Insomnia

Clinical Snapshot

Insomnia is dissatisfaction with sleep quality or quantity associated with 1 or more of: difficulty falling asleep, difficulty staying asleep, or early morning awakening without being able to return to sleep. The sleep disturbance must cause distress or impairment in daytime functioning to qualify as a disorder — poor sleep without daytime consequences is not, by itself, insomnia disorder. When these criteria are met and present at least 3 nights per week for at least 3 months, and are not substance-related, the diagnosis is chronic insomnia disorder; when the same criteria are met but the disturbance has lasted under 3 months, it is short-term insomnia disorder (sometimes still called acute insomnia).

Insomnia can be a standalone disorder, a symptom, or comorbid with another sleep disorder or a psychiatric or medical condition (sleep apnea, depression, anxiety, chronic pain). Identifying the presence or absence of comorbid conditions is central to management, since comorbid insomnia is common and usually needs the comorbidity addressed alongside the insomnia itself, not instead of it.

Behavioural intervention — culminating in cognitive behavioural therapy for insomnia (CBT-I) — is the foundation of treatment and the genuine first-line therapy for essentially every patient, not a fallback used only when medication fails or is declined.^[1] Hypnotic medications are comparably effective to CBT-I during acute treatment, and combining pharmacotherapy with CBT-I is an effective, reasonable approach when medication is needed — but CBT-I, not a drug, is where treatment starts.^[2]

Recognize the Condition

Core symptom domains

Sleep-onset difficulty — prolonged sleep latency (time to fall asleep).
Sleep-maintenance difficulty — frequent or prolonged awakenings during the night (wakefulness after sleep onset).
Early morning awakening — waking earlier than desired or intended and being unable to return to sleep.

Required daytime impairment (at least 1 domain)

Fatigue or malaise.
Attention, concentration, or memory impairment.
Impaired social, family, occupational, or academic performance.
Mood disturbance or irritability.
Daytime sleepiness.
Reduced motivation, energy, or initiative.

Short-term vs. chronic insomnia disorder

Short-term (acute) insomnia disorder

Meets the symptom and impairment criteria above but has been present for under 3 months. Often has an identifiable precipitant (acute stress, illness, travel, hospitalization). Frequently resolves once the precipitant resolves, but can become chronic if perpetuating behaviours (excess time in bed, irregular schedule, daytime napping) take hold.

Chronic insomnia disorder

Meets the symptom and impairment criteria at least 3 nights per week for at least 3 months, and is not substance-related. May be a standalone disorder or comorbid with another sleep disorder, a psychiatric condition, or a medical condition — a single diagnostic label applies whether or not a comorbidity is present, since the comorbidity must be identified and addressed either way rather than assumed to fully explain (or be fully explained by) the insomnia.

Insomnia develops and persists through 3 overlapping factors: predisposing factors that increase baseline risk (an anxious or ruminative temperament), precipitating factors that trigger an episode (an acute stressor, illness, or life change), and perpetuating factors that maintain the problem after the trigger resolves (learned negative sleep behaviours — excess time in bed, irregular schedule, sleep-related anxiety). CBT-I works primarily by dismantling the perpetuating factors.

Risk Factors

Anxious, ruminative, or worry-prone predisposition; family history of insomnia.
Female sex; older age.
Shift work, irregular sleep-wake schedule, jet lag.
Psychiatric comorbidity — mood disorders, anxiety disorders, ADHD, post-traumatic stress disorder, alcohol or substance use disorder.
Medical comorbidity causing nocturnal discomfort or pain — arthritis, fibromyalgia and other chronic pain, menopause, gastroesophageal reflux disease, migraine, stroke, COPD or asthma, congestive heart failure, hypothyroidism or hyperthyroidism.
Medications that disrupt sleep — stimulants, some antidepressants, antihypertensives, decongestants and antihistamines, analgesics, corticosteroids, and sedatives themselves (via rebound/withdrawal effects).
Caffeine, alcohol, nicotine, or recreational substance use, particularly close to bedtime.
Poor sleep hygiene and stimulus-control breaches (irregular schedule, screens/work in bed, napping, an unfavourable sleep environment).
Pregnancy and the postpartum period.
An untreated primary sleep disorder — obstructive sleep apnea, restless legs syndrome, a circadian rhythm disorder, or a parasomnia — presenting with an insomnia complaint.

Red Flags & Refer

Screen every patient with insomnia for these before committing to insomnia-specific treatment — several change the diagnosis and management entirely rather than simply adding a comorbidity to treat alongside insomnia.

Suspected obstructive sleep apnea — loud snoring, witnessed breathing pauses or gasping, morning headache, or treatment-resistant hypertension: arrange a sleep study rather than treating as primary insomnia; sedating hypnotics can worsen undiagnosed sleep apnea.
Suspected restless legs syndrome — an urge to move the legs, worse at rest or in the evening, relieved by movement: treat the underlying RLS specifically rather than the insomnia symptom in isolation.
Suicidal ideation or a severe, undertreated psychiatric illness — insomnia is both a symptom and a modifiable risk factor for mood and anxiety disorders; escalate for urgent psychiatric assessment when ideation is present rather than treating sleep alone.
Suspected parasomnia (sleepwalking, sleep talking, injury during sleep) or a circadian rhythm disorder (persistently unusual sleep timing): refer for specialized sleep assessment rather than generic hypnotic therapy.
Complex sleep-related behaviours (sleep-related eating, walking, driving, or other activity with no recollection) associated with a benzodiazepine receptor agonist (Z-drug) or other sedative-hypnotic: discontinue the agent immediately and do not rechallenge with the same drug or class.
Evidence of a substance use disorder involving hypnotics, alcohol, or other sedatives.
Insomnia in a child, especially with red-flag features, or any consideration of long-term hypnotic therapy in a child: refer given the limited pediatric evidence base.
Treatment-resistant insomnia — inadequate response despite genuine CBT-I and an adequate pharmacotherapy trial: refer to a sleep medicine specialist rather than continuing to escalate empirically.

Assessment & Diagnosis

Sleep history

A structured sleep history is essential to quantify daytime impairment, determine what previous pharmacologic and nonpharmacologic treatment has already been tried, and screen for other sleep pathologies and substances affecting sleep.

Domain	What to ask
Temporal aspects	Time the patient goes to bed, attempts to sleep, wakes up, and gets out of bed.
Quantitative aspects	Sleep latency (time to fall asleep); number and duration of awakenings; wakefulness after sleep onset; total sleep time.
Qualitative aspects	Subjective sleep quality and satisfaction.
Behavioural/environmental factors	Non-sleep activities in bed (phone, computer, television); bedroom environment (temperature, light, sound); bed partners and pets; perceived causes of awakening.
Symptoms of other sleep disorders	Obstructive sleep apnea (snoring, breathing pauses); restless legs syndrome (urge to move legs); parasomnias (sleepwalking, sleep talking); circadian rhythm disorders (unusual sleep timing).
Daytime causes/consequences	Napping; exercise; work and activities; social and family stressors; caffeine, alcohol, and tobacco use.

