Janna Mantua

Reliability of Sleep Measures from Four Personal Health Monitoring Devices Compared to Research-Based Actigraphy and Polysomnography

Polysomnography (PSG) is the “gold standard” for monitoring sleep. Alternatives to PSG are of interest for clinical, research, and personal use. Wrist-worn actigraph devices have been utilized in research settings for measures of sleep for over two decades. Whether sleep measures from commercially available devices are similarly valid is unknown. We sought to determine the validity of five wearable devices: Basis Health Tracker, Misfit Shine, Fitbit Flex, Withings Pulse O2, and a research-based actigraph, Actiwatch Spectrum. We used Wilcoxon Signed Rank tests to assess differences between devices relative to PSG and correlational analysis to assess the strength of the relationship. Data loss was greatest for Fitbit and Misfit. For all devices, we found no difference and strong correlation of total sleep time with PSG. Sleep efficiency differed from PSG for Withings, Misfit, Fitbit, and Basis, while Actiwatch mean values did not differ from that of PSG. Only mean values of sleep efficiency (time asleep/time in bed) from Actiwatch correlated with PSG, yet this correlation was weak. Light sleep time differed from PSG (nREM1 + nREM2) for all devices. Measures of Deep sleep time did not differ from PSG (SWS + REM) for Basis. These results reveal the current strengths and limitations in sleep estimates produced by personal health monitoring devices and point to a need for future development.

Age-related changes in the sleep-dependent reorganization of declarative memories

Consolidation of declarative memories has been associated with slow wave sleep in young adults. Previous work suggests that, in spite of changes in sleep, sleep-dependent consolidation of declarative memories may be preserved with aging, although reduced relative to young adults. Previous work on young adults shows that, with consolidation, retrieval of declarative memories gradually becomes independent of the hippocampus. To investigate whether memories are similarly reorganized over sleep at the neural level, we compared functional brain activation associated with word pair recall following a nap and equivalent wake in young and older adults. SWS during the nap predicted better subsequent memory recall and was negatively associated with retrieval-related hippocampal activation in young adults. In contrast, in older adults there was no relationship between sleep and memory performance or with retrieval-related hippocampal activation. Furthermore, compared with young adults, postnap memory retrieval in older adults required strong functional connectivity of the hippocampus with the PFC, whereas there were no differences between young and older adults in the functional connectivity of the hippocampus following wakefulness. These results suggest that, although neural reorganization takes place over sleep in older adults, the shift is unique from that seen in young adults, perhaps reflecting memories at an earlier stage of stabilization.

The interactive effects of nocturnal sleep and daytime naps in relation to serum C-reactive protein

BACKGROUND AND AIM C-reactive protein (CRP) is a general marker of inflammation that has been differentially linked with sleep. Elevated CRP (ie, high inflammation) has been associated with either short/insufficient sleep duration or long sleep duration, both, or neither. Daytime napping has also been tied to increased and decreased inflammation. We attempted to unify these findings by examining the relationship between CRP and sleep duration in conjunction with napping in a healthy young adult cohort. PARTICIPANTS Participants were young adults (mean age = 29.05 years, n = 2147) from the National Longitudinal Study of Adolescent Health (Add Health) cohort, a nationally representative longitudinal sample. METHODS/RESULTS Analysis of covariance (ANCOVA) tests examined whether self-reported sleep duration (short, medium, or long) and nap frequency (none-few days/week; most days/week; every day) interacted in relation to CRP. Standard covariates (ie, age, gender, race/ethnicity, body mass index, physical activity, depression, snoring, systolic blood pressure, clinical symptoms, and household income) were used. There was a linear increase in CRP with increased napping [contrast estimate = 0.265, 95% confidence interval (CI) (0.045-0.485), P = 0.018]. There was also an interaction between sleep duration and napping frequency in relation to CRP (F4,2128 = 2.90, P = 0.021). Inflammation differed between nap groups within the long and short sleep groups. CONCLUSIONS Our results suggest that increased napping is an independent predictor of inflammation in young adults. These results also provide evidence for interactive effects of inflammation, nocturnal sleep, and daytime naps. Our findings confirm that excess sleep, insufficient sleep, frequent napping, and infrequent napping can all be linked with elevated CRP, but these relationships depend on both nocturnal and daytime sleep patterns. These analyses will guide future work to more specifically examine sleep-inflammation processes and directionality.

