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The Journal of Family Practice Jul 2023Insomnia is a distinct disorder that is common, yet underrecognized and undertreated in primary care. Treating insomnia has been shown to improve outcomes, including... (Review)
Review
Insomnia is a distinct disorder that is common, yet underrecognized and undertreated in primary care. Treating insomnia has been shown to improve outcomes, including reduced risk of developing cardiovascular and mental health disorders. Insomnia is influenced by the brain's regulation of sleep and wake, which are mutually exclusive events. Insomnia should be treated as a distinct condition, even when occurring with a comorbid diagnosis such as depression or anxiety. Clinicians should implement a multimodal approach to insomnia management, including nonpharmacologic interventions and pharmacologic therapy (when indicated). Pharmacologic agents that are approved by the US Food and Drug Administration for insomnia include benzodiazepine receptor agonists (zolpidem, eszopiclone, and zaleplon), low-dose doxepin (tricyclic antidepressant), ramelteon (melatonin receptor agonist), and dual orexin receptor agonists (DORAs, daridorexant, lemborexant, and suvorexant). Unlike other pharmacologic agents, DORAs inhibit wakefulness rather than induce sedation. Additionally, these medications have no evidence of rebound insomnia or withdrawal, and little to no abuse potential. Daridorexant is the newest DORA, has an ideal half-life of 8 hours, and has demonstrated continued efficacy over a 12-month period. Selection of pharmacologic agent should be based on the patient's comorbid conditions, treatment goals and preferences, and other clinical characteristics.
Topics: Humans; Sleep Initiation and Maintenance Disorders; Sleep; Zolpidem; Doxepin
PubMed: 37549414
DOI: 10.12788/jfp.0620 -
Journal of Sleep Research Dec 2023Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and... (Review)
Review
Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential-diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders, etc.), treatment-resistant insomnia (A) and for other indications (B). Cognitive-behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in-person or digitally (A). When cognitive-behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low-dose sedating antidepressants (B) can be used for the short-term treatment of insomnia (≤ 4 weeks). Longer-term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged-release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast-release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive-behavioural therapy for insomnia (B).
Topics: Adult; Humans; Sleep Initiation and Maintenance Disorders; Melatonin; Sleep; Benzodiazepines; Antidepressive Agents
PubMed: 38016484
DOI: 10.1111/jsr.14035 -
JAMA Psychiatry Oct 2023Insomnia has been associated with altered inflammatory response as well as increased risk of infections and sepsis in observational studies. However, these studies are...
IMPORTANCE
Insomnia has been associated with altered inflammatory response as well as increased risk of infections and sepsis in observational studies. However, these studies are prone to bias, such as residual confounding. To further understand the potential causal association between insomnia and sepsis risk, a 2-sample Mendelian randomization (MR) approach should be explored.
OBJECTIVE
To evaluate whether genetically predicted insomnia is associated with risk of sepsis.
DESIGN, SETTING, AND PARTICIPANTS
Two-sample MR was performed to estimate the association between genetically predicted insomnia and sepsis risk. Data were obtained from a genome-wide association study identifying 555 independent genetic variants (R2 < 0.01) strongly associated with insomnia (P < 5 × 10-8). Sensitivity analyses were conducted to address bias due to pleiotropy and sample overlap, along with mediation analyses and sex-stratified analyses. The insomnia data set included 2.4 million individuals of European ancestry from the UK Biobank and 23andMe. For sepsis, 462 918 individuals of European ancestry from the UK Biobank were included. Data were extracted between February and December 2022 and analyzed between March 2022 and March 2023.
EXPOSURE
Genetically predicted insomnia.
MAIN OUTCOME AND MEASURE
Sepsis.
RESULTS
There were 593 724 individuals with insomnia and 10 154 cases of sepsis. A doubling in the population prevalence of genetically predicted insomnia was associated with an odds ratio of 1.37 (95% CI, 1.19-1.57; P = 7.6 × 10-6) for sepsis. Sensitivity analyses supported this observation. One-third of the association between genetically predicted insomnia and risk of sepsis was mediated through a combination of cardiometabolic risk factors for sepsis (body mass index, type 2 diabetes, smoking, or cardiovascular disease; overall proportion, 35.2%; 95% CI, 5.1-76.9). The association between insomnia and sepsis was more pronounced among women compared with men (women: odds ratio, 1.44; 95% CI, 1.24-1.68; men: OR, 1.10; 95% CI, 0.86-1.40).
