Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “insomnia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

The Zurich study. VIII. Insomnia: association with depression, anxiety, somatic syndromes, and course of insomnia.

The association of three subtypes of insomnia with psychic and functional syndromes, and the course of insomnia over 7 years were examined in a Swiss cohort of young adults interviewed three times. Specific associations were found between repeated brief insomnia (RBI) and recurrent brief depression (RBD). Continued insomnia (CI) was associated with major depression. All three subtypes of insomnia were associated with anxiety disorders; 52% of insomniacs were free of concurrent anxiety and depression. Insomnia--especially RBI and CI--was also associated with a number of functional complaints, but not with the consumption of alcohol, medicine, or illegal drugs. Insomniacs with RBI and occasional insomnia (OI) experienced more life events and interpersonal conflicts than controls. These findings support the subdivision of insomnia into different subtypes. The longitudinal analysis showed that insomnia tends to reoccur. For subjects with insomnia either at age 21 or 23 years, there was a higher risk of further insomnia at follow-ups. The specific subtype of insomnia at the first occurrence was not predictive for the outcome: all subtypes of insomnia enhance the risk of relapses in a similar way. Insomnia at age 21 is no precursor of the first onset of a depressive or anxiety disorder within a 2-year follow-up. With respect to the course of insomnia over 7 years, the subtypes did not differentiate.

Adult↗
PubMed1992

Long-term study of the sleep of insomnia patients with sleep state misperception and other insomnia patients.

OBJECTIVE: The objectives were 1) to investigate differences among patients with subjective insomnia (sleep state misperception), patients with objective findings of insomnia, and normal volunteers and 2) to assess the consistency of the sleep findings during a 2-month period. METHOD: Twenty-one subjects were studied. Subjects with sleep state misperception (N = 7) had insomnia complaints for more than 1 year, no objective sleep disturbance, and sleep efficiency of 90% or greater (on the diagnostic screening sleep recording), while subjectively estimating that sleep time was less than 6.5 hours. Subjects with objective insomnia (N = 7) met the same subjective criteria, but objectively sleep efficiency was 85% or less. Normal subjects (N = 7) had no insomnia complaints and objective sleep efficiency of 90% or greater. All subjects were recorded on 2 consecutive nights three times with a 3-week period between each pair of nights (6 standard all-night polysomnographic sessions of 8 hours). A subjective sleep questionnaire was administered after each sleep recording night. RESULTS: Sleep stage variables (percentages) were similar between the two insomnia groups, and both were different from the normal subjects. Sleep continuity variables were disturbed in the objective insomnia group, but they were similar in the sleep state misperception and normal groups. Both insomnia groups rated their sleep as inadequate on the questionnaires and differed from the normal subjects. The distinct sleep patterns of each of the three groups did not vary over the 6 nights of assessment. CONCLUSIONS: Sleep state misperception may be a prodromic or transitional state of sleep dysfunction between normal sleep and the sleep pattern of objective insomnia.

Adult↗
PubMed1992

Risk factors associated with complaints of insomnia in a general adult population. Influence of previous complaints of insomnia.

BACKGROUND: Insomnia is a common complaint both in the general population and also in physician's offices. However, risk factors for the development of insomnia complaints have not been completely identified. METHODS: To identify population characteristics associated with increased prevalence of insomnia complaints, we surveyed a large general adult population in 1984 through 1985. We evaluated the relationship among current complaints of initiating and maintaining sleep and obesity, snoring, concomitant health problems, socioeconomic status, and documented complaints of difficulty with insomnia 10 to 12 years previously. RESULTS: The strongest risk factor for complaints of initiating and maintaining sleep was previous complaints of insomnia (odds ratio, 3.5). In addition, female gender (odds ratio, 1.5), advancing age (odds ratio, 1.3), snoring (odds ratio, 1.3), and multiple types of concomitant health problems (odds ratios, 1.1 to 1.7) were all risk factors associated with an increased rate of complaints of initiating and maintaining sleep. CONCLUSION: Complaints of insomnia tend to be a persistent or recurrent problem over long periods of time. Female gender, advancing age, and concomitant health problems also are important risk factors.

