When Insomnia Becomes an Economic Disease: Linking Phenotype, Comorbidity, Treatment, and Societal Cost—An Evidence-Based Narrative Review

1. Introduction: From Sleep Complaint to Economic Disease

Insomnia—difficulty initiating or maintaining sleep, or early-morning awakening, accompanied by daytime impairment—is the most common sleep disorder in adults, yet it has historically been undertreated, under-coded, and under-resourced. This review deliberately frames insomnia not merely as a clinical condition but as an economic one. Its costs are not confined to prescriptions and consultations; they propagate through reduced productivity, workplace absence, accidents, and the treatment of the illnesses with which insomnia is prospectively associated—depression, cardiovascular disease, diabetes, and dementia. Each of these downstream outcomes is itself expensive, which means that the economic footprint of insomnia is largely determined by what happens after the phenotype is established.

The evidence reviewed here links four domains: the phenotype (what insomnia is, biologically and nosologically), the comorbidity dimension (what insomnia does to physical and mental health), treatment (what can be done and at what risk), and societal cost (what insomnia costs, and what treating it is worth). The central thesis is that these four domains are closely and plausibly causally connected: the phenotype drives the comorbidities, the comorbidities drive the costs, and treatment—particularly cognitive behavioral therapy for insomnia (CBT-I)—is the principal lever that can interrupt the sequence.

2. The Phenotype of Insomnia: From Symptom to Disorder

2.1. Definition, Diagnosis, and Epidemiology

Modern nosology has decisively reframed insomnia as a disorder in its own right. Both the International Classification of Sleep Disorders, third edition (ICSD-3), and the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5), removed the distinction between primary and secondary insomnia in favor of an umbrella category of insomnia disorder that is diagnosed “whether or not there is a coexisting physical, mental or sleep disorder” [1]. This shift reflects the recognition that insomnia frequently precedes its comorbid conditions, persists after they are treated, and can aggravate their course [1].

The prevalence of insomnia depends heavily on how it is defined. Symptoms of acute insomnia are reported by up to 37% of the general population each year, whereas chronic insomnia disorder affects approximately 10–20%, with higher rates among women, older adults, and individuals of lower socioeconomic status [1]. Earlier estimates placed chronic insomnia at 10–15% of adults, with an additional 25–35% experiencing transient or occasional insomnia [2]. A 2025 meta-analysis of general-population studies found a pooled prevalence of insomnia disorder of 12.4% when DSM criteria were established by diagnostic interview and 16.3% when based on self-reported DSM criteria, with estimates ranging from 7.5% to 32.3% across validated questionnaires [3]. Applying pooled prevalence estimates to global population data yields approximately 852 million adults with insomnia worldwide—16.2% of the adult population—of whom an estimated 415 million (7.9%) have severe insomnia [4].

Chronicity is the epidemiological feature that converts a complaint into a disease. In population studies, insomnia lasted at least one year in 85% of cases [5]. The same body of work shows that insomnia complaints frequently arise from, or coexist with, other conditions: breathing-related sleep disorders account for 5–9% of insomnia complaints, periodic limb movement disorder or restless legs syndrome for about 15%, medical or neurological conditions for 4–11%, and poor sleep hygiene or environmental factors for approximately 10% [5].

2.2. Pathophysiology: Hyperarousal and the 3-P Model

The dominant pathophysiological construct in insomnia research is hyperarousal—a state of elevated cognitive, physiological, and emotional activation that persists across the 24-hour day and impedes the normal transition into sleep [6]. The hyperarousal model posits that heightened arousal alters cognitive and physiological state and thereby disturbs sleep; it has been complemented by the observation that individuals with persistent hyperarousal are prone to instability of rapid eye movement (REM) sleep, resulting in sleep fragmentation and subjective sleep complaints [6]. Psychophysiologically, people with insomnia develop a “fear of sleeplessness” that intensifies emotional arousal and perpetuates the disorder in a self-reinforcing cycle [7].

The most widely cited integrative framework is Spielman’s “3-P” model, which explains the transition from acute to chronic insomnia through the interaction of predisposing factors (genetic, physiological, and psychological vulnerability), precipitating events (stressors that trigger the acute sleep disturbance), and perpetuating factors (behaviors and cognitions, such as spending excessive time in bed and worrying about sleeplessness, that maintain it) [6,7,8].