CONCLUSIONS AND RELEVANCE
The concordance between these findings and previous observational studies supports that insomnia is potentially causally associated with the risk of sepsis. Thus, insomnia is a potential preventable risk factor of sepsis that should be further investigated, also in non-European populations.
Topics: Male; Humans; Female; Sleep Initiation and Maintenance Disorders; Diabetes Mellitus, Type 2; Genome-Wide Association Study; Mendelian Randomization Analysis; Sepsis; Polymorphism, Single Nucleotide
PubMed: 37556136
DOI: 10.1001/jamapsychiatry.2023.2717 -
Nature Communications Nov 2023Disrupted circadian rhythms have been linked to an increased risk of hypertension and cardiovascular disease. However, many studies show inconsistent findings and are...
Disrupted circadian rhythms have been linked to an increased risk of hypertension and cardiovascular disease. However, many studies show inconsistent findings and are not sufficiently powered for targeted subgroup analyses. Using the UK Biobank cohort, we evaluate the association between circadian rhythm-disrupting behaviours, blood pressure (SBP, DBP) and inflammatory markers in >350,000 adults with European white British ancestry. The independent U-shaped relationship between sleep length and SBP/DBP is most prominent with a low inflammatory status. Poor sleep quality and permanent night shift work are also positively associated with SBP/DBP. Although fully adjusting for BMI in the linear regression model attenuated effect sizes, these associations remain significant. Two-sample Mendelian Randomisation (MR) analyses support a potential causal effect of long sleep, short sleep, chronotype, daytime napping and sleep duration on SBP/DBP. Thus, in the current study, we present a positive association between circadian rhythm-disrupting behaviours and SBP/DBP regulation in males and females that is largely independent of age.
Topics: Adult; Male; Female; Humans; Blood Pressure; Shift Work Schedule; Biological Specimen Banks; Sleep; Circadian Rhythm; Sleep Initiation and Maintenance Disorders; Inflammation; United Kingdom
PubMed: 37925459
DOI: 10.1038/s41467-023-42758-6 -
Journal of Sleep Research Dec 2023Despite the success of cognitive behavioural therapy for insomnia and recent advances in pharmacotherapy, many patients with insomnia do not sufficiently respond to... (Review)
Review
Despite the success of cognitive behavioural therapy for insomnia and recent advances in pharmacotherapy, many patients with insomnia do not sufficiently respond to available treatments. This systematic review aims to present the state of science regarding the use of brain stimulation approaches in treating insomnia. To this end, we searched MEDLINE, Embase and PsycINFO from inception to 24 March 2023. We evaluated studies that compared conditions of active stimulation with a control condition or group. Outcome measures included standardized insomnia questionnaires and/or polysomnography in adults with a clinical diagnosis of insomnia. Our search identified 17 controlled trials that met inclusion criteria, and assessed a total of 967 participants using repetitive transcranial magnetic stimulation, transcranial electric stimulation, transcutaneous auricular vagus nerve stimulation or forehead cooling. No trials using other techniques such as deep brain stimulation, vestibular stimulation or auditory stimulation met the inclusion criteria. While several studies report improvements of subjective and objective sleep parameters for different repetitive transcranial magnetic stimulation and transcranial electric stimulation protocols, important methodological limitations and risk of bias limit their interpretability. A forehead cooling study found no significant group differences in the primary endpoints, but better sleep initiation in the active condition. Two transcutaneous auricular vagus nerve stimulation trials found no superiority of active stimulation for most outcome measures. Although modulating sleep through brain stimulation appears feasible, gaps in the prevailing models of sleep physiology and insomnia pathophysiology remain to be filled. Optimized stimulation protocols and proof of superiority over reliable sham conditions are indispensable before brain stimulation becomes a viable treatment option for insomnia.
Topics: Adult; Humans; Sleep Initiation and Maintenance Disorders; Transcranial Magnetic Stimulation; Sleep; Polysomnography; Brain; Treatment Outcome
PubMed: 37202368
DOI: 10.1111/jsr.13927 -
Journal of Advanced Research Apr 2024The causal association between modifiable risk factors and erectile dysfunction (ED) remains unclear, which hinders the early identification and intervention of patients...
INTRODUCTION
The causal association between modifiable risk factors and erectile dysfunction (ED) remains unclear, which hinders the early identification and intervention of patients with ED. The present study aimed to clarify the causal association between 42 predominant risk factors and ED.
