Risk for depression tripled during the COVID-19 pandemic in emerging adults followed for the last 8 years.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has significantly increased depression rates, particularly in emerging adults. The aim of this study was to examine longitudinal changes in depression risk before and during COVID-19 in a cohort of emerging adults in the U.S. and to determine whether prior drinking or sleep habits could predict the severity of depressive symptoms during the pandemic. METHODS: Participants were 525 emerging adults from the National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA), a five-site community sample including moderate-to-heavy drinkers. Poisson mixed-effect models evaluated changes in the Center for Epidemiological Studies Depression Scale (CES-D-10) from before to during COVID-19, also testing for sex and age interactions. Additional analyses examined whether alcohol use frequency or sleep duration measured in the last pre-COVID assessment predicted pandemic-related increase in depressive symptoms. RESULTS: The prevalence of risk for clinical depression tripled due to a substantial and sustained increase in depressive symptoms during COVID-19 relative to pre-COVID years. Effects were strongest for younger women. Frequent alcohol use and short sleep duration during the closest pre-COVID visit predicted a greater increase in COVID-19 depressive symptoms. CONCLUSIONS: The sharp increase in depression risk among emerging adults heralds a public health crisis with alarming implications for their social and emotional functioning as this generation matures. In addition to the heightened risk for younger women, the role of alcohol use and sleep behavior should be tracked through preventive care aiming to mitigate this looming mental health crisis.

Prior test experience confounds longitudinal tracking of adolescent cognitive and motor development.

BACKGROUND: Accurate measurement of trajectories in longitudinal studies, considered the gold standard method for tracking functional growth during adolescence, decline in aging, and change after head injury, is subject to confounding by testing experience. METHODS: We measured change in cognitive and motor abilities over four test sessions (baseline and three annual assessments) in 154 male and 165 female participants (baseline age 12-21 years) from the National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) study. At each of the four test sessions, these participants were given a test battery using computerized administration and traditional pencil and paper tests that yielded accuracy and speed measures for multiple component cognitive (Abstraction, Attention, Emotion, Episodic memory, Working memory, and General Ability) and motor (Ataxia and Speed) functions. The analysis aim was to dissociate neurodevelopment from testing experience by using an adaptation of the twice-minus-once tested method, which calculated the difference between longitudinal change (comprising developmental plus practice effects) and practice-free initial cross-sectional performance for each consecutive pairs of test sessions. Accordingly, the first set of analyses quantified the effects of learning (i.e., prior test experience) on accuracy and after speed domain scores. Then developmental effects were  determined for each domain for accuracy and speed having removed the measured learning effects. RESULTS: The greatest gains in performance occurred between the first and second sessions, especially in younger participants, regardless of sex, but practice gains continued to accrue thereafter for several functions. For all 8 accuracy composite scores, the developmental effect after accounting for learning was significant across age and was adequately described by linear fits. The learning-adjusted developmental effects for speed were adequately described by linear fits for Abstraction, Emotion, Episodic Memory, General Ability, and Motor scores, although a nonlinear fit was better for Attention, Working Memory, and Average Speed scores. CONCLUSION: Thus, what appeared as accelerated cognitive and motor development was, in most cases, attributable to learning. Recognition of the substantial influence of prior testing experience is critical for accurate characterization of normal development and for developing norms for clinical neuropsychological investigations of conditions affecting the brain.

Recommendations for Identifying Valid Wear for Consumer-Level Wrist-Worn Activity Trackers and Acceptability of Extended Device Deployment in Children.

BACKGROUND: Self-reported physical activity is often inaccurate. Wearable devices utilizing multiple sensors are now widespread. The aim of this study was to determine acceptability of Fitbit Charge HR for children and their families, and to determine best practices for processing its objective data. METHODS: Data were collected via Fitbit Charge HR continuously over the course of 3 weeks. Questionnaires were given to each child and their parent/guardian to determine the perceived usability of the device. Patterns of data were evaluated and best practice inclusion criteria recommended. RESULTS: Best practices were established to extract, filter, and process data to evaluate device wear, r and establish minimum wear time to evaluate behavioral patterns. This resulted in usable data available from 137 (89%) of the sample. CONCLUSIONS: Activity trackers are highly acceptable in the target population and can provide objective data over longer periods of wear. Best practice inclusion protocols that reflect physical activity in youth are provided.

Adolescent alcohol use disrupts functional neurodevelopment in sensation seeking girls.

