Insomnia: What It Is, How It's Treated, and Why Sleeping Pills Aren't the Answer

What chronic insomnia actually is

Insomnia disorder, as defined in DSM-5-TR and ICSD-3, is difficulty initiating sleep, maintaining sleep, or waking too early, occurring at least three nights per week for at least three months, and causing clinically significant daytime impairment (fatigue, mood disturbance, cognitive difficulty, functional or occupational impact).

That definition matters. A bad week of sleep after a stressful event is not insomnia disorder. Insomnia disorder is what develops when sleep problems persist past the acute phase, become self-sustaining, and start meaningfully degrading life outside the bedroom.

Recent Canadian population data (Morin et al., 2024) put the prevalence of chronic insomnia disorder at 16.3 percent of adults, with meaningfully higher rates in women, Indigenous populations, and people with poor mental or physical health. Roughly 40 percent of people with chronic insomnia still have it five years later without effective treatment.

Insomnia is not a symptom to endure. It is a treatable disorder with a well-defined mechanism and an evidence-based first-line therapy that most Canadians never get offered.

The hyperarousal model: why the sleep system isn't broken

The dominant neurobiological model of chronic insomnia is hyperarousal. In insomnia disorder, the arousal systems that should quiet at night, cortical, autonomic, and HPA-axis, stay too active.

The evidence for this is consistent:

• Quantitative EEG studies show elevated high-frequency (beta) activity at sleep onset and during sleep in insomnia patients compared with matched controls
• Overnight cortisol is elevated in chronic insomnia
• Heart rate variability shows persistent sympathetic dominance
• Metabolic rate is higher, both during the day and at night, in people with insomnia
• Neuroimaging shows heightened activation in the ascending arousal system

The clinical experience is familiar: the body is tired, the mind won't stop. It is not a will problem. It is the arousal system being on when the sleep system is supposed to take over.

The 3P model: how acute insomnia becomes chronic

A widely used clinical framework (Spielman's 3P model) separates three types of factors that turn a bad patch of sleep into a chronic disorder:

Predisposing factors are baseline traits that raise your risk. Being female, being older, having a family history of insomnia, tendency toward hyperarousal or perfectionism, high trait anxiety.

Precipitating factors are what started this episode. Stress, a life change, illness, grief, a new medication, having a baby, a bereavement, a major work project.

Perpetuating factors are what keeps insomnia going after the precipitant has passed. This is where things get interesting, because the precipitant may be long gone, but the perpetuating factors are actively maintaining the disorder. Common ones:

• Spending more time in bed to "catch up" on lost sleep, which fragments sleep
• Anxious monitoring of sleep ("how many hours did I get, how am I going to function tomorrow")
• Unhelpful beliefs about sleep ("if I don't sleep 8 hours I can't function," "I have to be able to sleep on demand")
• Daytime napping to compensate
• Clock-checking
• The bed becoming associated with wakefulness and frustration rather than sleep
• Increasing use of alcohol, cannabis, or medication to force sleep

CBT-I targets the perpetuating factors directly. That is why it works even when the original precipitant is long gone.

Why sleeping pills are not the answer

Sleep medication has a role in short-term or crisis use. It is not the treatment for chronic insomnia disorder, and the guidelines are clear on this point.

The American Academy of Sleep Medicine 2021 clinical practice guideline strongly recommends CBT-I as first-line treatment for chronic insomnia in adults. The 2024 combination-therapy guideline reinforces this: CBT-I alone is preferred over combination with medication where possible, because behavioural-psychological treatment "often produces meaningful and durable improvements without the added risks associated with pharmacotherapy."

What the evidence actually shows about medication:

• Benzodiazepines and Z-drugs (zopiclone, zolpidem, eszopiclone): effect sizes on total sleep time and sleep quality are modest. Tolerance develops. Dependence and withdrawal are common. Rebound insomnia on discontinuation is well-documented. Long-term use is associated with cognitive impairment, falls in older adults, and other safety concerns.
• Newer dual orexin receptor antagonists (daridorexant, lemborexant): better tolerability profile than benzodiazepines and Z-drugs, but effect sizes remain modest and long-term data are still accumulating.
• Over-the-counter sleep aids and antihistamines: limited evidence of durable benefit, meaningful next-day cognitive effects.
• Cannabis for sleep: heavily used (about 15 percent of Canadians used cannabis-derived products for sleep in the past year), but disrupts REM sleep, produces tolerance, and can worsen insomnia over time.