METHODS
Univariate Mendelian Randomization (MR), multivariate MR, and mediation MR analyses were used to investigate the causal association between 42 modifiable risk factors and ED. Combined results were pooled from two independent ED genome-wide association studies to verify the findings.
RESULTS
Genetically predicted body mass index (BMI), waist circumference, trunk fat mass, whole body fat mass, poor overall health rating, type 2 diabetes, basal metabolic rate, adiponectin, cigarette consumption, insomnia, snoring, hypertension, stroke, ischemic stroke, coronary heart disease, myocardial infarction, heart failure, and major depressive disorder were found to increase the risk of ED (all P < 0.05). Additionally, genetic liability to higher body fat percentage and alcohol consumption were suggestively associated with an increased risk of ED (P < 0.05 and adjusted P > 0.05). Genetic predisposition to higher sex hormone-binding globulin (SHBG) levels could decrease the risk of ED (P < 0.05). No significant association was detected between lipid levels and ED. Multivariate MR identified type 2 diabetes, basal metabolic rate, cigarette consumption, hypertension, and coronary heart disease as risk factors for ED. The combined results confirmed that waist circumference, whole body fat mass, poor overall health rating, type 2 diabetes, basal metabolic rate, adiponectin, cigarette consumption, snoring, hypertension, ischemic stroke, coronary heart disease, myocardial infarction, heart failure, and major depressive disorder could increase the risk of ED (all P < 0.05), while higher SHBG decreased the risk of ED (P = 0.004). There were suggestive significances of BMI, insomnia, and stroke on ED (P < 0.05 and adjusted P > 0.05).
CONCLUSION
This comprehensive MR study supported the causal role of obesity, type 2 diabetes, basal metabolic rate, poor self-health rating, cigarette and alcohol consumption, insomnia and snoring, depression, hypertension, stroke, ischemic stroke, coronary heart disease, myocardial infarction, heart failure, SHBG, and adiponectin in the onset and development of ED.
Topics: Male; Humans; Diabetes Mellitus, Type 2; Adiponectin; Depressive Disorder, Major; Erectile Dysfunction; Genome-Wide Association Study; Mendelian Randomization Analysis; Sleep Initiation and Maintenance Disorders; Snoring; Risk Factors; Hypertension; Ischemic Stroke; Myocardial Infarction; Stroke; Coronary Disease; Heart Failure
PubMed: 37236543
DOI: 10.1016/j.jare.2023.05.008 -
BMC Women's Health Jul 2023Menopause is the time that marks passing 12 months after the last menstruation cycle in women between ages 40-50. Menopausal women often experience depression and...
BACKGROUND
Menopause is the time that marks passing 12 months after the last menstruation cycle in women between ages 40-50. Menopausal women often experience depression and insomnia that significantly impact their overall well-being and quality of life. This systematic review aims to determine the effects of different therapeutic physiotherapy modalities on insomnia and depression in perimenopausal, menopausal, and post-menopausal women.
METHODOLOGY
After identifying our inclusion/exclusion criteria, we conducted a database search in Ovid Embase, MIDRIS, PubMed, Cochrane, and ScienceOpen, where 4007 papers were identified. By using EndNote software, we excluded duplicates, unrelated, and non-full text papers. Adding more studies from manual search, we finally included 31 papers including 7 physiotherapy modalities: exercise, reflexology, footbath, walking, therapeutic and aromatherapy massage, craniofacial message, and yoga.
RESULTS
Reflexology, yoga, walking and aromatherapy massage showed an overall significant impact on decreasing insomnia and depression in menopausal women. Most of exercise and stretching interventions also showed improvement in sleep quality but inconsistent findings regarding depression. However, insufficient evidence was found regarding the effect of craniofacial massage, footbath, and acupressure on improving sleep quality and depression in menopausal women.
CONCLUSION
Using non-pharmaceutical interventions such as therapeutic and manual physiotherapy have an overall positive impact on reducing insomnia and depression in menopausal women.
