Introduction Many factors contribute to sleep disturbance among young adults. Social media (SM) use is increasing rapidly, and little is known regarding its association with sleep disturbance. Methods In 2014 we assessed a nationally-representative sample of 1788 U.S. young adults ages 19-32. SM volume and frequency were assessed by self-reported minutes per day spent on SM (volume) and visits per week (frequency) using items adapted from the Pew Internet Research Questionnaire. We assessed sleep disturbance using the brief Patient-Reported Outcomes Measurement Information System (PROMIS®) Sleep Disturbance measure. Analyses performed in Pittsburgh utilized chi-square tests and ordered logistic regression using sample weights in order to estimate effects for the total U.S. population. Results In models that adjusted for all sociodemographic covariates, participants with higher SM use volume and frequency had significantly greater odds of having sleep disturbance. For example, compared with those in the lowest quartile of SM use per day, those in the highest quartile had an AOR of 1.95 (95% CI = 1.37-2.79) for sleep disturbance. Similarly, compared with those in the lowest quartile of SM use frequency per week, those in the highest quartile had an AOR of 2.92 (95% CI = 1.97-4.32) for sleep disturbance. Associations all demonstrated a significant linear trend. Discussion The strong association between SM use and sleep disturbance has important clinical implications for the health and well-being of young adults. Future work should aim to assess directionality and to better understand the influence of contextual factors associated with SM use.

Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with diffi culty falling asleep, frequent nighttime awakenings with diffi culty returning to sleep, and/or awakening earlier in the morning than desired. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment.The aims of this report are (1) to summarize current knowledge on the pathophysiology of insomnia and (2) to present a model of the pathophysiology of insomnia that considers evidence from various domains of research. Working within several models of insomnia, evidence for the pathophysiology of the disorder is presented across levels of analysis, from genetic to molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and self-report. We discuss the role of hyperarousal as an overarching theme that guides our conceptualization of insomnia. Finally, we propose a model of the pathophysiology of insomnia that integrates the various types of evidence presented.

Serotonin reuptake inhibitors may increase symptoms of anxiety immediately following treatment initiation. The present study examined whether acute citalopram increased fear-potentiated startle to predictable and/or unpredictable shocks in healthy subjects. Eighteen healthy subjects each received two treatments, placebo and 20 mg citalopram in a crossover design. Participants were exposed to three conditions including one in which predictable aversive shocks were signaled by a cue, a second in which unpredictable shocks were anticipated, and a third in which no shocks were administered. Changes in aversive states were investigated using acoustic startle stimuli. Citalopram did not affect baseline startle. However, the phasic startle potentiation to the threat cue in the predictable condition was robustly increased by acute citalopram. The sustained startle potentiation in the unpredictable conditions was also increased by citalopram, but only when the drug was given during the first session. These results indicate that a single dose of citalopram is not anxiogenic in itself, but can exacerbate the expression of fear and anxiety.

SM use in the 30 minutes before bed is independently associated with disturbed sleep among young adults. Future work should use qualitative and experimental methods to further elucidate the directionality of-and mechanisms underlying-this association.

Objectives We conducted a randomized, controlled trial comparing the efficacy of an Integrated Risk Reduction Intervention (IRRI) to a control condition with the objective of improving mood stability and psychosocial functioning by reducing cardiometabolic risk factors in overweight/obese patients with bipolar I disorder. Methods A total of 122 patients were recruited from our outpatient services and randomly allocated to IRRI (n = 61) or psychiatric care with medical monitoring (n = 61). Individuals allocated to IRRI received psychiatric treatment and assessment, medical monitoring by a nurse, and a healthy lifestyle program from a lifestyle coach. Those allocated to the control condition received psychiatric treatment and assessment and referral, if indicated, for medical problems. A mixed-effects model was used to examine the impact of the interventions on body mass index (BMI). Exploratory moderator analyses were used to characterize those individuals likely to benefit from each treatment approach. Results Analyses were conducted on the IRRI (n = 58) and control (n = 56) participants with ≥ 1 study visit. IRRI was associated with significantly greater rate of decrease in BMI (d = −0.51, 95% confidence interval: −0.91 to −0.14). Three variables (C-reactive protein, total cholesterol, and instability of total sleep time) contributed to a combined moderator of faster decrease in BMI with IRRI treatment. Conclusions Overweight/obese patients with bipolar disorder can make modest improvements in BMI, even when taking medications with known potential for weight gain. Our finding that a combination of three baseline variables provides a profile of patients likely to benefit from IRRI will need to be tested further to evaluate its utility in clinical practice.

Objectives Disruptions in sleep and dysregulation in circadian functioning may represent core abnormalities in the pathophysiology of bipolar disorder (BP). However, it is not clear whether these dysfunctions are “state” or “trait” markers of BP. This report compared sleep and circadian phenotypes among three groups: offspring of bipolar parents diagnosed with (BP/OB; n=47) and without (non-BP/OB; n=386) BP at intake and offspring of matched control parents who did not have BP (controls; n=301). We also examined the association of baseline sleep parameters with subsequent development of BP among the non-BP/OB group. Methods Pittsburgh Bipolar Offspring Study youth (ages 6-18) and their parents completed assessments every two years pertaining to child's sleep and circadian phenotypes and current psychopathology. Mixed-effects models examined differences on baseline sleep and circadian variables among the three groups. Results BP/OB offspring who were in a mood episode differed significantly on sleep parameters from the non-BP/OB and the offspring of controls, such as having inadequate sleep. Mixed logistic regression procedures showed that baseline sleep and circadian variables, such as frequent waking during the night, significantly predicted the development of BP among non-BP/OB over longitudinal follow-up. Conclusions While lifetime diagnostic status accounted for differences among the groups on sleep and circadian disturbances, psychopathology explained the differences even further. Additionally, sleep disturbance may be a prognostic indicator of the development of BP in high-risk youth. Future studies are required to further disentangle whether sleep and circadian disruption are state or trait features of BP.

community stakeholders regarding obstructive sleep apnea. (3) Increase the proportion of students in grades 9 through 12 who get sufficient sleep and (4) Perform trials aimed at improving adherence to treatments for sleep-disordered breathing (particularly evaluating cognitive therapy approaches). The fourth priority area was identified as an important barrier to implementation science efforts in sleep.

Background Depressed patients with comorbid personality pathology may fare worse in treatment for depression than those without this additional pathology, and comorbid personality pathology may be associated with superior response in one form of treatment relative to another, though recent findings have been mixed. We aimed to evaluate the effect of personality pathology on time to remission of patients randomly assigned to 1 of 2 treatment strategies for depression and to determine whether personality pathology moderated the effect of treatment assignment on outcome. Method Individuals undergoing an episode of unipolar major depression (n = 275) received interpersonal psychotherapy (Klerman, Weissman, Rounsaville, & Chevron, 1984) or selective serotonin reuptake inhibitor (SSRI) pharmacotherapy for depression. Depressive symptoms were measured with the HRSD-17. Remission was a mean HRSD-17 score of 7 or below over a period of 3 weeks. Personality disorders were measured according to SCID-II diagnoses, and personality pathology was measured dimensionally by summing the positive probes on the SCID-II. Results The presence of at least 1 personality disorder was not a significant predictor of time to remission, but a higher level of dimensionally measured personality pathology and the presence of borderline personality disorder were associated with a longer time to remission. Personality pathology did not moderate the effect of treatment assignment on time to remission. Conclusions The findings suggest that depressed individuals with comorbid personality pathology generally fare worse in treatment for depression, although in this report, the effect of personality pathology did not differ by the type of treatment received.