Adult↗
PubMed1992

Rebound insomnia in normals and patients with insomnia after abrupt and tapered discontinuation.

Rebound insomnia was studied in subjects, aged 25-50 years, with insomnia complaints and normal sleep, insomnia complaints and disturbed sleep, and normal sleep with no complaints (N = 21, n = 7 per group). Standard sleep recordings were collected on a baseline night and after abrupt discontinuation of 6 nights of 0.50 mg triazolam, tapered discontinuation (3 nights of 0.50 mg, 2 nights of 0.25 mg, and 1 night of 0.125 mg triazolam) and 6 nights of placebo. Significantly disturbed sleep on the discontinuation night compared to the baseline night was found. The relative degree of rebound insomnia was greater in the abrupt condition than in either the tapered or placebo conditions. The tapered condition reduced sleep time by half that of the abrupt condition which was twice the reduction found in the placebo condition. An overall (regardless of group or condition) difference in baseline versus discontinuation sleep was found, suggesting that pill discontinuation itself leads to sleep disturbance. Subjects did not differ in rebound insomnia as a function of pre-existing sleep disturbance.

Adult↗
PubMed2026

Cognitive Behavior vs Bright Light Therapy for Insomnia in Women Undergoing Chemotherapy for Breast Cancer: A Randomized Clinical Trial.

IMPORTANCE: Women receiving chemotherapy for breast cancer experience insomnia and fatigue, which impair quality of life. To date, no randomized clinical trial (RCT) has evaluated the use of cognitive behavior therapy for insomnia (CBT-I) and bright light therapy (BLT) both alone and in combination, and few have evaluated the use of either during chemotherapy. OBJECTIVE: To determine the main effects of CBT-I and BLT on insomnia and fatigue symptoms in women undergoing chemotherapy for breast cancer. DESIGN, SETTING, AND PARTICIPANTS: Sleep, Cancer, Rest (SleepCARE) was a 6-week, 2 × 2 factorial, superiority, parallel RCT conducted at 5 metropolitan and regional hospitals in Australia from January 22, 2021, to August 21, 2024. Participants were women (aged ≥18 years) receiving chemotherapy for early or metastatic breast cancer. INTERVENTIONS: Two brief interventions were administered: CBT-I and BLT alone (using light glasses at 1500 lux) and in combination, creating 4 groups (CBT-I alone, BLT alone, CBT-I plus BLT, and sleep hygiene education [SHE]). All interventions included SHE. The interventions lasted 6 weeks and included a 1:1 consultation session, emails sent once or twice per week, and a midpoint call for all groups, as well as light glasses for the BLT groups. MAIN OUTCOMES AND MEASURES: Dual primary outcomes were Insomnia Severity Index (ISI) scores and Patient-Reported Outcomes Measurement Information System (PROMIS)-Fatigue T scores. Both are patient-reported outcome measures and measure insomnia and fatigue symptoms, respectively. Assessments occurred via surveys administered at baseline and at the midpoint (3 weeks), postintervention (6 weeks), and follow-up (3 months and 6 months) periods. Modified intention-to-treat analyses used latent growth models. RESULTS: Of the 219 women enrolled (mean [SD] age, 50.7 [10.8] years; 54 [26.9%] with metastatic cancer), 55 were randomized to CBT-I, 55 to BLT, 52 to CBT-I plus BLT, and 57 to SHE. A total of 208 women (95.0%) with any data at any time point were analyzed. Insomnia symptoms (ISI score mean difference [MD], -2.19 [95% CI, -3.33 to -1.05] points; P = .002) but not fatigue symptoms (PROMIS-Fatigue score MD, -0.90 [95% CI, -3.08 to 1.28] points; P = .52) improved more in the CBT-I groups compared with the non-CBT-I groups. The BLT groups (compared with the non-BLT groups) did not differ in insomnia symptoms (ISI score MD, -0.88 [95% CI, -2.02 to 0.26] points; P = .26) or fatigue symptoms (PROMIS-Fatigue score MD, -0.71 [95% CI, -2.89 to 1.47] points; P = .52). Comparable results emerged in the high-adherence subgroup and in the subgroups with high initial insomnia and fatigue symptoms. However, exploratory subgroup analyses in women with metastatic breast cancer showed that BLT (vs non-BLT) improved insomnia symptoms (ISI score MD, -2.87 [95% CI, -5.06 to -0.67] points; P = .01) and fatigue symptoms (PROMIS-Fatigue score MD, -5.16 [95% CI, -9.57 to -0.76] points; P = .02). CONCLUSIONS AND RELEVANCE: In the SleepCARE RCT of CBT-I and BLT administered for 6 weeks to women receiving chemotherapy for breast cancer, CBT-I improved insomnia but not fatigue compared with SHE or BLT. BLT did not produce greater improvements in fatigue or insomnia symptoms compared with non-BLT treatment. The study findings indicate that brief CBT-I, but not BLT, may reduce insomnia symptoms among women receiving chemotherapy for breast cancer. TRIAL REGISTRATION: ANZCTR Identifier: ACTRN12620001133921.