More recent neuroscience has begun to localize this vulnerability. Functional and structural evidence suggests that people who develop insomnia may carry genetically and experientially sensitized brain circuits—particularly involving the locus coeruleus and the salience network—that remain active during REM sleep, when they would normally be quiescent, producing a state aptly described as “sleeping with one eye open” [9]. This accumulating hyperarousal not only impedes restorative sleep but may also increase vulnerability to other mental health problems, providing a mechanistic bridge from phenotype to comorbidity [9].

2.3. Phenotypic Heterogeneity and Subtypes

Insomnia is not a homogeneous disorder, and its heterogeneity has direct economic relevance because different phenotypes carry different medical risks. The best-validated biological phenotype distinguishes insomnia with objective short sleep duration (ISSD; typically <6 hours on polysomnography) from insomnia with normal sleep duration. ISSD is characterized by activation of the stress system (the hypothalamic–pituitary–adrenal axis and sympathetic nervous system), significant medical sequelae—hypertension, diabetes, neurocognitive deficits, and increased mortality—and a persistent course; in contrast, the normal-sleep-duration phenotype shows cognitive-emotional arousal without physiological hyperarousal, lacks these medical sequelae, and is more likely to remit over time [10]. The ISSD subtype is also associated with a longer history of insomnia, more abnormal biomarkers, and greater treatment resistance, although the night-to-night stability of objective sleep duration is limited [1].

Complementing this biological subtyping, data-driven approaches using multivariate profiles of life history, mood, and personality have identified robust clusters of insomnia phenotypes with differing clinical and biological features [11]. These efforts, together with large population-based analyses of insomnia subtypes, promise to move beyond a single “lumped” diagnosis toward mechanism-based subtyping that could predict differential treatment response [1,12]. At the genetic level, insomnia is a highly polygenic trait: genome-wide association studies including more than 1.3 million individuals have confirmed a substantial heritable architecture, reinforcing the view of insomnia as a biological disorder rather than a psychological by-product [1].

3. The Comorbidity Dimension: How Insomnia Multiplies Disease Burden

3.1. Mental Disorders: Depression, Anxiety, and Suicide

The longitudinal association between insomnia and depression is among the most robust findings in psychiatric epidemiology. A meta-analysis of 21 longitudinal studies reported a pooled odds ratio (OR) of 2.60 (95% confidence interval [CI] 1.98–3.42; random-effects model) for insomnia predicting subsequent depression in people who were not depressed at baseline (fixed-effects OR 2.10, 95% CI 1.86–2.38) [13], and a subsequent meta-analysis of 34 prospective cohort studies confirmed an approximately twofold risk (relative risk [RR] 2.27, 95% CI 1.89–2.71) [14]. Interpreted against a background depression incidence of about 10% per year in the general population, these estimates imply a substantial number of depressive episodes potentially attributable to insomnia [15]. Subsequent work has confirmed—and even strengthened—the association, leading investigators to describe insomnia as a possible transdiagnostic process in psychopathology [16]. The relationship extends beyond depression: insomnia predicts a wide range of mental disorders, consistent with the Research Domain Criteria concept that dysfunction in a limited number of neurobiological systems—notably arousal—underlies many psychiatric conditions [17]. Anxiety is closely intertwined: 70–90% of patients with anxiety report insomnia, and combined anxiety and depression exert the strongest effect on sleep quality among individuals at high risk for insomnia, partly through poor sleep behaviors [18].

The economic stakes of this comorbidity are raised substantially by the suicide literature. A meta-analysis of 39 studies comprising 147,753 participants found that sleep disturbance was associated with relative risks of suicidal ideation, suicide attempts, and suicide ranging from 1.95 to 2.95 in unadjusted analyses, and depression did not moderate these associations [19]. A subsequent review estimated an overall relative risk of 2.79 (95% CI 2.44–3.19) for sleep disturbance and suicidal outcomes, with comparable risk ratios for insomnia (2.84), nightmares (2.61), and other sleep disorders (2.72) [20]. A meta-analysis of longitudinal studies confirmed that sleep disturbance, including insomnia, prospectively predicts suicidal thoughts and behaviors with small-to-medium to medium effect sizes [21], and a second longitudinal meta-analysis found that insomnia predicted suicidal ideation (OR 2.10, 95% CI 1.83–2.41), suicide attempts (OR 1.78, 95% CI 1.38–2.29), and suicide death (OR 1.54, 95% CI 1.04–2.29), although the authors cautioned that these are statistically significant but weak predictors [22]. Among patients with psychiatric diagnoses, comorbid sleep disturbance is associated with nearly twofold odds of suicidal behaviors (OR 1.99, 95% CI 1.72–2.30) [23]. Because suicide and depression are themselves leading contributors to lost productivity, disability, and premature mortality, this pathway alone makes insomnia a major economic risk factor.