Sleep diary

A 1-2 week sleep-wake diary tracking bedtime, sleep latency, awakenings and their likely cause, wake time, out-of-bed time, and a same-day rating of daytime functioning is useful for both initial assessment and ongoing CBT-I (particularly sleep restriction therapy, see Non-Pharmacologic Treatment). Take care not to let ongoing diary-keeping itself reinforce maladaptive preoccupation with sleep — refocus the patient on daytime function rather than nightly sleep totals.

Insomnia Severity Index (ISI)

The ISI is a brief, validated 7-item questionnaire assessing the severity of sleep-onset and sleep-maintenance difficulty, sleep satisfaction, noticeability and distress of the sleep problem to others, and interference with daily functioning — useful both to characterize severity at baseline and to track response to treatment.^[3] Each of the 7 items is rated from 0 (no problem) to 4 (very severe problem), for a total possible score of 0-28.

#	Item
1	Severity of difficulty falling asleep
2	Severity of difficulty staying asleep
3	Severity of early morning awakening problems
4	Satisfaction with current sleep pattern
5	How noticeable to others is the sleep problem in terms of impairing quality of life
6	How worried/distressed is the patient about the current sleep problem
7	Interference with daily functioning (fatigue, mood, concentration, work, memory)

Total score interpretation: 0-7 no clinically significant insomnia; 8-14 subthreshold insomnia; 15-21 clinical insomnia of moderate severity; 22-28 clinical insomnia of severe severity. The Pittsburgh Sleep Quality Index is a similar validated option; either is used alongside — never in isolation from — screening for comorbidities.

Objective measurement

Actigraphy (average motor activity measured over days to weeks via a wrist-worn accelerometer, often housed in a consumer smartwatch) can supplement a sleep diary but should not replace clinical assessment — its accuracy can be affected by medications or other sleep disorders, and consumer devices can exaggerate or misrepresent findings, which can itself reinforce maladaptive beliefs about sleep if not reviewed with a clinician. Any actigraphy or commercial wearable-sleep data is a rough estimate that needs clinical context, not a standalone diagnosis.

Polysomnography (PSG) is not indicated in the initial assessment of routine, uncomplicated insomnia. Reserve referral for PSG for patients with risk factors or symptoms of another sleep disorder (sleep apnea, periodic limb movements), resistant or chronic cases, and patients being considered for long-term hypnotic therapy. Home sleep apnea testing is an accepted option for uncomplicated suspected obstructive sleep apnea and is standard practice outside large urban centres, but it can only confirm moderate-to-severe obstructive sleep apnea — it does not diagnose the insomnia itself and a negative home test does not rule out a sleep disorder requiring in-lab PSG.

Screen for comorbidities

Screen every patient with insomnia for other sleep disorders, contributing medications, and comorbid conditions, particularly those causing nocturnal discomfort or pain.

Category	Examples
Psychiatric disorders	Mood disorders; anxiety disorders; attention-deficit hyperactivity disorder (ADHD); post-traumatic stress disorder (PTSD); alcohol/substance use disorders.
Other medical disorders	Neurologic (stroke, migraine); musculoskeletal (arthritis, fibromyalgia); pulmonary (COPD, asthma); endocrine (hypothyroidism, hyperthyroidism); digestive (GERD, colitis); cardiovascular (congestive heart failure); chronic pain.
Medications	Antidepressants; stimulants; antihypertensives; sedatives (via rebound/withdrawal); decongestants and antihistamines; analgesics; herbal supplements; substances of abuse.

Validated screening tools for the most common comorbidities:

Comorbidity	Screening tool
Obstructive sleep apnea	STOP-BANG, Berlin Questionnaire
Restless legs syndrome	sIRLS
Circadian rhythm disorders	mCTQ (Munich Chronotype Questionnaire)
Depression, mood disorders	PHQ-9; MDQ; Bipolar Spectrum Diagnostic Scale
Anxiety disorders	GAD-7
ADHD	ASRS
PTSD	PC-PTSD
Substance use	TAPS

Treatment Targets

Improve daytime function — the primary goal of any sleep intervention. How the patient's daytime functioning relates to sleep matters more than the raw quantity or quality of sleep reported.
Reduce daytime impairment: fatigue, dysphoria, decreased alertness, and cognitive complaints.
Promote subjectively sound, restorative sleep despite external (stress, noise, travel) or internal (pain, anxiety) disruptors — making sleep more resilient, not just better on a given night.
When pharmacotherapy is used, potentiate rather than replace CBT-I.
Use the lowest effective medication dose for the shortest duration required to meet the above goals.

Choose Initial Treatment

Direct treatment rule

First-line therapy

1st line for every patient cognitive behavioural therapy for insomnia (CBT-I) — regardless of insomnia duration (short-term or chronic) and regardless of whether a psychiatric or medical comorbidity is present. CBT-I is also effective for comorbid insomnia and may improve both the sleep complaint and the comorbid condition.^[1]^[2]

Sleep hygiene is incorporated into CBT-I but is not sufficient as a standalone treatment for insomnia disorder — deliver it as one component of full or brief CBT-I, not as the entire intervention.

When pharmacotherapy is added

Add time-limited pharmacotherapy when CBT-I is not accessible, has not been sufficient on its own, the patient cannot complete it, or daytime impairment is severe enough that faster symptom relief is needed while CBT-I is initiated. Confirm sleep education, discussion of CBT-I strategies, any needed diagnostic sleep studies, and optimization of major comorbidities before starting a hypnotic.^[4]

Base initial drug choice on the predominant symptom pattern: a short-acting Z-drug or melatonin for isolated sleep-onset difficulty; low-dose doxepin or eszopiclone for sleep-maintenance difficulty; a dual orexin receptor antagonist (lemborexant or daridorexant) when both onset and maintenance are affected. See Pharmacologic Treatment Options and Drug Tables for exact doses.

Duration and reassessment

Use the lowest effective dose for the shortest duration. A 7-10 day, up to 1-month, initial supply with frequent follow-up (3-6 weeks) and limited dispensing (30-60 days) is a reasonable default, even though this specific limit is not itself a hard evidence-based ceiling.

Re-evaluate if sleep performance and daytime functioning have not improved after 2-6 weeks — reassess the diagnosis and comorbidities, and consider referral to a sleep specialist, rather than simply escalating the dose or switching within the same drug class.

