Objective
Adolescence is a developmental stage of critical changes in sleep and its circadian timing when the contribution of abnormal sleep variability (amount) and sleep regularity (timing) to ...obesity and its associated adverse cardiometabolic health outcomes appears to increase. The aim of this study was to summarize findings from studies conducted in adolescents examining both sleep variability and regularity in relation to obesity and cardiometabolic health. Gaps in research and potential causal pathways that future studies should examine are highlighted.
Results
Nightly deviations in sleep duration and sleep midpoint appear to contribute to the development of obesity and associated adverse cardiometabolic outcomes in youth. Studies show that increased sleep variability and irregularity are associated with obesity, decreased physical activity, dysregulated eating and inadequate diet, metabolic dysfunction, impaired cardiac autonomic balance, and elevated blood pressure in adolescents.
Conclusions
A stable circadian timing of sleep is essential to the overall physical well‐being of youth. Emerging evidence supports that sleep variability and circadian misalignment, including sleep irregularity, contribute to adverse obesity‐related health outcomes early on in adolescence. Future studies should focus on the underlying behavioral and biological mechanisms in the causal pathway between day‐to‐day deviations in the amount and timing of sleep and obesity.
Summary
Insomnia nosology has significantly evolved since the Diagnostic and Statistical Manual (DSM)‐III‐R first distinguished between ‘primary’ and ‘secondary’ insomnia. Prior International ...Classification of Sleep Disorders (ICSD) nosology ‘split’ diagnostic phenotypes to address insomnia's heterogeneity and the DSM nosology ‘lumped’ them into primary insomnia, while both systems assumed causality for insomnia secondary to health conditions. In this systematic review, we discuss the historical phenotypes in prior insomnia nosology, present findings for currently proposed insomnia phenotypes based on more robust approaches, and critically appraise the most relevant ones. Electronic databases PsychINFO, PubMED, Web of Science, and references of eligible articles, were accessed to find diagnostic manuals, literature on insomnia phenotypes, including systematic reviews or meta‐analysis, and assessments of the reliability or validity of insomnia diagnoses, identifying 184 articles. The data show that previous insomnia diagnoses lacked reliability and validity, leading current DSM‐5‐TR and ICSD‐3 nosology to ‘lump’ phenotypes into a single diagnosis comorbid with health conditions. However, at least two new, robust insomnia phenotyping approaches were identified. One approach is multidimensional‐multimethod and provides evidence for self‐reported insomnia with objective short versus normal sleep duration linked to clinically relevant outcomes, while the other is multidimensional and provides evidence for two to five clusters (phenotypes) based on self‐reported trait, state, and/or life‐history data. Some approaches still need replication to better support whether their findings identify true phenotypes or simply different patterns of symptomatology. Regardless, these phenotyping efforts aim at improving insomnia nosology both as a classification system and as a mechanism to guide treatment.
Background
A high comorbidity between attention‐deficit/hyperactivity disorder (ADHD) and obstructive sleep apnea (OSA) as well as similar impairments across neurobehavioral outcomes has been ...described in children. However, there is a paucity of research examining the comorbidity of these two disorders in adolescents. This study examined the association of OSA with sleep, neurobehavioral, and cardiometabolic outcomes in adolescents with ADHD from the general population.
Methods
421 adolescents (16.9 ± 2.3 years, 53.9% male) underwent 9‐hr polysomnography, neurobehavioral, and physical evaluation. ADHD was ascertained by a parent‐or‐self‐report of a lifetime diagnosis/treatment of ADHD. OSA was defined as an apnea hypopnea index of ≥2 events/hour. Groups of controls (n = 208), OSA‐alone (n = 115), ADHD‐alone (n = 54), and ADHD+OSA (n = 44) were studied. Multivariable‐adjusted general linear models tested group differences in PSG parameters, neurobehavioral, and cardiometabolic outcomes after controlling for sex, race/ethnicity, age, and/or body mass index percentile.