Topics: Female; Humans; Sleep Initiation and Maintenance Disorders; Postmenopause; Perimenopause; Depression; Quality of Life; Menopause; Physical Therapy Modalities
PubMed: 37422660
DOI: 10.1186/s12905-023-02515-9 -
Emerging Topics in Life Sciences Dec 2023This review centres around the recent evidence in examining the intersection of sleep and cardiovascular disease (CVD). Sleep in this review will be further subdivided... (Review)
Review
This review centres around the recent evidence in examining the intersection of sleep and cardiovascular disease (CVD). Sleep in this review will be further subdivided to consider both sleep quantity and quality along and will also consider some of the more common sleep disorders, such as insomnia and obstructive sleep apnoea, in the context of CVD. Sleep disorders have been further explored in several specific populations which are both at risk of sleep disorders and CVD. Secondly, the review will present some of the risk factors for CVD that are affected by sleep and sleep disorders which include hypertension, diabetes, and obesity. It will also examine the potential underlying mechanisms including inflammation, appetite control, endocrine, and genetic processes that are affected by sleep and sleep disorders leading to increased risk of CVD development. In addition, we will consider the observed bi-directional relationships between sleep and cardiovascular risk factors. For example, obesity, a risk factor for CVD can be affected by sleep, but in turn can increase the risk of certain sleep disorder development which disrupts sleep, leading to further risk of obesity development and increased CVD risk. Finally, the review will explore emerging evidence around lifestyle interventions that have included a sleep component and how it impacts the management of CVD risk factor. The need for increased awareness of the health effects of poor sleep and sleep disorders will be discussed alongside the need for policy intervention to improve sleep to facilitate better health and well-being.
Topics: Humans; Cardiovascular Diseases; Sleep; Risk Factors; Obesity; Sleep Initiation and Maintenance Disorders; Sleep Wake Disorders
PubMed: 38084859
DOI: 10.1042/ETLS20230111 -
Ugeskrift For Laeger Mar 2024Improved survival after breast cancer treatment comes at a cost in the form of increased risk of late effects. A number of these are summarised in this review. The late... (Review)
Review
Improved survival after breast cancer treatment comes at a cost in the form of increased risk of late effects. A number of these are summarised in this review. The late effects can be divided in 1) late effects after locoregional treatment, e.g., lymphoedema, impaired shoulder movement, and pain; 2) consequences of systemic treatment, e.g. polyneuropathy, problems related to premature menopause, and increased risk of cardio-vascular disease; and 3) general late effects, commonly seen across all cancer types, including fatigue, insomnia, and cognitive impairment. There is a need for more knowledge about risk factors, prognoses, and the most effective treatments.
Topics: Female; Humans; Breast Neoplasms; Treatment Outcome; Sleep Initiation and Maintenance Disorders; Disease Progression; Lymphedema
PubMed: 38533874
DOI: 10.61409/V02230091 -
BMC Medicine Oct 2023Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian...
BACKGROUND
Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation, and measurement error. Thus, it is prudent to study joint effects using robust methods to propose sleep-targeted interventions which lower the risk of AMI.
METHODS
The causal interplay between combinations of two sleep traits (including insomnia symptoms, sleep duration, or chronotype) on the risk of AMI was investigated using factorial MR. Genetic risk scores for each sleep trait were dichotomized at their median in UK Biobank (UKBB) and the second survey of the Trøndelag Health Study (HUNT2). A combination of two sleep traits constituting 4 groups were analyzed to estimate the risk of AMI in each group using a 2×2 factorial MR design.
RESULTS
In UKBB, participants with high genetic risk for both insomnia symptoms and short sleep had the highest risk of AMI (hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.03, 1.18), although there was no evidence of interaction (relative excess risk due to interaction (RERI) 0.03; 95% CI -0.07, 0.12). These estimates were less precise in HUNT2 (HR 1.02; 95% CI 0.93, 1.13), possibly due to weak instruments and/or small sample size. Participants with high genetic risk for both a morning chronotype and insomnia symptoms (HR 1.09; 95% CI 1.03, 1.17) and a morning chronotype and short sleep (HR 1.11; 95% CI 1.04, 1.19) had the highest risk of AMI in UKBB, although there was no evidence of interaction (RERI 0.03; 95% CI -0.06, 0.12; and RERI 0.05; 95% CI -0.05, 0.14, respectively). Chronotype was not available in HUNT2.
CONCLUSIONS
This study reveals no interaction effects between sleep traits on the risk of AMI, but all combinations of sleep traits increased the risk of AMI except those with long sleep. This indicates that the main effects of sleep traits on AMI are likely to be independent of each other.
Topics: Humans; Sleep Initiation and Maintenance Disorders; Mendelian Randomization Analysis; Sleep; Myocardial Infarction; Risk Factors; Genome-Wide Association Study
PubMed: 37798698
DOI: 10.1186/s12916-023-03078-0