Exogenous causes, such as alcohol use, and endogenous factors, such as temperament and sex, can modulate developmental trajectories of adolescent neurofunctional maturation. We examined how these factors affect sexual dimorphism in brain functional networks in youth drinking below diagnostic threshold for alcohol use disorder (AUD). Based on the 3-year, annually acquired, longitudinal resting-state functional magnetic resonance imaging (MRI) data of 526 adolescents (12-21 years at baseline) from the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) cohort, developmental trajectories of 23 intrinsic functional networks (IFNs) were analyzed for (1) sexual dimorphism in 259 participants who were no-to-low drinkers throughout this period; (2) sex-alcohol interactions in two age- and sex-matched NCANDA subgroups (N = 76 each), half no-to-low, and half moderate-to-heavy drinkers; and (3) moderating effects of gender-specific alcohol dose effects and a multifactorial impulsivity measure on IFN connectivity in all NCANDA participants. Results showed that sex differences in no-to-low drinkers diminished with age in the inferior-occipital network, yet girls had weaker within-network connectivity than boys in six other networks. Effects of adolescent alcohol use were more pronounced in girls than boys in three IFNs. In particular, girls showed greater within-network connectivity in two motor networks with more alcohol consumption, and these effects were mediated by sensation-seeking only in girls. Our results implied that drinking might attenuate the naturally diminishing sexual differences by disrupting the maturation of network efficiency more severely in girls. The sex-alcohol-dose effect might explain why women are at higher risk of alcohol-related health and psychosocial consequences than men.

Influences of Age, Sex, and Moderate Alcohol Drinking on the Intrinsic Functional Architecture of Adolescent Brains.

The transition from adolescent to adult cognition and emotional control requires neurodevelopmental maturation likely involving intrinsic functional networks (IFNs). Normal neurodevelopment may be vulnerable to disruption from environmental insult such as alcohol consumption commonly initiated during adolescence. To test potential disruption to IFN maturation, we used resting-state functional magnetic resonance imaging (rs-fMRI) in 581 no-to-low alcohol-consuming and 117 moderate-to-high-drinking youth. Functional seed-to-voxel connectivity analysis assessed age, sex, and moderate alcohol drinking on default-mode, executive-control, salience, reward, and emotion networks and tested cognitive and motor coordination correlates of network connectivity. Among no-to-low alcohol-consuming adolescents, executive-control frontolimbicstriatal connectivity was stronger in older than younger adolescents, particularly boys, and predicted better ability in balance, memory, and impulse control. Connectivity patterns in moderate-to-high-drinking youth were tested mainly in late adolescence when drinking was initiated. Implicated was the emotion network with attenuated connectivity to default-mode network regions. Our cross-sectional rs-fMRI findings from this large cohort of adolescents show sexual dimorphism in connectivity and suggest neurodevelopmental rewiring toward stronger and spatially more distributed executive-control networking in older than younger adolescents. Functional network rewiring in moderate-to-high-drinking adolescents may impede maturation of affective and self-reflection systems and obscure maturation of complex social and emotional behaviors.

Reducing bedtime physiological arousal levels using immersive audio-visual respiratory bio-feedback: a pilot study in women with insomnia symptoms.

Hyperarousal is a critical component of insomnia, particularly at bedtime when individuals are trying to fall asleep. The current study evaluated the effect of a novel, acute behavioral experimental manipulation (combined immersive audio-visual relaxation and biofeedback) in reducing bedtime physiological hyperarousal in women with insomnia symptoms. After a clinical/adaptation polysomnographic (PSG) night, sixteen women with insomnia symptoms had two random-order PSG nights: immersive audio-visual respiratory bio-feedback across the falling asleep period (manipulation night), and no pre-sleep arousal manipulation (control night). While using immersive audio-visual respiratory bio-feedback, overall heart rate variability was increased and heart rate (HR) was reduced (by ~ 5 bpm; p < 0.01), reflecting downregulation of autonomic pre-sleep arousal, relative to no-manipulation. HR continued to be lower during sleep, and participants had fewer awakenings and sleep stage transitions on the manipulation night relative to the control night (p < 0.05). The manipulation did not affect sleep onset latency or other PSG parameters. Overall, this novel behavioral approach targeting the falling asleep process emphasizes the importance of pre-sleep hyperarousal as a potential target for improving sleep and nocturnal autonomic function during sleep in insomnia.

The Sleep of the Ring: Comparison of the OURA Sleep Tracker Against Polysomnography.

