Our findings suggest that a misalignment of sleep timing is associated with metabolic risk factors that predispose to diabetes and atherosclerotic cardiovascular disease.

ABSTRACT. Objective: During adolescence, neurobiological maturation occurs concurrently with social and interpersonal changes, including the initiation of alcohol and other substance use. The National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) is designed to disentangle the complex relationships between onset, escalation, and desistance of alcohol use and changes in neurocognitive functioning and neuromaturation. Method: A sample of 831 youth, ages 12-21 years, was recruited at five sites across the United States, oversampling those at risk for alcohol use problems. Most (83%) had limited or no history of alcohol or other drug use, and a smaller portion (17%) exceeded drinking thresholds. A comprehensive assessment of biological development, family background, psychiatric symptomatology, and neuropsychological functioning-in addition to anatomical, diffusion, and functional brain magnetic resonance imaging-was completed at baseline. Results: The NCANDA sample of youth is nationally representative of sex and racial/ethnic groups. More than 50% have at least one risk characteristic for subsequent heavy drinking (e.g., family history, internalizing or externalizing symptoms). As expected, those who exceeded drinking thresholds (n = 139) differ from those who did not (n = 692) on identified factors associated with early alcohol use and problems. Conclusions: NCANDA successfully recruited a large sample of adolescents and comprehensively assessed psychosocial functioning across multiple domains. Based on the sample's risk profile, NCANDA is well positioned to capture the transition into drinking and alcohol problems in a large portion of the cohort, as well as to help disentangle the associations between alcohol use, neurobiological maturation, and neurocognitive development and functioning. (J. Stud. Alcohol Drugs, 76, 895-908, 2015)

Substance abuse is linked to numerous mental and physical health problems, including disturbed sleep. The association between substance use and sleep appears to be bidirectional, in that substance use may directly cause sleep disturbances, and difficulty sleeping may be a risk factor for relapse to substance use. Growing evidence similarly links substance use to disturbances in circadian rhythms, although many gaps in knowledge persist, particularly regarding whether circadian disturbance leads to substance abuse or dependence. Given the integral role circadian rhythms play in regulating sleep, circadian mechanisms may account in part for sleep-substance abuse interactions. Furthermore, a burgeoning research base supports a role for the circadian system in regulating reward processing, indicating that circadian mechanisms may be directly linked to substance abuse independently of sleep pathways. More work in this area is needed, particularly in elucidating how sleep and circadian disturbance may contribute to initiation of, and/or relapse to, substance use. Sleep and circadian-based interventions could play a critical role in the prevention and treatment of substance use disorders.

Objective Emerging evidence suggests the existence of bidirectional links between sleep and relational processes in dyads, but to date, this research has been primarily cross-sectional. The present analyses were undertaken to prospectively examine the directionality of the association between daily relationship functioning and nightly sleep quality and the association between couples’ relationship functioning and concordance in sleep-wake rhythms. Methods Sleep was measured via both diaries and wrist actigraphy for 7 days in 29 heterosexual co-sleeping couples. Ecological momentary assessment methods were used to characterize daily relationship functioning. Dyadic, multilevel analyses were used to examine the degree to which nightly sleep efficiency or within-couple concordance in sleep timing predicted the next day’s relational functioning and vice versa. Results In the first set of analyses, for males, higher diary-based sleep efficiency predicted less negative partner interaction the following day. For females, less negative partner interaction during the day predicted greater actigraphy-based sleep efficiency that night. Furthermore, if females reported more positive and less negative daytime partner interaction during the day, this also predicted higher diary-based sleep efficiency for their male partners that night. In the second set of analyses, among females only, lower diary- or actigraphy-based sleep onset concordance respectively predicted less positive and more negative partner interactions the next day. Conclusions Bidirectional associations appear to exist between sleep parameters and interpersonal interaction, and may represent a novel pathway linking close relationships with physical and mental health.

There is considerable evidence of circadian rhythm abnormalities in mood disorders. Morningnesseveningness, the degree to which people prefer organizing their activity and sleep patterns toward the morning or evening, is related to circadian phase and is associated with mood, with relatively greater psychological distress among evening types. Given that circadian rhythms may also relate to the Behavioral Activation System (BAS) and positive affect (PA), but not to the Behavioral Inhibition System (BIS) or negative affect (NA), it was hypothesized that individual differences in BAS sensitivity and levels of PA, but not BIS and NA, would explain the association between morningness-eveningness and depression in a sample of 208 individuals with a range of depressive symptomatology. As predicted, increasing eveningness was associated with greater depression, lower BAS, and lower PA, but not directly associated with NA. Path analyses supported a model wherein morningness-eveningness is associated with depression via multi-step indirect paths including BAS reward responsiveness, PA, and NA. A path between BIS and depression was distinct from the one involving morningness-eveningness. A variety of alternative path models all provided a weaker fit to the data. Thus, results were consistent with the BAS and PA mediating the effects of morningnesseveningness on depression.

While evening chronotype is most consistently associated with severity of mood disorder symptoms, emerging evidence implicates evening chronotype as a transdiagnostic correlate of substance use severity, anxiety symptoms, attentional difficulties, and maladaptive behaviors such as aggression. Longitudinal studies point to the possibility that evening chronotype precedes problematic substance use, depression, and anxiety. Neural processes related to reward and affective regulation may underlie associations between evening chronotype and illness. The literature on chronotype and mental illness has evolved to (1) include associations with a broader range of psychiatric symptom profiles; (2) explore underlying mechanisms; and (3) expand on earlier research using objective measures and more sophisticated study designs. In addition to further mechanistic research, additional work is needed to examine the stability and key subcomponents of the chronotype construct, as well as more attention to pediatric and special populations. This research is needed to clarify the chronotype-mental health relationship, and to identify how, when, and what aspects of chronotype can be targeted via therapeutic interventions.

Misalignment between the timing of sleep and the circadian pacemaker has been linked to depression symptoms. This study sought to extend earlier findings by comparing sleep and circadian markers in healthy controls and individuals with major depression. Two markers of circadian misalignment correlated with depression severity in the depressed group.

Sleep homeostasis and circadian function are important maintaining factors for optimal health and well-being. Conversely, sleep and circadian disruptions are implicated in a variety of adverse health outcomes, including substance use disorders. These risks are particularly salient during adolescence. Adolescents require 8 to 10 hours of sleep per night, although few consistently achieve these durations. A mismatch between developmental changes and social/environmental demands contributes to inadequate sleep. Homeostatic sleep drive takes longer to build, circadian rhythms naturally become delayed, and sensitivity to the phase-shifting effects of light increases, all of which lead to an evening preference (i.e., chronotype) during adolescence. In addition, school start times are often earlier in adolescence and the use of electronic devices at night increases, leading to disrupted sleep and circadian misalignment (i.e., social jet lag). Social factors (e.g., peer influence) and school demands further impact sleep and circadian rhythms. To cope with sleepiness, many teens regularly consume highly caffeinated energy drinks and other stimulants, creating further disruptions in sleep. Chronic sleep loss and circadian misalignment enhance developmental tendencies toward increased reward sensitivity and impulsivity, increasing the likelihood of engaging in risky behaviors and exacerbating the vulnerability to substance use and substance use disorders. We review the neurobiology of brain reward systems and the impact of sleep and circadian rhythms changes on addiction vulnerability in adolescence and suggest areas that warrant additional research.