Non-Pharmacologic Treatment

Sleep hygiene

Good sleep hygiene is the cornerstone of any sleep intervention, though data indicates it is often insufficient as a standalone treatment for insomnia disorder — it is incorporated into, but does not replace, full CBT-I.

Keep a regular sleep-wake schedule with a consistent rising time within 60-90 minutes, 7 days per week — this reinforces the circadian sleep rhythm and prevents oversleeping.
Restrict time in bed to the average sleep time actually obtained over the preceding week.
Avoid sleeping in, extensive daytime horizontal rest, or daytime naps longer than about 15-20 minutes in the afternoon — these tend to worsen the following night's sleep.
Get regular exercise, about 30 minutes of activity intense enough to cause sweating; if evening exercise disrupts sleep, move it earlier in the day.
Avoid caffeine after mid-afternoon and alcohol after supper, and avoid recreational drugs; if smoking, stop by early evening.
Plan a quiet period before lights out (a warm bath can help); keep the bedroom around 16-20°C, which appears to signal the circadian rhythm toward sleep.
Avoid large meals late in the evening; a light carbohydrate snack before bed can be helpful.
Turn the clock face away — checking the time on awakening can cause performance anxiety or frustration that delays returning to sleep. Use an alarm instead.
Keep the bedroom dark, quiet, and free of phones, televisions, and computers; use earplugs or an eye mask if the environment can't otherwise be controlled.
Use the bedroom only for sleep and intimacy — using the bed as a reading, work, or media space conditions the patient to be alert there instead of drowsy. If awake and alert during the night, get up, leave the bedroom, and do something quiet until drowsy again before returning to bed.

Pharmacologic (or any) intervention is less effective when these guidelines are not followed. In mild insomnia, consistently applied sleep hygiene strategies alone may be enough to restore a normal sleep pattern.

Cognitive behavioural therapy for insomnia (CBT-I)

CBT-I is a multi-component intervention, typically delivered in up to 8 individual or group sessions, and is the genuine first-line treatment described above. Improvement is typically seen after 3-4 sessions, and consistent follow-up through the full course sets up successful treatment.^[1]

Component	Description
1. Stimulus control	Go to bed only when sleepy; get out of bed after about 15 minutes if sleep does not come; reinforce the bed-sleep association per sleep hygiene principles above.
2. Sleep hygiene	The 10-point sleep hygiene guidance above.
3. Sleep restriction (paradoxical approach)	Limit time in bed to actual time asleep, or 6-7 hours; increase time in bed by 20-30 minutes per week as sleep efficiency improves, or decrease it further if sleep remains fragmented. Usually best done under supervision of a trained provider given the short-term worsening of daytime sleepiness this can cause.
4. Relaxation techniques	Meditation, progressive muscle relaxation, or autogenic training to reduce hyperarousal at bedtime.
5. Cognitive therapy	Identify and change dysfunctional beliefs and attitudes about sleep (see below).

The Dysfunctional Beliefs and Attitudes about Sleep (DBAS) tool is a brief, useful way to assess maladaptive sleep-related cognitions before starting behaviour-change work.

Cognitive barrier	Reframe for the patient
Unrealistic expectations	Even good sleepers do not always get 8 hours of quality sleep, and individual sleep needs vary.
Blaming insomnia for all daytime impairments	Consider other contributors to daytime symptoms rather than attributing everything to sleep.
Catastrophizing after a poor night	Insomnia is unpleasant but not dangerous — the practical consequence of one bad night is usually just more sleepiness and sounder sleep the next night.
Giving too much importance to sleep	Even though sleep occupies roughly a third of life, it doesn't need to be the sole focus of daily attention.
Developing some tolerance to insomnia's effects	Rearrange the day's schedule as needed rather than cancelling planned activities.

Delivery and access

The strongest evidence for CBT-I comes from manualized, systematic therapy delivered by trained clinicians, but primary care providers have also successfully used modified, simplified versions. Barriers include a shortage of trained specialists, cost, and patient acceptability/adherence. More accessible delivery formats include digital CBT-I, an abbreviated 2-session version, and CBT-I print materials or mobile apps — internet-delivered CBT-I has proven as effective as other CBT-I formats and is often the most accessible option. Examples of digital/online CBT-I programs include Haleo, Sleepio, Somryst, CBT for Insomnia, Go! to Sleep, CBT-i Coach, and My Sleep Well. Even with good access, a meaningful minority of patients do not respond to CBT-I, and some drop out before completing it — pharmacotherapy remains a reasonable adjunct or alternative in these patients rather than a treatment failure on the clinician's part.

Other adjuncts

Aerobic exercise — a useful modifier of stress and dysphoric mood that also promotes deeper, more restful sleep; encourage patients with insomnia to increase exercise.
Mindfulness meditation and bright light therapy — both show modest improvement in sleep efficacy.
Weighted blankets — a randomized trial demonstrated a meaningful reduction in insomnia severity; a reasonable low-risk adjunct.
Acupuncture — efficacy has been shown across multiple studies, though the evidence quality is low.
Other adjunct strategies (music, foot baths, sound masking) — evidence quality is very low, but risk is minimal, so these can reasonably be offered as low-cost adjuncts if the patient is interested.

Natural health products and OTC agents

Of the natural supplements, melatonin has the most evidence, with a modest overall effect — see Pharmacologic Treatment Options and Drug Tables for dosing. Valerian and L-tryptophan have inconsistent trial results but are occasionally clinically useful; L-tryptophan is in the Drug Database (Tryptophan), while valerian root extract (typically 300-600 mg of standardized extract at bedtime) does not currently have a Pharmasist Drug Database monograph.

Screen every patient for use of OTC sleep agents containing diphenhydramine, dimenhydrinate, or doxylamine (e.g., store-brand "PM" analgesics, Nytol, Sleep-Eze, Unisom, Gravol, cold/flu night formulations). Routine or long-term use of these agents is discouraged given the risk of cognitive impairment, hangover effects, dizziness, anticholinergic delirium, and falls — especially in older adults — and they should generally be reserved for occasional, short-term use, or for insomnia genuinely driven by histamine-mediated symptoms (e.g., allergies, atopic dermatitis) rather than as a routine sleep aid. See Special Populations and Drug Tables for the specific caveats.

Cannabis — given legalization and heavy marketing of cannabis products for sleep, ask every patient about cannabis use. There is insufficient evidence to support routine clinical use of cannabis for insomnia, and the effects of its many components on sleep remain unclear. Reserve cannabis consideration for resistant insomnia with a comorbidity that itself has supporting evidence for cannabis (e.g., certain pain syndromes, resistant anxiety), and only after treatments with better evidence have failed. Cannabis products are mainly CBD (cannabidiol) and THC (tetrahydrocannabinol) — THC is more sedating but is psychoactive, so CBD-dominant products are usually preferred initially if cannabis is considered.

