Links Between Objectively-Measured Hourly Smartphone Use and Adolescent Wake Events Across Two Weeks.

PURPOSE: Psychosocial and bioregulatory pressures threaten sleep during adolescence. Although recent work suggests that the ubiquity of smartphone use throughout adolescence may also relate to poorer sleep outcomes, most existing research relies upon self-report and retrospective measures. This study drew upon objective measures of smartphone use and sleep at the hourly level to understand how smartphone use was associated with the duration of wake events during sleeping hours. METHODS: Across a 14-day daily study, 59 racially and ethnically diverse adolescents ages 15 to 18 had their sleep assessed via Fitbit Inspire 2 devices and uploaded screenshots of their screen time, pickups, and notifications as logged by their iPhone's iOS. Multi-level modeling was performed to assess hourly level associations between adolescent smartphone use and wake-events during their sleep sessions (N = 4,287 hourly cases). RESULTS: In hours during adolescents' sleep session with more screen time or pickups, adolescents had longer wake event duration. More notifications in a given hour were not associated with wake event duration in the same hour. CONCLUSIONS: Using objectively measured smartphone and sleep data collected at the hourly level, we found that during sleeping hours, when adolescents are actively engaging with their smartphones, their sleep is disrupted, such that their wake events are longer in that hour.

Linking video chatting, phone calling, text messaging, and social media with peers to adolescent connectedness.

For 14 days three times per day (6072 observations), adolescents (N = 207, Mage = 15.45 years) reported their digital (i.e., video chatting, texting, social media, and phone calling) communication with peers and their social connectedness. Controlling for in-person interactions, adolescents felt more connected in hours when they had communicated with peers by video chatting, texting, or social media, but not phone calling. Girls communicated with peers via text and social media more than boys, and boys talked on the phone more than girls. Boys who talked, texted, or video chatted more on average reported higher connectedness on average, whereas girls did not. As the links with connectedness were only found at the hourly- and not the daily level, results highlight that a sense of connectedness from digital media may be fleeting in nature.

ß-Adrenergic Contributions to Emotion and Physiology During an Acute Psychosocial Stressor.

OBJECTIVE: ß-Adrenergic receptor signaling, a critical mediator of sympathetic nervous system influences on physiology and behavior, has long been proposed as one contributor to subjective stress. However, prior findings are surprisingly mixed about whether ß-blockade (e.g., propranolol) blunts subjective stress, with many studies reporting no effects. We reevaluated this question in the context of an acute psychosocial stressor with more comprehensive measures and a larger-than-typical sample. We also examined the effects of ß-blockade on psychophysiological indicators of sympathetic and parasympathetic nervous system reactivity, given that ß-blockade effects for these measures specifically under acute psychosocial stress are not yet well established. METHODS: In a double-blind, randomized, placebo-controlled study, 90 healthy young adults received 40 mg of the ß-blocker propranolol or placebo. Participants then completed the Trier Social Stress Test, which involved completing an impromptu speech and difficult arithmetic in front of evaluative judges. Self-reported emotions and appraisals as well as psychophysiology were assessed throughout. RESULTS: Propranolol blunted Trier Social Stress Test preejection period reactivity (b = 9.68, p = .003), a marker of sympathetic nervous system activity, as well as salivary α-amylase reactivity (b = -0.50, p = .006). Critically, propranolol also blunted negative, high arousal emotions in response to the stressor (b = -0.22, p = .026), but cognitive appraisals remained intact (b values < -0.17, p values > .10). CONCLUSIONS: These results provide updated experimental evidence that ß-adrenergic blockade attenuates negative, high arousal emotions in response to a psychosocial stressor while also blunting sympathetic nervous system reactivity. Together, these findings shed light on the neurophysiological mechanisms by which stressors transform into the subjective experience we call "stress."Trial Registration: ClinicalTrials.gov Identifier: NCT02972554.

Beta-adrenergic blockade blunts inflammatory and antiviral/antibody gene expression responses to acute psychosocial stress.

Dysregulation of the immune system is one potential mechanism by which acute stress may contribute to downstream disease etiology and psychopathology. Here, we tested the role of ß-adrenergic signaling as a mediator of acute stress-induced changes in immune cell gene expression. In a randomized, double-blind, and placebo-controlled trial, 90 healthy young adults (44% female) received a single 40 mg dose of the ß-blocker propranolol (n = 43) or a placebo (n = 47) and then completed the Trier Social Stress Test (TSST). Pre- and post-stress blood samples were assayed for prespecified sets of pro-inflammatory and antiviral/antibody gene transcripts. Analyses revealed increased expression of both inflammatory and antiviral/antibody-related genes in response to the TSST, and these effects were blocked by pre-treatment with propranolol. Bioinformatics identified natural killer cells and dendritic cells as the primary cellular context for transcriptional upregulation, and monocytes as the primary cellular carrier of genes downregulated by the TSST. These effects were in part explained by acute changes in circulating cell types. Results suggest that acute psychosocial stress can induce an "acute defense" molecular phenotype via ß-adrenergic signaling that involves mobilization of natural killer cells and dendritic cells at the expense of monocytes. This may represent an adaptive response to the risk of acute injury. These findings offer some of the first evidence in humans that ß-blockade attenuates psychosocial stress-induced increases in inflammatory gene expression, offering new insights into the molecular and immunologic pathways by which stress may confer risks to health and well-being.