3.2. Cardiometabolic Disease: Hypertension and Cardiovascular Events

The bidirectional relationship between insomnia and physical health is now well established, and the European Insomnia Guideline emphasizes that insomnia should be evaluated and actively treated in the presence of comorbid conditions [24]. The physiological signature of hyperarousal—elevated sympathetic activity, abnormal hormone secretion, and increased whole-body metabolic rate across the 24-hour day—plausibly explains why chronic insomnia increases the risk of hypertension and related disorders [25]. Meta-analytic evidence from prospective cohorts shows that short sleep duration, difficulty maintaining sleep, early-morning awakening, and combined insomnia symptoms are each associated with an increased risk of incident hypertension, with insomnia chronicity strengthening the association [25].

For cardiovascular disease, a meta-analysis concluded that insomnia is associated with an increased risk of developing and/or dying from cardiovascular disease [26]. Symptom-specific pooled relative risks for cardio-cerebral vascular events were 1.27 (95% CI 1.15–1.40) for difficulty initiating sleep, 1.11 (95% CI 1.04–1.19) for difficulty maintaining sleep, and 1.18 (95% CI 1.05–1.33) for non-restorative sleep [27]. The reductions in sleep duration that accompany chronic insomnia disorder have also been linked to increased risk of coronary artery disease, incident myocardial infarction, type 2 diabetes, obesity, systemic hypertension, and all-cause mortality [28].

3.3. Diabetes and the Metabolic Phenotype

The sleep–diabetes link is one of the most quantitatively developed areas of sleep epidemiology. A meta-analysis of 10 prospective studies (107,756 participants) found that difficulty initiating sleep (RR 1.57, 95% CI 1.25–1.97) and difficulty maintaining sleep (RR 1.84, 95% CI 1.39–2.43) were both associated with an increased risk of incident type 2 diabetes [29]. Dose–response analyses show a U-shaped relationship between sleep duration and type 2 diabetes, with the lowest risk at 7–8 hours per night and significantly elevated risk at both extremes [30]. In the population-based MONICA/KORA Augsburg cohort, difficulty maintaining sleep predicted incident type 2 diabetes in both men and women, plausibly through insulin resistance and chronic low-grade systemic inflammation [31]. Crucially, the biological phenotype matters: insomnia with objective short sleep duration is associated with increased odds of diabetes, whereas insomnia with normal sleep duration is not, suggesting that the medical impact of the ISSD phenotype has been underestimated [32]. Epidemiological and administrative studies further indicate that insomnia symptoms are more common among people with type 2 diabetes than in the general population and that the risk of incident diabetes rises with the duration of insomnia [33].

3.4. Cognitive Decline and Dementia

Longitudinal and meta-analytic evidence increasingly implicates insomnia in cognitive aging. A systematic review and meta-analysis of 51 cohorts identified insomnia, sleep fragmentation, daytime dysfunction, prolonged sleep latency, REM sleep behavior disorder, and excessive time in bed as risk factors for all-cause cognitive decline or dementia, with a U-shaped relationship for sleep duration [34]. A multicenter study found that midlife insomnia was associated with an increased risk of developing dementia later in life, with terminal insomnia and longer sleep duration in late life also conferring risk [35]. Dose-dependent effects have been demonstrated at the symptom level: in a nationally representative sample of 13,833 US adults aged 51 years and older, each one-unit increase in an insomnia symptom index was associated with a 5% greater hazard of mild cognitive impairment (hazard ratio [HR] 1.05, 95% CI 1.04–1.06) and of dementia (HR 1.05) [36]. Given that dementia care is among the most expensive endpoints in modern health systems, the insomnia–dementia pathway is a compelling target for prevention-oriented sleep health policy.

3.5. Co-occurring Sleep Disorders: COMISA

Insomnia frequently coexists with other sleep disorders, most importantly obstructive sleep apnea (OSA). Approximately 30–40% of people with insomnia symptoms have comorbid OSA, and 30–50% of people with OSA report insomnia symptoms—a combination now termed comorbid insomnia and sleep apnea (COMISA) [24,37]. The clinical importance of this overlap is underscored by analysis of the Wisconsin Sleep Cohort, in which COMISA was associated with a higher prevalence of hypertension, diabetes, and cardiovascular disease and with more severe depression and anxiety symptoms than in people with neither condition, and with increased all-cause mortality over 20 years of follow-up (HR 1.71, 95% CI 1.00–2.93) [37]. Notably, the association between COMISA and mortality was no longer significant after further adjustment for depression and anxiety symptoms, suggesting that mental health may mediate much of the excess mortality associated with the combination [37]. From an economic perspective, COMISA represents a population in which untreated sleep pathology is compounded, and in which both disorders must be treated to halt the accrual of cardiovascular and psychiatric costs.