Humans↗
PubMed2026

Integrative multi-omics profiling of insomnia-related molecular features reveals microbiome, immune, and therapy-relevant heterogeneity in colorectal cancer.

Emerging evidence implicates insomnia as a potential risk factor in carcinogenesis, potentially involving systemic inflammation, circadian disruption, and microbiome alterations. However, the molecular associations linking insomnia-related features to colorectal cancer (CRC), particularly with respect to tumor biology, immune microenvironmental states, and therapy-relevant phenotypes, remain largely unexplored. Multi-omics integration of genomic, transcriptomic, and microbiome data from 3,026 CRC patients across seven independent cohorts, including a large, well-annotated Clinical Omics study of Colorectal Cancer in China (COCC) cohort, enabled insomnia-based molecular classification through unsupervised non-negative matrix factorization (NMF) clustering. The insomnia subtype (IS) was biologically characterized via pathway enrichment, immune deconvolution, microbial profiling, and single-cell transcriptomics. Furthermore, an insomnia score (ISscore) was developed and validated in multiple cohorts for risk stratification and assessment of treatment-response-related indicators in CRC. Unsupervised clustering revealed two distinct molecular subtypes (IS1/IS2), with IS2 demonstrating significantly poorer survival. IS2 exhibited marked activation of EMT/angiogenesis pathways versus cell cycle activation in IS1. The IS2 microenvironment showed increased immunosuppression-related infiltration and exhausted T cell signatures, together with intratumoral microbiome variation characterized by depletion of Ruminococcaceae UCG-002 and enrichment of Hungatella/Selenomonas. The ISscore system stratified survival risk and was associated with computational indicators of immunotherapy response. Single-cell analysis nominated PPIA-BSG as a potential cell-cell communication signal involving high-ISscore tumor cells, CXCL12+ endothelial cells, and CLEC9A+ dendritic cell subsets. This multi-omics characterization of insomnia-CRC interplay suggests that insomnia-related molecular features are associated with an immunologically distinct and microbiome-altered tumor ecosystem. The ISscore provides a reproducible framework for capturing insomnia-related molecular heterogeneity, supporting risk stratification and future evaluation of therapy-relevant phenotypes.IMPORTANCEChronic insomnia affects millions, but it is not typically considered a cancer risk factor. Our study, analyzing vast biological data from over 3,000 colorectal cancer patients, uncovers a potential link between a person's predisposition to insomnia and their risk of developing this disease. This suggests that the biological pathways related to sleep may play a role in cancer development. Understanding this connection opens up new avenues for identifying individuals at higher risk and developing novel prevention strategies for colorectal cancer.

colorectal cancer↗
PubMed2026

IL1B-centered immune dysregulation involving IL7R, CCR7, ITGB2 and IRF1 across insomnia and inflammatory bowel disease.