Objective/Background: To evaluate the performance of a multisensor sleep-tracker (OURA ring) against polysomnography (PSG) in measuring sleep and sleep stages. Participants: Forty-one healthy adolescents and young adults (13 females; Age: 17.2 ± 2.4 years). Methods: Sleep data were recorded using the OURA ring and standard PSG on a single laboratory overnight. Metrics were compared using Bland-Altman plots and epoch-by-epoch (EBE) analysis. Results: Summary variables for sleep onset latency (SOL), total sleep time (TST), and wake after sleep onset (WASO) were not different between OURA ring and PSG. PSG-OURA discrepancies for WASO were greater in participants with more PSG-defined WASO (p < .001). Compared with PSG, OURA ring underestimated PSG N3 (~20 min) and overestimated PSG REM (~17 min; p < .05). PSG-OURA differences for TST and WASO lay within the ≤ 30 min a-priori-set clinically satisfactory ranges for 87.8% and 85.4% of the sample, respectively. From EBE analysis, OURA ring had a 96% sensitivity to detect sleep, and agreement of 65%, 51%, and 61%, in detecting "light sleep" (N1), "deep sleep" (N2 + N3), and REM sleep, respectively. Specificity in detecting wake was 48%. Similarly to PSG-N3 (p < .001), "deep sleep" detected with the OURA ring was negatively correlated with advancing age (p = .001). OURA ring correctly categorized 90.9%, 81.3%, and 92.9% into PSG-defined TST ranges of < 6 hr, 6-7 hr, > 7 hr, respectively. Conclusions: Multisensor sleep trackers, such as the OURA ring have the potential for detecting outcomes beyond binary sleep-wake using sources of information in addition to motion. While these first results could be viewed as promising, future development and validation are needed.

Effects of sleep on substance use in adolescents: a longitudinal perspective.

Substance use (SU) and sleep problems appear interrelated, but few studies have examined the influence of adolescent sleep patterns on development of SU disorders. This study prospectively examined the influence of sleep habits on subsequent SU in youth who later transitioned into heavy drinking. At time 1 (T1), participants (n = 95) were substance-naive 12- to 14-year-olds. Path-analytic models examined whether the effects of T1 risk factors (familial SU disorder, inhibition control, and externalizing and internalizing traits) on time 3 (M = 19.8 years old) tobacco, alcohol, and cannabis were mediated by time 2 (M = 15.1 years old) sleep chronotype, daytime sleepiness, and erratic sleep/wake behaviors. Significant direct path effects of T1 risk factors and time 2 sleep behaviors on time 3 SU were found, Ps < 0.05. In models that examined the effect of each individual sleep behavior separately on SU, more erratic sleep/wake and greater daytime sleepiness predicted higher lifetime use events for all substances (Ps < 0.01). Higher evening chronotype tendencies predicted lower tobacco and higher alcohol and cannabis lifetime use events (Ps < 0.01). Erratic sleep/wake behaviors mediated the effect of inhibitory control on subsequent SU; less erratic sleep/wake behaviors predicted better inhibition control ( ß̂= -0.20, P < 0.05). Early-mid adolescent psychiatric health and sleep behaviors prior to drinking onset predicted greater SU 5 years later. Participants were substance-naïve at baseline, allowing for the examination of temporal order in the relationship between sleep problems and alcohol use. Early adolescent sleep problems may be an important risk factor for SU in later life.

Eveningness and Later Sleep Timing Are Associated with Greater Risk for Alcohol and Marijuana Use in Adolescence: Initial Findings from the National Consortium on Alcohol and Neurodevelopment in Adolescence Study.

BACKGROUND: Abundant cross-sectional evidence links eveningness (a preference for later sleep-wake timing) and increased alcohol and drug use among adolescents and young adults. However, longitudinal studies are needed to examine whether eveningness is a risk factor for subsequent alcohol and drug use, particularly during adolescence, which is marked by parallel peaks in eveningness and risk for the onset of alcohol use disorders. This study examined whether eveningness and other sleep characteristics were associated with concurrent or subsequent substance involvement in a longitudinal study of adolescents. METHODS: Participants were 729 adolescents (368 females; age 12 to 21 years) in the National Consortium on Alcohol and Neurodevelopment in Adolescence study. Associations between the sleep variables (circadian preference, sleep quality, daytime sleepiness, sleep timing, and sleep duration) and 3 categorical substance variables (at-risk alcohol use, alcohol bingeing, and past-year marijuana use [y/n]) were examined using ordinal and logistic regression with baseline age, sex, race, ethnicity, socioeconomic status, and psychiatric problems as covariates. RESULTS: At baseline, greater eveningness was associated with greater at-risk alcohol use, greater bingeing, and past-year use of marijuana. Later weekday and weekend bedtimes, but not weekday or weekend sleep duration, showed similar associations across the 3 substance outcomes at baseline. Greater baseline eveningness was also prospectively associated with greater bingeing and past-year use of marijuana at the 1-year follow-up, after covarying for baseline bingeing and marijuana use. Later baseline weekday and weekend bedtimes, and shorter baseline weekday sleep duration, were similarly associated with greater bingeing and past-year use of marijuana at the 1-year follow-up after covarying for baseline values. CONCLUSIONS: Findings suggest that eveningness and sleep timing may be under recognized risk factors and future areas of intervention for adolescent involvement in alcohol and marijuana that should be considered along with other previously identified sleep factors such as insomnia and insufficient sleep.