4. Treatment: The Economic Lever

4.1. Cognitive Behavioral Therapy for Insomnia: Efficacy and Components

CBT-I is the first-line treatment for insomnia disorder and is recommended by the principal international guidelines [6,24]. Its efficacy is supported by an extensive randomized evidence base: a meta-analysis of 87 randomized controlled trials (3724 treated patients versus 2579 controls) found significant effects on insomnia severity (Hedges’ g = 0.98), sleep efficiency (g = 0.71), Pittsburgh Sleep Quality Index scores (g = 0.65), wake after sleep onset (g = 0.63), sleep onset latency (g = 0.57), sleep quality (g = 0.40), and number of awakenings (g = 0.29), with the smallest effect on total sleep time (g = 0.16) [38]. Face-to-face treatment of at least four sessions appeared more effective than self-help or shorter face-to-face formats, and results were robust across patients with and without comorbid disease and across age groups [38]. In clinical terms, 70–80% of people with chronic insomnia improve with treatment, approximately 50% achieve clinically meaningful improvement, and approximately 30% become good sleepers [6].

A component network meta-analysis of 241 trials (31,452 participants) identified the critical active ingredients of CBT-I: cognitive restructuring (incremental OR 1.68, 95% CI 1.28–2.20), third-wave components (1.49, 95% CI 1.10–2.03), sleep restriction (1.49, 95% CI 1.04–2.13), and stimulus control (1.43, 95% CI 1.00–2.05) [39]. A randomized comparison of behavior therapy, cognitive therapy, and their combination showed that each component confers distinct benefits—behavior therapy producing faster improvement in sleep and cognitive therapy producing more durable gains—with the combined package providing the most balanced outcomes [40].

4.2. Pharmacotherapy and Its Risks

Where pharmacotherapy is indicated, the European Insomnia Guideline recommends benzodiazepines, benzodiazepine receptor agonists, daridorexant, and low-dose sedating antidepressants for short-term treatment (≤4 weeks), with orexin receptor antagonists usable for up to 3 months, or longer in selected cases [24]. Prolonged-release melatonin may be used for up to 3 months in patients aged 55 years and older, whereas antihistaminergic drugs, antipsychotics, fast-release melatonin, ramelteon, and phytotherapeutics are not recommended [24].

The economic logic of pharmacotherapy is complicated by its adverse-event profile, which is most consequential in older adults—the population with the highest prevalence of insomnia. Hypnotics measurably increase the risk of falls and fractures: pooled meta-analytic estimates for hip fracture are RR 1.52 (95% CI 1.37–1.68) for benzodiazepines and RR 1.90 (95% CI 1.68–2.13) for Z-drugs [41]. In adults aged 65 years and older, the risk of fracture requiring hospitalization in the 90 days after an initial zolpidem prescription (RR 2.55) was at least as high as that after diazepam (RR 1.97), indicating that Z-drugs are not a safer alternative [42]. In nursing home residents, non-benzodiazepine hypnotics are associated with elevated hip fracture risk (OR 1.66, 95% CI 1.45–1.90), especially in new users (OR 2.20) [43]. Cognitive harms compound the injury burden: benzodiazepines are implicated in impaired cognition, delirium, and motor vehicle crashes in older adults [44], and it has been estimated that about 10% of older adults referred to memory clinics have drug-related cognitive impairment, often attributable to benzodiazepines [45]. Once fractures, emergency admissions, and cognitive decline are costed, an inexpensive hypnotic prescription can generate substantial downstream costs—an inversion of the usual assumption that drug treatment is the low-cost option [41,43].

4.3. Delivery Innovation: Digital and Guided Formats

A major barrier to realizing the economic potential of CBT-I has been the scarcity of trained therapists. Digital CBT-I, delivered with or without coaching, addresses this bottleneck. In a randomized trial among employees (schoolteachers) with insomnia and work-related rumination, internet-based CBT-I significantly reduced insomnia symptoms and costs attributable to absenteeism and presenteeism compared with a wait-list control, with a high probability of cost-effectiveness from the employer’s perspective [46]. This finding is directly relevant to workplace health investment: because insomnia is common, measurable, and treatable with scalable technology, employers have both the data and the tools to act on it.