Pharmacologic Treatment Options

Drug / intervention	Role	Dose / use	Important adverse effects	Teaching points
Zopiclone 1st line	Sleep-onset and maintenance insomnia	Initial 3.75 mg PO QHS; usual max 7.5 mg QHS PO; max 5 mg QHS PO if ≥65 y, hepatic/renal impairment, or with a potent CYP3A4 inhibitor	Bitter/metallic taste, dry mouth, dizziness, somnolence; rare complex sleep behaviours	Use only when ≥7-8 hours are available before planned waking; wait ≥12 hours before driving; never combine with alcohol.
Zolpidem 1st line	Sleep-onset insomnia	Men: 5-10 mg PO QHS; Women: 5 mg PO QHS; max 10 mg QHS PO (5 mg if ≥65 y or mild-moderate hepatic impairment)	Similar Z-drug class effects; complex sleep behaviours; less bitter taste than zopiclone	Shorter half-life than zopiclone/eszopiclone — only 8 hours needed before driving. Avoid with a history of somnambulism.
Eszopiclone 1st line	Sleep-onset and maintenance insomnia, including longer-term use	Initial 1 mg PO QHS; max 3 mg QHS PO (max 2 mg QHS PO if ≥65 y, severe hepatic/renal impairment, or with a potent CYP3A4 inhibitor)	Same Z-drug class effects; minimal rebound/tolerance reported	Evidence supports use up to 12 months. Low-dose (2 mg) evidence in older adults shows a lower fall risk.
Lemborexant 1st line	Sleep-onset and maintenance insomnia	Initial/usual 5 mg PO QHS; max 10 mg QHS PO (max 5 mg QHS PO with a weak CYP3A inhibitor or moderate hepatic impairment)	Somnolence; rare sleep paralysis, hypnagogic/hypnopompic hallucinations, cataplexy-like symptoms	No dependence/rebound signal; efficacy data to 12 months. Favourable safety profile shown in older adults.
Daridorexant 1st line	Sleep-onset and maintenance insomnia	50 mg PO QHS (25 mg QHS PO with a moderate CYP3A4 inhibitor or moderate hepatic impairment)	Headache, somnolence, fatigue; rare sleep paralysis/hallucinations	No dependence/rebound signal; contraindicated with strong CYP3A4 inhibitors.
Doxepin (low-dose) 1st line for sleep-maintenance, especially older adults	Sleep-maintenance insomnia	3 mg PO 30 minutes before bedtime; may increase to 6 mg. Same 3 mg starting dose in older adults or hepatic impairment.	Somnolence, sedation, nausea	Minimal next-day impairment and no dependence/rebound at this low dose — a preferred hypnotic choice in older adults.
Temazepam Alternative	Sleep-onset and maintenance insomnia, short-term	Initial 15 mg PO QHS; max 30 mg QHS PO (max 15 mg QHS PO if ≥65 y)	Ataxia, dependence/withdrawal, impaired memory, next-day impairment	The preferred benzodiazepine when one is needed — half-life covers the sleep period without excessive accumulation. Avoid in older adults or respiratory disease when possible.
Melatonin Alternative	Sleep-onset insomnia; circadian-based insomnia	0.5-5 mg PO 1-2 hours before bedtime	Generally well tolerated; headache, daytime drowsiness	Modest overall evidence; a reasonable low-risk first pharmacologic option, especially in older adults.
Trazodone (off-label) Special situation	Widespread off-label use, especially with comorbid depression	25-100 mg PO QHS	Orthostatic hypotension, rare priapism, morning sedation	Evidence is limited to a few small studies; consider particularly when comorbid depression is present.
Doxylamine (OTC) Special situation — short-term/occasional only	OTC short-term sleep aid	25 mg PO at bedtime	Anticholinergic effects, next-day sedation	Avoid regular/long-term use; avoid in older adults per the Beers Criteria.
Diphenhydramine (OTC) Special situation — short-term/occasional only	OTC short-term sleep aid	25-50 mg PO, 30-60 minutes before bedtime	Anticholinergic effects, next-day sedation, delirium risk	Avoid regular/long-term use; avoid in older adults per the Beers Criteria.

Special Populations

Pregnancy

Disrupted sleep is a very common complaint in pregnancy and tends to worsen as pregnancy progresses; endocrine changes, physical discomfort, and bladder distension all contribute. Obstructive sleep apnea and restless legs syndrome both commonly worsen during pregnancy and can present as an insomnia complaint — screen for both rather than assuming the complaint is primary insomnia. Cognitive and behavioural techniques (CBT-I) are the treatment of choice when distress and impairment are mild to moderate.

If insomnia is severe or disabling in pregnancy, carefully weigh the risk-benefit ratio for both patient and fetus before using pharmacotherapy, and favour intermittent dosing of the safest option at the lowest effective dose alongside continued behavioural strategies.

Reasonable if clinically justified: zopiclone, eszopiclone, and trazodone do not appear to be teratogenic.

Avoid: benzodiazepines, particularly in the first trimester (increased oral cleft risk) and near term (neonatal withdrawal symptoms); zolpidem (associated with preterm delivery, small-for-gestational-age infants, and cesarean delivery, though not with congenital anomalies); melatonin (a theoretical concern for disrupting reproduction); lemborexant, L-tryptophan, and diphenhydramine (safety in pregnancy unknown).

Doxepin does not appear to be teratogenic but has not been specifically studied in pregnancy.

Breastfeeding

If pharmacotherapy is required while breastfeeding, intermittent low doses of a short-acting benzodiazepine (e.g., temazepam) or a Z-drug appear relatively safe with appropriate monitoring, though the effects of chronic exposure are unknown. Trazodone is transferred into breast milk in low amounts and is not expected to affect the breastfed infant, particularly beyond 2 months of age and at doses ≤100 mg/night. Doxepin and diphenhydramine should not be used while breastfeeding, based on adverse effects reported in case reports.

Children

Nonpharmacologic therapy is first-line for pediatric insomnia, especially in young children under 6 years. Graded extinction (gradual withdrawal of parental attention to a child crying rather than settling alone) is a useful additional behavioural technique in younger children and infants. Medication use for pediatric insomnia is not well evidence-based and is guided largely by clinical experience and treatment of comorbidities.