BACKGROUND: Insomnia is a prevalent sleep disorder that strongly affects one's quality of life and physical well-being. Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines, and a majority of IBD patients suffer from comorbid insomnia. However, the shared molecular features linking insomnia and IBD remain poorly characterized. METHODS: Common differentially expressed genes (DEGs) were identified in datasets of insomnia (GSE208668) and IBD (GSE179285) using the Limma package. Functional enrichment was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Protein-protein interaction (PPI) network construction and hub gene identification was subsequently performed. Furthermore, we validated the reliability of the hub genes using qRT-PCR and Enzyme-linked immunosorbent assay (ELISA). In addition, we constructed a TF-miRNA regulatory network of hub genes and assessed the abundance of immune cell infiltration in insomnia and IBD using CIBERSORT, EPIC, and xCell algorithms. Finally, we utilized the DsigDB to predict potential therapeutic candidates. RESULTS: The analysis revealed 75 upregulated and 32 downregulated common DEGs. Functional enrichment analysis revealed the inflammatory response and immune activation as pivotal drivers underlying the pathogenesis of both insomnia and IBD. Five hub DEGs, namely, IL1B, IL7R, CCR7, ITGB2, and IRF1, were subsequently screened and validated. The TF-miRNA-mRNA regulatory network consisted of 5 TFs, 14 miRNA nodes and 5 core mRNA nodes. Immune cell infiltration analysis revealed several patterns shared between insomnia and IBD. Additionally, 10 potential therapeutic drugs for insomnia and IBD were proposed. CONCLUSION: Integrative coexpression network analysis reveals convergent dysregulation of an IL1B-centered immune module (comprising IL7R, CCR7, ITGB2, and IRF1) across insomnia and IBD, a shared immune disturbance and candidate targets for simultaneous intervention upon further mechanistic validation.

Humans↗
PubMed1990

Insomnia.

Because sleep needs vary from person to person, insomnia is defined as the chronic inability to obtain the amount of sleep needed for optimal functioning and well-being. Insomnia, which is a symptom rather than a disease, can be classified into three main etiologic groups: insomnias related to other mental disorders (for example, depression and anxiety), insomnias related to known organic factors (for example, sleep apnea and "nonrestorative" sleep), and primary insomnia (for example, learned psychophysiologic insomnias and insomnia complaints without objective findings). The treatment for insomnia often involves a combination of pharmacotherapy, behavioral and short-term psychotherapy, and sleep hygiene guidelines. Sleep disorders centers can provide specialized knowledge and techniques for patients with severe chronic insomnia.

Circadian Rhythm↗
PubMed1991

Subtyping DSM-III-R primary insomnia: a literature review by the DSM-IV Work Group on Sleep Disorders.

OBJECTIVE: The authors review the usefulness, reliability, and validity of recently proposed subtypes of primary insomnia. DSM-III uses "primary insomnia" to indicate chronic insomnia not associated with other diagnosable mental or medical disorders, whereas the International Classification of Sleep Disorders (ICSD) recognizes three subtypes: psychophysiological insomnia, idiopathic insomnia, and sleep state misperception. METHOD: After reviewing all of the primary source references for each insomnia disorder in the ICSD and all of the additional primary sources cited in each of these, the authors conducted an automated literature search using Medline. Of the 48 primary sources located, the authors selected 27 studies that were reported in peer-reviewed journals, had the largest available subject groups, used diagnostic reliability procedures, and included control groups. RESULTS: The studies reviewed contained limited empirical support for the proposed distinction between idiopathic and psychophysiological insomnia. Sleep state misperception appears, however, to be a highly prevalent feature of chronic insomnia generally, rather than only a specific disorder per se. CONCLUSIONS: The authors conclude that there is not yet sufficient empirical evidence to warrant the abandonment of DSM-III-R "primary insomnia" and the adoption of the ICSD subtypes in DSM-IV. However, they affirm the heuristic value of the ICSD subtypes and the need for field trials to compare the performance characteristics of the DSM-III-R and ICSD systems with respect to 1) interrater reliability, 2) effects of rater expertise (generalist versus specialist) on rates of agreement, and 3) effects of polysomnographic data on rates of agreement.