Altered sleep composition after traumatic brain injury does not affect declarative sleep-dependent memory consolidation

Individuals with a history of traumatic brain injury (TBI) often report sleep disturbances, which may be caused by changes in sleep architecture or reduced sleep quality (greater time awake after sleep onset, poorer sleep efficiency, and sleep stage proportion alterations). Sleep is beneficial for memory formation, and herein we examine whether altered sleep physiology following TBI has deleterious effects on sleep-dependent declarative memory consolidation. Participants learned a list of word pairs in the morning or evening, and recall was assessed 12-h later, following an interval awake or with overnight sleep. Young adult participants (18–22 years) were assigned to one of four experimental groups: TBI Sleep (n = 14), TBI Wake (n = 12), non-TBI Sleep (n = 15), non-TBI Wake (n = 15). Each TBI participant was >1 year post-injury. Sleep physiology was measured with polysomnography. Memory consolidation was assessed by comparing change in word-pair recall over 12-h intersession intervals. The TBI group spent a significantly greater proportion of the night in SWS than the non-TBI group at the expense of NREM1. The TBI group also had marginally lower EEG delta power during SWS in the central region. Intersession changes in recall were greater for intervals with sleep than without sleep in both groups. However, despite abnormal sleep stage proportions for individuals with a TBI history, there was no difference in the intersession change in recall following sleep for the TBI and non-TBI groups. In both Sleep groups combined, there was a positive correlation between Intersession Change and the proportion of the night in NREM2 + SWS. Overall, sleep composition is altered following TBI but such deficits do not yield insufficiencies in sleep-dependent memory consolidation.

Novel word learning in older adults: A role for sleep?

HighlightsSleep is beneficial for language learning in children and young adults.Older adults have deficits in both sleep quality and language usage.Language learning may be reduced as a consequence of sleep deficits associated with aging. Abstract Sleep is an offline period during which newly acquired semantic information is transformed into longer‐lasting memories. Language acquisition, which requires new word learning and semantic integration, is preferentially benefitted by a period of sleep in children and young adults. Specific features of sleep (e.g., sleep stage characteristics) have been associated with enhanced language acquisition and generalization. However, with increasing age, even in healthy individuals, sleep quality and quantity decrease. Simultaneously, deficits in word retrieval and new word learning emerge. Yet it is unknown whether age‐related alterations in language ability are linked with alterations in sleep. The goal of this review is to examine changes in language learning and sleep across the lifespan. We consider how sleep detriments that occur with aging could affect abilities to learn novel words and semantic generalization and propose hypotheses to motivate future research in this area.

A systematic review and meta-analysis of sleep architecture and chronic traumatic brain injury

Sleep quality appears to be altered by traumatic brain injury (TBI). However, whether persistent post-injury changes in sleep architecture are present is unknown and relatively unexplored. We conducted a systematic review and meta-analysis to assess the extent to which chronic TBI (>6 months since injury) is characterized by changes to sleep architecture. We also explored the relationship between sleep architecture and TBI severity. In the fourteen included studies, sleep was assessed with at least one night of polysomnography in both chronic TBI participants and controls. Statistical analyses, performed using Comprehensive Meta-Analysis software, revealed that chronic TBI is characterized by relatively increased slow wave sleep (SWS). A meta-regression showed moderate-severe TBI is associated with elevated SWS, reduced stage 2, and reduced sleep efficiency. In contrast, mild TBI was not associated with any significant alteration of sleep architecture. The present findings are consistent with the hypothesis that increased SWS after moderate-severe TBI reflects post-injury cortical reorganization and restructuring. Suggestions for future research are discussed, including adoption of common data elements in future studies to facilitate cross-study comparability, reliability, and replicability, thereby increasing the likelihood that meaningful sleep (and other) biomarkers of TBI will be identified.

Sleep Physiology Correlations and Human Memory Consolidation: Where Do We Go From Here?