4.4. Guideline Synthesis: A Stepped, Safety-Aware Approach

Taken together, the treatment evidence supports stepped care as the optimal economic strategy: CBT-I (face-to-face, group, or digital) as first-line treatment; pharmacotherapy reserved for short-term relief or CBT-I non-response, with orexin receptor antagonists considered where longer use is contemplated; and systematic deprescribing of benzodiazepines and Z-drugs in older patients, who bear the greatest fracture and cognitive risk [24,41,44]. Because CBT-I targets the maintaining mechanisms (hyperarousal and perpetuating behaviors) rather than merely inducing sedation, its benefits extend beyond sleep to mood, fatigue, and quality of life—outcomes that are themselves major cost drivers [6].

5. The Societal Cost of Insomnia

5.1. Direct Costs

Direct costs—medical consultations, sleep studies, hypnotic prescriptions, and hospitalizations attributable to insomnia—were among the first to be quantified. The US National Commission on Sleep Disorders Research estimated the direct costs of insomnia at $15.4 billion in 1990 [47]. A subsequent analysis estimated US direct costs in 1995 at $13.9 billion, comprising $1.97 billion for sleep-promoting substances and $11.96 billion for health care services [48]. In France, the direct costs of insomnia were estimated at more than $2 billion for 1995 [49]. Although methodologically heterogeneous, these figures consistently show that insomnia consumes substantial health-system resources even before its consequences—absenteeism, presenteeism, accidents, and downstream disease—are counted [50,51].

5.2. Indirect Costs: Absenteeism and Presenteeism

The indirect costs of insomnia far exceed its direct costs. In a population-based study in the Canadian province of Quebec, the total annual cost of insomnia was estimated at CAD 6.5 billion, 76% of which was attributable to insomnia-related work absences and reduced productivity [52]. Aggregate estimates of direct plus indirect costs in the United States have ranged from $92.5–107.5 billion annually in earlier analyses [53] to as much as approximately $100 billion in more recent syntheses [54]. The costs of accidents related to sleep disorders, including property damage, have been estimated separately at $43.15–56.02 billion [47].

Workplace evidence quantifies the mechanism behind these totals. People with insomnia report two to three times as many days of poor productivity and impaired concentration as good sleepers [47]. Among employed populations, insomnia is associated with significantly higher absenteeism: in France, employees with insomnia were absent for 5.8 days per year compared with 2.4 days for good sleepers, and 88% of the resulting cost was borne by employers [55]. In the United States, the annual cost of insomnia in the civilian labor force was estimated at approximately $15.0–17.7 billion [56]. Presenteeism—productivity loss while present at work—shows a dose–response relationship with insomnia severity, with moderate and severe insomnia associated with greater presenteeism than mild insomnia [57]. Even subclinical sleep disturbance matters: a longitudinal analysis of more than 11,000 state employees found that greater trouble sleeping predicted absenteeism, lower work performance ratings, and higher health care costs over a two-year period [58].

5.3. Quality of Life and Daytime Functioning as Economic Inputs

The economic case is underpinned by consistent evidence that insomnia degrades health-related quality of life. Insomnia is independently associated with impaired health-related quality of life to almost the same extent as chronic conditions such as congestive heart failure and clinical depression [59]. National survey data show that people with insomnia report impaired concentration, impaired memory, decreased ability to accomplish daily tasks, and decreased enjoyment of interpersonal relationships, with impairment increasing with the frequency of sleep disturbance [60]. Qualitative research articulates the lived experience: participants with persistent insomnia described daily difficulties with cognitive, emotional, and physical functioning, reduced work performance and social participation, and a sense of being “isolated” and “obstructed” from their desired selves [61]. These functional decrements are precisely what presenteeism instruments attempt to monetize.

5.4. Mortality as an Economic Outcome

Mortality risk converts insomnia from a productivity problem into a population-health problem with actuarial consequences. In the Hordaland Health Study of 6236 adults aged 40–45 years at baseline, insomnia was associated with an almost threefold increase in all-cause mortality over 13–15 years of follow-up (HR 2.74, 95% CI 1.75–4.30), which was not attenuated after full adjustment (HR 3.34, 95% CI 1.67–6.69) [62]. In a large prospective cohort of US men, difficulty initiating sleep and non-restorative sleep were associated with a modestly higher risk of mortality [63]. When premature death, disability, and lost working life are valued economically, mortality is among the largest—and most frequently omitted—components of the societal cost of insomnia.