Humans↗
PubMed1992

Fatal familial insomnia, a prion disease with a mutation at codon 178 of the prion protein gene.

BACKGROUND: We previously described two members of a family affected by an apparently genetically determined fatal disease characterized clinically by progressive insomnia, dysautonomia, and motor signs and characterized pathologically by severe atrophy of the anterior ventral and mediodorsal thalamic nuclei. Five other family members who died of this disease, which we termed "fatal familial insomnia," had broader neuropathologic changes suggesting that fatal familial insomnia could be a prion disease. METHODS: We used antibodies to prion protein (PrP) to perform dot and Western blot analyses, with and without proteinase K, on brain tissue obtained at autopsy from two patients with fatal familial insomnia, three patients with sporadic Creutzfeldt-Jakob disease, and six control subjects. The coding region of the PrP gene was amplified and sequenced in the samples from the two patients with fatal familial insomnia. Restriction-enzyme analysis was carried out with amplified PrP DNA from 33 members of the kindred. RESULTS: Protease-resistant PrP was found in both patients with fatal familial insomnia, but the size and number of protease-resistant fragments differed from those in Creutzfeldt-Jakob disease. In the family with fatal familial insomnia, all 4 affected members and 11 of the 29 unaffected members had a point mutation in PrP codon 178 that results in the substitution of asparagine for aspartic acid and elimination of the Tth111 I restriction site. Linkage analysis showed a close relation between the point mutation and the disease (maximal lod score, 3.4 when theta was zero). CONCLUSIONS: Fatal familial insomnia is a prion disease with a mutation in codon 178 of the PrP gene, but the disease phenotype seems to differ from that of previously described kindreds with the same point mutation.

Adolescent↗
PubMedDate not supplied

Detection and assessment of insomnia.

Insomnia is one of the most common complaints encountered by the primary care physician. Yet, in many cases, physicians treat the symptom of insomnia rather than evaluating and treating the underlying causes of insomnia. Because the subjective complaint of insomnia does not always correlate with evidence of objective sleep disruption, a careful history and evaluation are required. Assessment of the duration of insomnia and quantification of the impact of nocturnal sleep disruption on daytime functioning provide the most reliable indices of severity. Primary insomnia may be due to a number of different causes, such as poor sleep hygiene or circadian rhythm disruption. Insomnia may also be the presenting symptom of other primary sleep disorders, such as sleep apnea syndrome or nocturnal myoclonus, or of a variety of medical or psychiatric illnesses. The treatment of the patient with insomnia should address the underlying cause, when identifiable. When the cause cannot be identified, treatment should be conservative; nonpharmacologic therapies should be used whenever possible. When pharmacologic approaches are indicated, short-acting benzodiazepines should be administered in concordance with strict prescribing guidelines. Frequent follow-up is necessary to ensure continued therapeutic efficacy of the prescribed therapy.

Age Factors↗
PubMed1989

Rebound insomnia: a critical review.