Adolescent Development of Cortical and White Matter Structure in the NCANDA Sample: Role of Sex, Ethnicity, Puberty, and Alcohol Drinking.

Brain structural development continues throughout adolescence, when experimentation with alcohol is often initiated. To parse contributions from biological and environmental factors on neurodevelopment, this study used baseline National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) magnetic resonance imaging (MRI) data, acquired in 674 adolescents meeting no/low alcohol or drug use criteria and 134 adolescents exceeding criteria. Spatial integrity of images across the 5 recruitment sites was assured by morphological scaling using Alzheimer's disease neuroimaging initiative phantom-derived volume scalar metrics. Clinical MRI readings identified structural anomalies in 11.4%. Cortical volume and thickness were smaller and white matter volumes were larger in older than in younger adolescents. Effects of sex (male > female) and ethnicity (majority > minority) were significant for volume and surface but minimal for cortical thickness. Adjusting volume and area for supratentorial volume attenuated or removed sex and ethnicity effects. That cortical thickness showed age-related decline and was unrelated to supratentorial volume is consistent with the radial unit hypothesis, suggesting a universal neural development characteristic robust to sex and ethnicity. Comparison of NCANDA with PING data revealed similar but flatter, age-related declines in cortical volumes and thickness. Smaller, thinner frontal, and temporal cortices in the exceeds-criteria than no/low-drinking group suggested untoward effects of excessive alcohol consumption on brain structural development.

Harmonizing DTI measurements across scanners to examine the development of white matter microstructure in 803 adolescents of the NCANDA study.

Neurodevelopment continues through adolescence, with notable maturation of white matter tracts comprising regional fiber systems progressing at different rates. To identify factors that could contribute to regional differences in white matter microstructure development, large samples of youth spanning adolescence to young adulthood are essential to parse these factors. Recruitment of adequate samples generally relies on multi-site consortia but comes with the challenge of merging data acquired on different platforms. In the current study, diffusion tensor imaging (DTI) data were acquired on GE and Siemens systems through the National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA), a multi-site study designed to track the trajectories of regional brain development during a time of high risk for initiating alcohol consumption. This cross-sectional analysis reports baseline Tract-Based Spatial Statistic (TBSS) of regional fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (L1), and radial diffusivity (LT) from the five consortium sites on 671 adolescents who met no/low alcohol or drug consumption criteria and 132 adolescents with a history of exceeding consumption criteria. Harmonization of DTI metrics across manufacturers entailed the use of human-phantom data, acquired multiple times on each of three non-NCANDA participants at each site's MR system, to determine a manufacturer-specific correction factor. Application of the correction factor derived from human phantom data measured on MR systems from different manufacturers reduced the standard deviation of the DTI metrics for FA by almost a half, enabling harmonization of data that would have otherwise carried systematic error. Permutation testing supported the hypothesis of higher FA and lower diffusivity measures in older adolescents and indicated that, overall, the FA, MD, and L1 of the boys were higher than those of the girls, suggesting continued microstructural development notable in the boys. The contribution of demographic and clinical differences to DTI metrics was assessed with General Additive Models (GAM) testing for age, sex, and ethnicity differences in regional skeleton mean values. The results supported the primary study hypothesis that FA skeleton mean values in the no/low-drinking group were highest at different ages. When differences in intracranial volume were covaried, FA skeleton mean reached a maximum at younger ages in girls than boys and varied in magnitude with ethnicity. Our results, however, did not support the hypothesis that youth who exceeded exposure criteria would have lower FA or higher diffusivity measures than the no/low-drinking group; detecting the effects of excessive alcohol consumption during adolescence on DTI metrics may require longitudinal study.

