Male Sexual Dysfunction

Erectile dysfunction (ED) is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual activity, on all or almost all attempts.^[1] It is common, has vascular, neurogenic, structural, hormonal, and psychogenic causes that frequently coexist, and is far more than a quality-of-life issue: vascular ED often precedes the clinical diagnosis of coronary artery disease, so its presence should prompt a genuine cardiovascular risk assessment, not just a prescription.^[2] This chapter focuses on the assessment and stepwise pharmacologic management of ED — phosphodiesterase type 5 (PDE5) inhibitors as first-line therapy, the essential nitrate-interaction safety check, second-line options when PDE5 inhibitors fail or are contraindicated, and testosterone replacement therapy for confirmed hypogonadism — with brief, distinct coverage of premature ejaculation, delayed ejaculation, and low sexual desire, since more than one of these conditions can be present in the same patient and a focused sexual history is needed to tell them apart.

Erectile dysfunction

ED is classified by underlying mechanism, since this shapes both workup and counselling.

Premature ejaculation

Ejaculation that occurs sooner than desired with a sense of lack of control, causing distress. Lifelong premature ejaculation is present from a person's first sexual experiences, typically with ejaculation within about 1-2 minutes of penetration nearly every time; acquired premature ejaculation is a clinically significant reduction in ejaculatory latency from a patient's own previous pattern, with associated distress.^[3]

Delayed ejaculation

A marked delay in, or inability to achieve, ejaculation despite adequate sexual stimulation and the desire to ejaculate. Uncommon before age 50, with incidence increasing with age.

Male hypoactive sexual desire disorder

A persistent or recurrent lack of sexual thoughts, fantasies, and desire that causes distress. Depression, low testosterone, anxiety, insomnia, and insufficient physical activity are commonly associated.

More than one of these conditions can be present in the same patient at once — a focused sexual history covering desire, erection, ejaculation, and satisfaction is needed to identify all of them, since treating only the presenting complaint risks leaving a coexisting condition unaddressed.

• Advancing age.
• Cardiovascular risk factors that overlap heavily with vasculogenic ED: diabetes mellitus, dyslipidemia, hypertension, obesity, metabolic syndrome, sedentary lifestyle, and smoking.
• Pelvic or prostate surgery (radical prostatectomy), pelvic radiation therapy, pelvic trauma, or penile fracture.
• Neurologic disease — multiple sclerosis, Parkinson disease, spinal cord injury, diabetic neuropathy.
• Peyronie disease and other structural penile abnormalities.
• Lower urinary tract symptoms/benign prostatic hyperplasia and chronic prostatitis/chronic pelvic pain syndrome.
• Psychological factors — depression, anxiety, performance anxiety, relationship distress.
• Testosterone deficiency.
• Alcohol use, both acute intoxication and chronic heavy use; cannabis use.
• Medications — a major and frequently overlooked cause. Always review the medication list as part of the workup; the table below reproduces the drug classes most consistently associated with each type of male sexual dysfunction.

Medication-associated male sexual dysfunction

Abbreviations: GnRH = gonadotropin-releasing hormone; MAOI = monoamine oxidase inhibitor; SSRI = selective serotonin reuptake inhibitor. When a temporal link is plausible, discuss an alternative agent or dose adjustment with the prescriber before assuming the sexual dysfunction is unrelated to therapy.

History

• A focused sexual history distinguishing ED, premature ejaculation, delayed ejaculation, and low desire, including onset (lifelong vs. acquired), whether it is generalized or situational, and erection quality with self-stimulation and on waking versus with a partner.
• Medical, surgical, and psychiatric history, including pelvic/prostate surgery or radiation, pelvic trauma, and previously tried treatments.
• A complete medication review against the table in Risk Factors, plus tobacco, alcohol, cannabis, and other substance use.
• Screening for comorbid sexual conditions — premature ejaculation, delayed ejaculation, low desire, and Peyronie disease — since their presence changes management.
• Partner involvement in the history, when possible — it improves both assessment accuracy and treatment outcomes.

Physical examination

• Cardiovascular signs suggesting vascular disease — bruits, hypertension, poor peripheral pulses, heart failure.
• Neurologic signs suggesting an irreversible neurogenic cause.
• Signs of hypogonadism — reduced body/facial hair, gynecomastia, small or atrophic testes.
• Genital examination for penile plaques/curvature (Peyronie disease) and testicular size/consistency.