Rebound insomnia, a worsening of sleep compared with pretreatment levels, has been reported upon discontinuation of short half-life benzodiazepine hypnotics. This paper reviews the existing sleep laboratory studies for the presence or absence of rebound insomnia following treatment with triazolam, temazepam, and flurazepam in insomniac patients or poor sleepers and, when possible, in normals. The results indicate that rebound insomnia is a distinct possibility after discontinuation of triazolam in both insomniacs and normal controls. Compared with baseline, disturbed sleep was reported in insomniacs or poor sleepers for the first 1 or 2 nights of withdrawal in seven of nine polygraphically recorded sleep studies following triazolam 0.5 mg and in one of two studies following triazolam 0.25 mg. In one study conducted in normal volunteers, rebound insomnia was observed following triazolam 0.5 mg but not triazolam 0.25 mg. In another study, which used subjective reports of sleep rather than polygraphic recordings, rebound insomnia was significantly attenuated after triazolam 0.5 mg by tapering the dose over 4 nights. The risk of rebound insomnia after temazepam 15 or 30 mg was low. In keeping with its long elimination half-life, flurazepam (30 mg) continued to exert beneficial effects for the first 2-3 withdrawal nights, but the possibility of a mild rebound insomnia cannot be dismissed during the intermediate withdrawal period (nights 4-10) following prolonged, consecutive, nightly administration (more than 30 nights). The benzodiazepine hypnotics are generally preferred over other types (barbiturates or nonbenzodiazepine, nonbarbiturate), but there are advantages and disadvantages related to half-life of the benzodiazepines. The risk of rebound insomnia is greater with the short half-life as compared with the long half-life benzodiazepines.

Anti-Anxiety Agents↗
PubMedDate not supplied

Insomnia and depression prior to myocardial infarction.

Insomnia is common among patients who subsequently experience an acute myocardial infarction (MI), and is a major symptom of psychiatric depression. The purpose of this study was to determine what proportion of patients reporting insomnia prior to MI have depression. Of 70 patients with a recent MI, 27 (39%) reported having had insomnia for two weeks or longer prior to their MI, 13 of whom (48%) met diagnostic criteria for a major depressive episode (MDE). MDE accounted for a significant proportion of the patients reporting insomnia prior to MI (p less than 0.0001). Furthermore, those patients with insomnia who did not meet diagnostic criteria for MDE nevertheless had three times as many depressive symptoms, excluding sleep disturbance, as did those patients who did not experience insomnia prior to their MI (p less than 0.0009). The implications of this finding are discussed, as well as possible explanations for the relationship between insomnia, depression, and subsequent MI.

Aged↗
PubMed1992

Diagnosis and treatment of insomnia and risks associated with lack of treatment.

Despite the fact that the prevalence rate for insomnia in the United States is high (35.2%), the number of patients with this condition do not represent a large percentage of patients evaluated and treated in sleep disorders clinics. On the other hand, the great majority of patients with insomnia do not seek treatment for their condition from their physicians. Several hypotheses have been created to explain this phenomenon: (1) lack of training for physicians in the area of sleep disorders, (2) pessimism in relation to treatment outcome shared by patients and physicians, and (3) time constraints and other reasons on the part of the physicians. Insomniacs, however, deserve accurate diagnosis and effective treatments for their condition. Insomnia is often the result of multiple factors converging rather than one single cause. For academic purposes, however, different disorders in difficulties with initiation and maintenance of sleep are discussed. Among them, adjustment sleep disorder, obstructive sleep apnea, periodic limb movements in sleep, circadian abnormalities, and psychiatric disturbances. Emphasis is placed on the treatment of each, along with the treatment of the other factors that are commonly found in patients with insomnia: poor sleep hygiene, use of medications that disrupt sleep, performance anxiety, deficient exposure to entrainers of circadian rhythms, diet, and exercise. A comprehensive treatment that includes a multifactorial approach is the ideal way to treat patients with insomnia. Research that will enhance our knowledge of the biological substrate of insomnia will provide clinicians with additional tools to improve the outcome of their treatments of patients with insomnia.

Age Factors↗
PubMed1988

The prevalence of insomnia: the importance of operationally defined criteria.