Results
The ADHD+OSA group had significantly longer sleep onset latency, shorter total sleep time, lower sleep efficiency, and higher percent of stage 1 sleep, as compared with all other groups, however, these differences were diminished by excluding adolescents on psychoactive medication. The ADHD‐alone group showed significantly higher periodic limb movements than controls. The ADHD+OSA and ADHD‐alone groups did not significantly differ on any measure of neurocognitive or behavioral functioning. The ADHD+OSA and OSA‐alone groups showed significantly worse cardiometabolic and inflammatory biomarkers when compared to controls or the ADHD‐alone, but did not significantly differ between each other.
Conclusions
Adolescents with a diagnosis ADHD+OSA showed phenotypic risk factors for OSA (i.e., overweight/obesity, visceral adiposity, metabolic syndrome, and inflammation) but not worse neurobehavioral outcomes when compared with ADHD‐alone. While comorbidity is possible, these data support that adolescents with a suspicion of ADHD should be screened for OSA, before a diagnosis is reached and psychoactive medication initiated.
Summary
Longitudinal studies that have examined the association of insomnia with incident depression using objective sleep measures are very limited. The aim of this study was to examine the ...predictive role of the severity of insomnia for incident depression in a general population sample using psychometric and polysomnographic data. From a random, general population sample of 1741 individuals of the Penn State Adult Cohort, 1137 adults without depression were followed up with a structured telephone interview after 7.5 years. All subjects completed a full medical evaluation, 1‐night polysomnogram and Multiphasic Minnesota Personality Inventory at baseline. The incidence of depression was 15%. Poor sleep (odds ratio = 1.5, P = 0.001) and insomnia (odds ratio = 1.9, P = 0.031) were significantly associated with incident depression. The odds of incident depression were highest (odds ratio = 2.2, P = 0.019) in insomnia with objective short sleep duration and independent of Multiphasic Minnesota Personality Inventory Ego Strength scores, an index of poor coping resources. The persistence of insomnia and worsening of poor sleep into insomnia significantly increased the odds of incident depression (odds ratios ranged from 1.8 to 6.3), whereas their full remission did not (odds ratio ranged from 1.2 to 1.8). Insomnia with short sleep duration is associated with incident depression independent of poor coping resources, whereas the association of insomnia with normal sleep duration with incident depression was mediated by poor coping resources. Persistence and worsening of poor sleep or insomnia, but not their full remission, are significant predictors of incident depression. These data suggest that there is a significant relationship between the severity of insomnia and incident depression.
Because insomnia with objective short sleep duration is associated with increased morbidity, we examined the effects of this insomnia subtype on all-cause mortality.
Longitudinal.
Sleep laboratory.
...1,741 men and women randomly selected from Central Pennsylvania.
Participants were studied in the sleep laboratory and were followed-up for 14 years (men) and 10 years (women). "Insomnia" was defined by a complaint of insomnia with duration > or = 1 year. "Normal sleeping" was defined as absence of insomnia. Polysomnographic sleep duration was classified into two categories: the "normal sleep duration group" subjects who slept > or = 6 h and the "short sleep duration group" subjects who slept < 6 h. We adjusted for age, race, education, body mass index, smoking, alcohol, depression, sleep disordered breathing, and sampling weight.
The mortality rate was 21% for men and 5% for women. In men, mortality risk was significantly increased in insomniacs who slept less than 6 hours compared to the "normal sleep duration, no insomnia" group, (OR = 4.00, CI 1.14-13.99) after adjusting for diabetes, hypertension, and other confounders. Furthermore, there was a marginally significant trend (P = 0.15) towards higher mortality risk from insomnia and short sleep in patients with diabetes or hypertension (OR = 7.17, 95% CI 1.41-36.62) than in those without these comorbid conditions (OR = 1.45, 95% CI 0.13-16.14). In women, mortality was not associated with insomnia and short sleep duration.
Insomnia with objective short sleep duration in men is associated with increased mortality, a risk that has been underestimated.
To examine whether cognitive-emotional hyperarousal is a premorbid characteristic of middle-aged and young good sleepers vulnerable to stress-related insomnia.