Laboratory testing

• Fasting glucose or A1c and a lipid profile in suspected vasculogenic or idiopathic ED, to identify occult diabetes and dyslipidemia.^[1]
• Morning total testosterone in patients with symptoms of testosterone deficiency (low desire, fatigue) or an unsatisfactory response to a PDE5 inhibitor.^[1] Diagnose testosterone deficiency only after two total testosterone measurements, both drawn before 11 a.m. after an overnight fast on separate days, showing a level under 300 ng/dL (approximately under 10.4 nmol/L) together with compatible symptoms or signs.^[4] If testosterone is low, check LH; if LH is low or low-normal, check prolactin.^[4]
• Screening questionnaires support diagnosis and follow-up but are not a substitute for laboratory testing, and are not a validated tool for deciding who is a candidate for testosterone therapy.^[4]

When testing is not indicated

Specialized testing — nocturnal penile tumescence and penile duplex ultrasound — provides little information beyond a detailed history and should be reserved for sub-specialist use in conflicting histories or medico-legal cases; it is not part of routine ED assessment.^[1]

Cardiovascular risk stratification before treating ED

ED is an independent cardiovascular risk marker, and every patient starting ED therapy should be stratified before treatment using a framework such as the Princeton IV Consensus.^[2]

Coronary artery calcium scoring is a reasonable adjunct for further risk assessment in men with ED and no known cardiovascular disease who fall in a borderline-to-intermediate risk category.^[2]

Validated questionnaires

The International Index of Erectile Function (IIEF) and its abridged 5-item version (IIEF-5, also called the Sexual Health Inventory for Men, SHIM) are validated tools that support diagnosis and track response to treatment without replacing a detailed history. The abridged version scores 5 domains — confidence in achieving an erection, erection firmness for penetration, ability to maintain an erection until completion of intercourse, difficulty maintaining an erection, and satisfaction with intercourse — each from 1 (or 0, if there was no sexual activity) to 5, for a total score of 5-25.

The clinically meaningful change in score depends on baseline severity — a smaller absolute change is meaningful in mild ED than in severe ED — so use the score to track trend and treatment response in an individual patient rather than as a single pass/fail cutoff.^[1]

• Achieve and maintain an erection sufficient for satisfactory sexual activity, using the lowest effective dose or least invasive option that works for the patient.
• Identify and correct reversible contributing factors — causative medications, uncontrolled diabetes/hypertension/dyslipidemia, and lifestyle factors — alongside, not instead of, pharmacologic therapy.
• Use the ED assessment as an opportunity for cardiovascular risk-factor review, given the link between vasculogenic ED and cardiovascular disease.
• Confirm testosterone deficiency biochemically before treating it, and treat it on its own merits (sexual and non-sexual symptoms) rather than as a substitute for standard ED therapy.
• Address the psychological and relationship dimension of sexual dysfunction alongside any organic cause, involving the partner where appropriate.
• For premature ejaculation, delayed ejaculation, and low sexual desire — achieve a pattern and degree of sexual satisfaction that is acceptable to the patient and their partner, combining behavioural and pharmacologic approaches as needed.

Lifestyle measures (erectile dysfunction)

• Increase physical activity/exercise — supported by evidence as improving erectile function, and a reasonable recommendation given its safety, low cost, and broader cardiovascular benefit.^[1]
• Smoking cessation, and reducing alcohol and cannabis consumption.
• Weight management and dietary changes, particularly with comorbid obesity or metabolic syndrome.
• L-arginine and citrulline (nitric oxide synthase substrates) have limited supporting evidence and are not currently recommended.^[1]

Psychological and relationship counselling

• Offer early referral for sexual counselling, especially when a psychogenic component is suspected — cognitive behavioural therapy or mindfulness-based approaches can be sufficient for situational ED.
• Address sexual avoidance directly: making time and context for intimacy, reintroducing affectionate/sexual communication throughout the day, and normalizing a broader range of sexual activity beyond penetrative intercourse.
• Involve the partner in assessment and counselling whenever possible — it improves both diagnostic accuracy and treatment outcomes, and sexual dysfunction affects the couple, not only the patient.
• Combining psychological treatment with a PDE5 inhibitor is common in practice and appears more effective than either approach alone.