Previous studies on the prevalence of sleep disturbances have shown that insomnia occurs in 3.2-42% of different populations. The wide reported variation in prevalence prompted a rigorous definition of insomnia to be introduced in this study. Randomly selected members of the population aged 30 to 65 years from two geographically different rural parts of central Sweden answered a sleep questionnaire. The response rates were 69.2% and 70.2%, respectively. Females significantly more often reported difficulty in falling asleep (7.1% of the women and 5.1% of the men). Among women 8.9 and among men 7.7% of individuals reported trouble with nocturnal awakenings. Using a stringently defined concept of insomnia as a disorder of initiating sleep (DIS), the prevalence rate of insomnia among women was 1.1% and among men 0.5%. Defining insomnia as a disorder of maintaining sleep (DMS), the prevalence among both women and men was 1.1%. Defining insomnia as a disorder of initiating and maintaining sleep (DIMS), the prevalence rate was 1.7% among women and 1.4% among men. This prevalence, which is lower than previously reported, demonstrate the importance of an operational definition of insomnia.

Adult↗
PubMed2026

Effectiveness of Wearable Digital Therapeutics in Improving Sleep Outcomes Among Individuals With Insomnia: Systematic Review and Meta-Analysis of Randomized Controlled Trials.

BACKGROUND: Wearable devices are increasingly used for sleep monitoring and as adjunctive treatment. Existing meta-analyses mostly pool composite digital therapies and rarely isolate stand-alone wearables or distinguish between objective and subjective end points. Whether stand-alone wearable interventions improve sleep outcomes in adults with insomnia, and which factors moderate treatment heterogeneity, remains unclear. OBJECTIVE: This study aims to evaluate the effectiveness of wearable digital interventions on sleep outcomes in adults with insomnia versus control strategies and explore moderators of effectiveness, including device-wearing position, intervention duration, and control type, using meta-regression. METHODS: This systematic review and meta-analysis was conducted in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta‑Analyses) 2020 statement and the PRISMA-S (Preferred Reporting Items for Systematic Reviews and Meta‑Analyses Literature Search Extension) guideline. Five electronic databases and clinical trial registries were searched from inception to May 18, 2026. Eligible studies were randomized controlled trials (RCTs) evaluating wearable digital interventions in adults with insomnia compared with sham, waitlist, usual care, or active control conditions and had an intervention duration of at least 1 week. Study screening, data extraction, and risk-of-bias assessment were carried out independently by 2 reviewers. Pooled estimates were calculated using a restricted maximum likelihood random-effects model with the Hartung-Knapp-Sidik-Jonkman correction. Heterogeneity was assessed using the I² statistic, and 95% prediction intervals (PIs) were calculated for the primary analyses. The certainty of evidence was rated using the GRADE (Grading of Recommendations, Assessment, Development, and Evaluation) approach. RESULTS: Sixteen RCTs (N=910) were included. Wearable digital interventions were associated with a significant reduction in objective sleep-onset latency (SOL; mean difference [MD] -4.52, 95% CI -8.38 to -0.67, PI -9.52 to 0.47 min) and a significant improvement in subjective sleep efficiency (SE; MD 2.00%, 95% CI 1.90%-2.11%, PI 1.85%-2.15%). Subjective total sleep time (TST) also showed a significant increase (MD 19.11, 95% CI 2.98-35.24, PI -16.20 to 54.43 minutes). Meta-regression showed that control type, intervention duration, and device location did not explain the heterogeneity of the insomnia severity index (ISI) (R²=0). Sensitivity analysis confirmed the robustness of pooled ISI estimates, and an Egger test indicated no small-study effects (P=.07). Certainty of evidence ranged from moderate to high. CONCLUSIONS: Wearable digital interventions provide selective benefits for objective SOL, subjective SE, and subjective TST in adults with insomnia, with no improvement in overall ISI. Despite statistically significant effects on several sleep parameters, wide PIs, substantial heterogeneity, and limited study numbers indicate preliminary, nonconclusive findings. Wearables should be viewed as affordable adjunctive tools requiring further validation, not substitutes for first-line cognitive behavioral therapy for insomnia. Large-scale, long-term RCTs with standardized protocols and patient-level external validation are required to consolidate the evidence base.

Humans↗