Chronic insomnia — difficulty initiating sleep, maintaining sleep, or experiencing restorative sleep for three or more nights weekly across three months or more — affects approximately 10–15% of adults at any given time. The figure rises with age, reaches near-30% in adults over 65, and is substantially higher in psychiatric populations. Chronic insomnia is not merely a symptom of an underlying condition; it is independently associated with elevated risk of depression, anxiety, cardiovascular disease, and — relevant to this volume — cognitive decline and dementia. The clinical task is to treat insomnia as the cognitive risk factor that it is, not as a complaint to be silenced with a hypnotic.
Cognitive Behavioral Therapy for Insomnia (CBT-I) is the first-line treatment, supported by stronger evidence than any pharmacological intervention. CBT-I addresses the cognitive and behavioral factors that maintain insomnia: sleep restriction, stimulus control, cognitive restructuring of catastrophic thinking about sleep, sleep hygiene, and relaxation training. Effect sizes are comparable to or larger than those of hypnotic medications, and benefits persist after treatment ends — unlike pharmacological interventions, which generally require ongoing use. The clinical problem is access: CBT-I requires trained providers, takes six to eight sessions, and is unevenly covered by insurance. Digital CBT-I platforms (Somryst, Sleepio, SHUTi) have closed some of this access gap with FDA-cleared options that produce comparable outcomes for many patients.
The pharmacological landscape is layered and should be deployed accordingly. Trazodone (25–100mg qhs) is the workhorse first-line pharmacological agent — cheap, generic, no respiratory depression, weight-neutral, minimal hangover, and useful in patients with comorbid depression. Mirtazapine (7.5–15mg qhs) is useful when appetite stimulation or anxiolysis is also desired; its dose paradox (more sedating at lower doses) is clinically important. Low-dose doxepin (3–6mg) is selective for histamine-1 receptors at low doses and is approved specifically for sleep maintenance; the cost-versus-effect calculation depends on whether brand or compounded generic is used. The dual orexin receptor antagonists (DORAs) — suvorexant, lemborexant, daridorexant — are newer agents with favorable safety profiles, particularly in older adults, and represent the most significant pharmacological advance in sleep medicine in two decades.
Benzodiazepines and Z-drugs deserve specific caution. Both classes work — they reliably produce sleep — but the cognitive cost over chronic use is substantial. Benzodiazepines have been linked in observational studies to elevated dementia risk, particularly with chronic use, and the cognitive impact is mechanistically plausible (GABA-mediated effects, residual sedation, impaired memory consolidation). Z-drugs (zolpidem, eszopiclone, zaleplon) carry similar concerns. The clinical principle is that both classes are appropriate for short-term use in acute insomnia or transient situations; their use as chronic, indefinite sleep aids is not consistent with longevity-psychiatry principles. The patient on chronic zolpidem for years should be reevaluated for alternatives.
Quetiapine 25–50mg for sleep is widespread and problematic. Low-dose quetiapine is widely prescribed off-label for insomnia despite limited evidence for efficacy at sleep-dose ranges and meaningful concerns about metabolic effects (weight gain, glucose dysregulation, lipid effects) and anticholinergic burden (cognitive cost). For psychiatric indications that justify quetiapine, it has a clear role. As a sleep medication in patients without psychiatric indication for it, the risk-benefit calculation is unfavorable for longevity psychiatry. The patient on quetiapine 25mg for sleep — a common scenario — should be evaluated for alternatives.
Special populations deserve specific considerations. Elderly patients are particularly sensitive to anticholinergic burden, falls risk from sedatives, and the cognitive cost of chronic hypnotic use; DORAs and low-dose doxepin are typically preferred. Patients with PTSD often benefit from prazosin for nightmares (covered in detail in L11.3). Patients with comorbid depression may have insomnia that responds primarily to depression treatment; durable remission of depression often resolves the insomnia. Perimenopausal and postmenopausal women have insomnia patterns driven partly by hormonal transitions; the conversation may need to include hormonal evaluation (covered in Stage 19). ADHD patients on stimulants need attention to the timing of the last stimulant dose.
The longevity-psychiatry approach to chronic insomnia is layered, patient — many "refractory" patients have not actually had CBT-I — and conservative about chronic pharmacology. The aim is restorative sleep that supports cognitive trajectory across decades, not just nightly sedation.