If pharmacotherapy is genuinely needed, melatonin can be considered, starting at 0.5-1 mg at bedtime — a reasonably sized meta-analysis found it effective and tolerable for short-term treatment of sleep-onset insomnia in children and adolescents, particularly with comorbid ADHD or autism spectrum disorder, with no significant adverse effects observed in follow-up out to 7 years. L-tryptophan has shown potential efficacy specifically for pediatric parasomnias. OTC antihistamines are not recommended in children given the risk of rapid tolerance, next-day sedation, cognitive impairment, and paradoxical reaction. Prescription medication should be used extremely judiciously and targeted at a specific comorbidity — clonidine (Clonidine) has shown efficacy in a case series of children with comorbid ADHD and insomnia. Z-drugs have not demonstrated efficacy in children, and benzodiazepines and TCAs are not recommended given an unfavourable benefit-to-risk ratio in this age group.

Older adults

Older patients face higher polypharmacy and drug-interaction risk, and the deleterious effects of hypnotics (cognitive impairment, falls) are amplified — making CBT-I as first-line therapy even more essential in this population.

The 2023 AGS Beers Criteria recommend avoiding benzodiazepines and first-generation antihistamines (including diphenhydramine and doxylamine) in adults 65 and older given markedly increased confusion, delirium, falls, and — for benzodiazepines specifically — impaired metabolism and cognitive impairment. Z-drugs are generally avoided as well given increased fall and confusion risk, though this specific warning is drawn largely from retrospective data with substantial confounding.^[5]

Safer pharmacologic options include low-dose doxepin (under 6 mg) for sleep-maintenance insomnia, or melatonin for sleep-onset insomnia. Lemborexant has also shown a favourable 6-month safety and efficacy profile specifically in older adults. If a benzodiazepine receptor agonist genuinely must be used, zolpidem is generally preferred for its shorter half-life; low-dose eszopiclone (2 mg) has shown short-term efficacy (up to 24 weeks) with a comparatively low fall risk. Low-dose trazodone and mirtazapine are commonly used off-label but have limited evidence specifically in older adults — reserve for comorbid depression/anxiety or resistant cases, with attention to fall and fracture risk.

Deprescribing of long-term hypnotic therapy should be discussed and offered, but rigid, mandatory discontinuation in a stable, functional, long-term low-dose user is not always the right answer — an overly rigid approach can push a patient toward more harmful, unmonitored substitutes (high-anticholinergic-burden OTC drugs, cannabis, or alcohol). Remember that off-label psychotropics used for insomnia, and indicated drugs used for other conditions (antihypertensives, antidepressants, antipsychotics), carry their own fall risk in this population — the comparison is never "hypnotic vs. nothing," but "this drug vs. the realistic alternative."

Renal and hepatic impairment

Zopiclone, eszopiclone, and zolpidem all require dose reduction in hepatic impairment (see Drug Tables); zopiclone also requires dose reduction in renal impairment. Lemborexant and daridorexant require dose reduction with moderate hepatic impairment or with a co-administered CYP3A inhibitor, and are not recommended with severe hepatic impairment.

Monitoring & Follow-Up

Follow up frequently (every 3-6 weeks) and dispense limited hypnotic quantities (30-60 days), especially early in treatment. Reassess daytime functioning, not just reported sleep quantity, at every visit — this is the primary treatment target. If sleep performance and daytime functioning have not returned to normal after 2-6 weeks, re-evaluate the diagnosis and comorbidities and consider referral to a sleep specialist.

For patients continuing hypnotic therapy longer-term, periodically reassess ongoing need with a clear documented rationale and an explicit review of risks and benefits — long-term sedative use should be the exception, reserved for cases with significant comorbidity or failure/inability to complete nonpharmacologic therapy, not a default outcome of an initial short-term prescription. Polysomnography should be considered in resistant or chronic cases and in patients on long-term hypnotic therapy.

Monitor specifically for complex sleep-related behaviours with any Z-drug — discontinue immediately if these occur and do not rechallenge with the same drug or class.

Counsel on driving and machinery-operation timing after every hypnotic dose — follow the recommended pre-driving interval for the specific agent (generally ≥7-8 hours for zopiclone/eszopiclone/zolpidem/lemborexant/daridorexant, ≥12 hours for longer-acting benzodiazepines such as temazepam), while recognizing that sleep deprivation itself also impairs driving. Some habituation to a hypnotic's driving-impairment effect develops with regular use, but off-label sedatives used for insomnia have not been rigorously tested for this and may be more impairing than expected. Use clinical judgment, factor in the nature of the patient's driving (commercial drivers need more vigilance), and be aware of provincial requirements for reporting an unfit driver.

Screen for emerging mood or anxiety disorders throughout treatment, not just at diagnosis — chronic sleep disturbance lasting at least 1 year increases the risk of a subsequent mood disorder, and insomnia often occurs as a symptom, comorbidity, or prodrome of depression or anxiety. A reduced response to insomnia treatment should specifically prompt re-screening for these.

Treatment Failure / Next Step

Confirm CBT-I components were genuinely implemented — stimulus control, sleep restriction, and cognitive therapy, not just generic sleep hygiene advice given in isolation, which is not sufficient as monotherapy.
For any pharmacotherapy trialed, confirm adherence, correct timing (30-60 minutes before the intended bedtime, with awareness that taking a Z-drug with food delays and blunts absorption), and correct dose.
Explicitly screen or re-screen for sleep apnea, restless legs syndrome, depression, anxiety, and medication-induced insomnia using the tools above — these are the most common reasons for apparent treatment failure.
If a comorbidity is newly identified or undertreated, treat or optimize it — insomnia often improves once the comorbidity is addressed, and CBT-I remains effective alongside comorbidity treatment rather than needing to wait for it.
If an adequate CBT-I trial and an adequate pharmacotherapy trial have both failed, consider switching drug class (e.g., a dual orexin antagonist if a Z-drug was ineffective or not tolerated) rather than repeatedly escalating within the same class.
Refer to a sleep medicine specialist for resistant or chronic cases, suspected other primary sleep disorder, or before committing to open-ended long-term hypnotic therapy.

Common Errors to Avoid

Treating insomnia with medication alone without ever offering CBT-I as genuine first-line therapy.
Delivering sleep hygiene advice alone and calling it "CBT-I" — sleep hygiene is only 1 of 5 components and is not sufficient as monotherapy for insomnia disorder.
Reflexively recommending diphenhydramine or doxylamine as a routine, indefinite "OTC-safe" solution — anticholinergic burden, tolerance, and next-day impairment make these poor choices beyond occasional, short-term use, especially in older adults.
Prescribing a benzodiazepine or Z-drug in an older adult without discussing fall, confusion, and cognitive risk and safer alternatives first, per the Beers Criteria.
Reaching for flurazepam, nitrazepam, or triazolam as a first-choice hypnotic — the longer-acting agents (flurazepam, nitrazepam) accumulate and cause more next-day impairment, and triazolam carries a distinct risk of amnesia, agitation, and rebound insomnia.
Applying rigid, mandatory deprescribing to a stable, functional, long-term low-dose hypnotic user — an overly rigid approach can push the patient toward more harmful, unmonitored substitutes.
Missing an underlying sleep apnea, restless legs syndrome, depression, or medication-induced cause and treating the insomnia symptom indefinitely in isolation.
Failing to counsel on driving/machinery-operation timing after a hypnotic dose, particularly since patients can feel "fully awake" despite measurable next-day impairment.
Combining any hypnotic with alcohol or another CNS depressant.
Continuing an ineffective or poorly tolerated hypnotic past the planned reassessment point instead of stopping and reassessing the diagnosis.