Vacuum erection device

Creates negative pressure to draw blood into the penis, trapped by a constriction ring at the base to maintain firmness; safe for up to 30 minutes once the ring is applied — the ring must be removed by 30 minutes. There is a learning curve, and some patients cannot tolerate the degree of constriction required. It has no absolute contraindications, making it a reasonable option for patients who cannot use or have contraindications to pharmacologic therapy, though caution is reasonable in patients on anticoagulation or with a bleeding disorder given the local trauma potential.^[1]

Low-intensity shockwave therapy — not currently recommended

Despite being widely offered, including by non-urologists, low-intensity shockwave therapy is not Health Canada or FDA approved for ED, and current evidence does not support a clinically meaningful benefit — do not present it as an evidence-based option outside of a clinical trial.^[1]

Investigational regenerative therapies

Stem cell therapy, platelet-rich plasma, and amniotic fluid matrices are being studied for ED but remain experimental; do not recommend them outside of a clinical trial.^[1]

Premature ejaculation — behavioural techniques

• Stop-start technique: pause stimulation on reaching moderate arousal, repeated several times before allowing ejaculation, to build tolerance of higher arousal states.
• Squeeze technique: a firm squeeze to the glans at the point of stopping — most clinicians do not recommend adding the squeeze given the discomfort involved, and the stop-start technique alone is generally preferred.
• Referral for sex therapy/relationship counselling, particularly when premature ejaculation is affecting a partnered relationship.
• Combining behavioural techniques with pharmacotherapy is recommended to prolong benefit and allow eventual dose reduction.

Adolescents

ED is uncommon before age 50 and rare in adolescence; a young patient presenting with generalized, lifelong ED should be referred for specialist evaluation rather than managed with a standard stepwise approach, since a structural or congenital vascular cause is more likely.

Renal impairment

Reduce the starting dose of all three PDE5 inhibitors in significant renal impairment (see Drug Tables for specifics); tadalafil is not recommended in severe renal impairment.

Hepatic impairment

Reduce the starting dose of all three PDE5 inhibitors in hepatic impairment; tadalafil is not recommended in severe hepatic impairment.

Older adults

Start PDE5 inhibitors at the lower end of the dose range in patients over 65. Cardiovascular risk stratification (see Assessment & Diagnosis) is especially important in this group, and polypharmacy increases the chance of an unrecognized nitrate or interacting antihypertensive.

Fertility-desiring patients

Do not prescribe exogenous testosterone to a man who is currently trying to conceive — it suppresses spermatogenesis and can produce severe oligospermia or azoospermia.^[4] Men with testosterone deficiency who want to preserve fertility should be referred for options that raise endogenous testosterone instead (human chorionic gonadotropin, selective estrogen receptor modulators, or aromatase inhibitors, alone or combined) — specialist-directed.^[4]

Prostate cancer history

Testosterone therapy is not appropriate in men with untreated or active prostate cancer. In men with a history of treated, localized prostate cancer with favourable pathology and an undetectable PSA, testosterone therapy can be considered on an individualized basis with urology/oncology involvement rather than treated as an automatic exclusion.^[4]

Post-radical-prostatectomy erectile dysfunction

Do not default to a scheduled, prophylactic (penile rehabilitation) PDE5 inhibitor regimen after radical prostatectomy — current evidence does not support a meaningful benefit over treating ED as it presents.^[1]

PDE5 inhibitor therapy

At follow-up, confirm an adequate trial before concluding a drug has failed — correct dose, correct timing relative to food and sexual activity, and adequate sexual stimulation. Reassess cardiovascular risk periodically, particularly if new symptoms or risk factors emerge.

Testosterone replacement therapy

• Hemoglobin/hematocrit at baseline, then at 3-6 months, then annually — a hematocrit reaching 54% or higher on treatment warrants dose reduction or temporary discontinuation.^[4]
• PSA and digital rectal exam at baseline in men over 40, then per shared decision-making using standard prostate-cancer-screening guidance.^[4]
• Testosterone level rechecked once the patient is established on a stable dosing regimen (timing depends on formulation — e.g., partway through the interval between doses for short-acting injectable esters), then every 6-12 months once the target range is reached, approximately 450-600 ng/dL (15.6-20.8 nmol/L).^[4][5]
• Discuss stopping therapy if the patient does not feel meaningfully better after 3-6 months despite achieving target testosterone levels — persistence of symptoms at target levels suggests testosterone deficiency was not the (sole) cause.^[4]

Premature ejaculation, delayed ejaculation, and low desire

Reassess response and tolerability at follow-up, and adjust regimen (on-demand versus daily dosing, dose) as needed. When using an SSRI or clomipramine for premature ejaculation, counsel that delayed ejaculation and reduced desire are expected — and here, therapeutically useful — effects, distinct from an unwanted adverse effect in other indications.

