Insomnia: What Could Be Causing It

How Common Is Insomnia, and Who Gets It?

Insomnia is the most frequently reported sleep complaint worldwide. Population-based surveys consistently place the prevalence of chronic insomnia disorder between 10% and 15% of adults, with an additional 30-35% experiencing short-term symptoms [1]. Women are 1.4 times more likely than men to develop insomnia, and the risk climbs with age, peaking after 60 [2].

The Spielman 3P model (predisposing, precipitating, perpetuating factors) remains the standard framework for understanding why one person develops transient sleep trouble while another spirals into a chronic pattern. Predisposing factors include genetic variants in circadian clock genes, trait hyperarousal, and female sex. Precipitating events range from job loss to acute illness. Perpetuating behaviors, such as spending excessive time in bed or relying on alcohol as a sedative, are what convert an acute episode into a disorder that persists long after the original stressor resolves [3].

Race and socioeconomic status also matter. A 2015 analysis from the National Health Interview Survey (N=444,306) found that Black adults reported significantly higher rates of short sleep duration and insomnia symptoms compared with white adults, even after adjusting for income and education [4]. Access to behavioral sleep medicine specialists is limited: fewer than 1,000 board-certified behavioral sleep medicine providers practice in the United States.

Psychiatric and Psychological Causes

Depression and anxiety are the two most common comorbidities found alongside chronic insomnia, present in roughly half of all cases. The relationship is bidirectional: insomnia doubles the risk of developing a new depressive episode, and depression frequently manifests as early-morning awakening or difficulty falling asleep [5].

Generalized anxiety disorder (GAD) drives pre-sleep cognitive hyperarousal. Patients describe racing thoughts, catastrophic worry about the next day, and physical tension that blocks the transition from wakefulness to sleep. Post-traumatic stress disorder (PTSD) adds nightmares and hypervigilance. A meta-analysis published in Sleep Medicine Reviews (2019) found that 70% of individuals with PTSD met criteria for clinically significant insomnia [6].

Bipolar disorder complicates the picture because sleep loss can trigger manic episodes. Clinicians evaluating insomnia should screen for a history of mania or hypomania before prescribing stimulants or activating antidepressants. Substance use disorders (alcohol, cannabis, opioids, stimulants) each produce distinct insomnia phenotypes. Alcohol shortens sleep latency initially but fragments sleep architecture in the second half of the night, reducing REM and increasing stage-1 transitions [7].

Chronic psychophysiological insomnia (also called conditioned insomnia or learned insomnia) deserves separate mention. These patients sleep better in unfamiliar environments, on the couch, or when not "trying" to sleep. The bed has become a conditioned cue for wakefulness. This pattern responds well to stimulus control therapy, a core component of CBT-I.

Medical Conditions That Disrupt Sleep

A long list of medical diagnoses can cause or worsen insomnia. The most frequent offenders, grouped by organ system:

Pain syndromes. Chronic low back pain, osteoarthritis, fibromyalgia, and migraine all fragment sleep. A 2019 study in the Journal of Clinical Sleep Medicine (N=2,095 adults with chronic pain) found that 72.7% screened positive for at least one sleep disorder, with insomnia being the most prevalent [8].

Respiratory disease. Obstructive sleep apnea (OSA) and insomnia overlap more than most patients realize. The term COMISA (comorbid insomnia and sleep apnea) describes a phenotype affecting 39-58% of OSA patients [9]. Asthma, COPD, and chronic cough also cause nocturnal awakenings. Nighttime GERD exacerbates both asthma and insomnia.

Endocrine and metabolic disorders. Hyperthyroidism accelerates metabolic rate and raises core body temperature, making sleep onset difficult. Uncontrolled type 2 diabetes causes nocturia and neuropathic pain. Cushing syndrome produces cortisol excess that disrupts circadian rhythmicity.

Cardiovascular disease. Heart failure causes orthopnea, paroxysmal nocturnal dyspnea, and Cheyne-Stokes respiration, each of which fragments sleep. Nocturnal angina awakens patients with chest pressure.

Neurological disease. Restless legs syndrome (RLS) affects 5-10% of adults and is a classic cause of sleep-onset insomnia [10]. Parkinson disease, Alzheimer disease, and multiple sclerosis each carry insomnia rates above 40%.

Urologic conditions. Nocturia (waking two or more times per night to urinate) is the single most common reason older adults report middle-of-the-night awakenings. Benign prostatic hyperplasia, overactive bladder, and poorly controlled diabetes are common culprits.

Medications and Substances That Cause Insomnia

Drug-induced insomnia is underrecognized. A thorough medication reconciliation should be part of every insomnia evaluation.