Self-reported information was collected ...from two samples of 305 middle-aged and 196 young adults. From those adults, 149 middle-aged (50.34 +/- 4.47 years) and 85 young (20.19 +/- 1.31 years) good sleepers were selected for the present study. The Ford Insomnia Response to Stress Test (FIRST) was used to measure vulnerability to stress-related insomnia. Trait measures of personality, arousability, rumination, presleep arousal, and coping skills were entered as predictors in the linear regression models, at the same time controlling for gender, depression, and anxiety.
The regression models showed that arousability (beta = 0.546), neuroticism (beta = 0.413), perceived stress (beta = 0.375), and rumination (beta = 0.214) were associated with FIRST scores in middle-aged adults. Among young adults, the regression models revealed that presleep cognitive arousal (beta = 0.448), arousability (beta = 0.426), neuroticism (beta = 0.320), presleep somatic arousal (beta = 0.290), emotion-oriented coping (beta = 0.220), and rumination (beta = 0.212) were associated with FIRST scores. Finally, individuals with high FIRST scores did not show lower scores in measures of cognitive-emotional hyperarousal compared with chronic insomniacs.
These data suggest that cognitive-emotional hyperarousal may be a premorbid characteristic of subjects vulnerable to insomnia. It seems that maladaptive coping stress strategies and cognitive-emotional hyperarousal predispose to the development of insomnia and that interventions targeting these characteristics may be important in the prevention and treatment of chronic insomnia.
Obstructive sleep apnea (OSA) is an increasingly prevalent sleep disorder characterized by upper airway obstruction during sleep, resulting in breathing pauses, intermittent hypoxia, and fragmented ...sleep. In parallel, the constellation of adverse health outcomes associated with prolonged obesity, such as insulin resistance, elevated blood pressure, triglycerides, and reduced high-density lipoprotein cholesterol – termed metabolic syndrome –raises the risk of cardiovascular morbidity and mortality, type 2 diabetes, and all-cause mortality. Affecting 35–40% of U.S. adults, risk factors for metabolic syndrome, including obesity, middle age, sedentary behavior, and genetics, share considerable overlap with those for OSA. Thus, it has been difficult to disentangle cause, effect, and whether certain treatments, such as CPAP, can improve these outcomes. In this paper, we provide an update to our 2005 review which explored the association between OSA and metabolic syndrome, highlighting visceral obesity as the common etiological factor of both conditions. This update includes (a) recent data on physiological and biochemical mechanisms, (b) new data in nonobese men and women as well as children and adolescents, (c) insight from the latest treatment studies, (d) the role of aging in understanding clinically-meaningful phenotypes of the disorder, and (e) the potential diagnostic/prognostic utility of biomarkers in identifying OSA patients with the strongest cardiometabolic risk.
About 5.4%-45.7% of the general population has mild-to-moderate obstructive sleep apnea (mmOSA), which is highly comorbid with cardiovascular and/or cerebrovascular diseases (CBVD). We examined the ...association between mmOSA and all-cause mortality and the modifying effect of age and CBVD. A total of 1681 adults 20-88 years old from the Penn State Adult Cohort (PSAC) (41.9% male) were followed up for 20.1 ± 6.2 years for all-cause mortality. Mild and moderate OSA were defined as an apnea/hypopnea index (AHI) 5-14.9 and 15-29.9 events/hour, respectively. CBVD was defined as a report of a physician diagnosis or treatment for heart disease and/or stroke. Cox proportional hazards regression models were used to estimate all-cause mortality adjusted for confounders. All-cause mortality risk was significantly increased in the mmOSA group in young and middle-aged adults (<60 years) (HR = 1.59, 95%CI 1.08-2.04) but not in older adults (≥60 years) (HR = 1.05, 95%CI 0.80-1.39). A synergistic effect between mmOSA and CBVD was stronger in those <60 years (HR = 3.82, 95%CI 2.25-6.48 in <60 years vs 1.86 95%CI 1.14-3.04 in ≥60 years). There was an additive effect between moderate OSA and hypertension in <60 but not in those ≥60 years. Mild OSA was associated with all-cause mortality only in the presence of CBVD. Mortality risk is increased in young and middle-aged adults with moderate OSA, whereas the mortality risk associated with mild OSA is elevated only, regardless of age, in the presence of comorbid CBVD. AHI cut-offs warranting treatment of mmOSA may need to be adjusted based on age and comorbidities.