Clinical Decision Algorithm

Initial assessment and treatment selection

Dissatisfaction with sleep quality/quantity: difficulty falling asleep, staying asleep, or early waking, with daytime impairment

Take a full sleep history; screen for OSA, RLS, mood/anxiety disorder, medication-induced causes, and substance use

Red flag identified (suspected OSA, RLS, suicidal ideation, severe psychiatric illness, parasomnia)

Manage or refer for the specific underlying cause — do not treat as primary insomnia alone

No red flags; primary or comorbid insomnia confirmed

Classify: short-term insomnia (under 3 months) vs. chronic insomnia disorder (≥3 nights/week for ≥3 months)

Start CBT-I (or CBT-I components) for every patient, regardless of duration or comorbidity — 1st line^[1]

Reassess in 3-4 weeks: daytime functioning and sleep pattern

Adequate response

Continue CBT-I; taper any short-term hypnotic that was co-started

Inadequate response, or severe/acute impairment from the start

Consider adding time-limited pharmacotherapy alongside continued CBT-I

Pharmacotherapy selection when medication is added

Decision made to add pharmacotherapy alongside CBT-I

Determine the predominant symptom pattern

Sleep-onset difficulty

Zopiclone 3.75-7.5 mg QHS, zolpidem 5-10 mg QHS (sex-specific dosing), or melatonin 0.5-5 mg 1-2h before bed

Sleep-maintenance difficulty

Low-dose doxepin 3-6 mg QHS, or eszopiclone 1-3 mg QHS

Both sleep-onset and maintenance affected

Lemborexant 5-10 mg QHS or daridorexant 50 mg QHS (dual orexin antagonist)

Prescribe the lowest effective dose for the shortest duration; plan follow-up at 3-6 weeks; document an explicit rationale if continuing beyond 1 month

Good response, functional improvement

Continue with periodic reassessment; discuss a deprescribing plan at a low-stress time when appropriate

No daytime-function improvement after 2-6 weeks, or a complex sleep behaviour/other red flag emerges

Stop the agent, re-evaluate the diagnosis and comorbidities, and refer to sleep medicine

Drug Tables

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment and reassessment against the Beers Criteria in older adults. Select any drug name to open its complete Pharmasist Drug Database page. All benzodiazepine receptor agonists (Z-drugs), benzodiazepines, and orexin antagonists require a planned sleep opportunity of at least 7-8 hours before the patient needs to be fully alert.

Benzodiazepines officially indicated for insomnia in Canada

4 benzodiazepines carry a Health Canada insomnia indication. Only temazepam is generally recommended as a first-choice agent within this class.

Drug	Dosage	Adverse effects	Comments
Temazepam	Initial: 15 mg PO QHS Maximum: 30 mg PO QHS Maximum, older adults (≥65 y): 15 mg PO QHS	Dose-dependent ataxia, dizziness; dependence/withdrawal symptoms; impaired memory; next-day impairment of activities requiring alertness (including driving) despite feeling fully awake	Preferred within this class — a half-life sufficient to cover the sleep period without significant accumulation or hangover effects. Substrate of CYP3A4. Significant rebound reported after discontinuation. Advise patients to wait at least 12 hours before driving or operating machinery.
Flurazepam	Adults: 15-30 mg PO QHS Older adults: Avoid — long-acting metabolite accumulation	Dose-dependent ataxia, dizziness, next-day impairment; dependence/withdrawal	Not recommended — a long-acting metabolite accumulates with repeated dosing, causing more next-day impairment than shorter-acting agents; higher risk of cortical impairment, confusion, and falls in older adults.
Nitrazepam	Adults: 5-10 mg PO QHS	Dose-dependent ataxia, dizziness, next-day impairment; dependence/withdrawal	Not recommended for the same reasons as flurazepam — a longer half-life that accumulates with repeated dosing and causes more next-day impairment, confusion, and falls, particularly in older adults.
Triazolam	Adults: 0.125-0.25 mg PO QHS; maximum 0.25 mg	Dose-related confusion, agitation, amnesia (a distinct adverse-effect profile from other benzodiazepines); dependence/withdrawal	Not recommended — pharmacokinetic properties may confer a higher risk of abuse, dependence, and rebound insomnia than other benzodiazepines.

Benzodiazepine receptor agonists (Z-drugs)

Act at the benzodiazepine receptor but are a distinct drug class with 10-40 times less myorelaxant effect than benzodiazepines and no demonstrated worsening of sleep apnea. Complex sleep behaviours (e.g., sleep-related eating or driving with no recollection) have been reported with zopiclone and zolpidem — review this risk with every patient and counsel that the medication should be taken in bed with limited access to dangerous items (car keys, kitchen tools). Combination with alcohol increases the risk of all adverse events, including complex sleep behaviours.

Drug	Dosage	Adverse effects	Comments
Zopiclone	Initial: 3.75 mg PO QHS Maximum: 7.5 mg PO QHS Maximum, older adults/hepatic or renal impairment/potent CYP3A4 inhibitor: 5 mg PO QHS	Bitter/metallic taste, dry mouth, dizziness, somnolence; dose-dependent ataxia; next-day impairment despite feeling awake; rare complex sleep behaviours	The most commonly prescribed Z-drug in Canada. Does not accumulate; may cause less rebound on withdrawal than other agents. Substrate of CYP3A4. Advise ≥12 hours before driving or operating machinery.
Eszopiclone	Initial: 1 mg PO QHS Maximum: 3 mg PO QHS Maximum, older adults/severe hepatic or renal impairment/potent CYP3A4 inhibitor: 2 mg PO QHS	Same class effects as zopiclone; complex sleep behaviours	The active (S+) isomer of zopiclone; may have a faster onset and less next-day effect than zopiclone, with minimal rebound and tolerance. Substantial evidence supports use across a wide variety of comorbidities, and for up to 24 weeks in older adults specifically.
Zolpidem	Men: 5-10 mg PO QHS Women: 5 mg PO QHS Maximum: 10 mg PO QHS Maximum, older adults/mild-moderate hepatic impairment: 5 mg PO QHS	Same class effects; much lower incidence of bitter/metallic taste than zopiclone	Specific affinity for the alpha-1 GABA-A subunit; a shorter half-life than zopiclone/eszopiclone, needing only 8 hours before driving/operating machinery. Considered a controlled substance in Canada, unlike zopiclone and eszopiclone. Minimal rebound and tolerance. Avoid with a history of somnambulism or complex sleep behaviours.
Zaleplon	Typical range: 5-10 mg PO QHS; maximum 20 mg	Similar class effects, with an even shorter half-life than zolpidem	Discontinued as a commercial Canadian product but sometimes available through compounding pharmacies. Its very short half-life can make it useful specifically for sleep-onset difficulty with minimal next-day effects.