Antidepressants. SSRIs (fluoxetine, sertraline) and SNRIs (venlafaxine, duloxetine) can cause insomnia in 10-20% of patients, often by suppressing REM sleep and increasing nocturnal arousals [11]. Bupropion is particularly activating. Mirtazapine and trazodone, by contrast, are sedating and sometimes prescribed off-label for insomnia.

Cardiovascular drugs. Beta-blockers (metoprolol, atenolol) suppress melatonin secretion via beta-1 receptor blockade in the pineal gland. A randomized crossover trial showed that adding 2.5 mg of exogenous melatonin reversed beta-blocker-induced insomnia in hypertensive patients [12]. Diuretics taken in the evening worsen nocturia.

Corticosteroids. Prednisone and dexamethasone cause dose-dependent insomnia, agitation, and sometimes frank psychosis. Patients on burst courses frequently report two to three nights of near-total sleeplessness.

Stimulants and related drugs. Methylphenidate, amphetamine salts, and modafinil used for ADHD or narcolepsy can push sleep onset past midnight when dosed too late. Decongestants containing pseudoephedrine and bronchodilators such as albuterol are also activating.

Recreational substances. Caffeine has a mean half-life of 5 to 6 hours, but CYP1A2 slow metabolizers may still have active serum levels 9 to 10 hours post-ingestion [13]. Nicotine is a stimulant that shortens total sleep time and fragments sleep architecture. Cannabis withdrawal after regular use produces rebound insomnia lasting 2 to 6 weeks.

Hormonal and Life-Stage Factors

Sleep changes predictably across the lifespan, with hormonal transitions serving as common inflection points.

Perimenopause and menopause. Up to 60% of women in the menopausal transition report new or worsened insomnia [14]. Vasomotor symptoms (hot flashes, night sweats) account for a large share of nocturnal awakenings, but declining estradiol and progesterone also affect GABA-A receptor sensitivity and thermoregulation independent of hot flashes. The Study of Women's Health Across the Nation (SWAN) followed 3,045 women longitudinally and documented a clear rise in self-reported sleep difficulty beginning in the early perimenopausal stage. Hormone therapy with estradiol (with or without micronized progesterone) has been shown to reduce wake-after-sleep-onset time by 15-20 minutes in symptomatic menopausal women [15].

Testosterone deficiency in men. Low testosterone (total T <300 ng/dL) is associated with increased sleep fragmentation and higher rates of obstructive sleep apnea. The relationship between TRT and sleep is complex: testosterone replacement may worsen OSA in some men by increasing upper-airway collapsibility, while improving subjective sleep quality in others [16].

Pregnancy. Insomnia prevalence rises from roughly 12% in the first trimester to 40% in the third trimester, driven by nocturia, back pain, fetal movement, and elevated progesterone.

Aging. Older adults experience a natural reduction in slow-wave (N3) sleep, increased sleep fragmentation, and an advanced circadian phase (earlier bedtime, earlier wake time). These changes are physiological, not pathological. They become clinically significant only when accompanied by daytime impairment.

Circadian Rhythm Disruptions

Not all insomnia is classic insomnia disorder. Misalignment between the internal circadian clock and the desired sleep schedule produces symptoms that mimic insomnia but require different treatment.

Delayed sleep-wake phase disorder (DSWPD) is common in adolescents and young adults. The patient falls asleep easily at 2:00 or 3:00 a.m. and wakes naturally at 10:00 or 11:00 a.m. but cannot fall asleep at a conventional bedtime. Treatment involves timed bright-light exposure in the morning and low-dose melatonin (0.5-3 mg) administered 5 to 7 hours before the desired sleep onset, not at bedtime [17].

Shift-work disorder affects 10-38% of rotating or night-shift workers. The circadian system never fully adapts to a nocturnal schedule, producing both insomnia during daytime sleep attempts and excessive sleepiness on the job. Strategic napping, timed light exposure, and, in select cases, prescription wakefulness-promoting agents (modafinil 200 mg) may help [18].

Jet lag disorder is transient. Eastward travel is harder to adapt to than westward travel because the endogenous circadian period averages slightly longer than 24 hours. A general rule: recovery takes approximately one day per time zone crossed eastward.

Irregular sleep-wake rhythm disorder is seen primarily in patients with neurodegenerative disease or intellectual disability. There is no single consolidated sleep period; instead, sleep and wake bouts scatter across the 24-hour day.