None of this means anyone currently on sleep medication has done something wrong. It means the treatment landscape has changed, and CBT-I should now be the offered starting point.

What CBT-I actually is

Cognitive Behavioural Therapy for Insomnia (CBT-I) is a structured, short-term treatment typically delivered over 4 to 8 sessions. It has the strongest evidence base of any insomnia treatment and produces gains that persist after therapy ends.

The active components (in order of the most recent 2024 network meta-analysis showing which components carry the most benefit):

Sleep restriction therapy. Temporarily narrowing the time you spend in bed to match the sleep you are actually getting. This increases sleep drive and consolidates sleep. Counterintuitive but powerful, and identified in a 2024 component network meta-analysis of 241 RCTs as the single most impactful component.

Stimulus control. Rebuilding the automatic association between bed and sleep by getting out of bed when you cannot sleep, reserving the bed for sleep and intimacy only, and maintaining a consistent wake time regardless of how the night went.

Cognitive restructuring. Examining and updating the anxious beliefs about sleep that keep the arousal system activated ("if I don't sleep I'll fall apart tomorrow"). The 2024 meta-analysis identified this as the second most effective component.

Third-wave components (acceptance-based approaches, mindfulness for insomnia). Increasingly integrated into CBT-I with growing evidence.

Psychoeducation and sleep hygiene. Necessary background, but on its own, not sufficient. Meta-analyses now show sleep hygiene education alone is essentially ineffective as a treatment for chronic insomnia. Sleep hygiene is a component, not a treatment.

Relaxation training. Mixed evidence. Some benefit for the physiological arousal piece, but not a strong stand-alone component.

CBT-I is not gentle in the first two weeks (sleep restriction usually means less sleep before it means more), but the trajectory is reliable. Most people begin to see improvement by session 3 or 4.

Insomnia rarely comes alone

Comorbidity is the rule, not the exception:

Depression. Insomnia is one of the strongest predictors of new-onset depression, and treating insomnia meaningfully improves depression outcomes. The relationship is bidirectional. See our companion piece on insomnia and depression.

Anxiety. High trait anxiety is a strong risk factor. The hyperarousal that maintains insomnia is essentially anxiety expressed in the sleep-wake system.

Chronic pain. Pain disrupts sleep and poor sleep amplifies next-day pain. Untreated insomnia sustains chronic pain conditions.

ADHD. Adult ADHD has a strong sleep component. Up to 80 percent of adults with ADHD report significant sleep disturbance, and up to 78 percent have delayed sleep-wake timing. See our companion piece on insomnia and ADHD.

Post-concussion syndrome. Sleep disruption is very common after concussion (roughly 60 percent of concussion patients experience chronic sleep problems) and is one of the highest-leverage things to treat.

Menopause and perimenopause. Hot flashes, hormonal shifts, and secondary hyperarousal are common precipitants of chronic insomnia in mid-life.

PTSD. Insomnia and nightmares are core features. CBT-I adapted for PTSD is effective.

Treating insomnia in the context of these conditions often unlocks improvement across the board.

What actually works: the current standard of care

Modern insomnia management is structured and layered:

1. Assessment. A proper history to distinguish insomnia disorder from other sleep disorders (sleep apnea, restless legs, circadian rhythm disorders), identify the 3P factors, and screen for comorbidities.

2. CBT-I as the first-line treatment. In-person or via therapist-guided digital programs. Brief Behavioural Treatment for Insomnia (BBT-I) is a shorter, more accessible variant that is well-evidenced when time or access are barriers.

3. Medication in specific circumstances only. For short-term crisis use, when CBT-I is truly unavailable, or in combination when a specific comorbidity requires it, under medical supervision.

4. Careful management of comorbid conditions and the mood/anxiety symptoms that often accompany insomnia.

When to seek care

If sleep problems have persisted more than a few weeks and are affecting your day-to-day life, mood, or functioning, and you have not had a proper conversation about CBT-I, that is the gap to close. This is not something to just live with.

References

• American Academy of Sleep Medicine. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. 2021.
• American Academy of Sleep Medicine. Combination treatment guideline for chronic insomnia. 2024.
• Morin CM et al. Prevalence of insomnia and use of sleep aids among adults in Canada. Sleep Medicine, 2024.
• Furukawa Y et al. Components of cognitive behavioural therapy for insomnia: network meta-analysis of 241 trials. JAMA Psychiatry, 2024.
• Riemann D et al. European insomnia guideline update, 2023.