Dual orexin receptor antagonists (DORA)

Reduce wakefulness and unwanted wake-sleep transitions rather than directly sedating via GABA-A. Indicated for both sleep-onset and sleep-maintenance insomnia. No evidence of withdrawal symptoms or rebound insomnia on discontinuation, efficacy data to 12 months, and minimal abuse potential — they are not controlled substances. Not recommended in combination with alcohol or other CNS depressants; contraindicated in narcolepsy.

Drug	Dosage	Adverse effects	Comments
Lemborexant	Initial/usual: 5 mg PO QHS Maximum: 10 mg PO QHS Maximum, weak CYP3A inhibitor or moderate hepatic impairment: 5 mg PO QHS	Somnolence; less commonly sleep paralysis, hypnagogic/hypnopompic hallucinations, cataplexy-like symptoms; rare complex sleep behaviours	Advise ≥7 hours before driving/operating machinery, with limited residual impairment reported after 9 hours. Favourable 6-month safety/efficacy profile in older adults specifically.
Daridorexant	Usual dose: 50 mg PO QHS Maximum, moderate hepatic impairment or moderate CYP3A4 inhibitor: 25 mg PO QHS	Headache, nasopharyngitis, somnolence, dizziness, nausea, fatigue; less commonly sleep paralysis, hypnagogic/hypnopompic hallucinations, cataplexy-like symptoms	Contraindicated with strong CYP3A4 inhibitors; dose reduction required with a moderate CYP3A4 inhibitor. Advise ≥7 hours before driving/operating machinery.

Low-dose tricyclic antidepressant

At the very low doses used for insomnia, doxepin acts as a selective H1-receptor antagonist rather than through its antidepressant mechanism, avoiding typical TCA adverse effects. Indicated specifically for sleep-maintenance difficulty, with trial data to 3 months. Not associated with rebound or dependence, and has minimal next-day sedation.

Drug	Dosage	Adverse effects	Comments
Doxepin (low dose, insomnia)	Usual dose: 3-6 mg PO, 30 minutes before bedtime Older adults (≥65 y) or hepatic impairment: Start 3 mg QHS; may increase to 6 mg if needed	Somnolence, sedation, nausea; TCA-type adverse effects become possible above 10 mg	Recommended specifically for older adults. Metabolized by CYP2D6/CYP2C19 — inhibitors of these enzymes may increase exposure. Should not be taken within 3 hours of a meal.

Antihistamines (OTC)

First-generation, sedating antihistamines with a flat dose-response above the doses listed and significant anticholinergic burden. The 2023 AGS Beers Criteria specifically recommend against routine use in adults 65 and older given markedly increased anticholinergic toxicity, delirium, and CNS adverse effects. Recommend intermittent use only (no more than about 4 nights per week) and advise patients to seek professional advice if a sleep aid is needed for more than about a week.

Drug	Dosage	Adverse effects	Comments
Diphenhydramine (oral)	Usual dose: 12.5-50 mg PO, 30-60 minutes before bedtime	Dizziness, grogginess, morning drowsiness; anticholinergic effects (urinary retention, dry mouth, constipation), particularly in older adults; impaired psychomotor/cognitive function; increased delirium risk in older adults; may lower seizure threshold	Optimal single dose is 50 mg, with a flat dose-response above this. Inhibits CYP2D6, increasing serum levels of many co-administered drugs. Contraindicated in benign prostatic hyperplasia, significant constipation, dementia/cognitive impairment, dry mouth/eyes, and glaucoma.
Doxylamine	Usual dose: 25 mg PO, about 30 minutes before bedtime	Same class effects as diphenhydramine	The active ingredient in Unisom SleepTabs; a distinct product from the doxylamine/pyridoxine combination (Diclectin) used for nausea and vomiting of pregnancy, which is dosed and used differently.
Dimenhydrinate	Typical range used off-label: 25-50 mg PO at bedtime	Same class effects as diphenhydramine	Contains approximately 50-55% diphenhydramine by weight; not a distinct mechanism from diphenhydramine itself.

Off-label sedating antidepressants

Rational for comorbid insomnia despite limited direct evidence — e.g., for insomnia with a depressive disorder. All are associated with next-day sedation and, for TCAs and mirtazapine, weight gain.

Drug	Dosage	Adverse effects	Comments
Mirtazapine (low dose)	Typical low-dose range: 7.5-15 mg PO QHS	Next-day sedation, motor restlessness, weight gain	May be particularly useful when low appetite or comorbid alcohol-use issues are also present.
Trazodone	Typical range: 25-100 mg PO QHS	Orthostatic hypotension, rare priapism, morning sedation	Widespread off-label use with apparent success reported by experts, though supporting trial evidence is limited to a few small studies. May be better for sleep maintenance than for overall sleep efficiency.

Off-label anticonvulsants

Rational specifically for insomnia associated with centralized pain syndromes (fibromyalgia, neuropathic pain, restless legs syndrome). Weight gain and next-day sedation are common; CNS depression and cognitive impairment can also occur.

Drug	Dosage	Adverse effects	Comments
Gabapentin (low dose)	Typical low-dose range: 100-300 mg PO QHS	Next-day sedation, dizziness, weight gain	Consider specifically when insomnia coexists with a centralized pain syndrome the drug also treats.
Pregabalin (low dose)	Typical low-dose range: 25-75 mg PO QHS	Next-day sedation, dizziness, weight gain	Same rationale as gabapentin; consider particularly for fibromyalgia-associated insomnia.

Off-label antipsychotics

Not recommended for insomnia in the absence of a comorbidity that itself indicates antipsychotic therapy, given unacceptable anticholinergic/neurological toxicity risk (first-generation) or metabolic syndrome risk (second-generation) relative to any sleep benefit. Reserve for insomnia with very resistant bipolar disorder, schizophrenia, or (for low-dose quetiapine/olanzapine) major depressive disorder augmentation — dosed per the treatment of the underlying disorder, monitoring for metabolic effects as usual, not independently dosed for insomnia alone.