How Insomnia Is Diagnosed

Diagnosis is clinical. No blood test or imaging study confirms insomnia disorder. The International Classification of Sleep Disorders, Third Edition (ICSD-3) requires all of the following: (1) difficulty initiating sleep, maintaining sleep, or waking too early; (2) adequate opportunity and circumstances for sleep; (3) daytime consequences (fatigue, mood disturbance, cognitive impairment, social or occupational dysfunction); and (4) symptoms present at least three nights per week for at least three months for a chronic diagnosis [19].

Sleep diary. Two weeks of a standardized sleep diary (bedtime, lights-out time, estimated sleep-onset latency, number and duration of awakenings, final wake time, rise time) is the single most useful diagnostic tool. It costs nothing and often reveals patterns invisible to the patient. The Consensus Sleep Diary is freely available and validated [20].

Actigraphy. Wrist-worn accelerometers estimate sleep-wake patterns over 1 to 2 weeks. Actigraphy is especially helpful for circadian rhythm disorders and for patients whose self-reported sleep times diverge markedly from objective measures.

Polysomnography (PSG). An overnight sleep study is not routinely indicated for insomnia. The American Academy of Sleep Medicine (AASM) recommends PSG only when a comorbid sleep disorder (OSA, periodic limb movement disorder, or parasomnias) is suspected [19].

Questionnaires. The Insomnia Severity Index (ISI) is a 7-item, validated self-report measure. A score of 15 or higher indicates moderate clinical insomnia. The Epworth Sleepiness Scale and STOP-BANG questionnaire help screen for OSA.

A clinician should also obtain a full medical history, medication list, psychiatric screening (PHQ-9 for depression, GAD-7 for anxiety), substance use history, and a review of sleep environment and habits.

Evidence-Based Treatment Options

The 2016 American College of Physicians (ACP) guideline recommends CBT-I as the first-line treatment for chronic insomnia in all adults [21]. This is a strong recommendation based on moderate-quality evidence.

CBT-I is a structured, typically 6- to 8-session intervention that combines sleep restriction therapy, stimulus control, cognitive restructuring, relaxation training, and sleep hygiene education. A meta-analysis of 20 RCTs (N=1,162) published in Annals of Internal Medicine found that CBT-I reduced sleep-onset latency by a mean of 19 minutes and wake-after-sleep-onset by 26 minutes, with effects sustained at 12-month follow-up [22]. Digital CBT-I platforms (such as FDA-cleared Pear Therapeutics Somryst) have shown comparable efficacy to in-person delivery.

"CBT-I should be offered to all patients with chronic insomnia as the initial intervention, regardless of whether they also have comorbid conditions," states the ACP guideline panel [21].

Pharmacotherapy is recommended only when CBT-I alone is insufficient or unavailable. Options include:

• Dual orexin receptor antagonists (DORAs). Suvorexant (10-20 mg) and lemborexant (5-10 mg) block wake-promoting orexin signaling. In the SUNRISE-2 trial (N=949), lemborexant 5 mg improved sleep onset and sleep maintenance vs. placebo over 12 months with no evidence of rebound insomnia on discontinuation [23].
• Low-dose doxepin (3-6 mg) is the only FDA-approved antidepressant for insomnia. It targets histamine H1 receptors selectively at these doses.
• Melatonin receptor agonists. Ramelteon (8 mg) reduces sleep-onset latency by approximately 9 minutes vs. placebo. It carries no abuse potential and no next-morning impairment.
• Benzodiazepine receptor agonists (Z-drugs). Zolpidem, zaleplon, and eszopiclone remain widely prescribed but carry FDA black-box warnings for complex sleep behaviors (sleepwalking, sleep-driving). The AASM 2017 clinical practice guideline suggests these agents only when CBT-I and newer medications are ineffective [24].
• Benzodiazepines (temazepam, triazolam) are generally avoided for chronic insomnia due to tolerance, dependence, falls, and cognitive impairment in older adults.

"Short-term use of medications may be appropriate in some patients, but clinicians should discuss the limited benefits and significant harms of pharmacotherapy," notes Andrew D. Krystal, MD, MS, of the UCSF Weill Institute for Neurosciences [21].

Treating the underlying cause is always the highest-yield intervention. CPAP adherence in COMISA patients improves both apnea metrics and insomnia severity. Adequate pain management, thyroid hormone optimization, hormone therapy for symptomatic menopausal insomnia, and medication timing adjustments (moving an SSRI from bedtime to morning) can each resolve insomnia without adding a sleep-specific drug.

Patients with insomnia lasting more than three months who have not responded to sleep hygiene changes alone should request a formal evaluation, including a sleep diary review and screening for comorbid conditions, from a provider trained in behavioral sleep medicine.