Background Cardiovascular and cerebrovascular diseases (CBVDs) and cancer are leading causes of death. Short sleep is a potential contributor to health; however, its role in predicting mortality ...associated with cardiometabolic risk factors (CMRs) and CBVD remains poorly understood. We tested whether objective short sleep duration increases the risk of mortality associated with CMRs and CBVD. Methods and Results A total of 1654 adults (aged 20-74 years) from the Penn State Adult Cohort (47.5 years, 52.5% women, and 89.8% white) whose cause of death was determined after 19.2 years (5.2 years). CMR was defined as stage 2 hypertension and/or type 2 diabetes mellitus on the basis of blood pressure and glucose levels or a report of diagnosis or treatment for these conditions. CBVD was defined as a report of diagnosis or treatment for heart disease and/or stroke. Objective short sleep duration was defined as polysomnographic total sleep time <6 hours. Cox proportional hazard models estimated multivariable-adjusted hazard ratios (HRs) and 95% CIs. Risk of all-cause mortality associated with CMR or CBVD was significantly modified by objective sleep duration (
<0.05), and it was significantly higher in subjects who slept <6 hours (HR, 2.14 95% CI, 1.52-3.02 and HR, 3.17 95% CI=2.16-4.65, respectively). In subjects who slept <6 hours, CMR was associated with a 1.83 higher (95% CI, 1.07-3.13) risk of CBVD mortality and CBVD with a 2.92 higher (95% CI, 1.28-6.65) risk of cancer mortality. In subjects who slept ≥6 hours, CMR was not significantly associated with CBVD mortality (HR, 1.35; 95% CI, 0.70-2.63) nor was CBVD significantly associated with cancer mortality (HR, 0.55; 95% CI, 0.18-1.64). Conclusions Objective short sleep duration predicts the all-cause mortality prognosis of middle-aged adults with CMR and the cancer-specific mortality prognosis of those with CBVD.
Background
Insomnia has been associated in cross‐sectional studies with increased beta (15–35 Hz) electroencephalogram (EEG) power during nonrapid eye movement (NREM) sleep, an index of cortical ...hyperarousal. However, it is unknown whether this cortical hyperarousal is present before individuals with insomnia develop the disorder. To fill this gap, we examined the association of childhood sleep high‐frequency EEG activity with incident insomnia symptoms (i.e., absence of insomnia symptoms in childhood but presence in adolescence).
Methods
We studied a case–control subsample of 45 children (6–11 years) from the Penn State Child Cohort, a population‐based random sample of 421 children, who were followed up after 8 years as adolescents (13–20 years). We examined low‐beta (15–25 Hz) and high‐beta (25–35 Hz) relative power at central EEG derivations during NREM sleep and, in secondary analyses, during sleep onset latency, sleep onset, and REM sleep. Incident insomnia symptoms were defined as the absence of parent‐reported difficulty falling and/or staying asleep during childhood and a self‐report of these insomnia symptoms during adolescence.
Results
Childhood high‐beta power during NREM sleep was significantly increased in children who developed insomnia symptoms in adolescence (n = 25) as compared to normal sleeping controls (n = 20; p = .03). Multivariable‐adjusted logistic regression models showed that increased childhood high‐beta EEG power during NREM sleep was associated with a threefold increased odds (95% CI = 1.12–7.98) of incident insomnia symptoms in adolescence. No other significant relationships were observed for other sleep/wake states or EEG frequency bands.
Conclusions
Increased childhood high‐frequency EEG power during NREM sleep is associated with incident insomnia symptoms in adolescence. This study indicates that cortical hyperarousal during sleep may be a premorbid neurophysiological sign of insomnia, which may mediate the increased risk of psychiatric disorders associated with insomnia.
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