1. Before declaring PDE5 inhibitor failure, confirm a genuinely adequate trial: correct dose (titrated to the maximum tolerated/approved dose), correct timing relative to food and sexual activity, and adequate sexual stimulation — many apparent failures reflect technique or expectations rather than true nonresponse.
2. If there is genuinely inadequate response at the maximum tolerated dose of one PDE5 inhibitor, trial an alternative PDE5 inhibitor before abandoning the class.
3. Screen or re-screen for an unaddressed contributing cause: unconfirmed testosterone deficiency, an unrecognized causative medication, uncontrolled diabetes or cardiovascular risk factors, or a significant psychological/relationship component.
4. If the patient requires ongoing nitrate therapy for cardiac symptoms, do not attempt to combine it with a PDE5 inhibitor under any timing strategy — refer for an alternative anti-anginal approach instead.
5. For confirmed PDE5 inhibitor failure or contraindication, move to a second-line option: intracavernosal alprostadil, a vacuum erection device, or intraurethral alprostadil.
6. If second-line therapy fails, is not tolerated, or is unacceptable to the patient, refer for urologic evaluation of a penile prosthesis.
7. For premature ejaculation not responding to first-line topical anesthetic, SSRI, or on-demand clomipramine therapy, refer for a sexual-medicine or urology evaluation before escalating further.

• Prescribing or dispensing a PDE5 inhibitor without asking about nitrate use, including intermittent and recreational nitrite use.
• Treating ED with testosterone therapy alone without confirming deficiency on two separate morning fasting measurements plus compatible symptoms.
• Assuming ED is purely psychological, or purely organic, without a history that genuinely covers both.
• Missing a medication cause because the causative drug was started long before the ED complaint was raised — always cross-check the current medication list.
• Not counselling on the high-fat-meal delay with sildenafil, or on the need for adequate sexual stimulation regardless of which PDE5 inhibitor is used — none of them produce an erection without arousal.
• Presenting low-intensity shockwave therapy as an evidence-based option — current evidence does not support it and it is not Health Canada or FDA approved for this use.
• Continuing testosterone therapy indefinitely without rechecking hematocrit, PSA, and testosterone levels on schedule.
• Prescribing exogenous testosterone to a man who is actively trying to conceive.
• Not asking about cardiovascular symptoms with exertion or sexual activity before starting any ED therapy.
• Treating only the presenting complaint without screening for a coexisting sexual dysfunction — ED, premature ejaculation, delayed ejaculation, and low desire frequently overlap.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

PDE5 Inhibitors — 1st line

First-line for essentially all erectile dysfunction. Absolute contraindication: any nitrate use. Use caution with alpha-blockers (additive hypotension) and strong CYP3A4 inhibitors/inducers.

Adjunctive folic acid 5 mg PO daily has limited trial evidence for improving PDE5 inhibitor response specifically in men with diabetes-related ED and is not a substitute for standard therapy or diabetes management.^[6]

Prostaglandin E1 (PGE1) Analogues — 2nd line

Used when PDE5 inhibitors fail after an adequate trial or are contraindicated. Dosing is individualized during in-office titration by the prescriber, not the pharmacist.

Androgen Replacement — special situation, confirmed testosterone deficiency only

Never a substitute for standard ED therapy in a man with a normal testosterone level. Confirm deficiency (two low morning fasting levels plus symptoms) before starting; exclude untreated prostate/breast cancer, a current desire for fertility, and a baseline hematocrit over 50% first.

Premature Ejaculation — SSRIs (off-label)

Regular daily dosing is more effective than on-demand dosing and may take 2-3 weeks for full benefit; on-demand dosing gives more timing flexibility for infrequent sexual activity.

Premature Ejaculation — tricyclic (off-label)

Premature Ejaculation — topical and other adjuncts

Compounded alprostadil combined with papaverine and phentolamine (informally known as "Trimix") is more effective than alprostadil alone but is not Health Canada approved and is prescribed only by specialists experienced in intracavernosal therapy — not included as a standard table row above.^[1]

Evidence note: Comparative PDE5 inhibitor dosing and second-line therapy content reflect the CUA 2021 Canadian guideline, cross-checked against the AUA 2018 erectile dysfunction guideline.^[7] Testosterone dosing and monitoring reflect the AUA Testosterone Deficiency guideline. Premature ejaculation dosing reflects the AUA/SMSNA 2022 ejaculation disorders guideline.