Drug	Dosage	Adverse effects	Comments
Chlorpromazine (low dose)	Typical low-dose range: 25-50 mg PO QHS	Anticholinergic and extrapyramidal effects, orthostatic hypotension, sedation	Reserve for very resistant bipolar disorder or schizophrenia with prominent insomnia.
Methotrimeprazine	Typical low-dose range: 5-25 mg PO QHS	Anticholinergic and extrapyramidal effects, orthostatic hypotension, sedation	Reserve for very resistant bipolar disorder or schizophrenia with prominent insomnia.
Loxapine	Typical low-dose range: 5-25 mg PO QHS	Anticholinergic and extrapyramidal effects, orthostatic hypotension, sedation	Reserve for very resistant bipolar disorder or schizophrenia with prominent insomnia.
Olanzapine	Typical low-dose range: 2.5-5 mg PO QHS	Weight gain, metabolic syndrome, sedation	Consider for insomnia with comorbid bipolar disorder or schizophrenia; dose per the underlying disorder, not independently for insomnia.
Quetiapine (low dose)	Typical low-dose range: 25-50 mg PO QHS	Weight gain, metabolic syndrome, sedation, orthostatic hypotension	Not recommended for isolated insomnia without an indicated comorbidity, given metabolic risk relative to limited direct insomnia evidence; consider for comorbid bipolar disorder, schizophrenia, or generalized anxiety disorder.
Brexpiprazole	Dosing: Per the treatment of the underlying disorder	Weight gain, akathisia, sedation	Considered specifically as augmentation for major depressive disorder with insomnia; dose per the underlying disorder.
Paliperidone	Dosing: Per the treatment of the underlying disorder	Weight gain, extrapyramidal effects, sedation	Consider only for insomnia with comorbid bipolar disorder or schizophrenia; dose per the underlying disorder.
Clozapine	Dosing: Per the treatment of the underlying disorder	Weight gain, metabolic syndrome, agranulocytosis (requires mandatory monitoring), sedation	Consider only for insomnia with treatment-resistant schizophrenia already indicating clozapine; dose per the underlying disorder and mandatory hematologic monitoring program.
Risperidone	Dosing: Per the treatment of the underlying disorder	Extrapyramidal effects, weight gain, sedation	Consider only for insomnia with comorbid bipolar disorder or schizophrenia; dose per the underlying disorder.
Lurasidone	Dosing: Per the treatment of the underlying disorder	Akathisia, sedation, GI upset	Consider only for insomnia with comorbid bipolar disorder; dose per the underlying disorder. Take with food.
Asenapine	Dosing: Per the treatment of the underlying disorder	Sedation, oral hypoesthesia, weight gain	Consider only for insomnia with comorbid bipolar disorder or schizophrenia; dose per the underlying disorder.

Other off-label agents

Drug	Dosage	Adverse effects	Comments
Hydroxyzine	Typical low-dose range: 25-50 mg PO QHS	Anticholinergic effects, next-day sedation	A sedating antihistamine sometimes used off-label for insomnia associated with anxiety or histamine-mediated symptoms.
Chlorpheniramine	Typical dose: 4 mg PO QHS	Anticholinergic effects, next-day sedation	No single-ingredient Pharmasist Drug Database monograph — only combination decongestant products are catalogued. Similar caveats to diphenhydramine apply.
Diazepam	Typical range: 2-10 mg PO QHS	Sedation, dependence/withdrawal, next-day impairment	Off-label; consider specifically for insomnia with a comorbid anxiety disorder or severe hyperarousal rather than as a primary hypnotic.
Clonazepam	Typical range: 0.25-1 mg PO QHS	Sedation, dependence/withdrawal, next-day impairment	Off-label; considered for insomnia with comorbid anxiety disorder; also used (with minimal supporting evidence) for restless-legs-associated insomnia.
Lorazepam	Typical range: 0.5-2 mg PO QHS	Sedation, dependence/withdrawal, next-day impairment	Off-label; consider specifically for insomnia with a comorbid anxiety disorder or severe hyperarousal.
Alprazolam	Typical range: 0.25-0.5 mg PO QHS	Sedation, dependence/withdrawal, next-day impairment	Off-label; consider specifically for insomnia with a comorbid anxiety disorder.
Oxazepam	Typical range: 15-30 mg PO QHS	Sedation, dependence/withdrawal, next-day impairment	Off-label; consider specifically for insomnia with a comorbid anxiety disorder.

Natural health products

Melatonin has the most consistent evidence of the natural supplements, with a modest overall effect; valerian and L-tryptophan have inconsistent trial evidence but are occasionally clinically useful.

Drug	Dosage	Adverse effects	Comments
Melatonin	Adults: 0.5-5 mg PO, 1-2 hours before bedtime Children (if needed): 0.5-1 mg PO at bedtime, initial dose	Generally well tolerated; headache, daytime drowsiness	Reasonable low-risk first pharmacologic option, especially in older adults. In children, start at 0.5-1 mg QHS if pharmacotherapy is genuinely needed. Avoid in pregnancy.
Tryptophan (L-tryptophan)	Typical dose: 1-2 g PO at bedtime (product-dependent)	Generally well tolerated; mild GI upset, drowsiness	Evidence is inconsistent overall; has shown potential efficacy specifically in pediatric parasomnias.
Valerian	Typical dose: 300-600 mg of standardized extract PO at bedtime	Generally well tolerated; mild GI upset, headache	No Pharmasist Drug Database monograph currently exists for this natural health product. Evidence for efficacy is inconsistent but risk is low.

References

Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline — Journal of Clinical Sleep Medicine (Edinger JD, Arnedt JT, Bertisch SM, et al.). J Clin Sleep Med 2021;17(2):255-262
Delphi consensus recommendations for the management of chronic insomnia in Canada — Sleep Medicine (Morin CM, Khullar A, Robillard R, et al.). Sleep Med 2024;124:598-605
Validation of the Insomnia Severity Index as an outcome measure for insomnia research — Sleep Medicine (Bastien CH, Vallières A, Morin CM). Sleep Med 2001;2(4):297-307
Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: an American Academy of Sleep Medicine clinical practice guideline — Journal of Clinical Sleep Medicine (Sateia MJ, Buysse DJ, Krystal AD, Neubauer DN, Heald JL). J Clin Sleep Med 2017;13(2):307-349
American Geriatrics Society 2023 updated AGS Beers Criteria® for potentially inappropriate medication use in older adults — Journal of the American Geriatrics Society (2023 American Geriatrics Society Beers Criteria® Update Expert Panel). J Am Geriatr Soc 2023;71(7):2052-2081

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.