Dear Editor, The search for a reliable link between sleep physiology and improvement in memory performance attributed to sleep (i.e., sleep-dependent memory consolidation) has spanned several decades [1]. In the late 1990s, in an attempt to probe causality, researchers began correlating sleep markers (e.g., time in a sleep stage) with memory enhancement over sleep. From these studies, and from corresponding work in animal models (e.g., Ref. [2]), hypotheses of sleep physiology-dependent memory consolidation in humans were established and have endured. Put simply, it is generally believed that declarative memory consolidation predominantly relies on SWS duration or features (e.g., spectral power in the δ frequency range), motor consolidation predominantly relies on N2 duration or features (e.g., sleep spindles and σ power), and emotional processing or consolidation predominantly relies on REM duration or features (e.g., θ power). However, since the establishment of these hypotheses, countless empirical human investigations have failed to detect hypothesized correlations between sleep and memory consolidation, even when sleep-dependent consolidation has clearly occurred. Moreover, various studies have detected negative correlations when a positive correlation is expected [3–5] or have conducted more correlations than statistically appropriate [6– 10], resulting in findings that are likely spurious and thus not credible (the author of this letter is guilty of the latter transgression). Often, when hypothesized correlations are not detected, researchers attempt to find a post hoc explanation for results, either by adjusting hypotheses or by attributing findings to subtle differences or inadequacies in study design [3,8,11]. Although this may not seem to be a substantial issue in the field, null, negative, or spurious correlations are not without cost, as they may lead to timeand resource-consuming experimentation based on results from previous work. Additionally, at times, investigations that do not detect a hypothesized correlation (i.e., a purportedly causal link) between sleep physiology and behavior are considered substandard (e.g., less worthy of a high-impact journal). As such, the continued use of this convention could be detrimental to the field. At academic conferences and through personal correspondence, researchers freely discuss the need to move away from the over-utilization of sleep physiology correlations. Nevertheless, many feel that they are expected to conduct these analyses, either by colleagues or by a manuscript reviewer. Herein, in response to this issue, findings that demonstrate there is not a direct (i.e., 1:1) relationship between sleep physiology and human memory consolidation are discussed. This evidence is presented in an attempt to demonstrate that correlations should not be used to link sleep physiology with sleep-dependent memory consolidation. Subsequently, alternative statistical and methodological approaches are presented. It is hoped that this letter will (1) provide justification for researchers to move away from this convention and (2) propel the field in a more conservative, yet informative, direction.

The role of sleep in emotional memory processing in middle age

&NA; Sleep benefits memory in young adults, and this effect may be particularly strong for representations associated with negative emotion. Many aspects of sleep important for memory consolidation change with aging, particularly by middle age, suggesting that sleep‐related consolidation may be reduced. However, the influence of sleep on memory has rarely been investigated in a middle‐aged population. In the current study, young and middle‐aged adults viewed negative and neutral pictures and underwent a recognition test after sleep or wake. Subjective emotional reactivity was also measured. Compared to waking, sleep benefited memory in young adults. Performance did not differ between sleep and wake groups in middle‐aged adults, and it matched the level of young adults who slept. The effect of sleep versus wake was not influenced by memory valence in either age group. These results suggest the relative influence of sleep compared to wake on memory declines with aging, specifically by middle age, and that this decline extends to negative memory.

Sleep Quality and Emotion Regulation Interact to Predict Anxiety in Veterans with PTSD

Posttraumatic stress disorder (PTSD) is a debilitating and common consequence of military service. PTSD is associated with increased incidence of mood disturbances (e.g., anxiety). Additionally, veterans with PTSD often have poor-quality sleep and poor emotion regulation ability. We sought to assess whether such sleep and emotion regulation deficits contribute to mood disturbances. In 144 veterans, using a double moderation model, we tested the relationship between PTSD and anxiety and examined whether sleep quality and emotion regulation interact to moderate this relationship. We found that PTSD predicts higher anxiety in veterans with poor and average sleep quality who utilize maladaptive emotion regulation strategies. However, there was no relationship between PTSD and anxiety in individuals with good sleep quality, regardless of emotion regulation. Similarly, there was no relationship between PTSD and anxiety in individuals with better emotion regulation, regardless of sleep quality. Results were unchanged when controlling for history of traumatic brain injury (TBI), despite the fact that those with both PTSD and TBI had the poorest emotion regulation overall. Taken together, these results suggest that good-quality sleep may be protective against poor emotion regulation in veterans with PTSD. Sleep may therefore be a target for therapeutic intervention in veterans with PTSD and heightened anxiety.