syndrome); femoral and peripheral pulses (arterial disease); neurological assessment including perineal and penile sensation; penile anatomy (phimosis, chordee, Peyronie's plaques). Blood investigations: fasting plasma glucose and HbA1c (diabetes), lipid panel (dyslipidaemia), total testosterone (morning sample — 8–10 am for diurnal variation; if low, repeat with LH, FSH, and prolactin to classify hypogonadism), thyroid function (TSH), FBC and renal function. PSA in appropriate patients with prostate cancer risk who are being considered for testosterone therapy. Nocturnal penile tumescence (NPT) testing (RigiScan): distinguishes organic from psychogenic ED — 3 nights of measurement; organic ED shows absent or inadequate tumescence. Penile Duplex Doppler ultrasound: following intracavernosal injection of alprostadil (prostaglandin E1 — 10–20 mcg), peak systolic velocity above 30 cm/s = normal arterial inflow; below 25 cm/s = arterial insufficiency; elevated diastolic flow or end-diastolic velocity = venous leak. Selective pudendal arteriography is reserved for young patients with post-traumatic pelvic arterial injury before reconstructive surgery.

Phosphodiesterase type 5 (PDE5) inhibitors are the first-line pharmacological treatment for ED in the absence of contraindications. They enhance the nitric oxide-cGMP pathway by preventing cGMP degradation, causing cavernosal smooth muscle relaxation and sustained arterial inflow during sexual stimulation: Sildenafil (Viagra) 25–100 mg — taken 30–60 minutes before intercourse; on-demand use; food reduces absorption; duration 4–6 hours. Tadalafil (Cialis) 10–20 mg on demand or 2.5–5 mg daily (the only PDE5 inhibitor licensed for daily use — provides continuous readiness regardless of timing of intercourse; also reduces BPH-related LUTS). Vardenafil 10–20 mg. Avanafil 100–200 mg — fastest onset (15 minutes), fewer visual disturbances (less PDE6 cross-reactivity). PDE5 inhibitors are ABSOLUTELY CONTRAINDICATED with all nitrate medications (isosorbide mononitrate, glyceryl trinitrate, amyl nitrite — risk of profound and potentially fatal hypotension). Testosterone replacement therapy (TRT): indicated for confirmed hypogonadism (total testosterone below 12 nmol/L with symptoms); forms include IM testosterone undecanoate (Nebido — every 10–14 weeks), testosterone gel (Testogel, Tostran — daily); restores libido and may improve PDE5 inhibitor responsiveness; contraindicated in active prostate cancer and prostate cancer risk (PSA assessment required before TRT). Second-line treatments: Intracavernosal injection (ICI): self-administered injection of alprostadil (Caverject) or combination papaverine/phentolamine/alprostadil (Trimix — not licensed in UK/EU but used widely); erection onset in 5–20 minutes; highly effective (75–90%) including in post-prostatectomy ED; risk of priapism (1–5% — requires education on self-management). Vacuum erection devices (VEDs): a cylinder placed over the penis creates negative pressure drawing blood in; a constriction ring maintains the erection; effective in 90% but less preferred by patients due to unnatural erection. Intraurethral alprostadil suppository (MUSE — Medicated Urethral System for Erection): less effective than ICI. Penile prosthesis (inflatable 3-piece IPP or malleable rod): the most effective definitive treatment for severe, refractory organic ED — satisfaction rates above 90% in appropriately selected patients; requires surgical implantation; not reversible.

ED significantly impairs quality of life, self-esteem, and intimate relationships, with high rates of depression and anxiety in affected men and their partners. ED is an independent marker of cardiovascular risk — men with ED have a 2–5 times higher risk of major cardiac events within 10 years. Untreated underlying causes (diabetes, hypertension, atherosclerosis) will continue to progress. Priapism (prolonged unwanted erection exceeding 4 hours) is a urological emergency that can result in permanent erectile dysfunction if not promptly treated.

Erectile dysfunction is a largely preventable condition in many men — the same lifestyle modifications that reduce cardiovascular disease risk protect erectile function. Smoking cessation: smoking doubles the risk of ED from endothelial damage, reduced nitric oxide bioavailability, and cavernosal smooth muscle fibrosis — cessation at any age reduces ED risk and improves severity in established disease. Regular physical exercise (at least 150 minutes of moderate-intensity aerobic activity per week): the single most effective lifestyle intervention for ED — a 2018 meta-analysis showed exercise equivalent to running 30 minutes/day 5 times per week reduced ED risk by 40% in men with cardiovascular disease. Weight management: obesity causes ED through dyslipidaemia, hypogonadism (aromatisation of testosterone to oestradiol in adipose tissue), elevated inflammatory cytokines, and sleep apnoea — weight loss of 10% body weight significantly improves ED severity and PDE5 inhibitor responsiveness. Blood pressure, blood sugar, and lipid control: each 1% reduction in HbA1c improves erectile function in diabetic men; statin therapy (particularly atorvastatin) improves endothelial function and ED in men with dyslipidaemia. Limiting alcohol: chronic heavy alcohol consumption causes autonomic neuropathy, hypogonadism, and direct testicular toxicity — moderate consumption (2 units/day maximum) does not worsen ED. Psychological and relationship health: addressing performance anxiety, depression, and relationship conflict through psychosexual therapy and couples counselling improves ED in men with predominantly psychogenic cause and enhances the efficacy of pharmacological treatment in those with mixed aetiology. Medication review: if a suspected causative medication (SSRI, beta-blocker, thiazide diuretic) can be safely changed to an alternative with lower sexual side effects (mirtazapine, amlodipine, ACE inhibitor), this should be considered in consultation with the prescribing clinician.

See a GP for: persistent erectile dysfunction (difficulty achieving or maintaining erections) lasting more than 3 months — particularly in men under 50 where cardiovascular risk assessment is indicated, as ED is an early marker of endothelial dysfunction and atherosclerosis. Erectile dysfunction is associated with 1.5-2x higher risk of cardiovascular events; a young man with new ED should have blood pressure, lipids, and HbA1c checked. Seek urgent assessment for: sudden loss of erections with no psychological explanation in a man over 50 (may indicate new cardiovascular disease or undiagnosed diabetes); new penile curvature with painful erections (Peyronie's disease — requires early urological assessment); or priapism (a prolonged unwanted erection lasting more than 4 hours — a medical emergency requiring immediate emergency department attendance to prevent permanent erectile damage). Online prescription services for PDE5 inhibitors (sildenafil, tadalafil) may be appropriate for low-risk men, but a GP assessment is strongly recommended first to exclude cardiovascular contraindications (particularly nitrate use) and identify treatable causes.