5.5. Cost-Effectiveness of Treatment: The Return on Investment

The final element of the economic case is the favorable cost-effectiveness of treating insomnia. In a randomized trial among long-term hypnotic users in general practice, psychological treatment for insomnia improved sleep quality, reduced hypnotic use, and improved health-related quality of life at a mean incremental cost of £3418 per quality-adjusted life-year (QALY) at 6 months, with a probability of cost-effectiveness exceeding 80% at willingness-to-pay thresholds of around £12,500 per QALY—well within the range historically considered acceptable by UK decision-makers [64]. In a trial of guided internet-based CBT-I among schoolteachers, the intervention had a 94% probability of dominating the wait-list control (better outcomes at lower cost) from the societal perspective; from the public health care perspective, the incremental cost-effectiveness ratio was €650 per symptom-free individual and €11,285 per QALY gained, with an 89% probability of cost-effectiveness at a threshold of €20,000 per QALY [65]. These ratios fall well below commonly applied willingness-to-pay thresholds and strengthen the argument that treating insomnia is not a cost but an investment.

6. Synthesis: The Economic Case for Treating Insomnia

The connections developed across the preceding sections form a coherent chain with clear economic implications. The insomnia phenotype—a hyperarousal disorder, chronic in most cases, with a biologically severe short-sleep variant—predisposes to comorbidity: depression (OR ≈ 2.6), suicidal thoughts and behaviors (RR ≈ 2–3), hypertension, cardio-cerebral vascular events (RR 1.11–1.27 by symptom), type 2 diabetes, and dementia (HR 1.05 per symptom-index unit) [13,19,27,36]. Each comorbid outcome is itself a high-cost disease, financed through the same health care budgets and employer productivity accounts that must also absorb the direct costs of insomnia. Treatment can modulate the links in this chain: CBT-I reduces insomnia severity with large effect sizes, improves mood and daytime function, and can be delivered at scale digitally, whereas inappropriate hypnotic use adds fracture and cognitive costs of its own [38,41,46]. The societal cost—estimated at up to approximately $100 billion annually in the United States, with three-quarters of costs in a Canadian population arising from lost productivity—is therefore not a fixed burden but a modifiable one [52,54].

Three structural observations follow. First, insomnia is systematically undervalued because its costs are distributed across psychiatric, cardiometabolic, geriatric, and occupational silos, so that no single budget holder sees the full bill. Second, because insomnia is a modifiable antecedent of expensive diseases, its treatment could function as primary prevention—for depression, hypertension, diabetes, and possibly dementia—yet it is rarely funded from prevention budgets. Third, the workplace is a natural venue for intervention: employers bear a large share of the indirect costs of insomnia and have access to scalable digital CBT-I with demonstrated cost-effectiveness from the employer’s perspective [46,55].

7. Conclusions and Future Directions

Insomnia meets the defining criteria of an economic disease: it is prevalent (insomnia disorder in approximately 10–20% of adults), chronic (lasting at least one year in 85% of cases), costly (up to approximately $100 billion per year in the United States), and treatable at favorable cost-effectiveness [1,5,54,64]. Its phenotype is increasingly well characterized—hyperarousal, the 3-P model, and the ISSD subtype provide actionable biological and clinical targets [7,10]. The comorbidity evidence is consistent across large prospective studies and meta-analyses: insomnia approximately doubles the risk of depression and is associated with materially higher risks of cardiometabolic disease, suicidal behavior, and dementia [13,20,26,34]. Effective treatment exists—CBT-I works in meta-analyses, in clinical practice, and in digital form [38,46].

What remains is a policy and implementation gap. Future research should prioritize trials testing whether insomnia treatment reduces incident depression, cardiovascular events, and cognitive decline—the outcomes that would transform the cost calculus; employer-based implementation studies of digital CBT-I with productivity endpoints; health-economic modeling that captures the full cross-sectoral cost offsets of insomnia treatment; and personalization research linking insomnia subtypes to differential treatment response, so that resources are directed to those most likely to benefit [11,39]. Governments, payers, and employers who continue to treat insomnia as a trivial complaint are, in effect, absorbing the downstream costs of depression, cardiovascular disease, diabetes, dementia, and workplace dysfunction—a position that the current evidence does not support. When insomnia is reframed as the modifiable economic disease that it is, the investment case for treating it becomes compelling.