Partial K-Complex Recovery Following Short-Term Abstinence in Individuals with Alcohol Use Disorder.

BACKGROUND: The K-complex (KC) is a brain potential characteristic of nonrapid eye movement (NREM) sleep resulting from the synchronous activity of a large population of neurons and hypothesized to reflect brain integrity. KC amplitude is lower in individuals with alcohol use disorder (AUD) compared with age-matched controls, but its recovery with short-term abstinence has not been studied. Therefore, we investigated whether the KC shows significant recovery over the first 4 months of abstinence in individuals with AUD. METHODS: A total of 16 recently abstinent AUD individuals (46.6 ± 9.3 years) and 13 gender and age-matched healthy controls (41.6 ± 8.3 years) were studied on 3 occasions: the Initial session was within 1 month of the AUD individuals' last drink, then 1 and 3 months later. Overnight electroencephalogram was recorded while participants were presented with tones during stage 2 NREM sleep to elicit KCs. RESULTS: At the Initial session, AUD participants showed significantly lower KC amplitude and incidence compared with controls. In the AUD individuals, KC amplitude increased significantly from the Initial to the 1-month session. KC incidence showed a marginally significant increase. Neither KC amplitude nor incidence changed from the 1-month to the 3-month session. No changes in KC amplitude or incidence across sessions were observed in the control group. CONCLUSIONS: Our results demonstrate partial KC recovery during the first 2 months of abstinence. This recovery is consistent with the time course of structural brain recovery in abstinent AUD individuals demonstrated by recent neuroimaging results.

The acute effects of alcohol on sleep electroencephalogram power spectra in late adolescence.

BACKGROUND: Alcohol's effect on sleep electroencephalogram (EEG) power spectra during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption and major sleep-related developmental changes in quantitative EEG measures. This study examined the effect of alcohol on sleep EEG power spectra in 18- to 21-year-old college students. METHODS: Participants were 24 (12 female) healthy 18- to 21-year-old social drinkers. Participants underwent 2 conditions: presleep alcohol and placebo, followed by standard polysomnography with comprehensive EEG recordings. RESULTS: After alcohol, mean breath alcohol concentration at lights-out was 0.084%. Interaction effects indicated simultaneous increases in frontal non-rapid eye movement sleep (NREM) delta (p = 0.031) and alpha (p = 0.005) power in the first sleep cycles following alcohol consumption which was most prominent at frontal scalp sites (p < 0.001). A decrease in sigma power (p = 0.001) was also observed after alcohol. CONCLUSIONS: As hypothesized, alcohol increased slow wave sleep-related NREM delta power. However, there was a simultaneous increase in frontal alpha power. Results suggest that alcohol may exert an arousal influence which may compete with the sleep maintenance influence of increased delta activity. The phenomenon is similar to, or the same as, alpha-delta sleep which has been associated with the presence of disruptive stimuli during sleep. This may have negative implications for the impact of presleep alcohol consumption on sleep and consequent daytime functioning.

Poor autonomic nervous system functioning during sleep in recently detoxified alcohol-dependent men and women.

BACKGROUND: Alcoholism is considered an important risk factor for cardiovascular (CV) disease. Autonomic nervous system (ANS) function is a major indicator of CV health. Sleep is a suitable model to investigate ANS activity free from wake-related confounders. We investigated nighttime ANS functioning, and the relation between ANS activity and severity of alcohol dependence in chronic alcoholism. METHODS: Fourteen recently abstaining alcoholics (age: 42.0 ± 9.0 years, 7 women) and 16 age- and sex-matched controls (age: 45.2 ± 9.1 years, 8 women) underwent a night of standard clinical polysomnography, including electrocardiographic recording. Time- and frequency-domain spectral analysis of heart rate variability (HRV) was performed across hours of the night and during artifact-free epochs of stable sleep and wakefulness (presleep wakefulness, rapid-eye-movement [REM], and non-REM sleep). RESULTS: Alcoholics had a poorer subjective and objective sleep quality compared to controls. Across the night, alcoholic men and women had elevated heart rate, reduced total HRV, that is, lower standard deviation of normal-to-normal interbeat intervals, and reduced high frequency (HF) activity (assessed by the HF power and by the square root of the mean squared of successive heart period differences). This ANS pattern was most apparent at the beginning of the night. None of the ANS measures was associated with lifetime alcohol consumption or duration of alcohol dependence. CONCLUSIONS: Our results show that ANS functioning is disrupted during the night, even in undisturbed sleep periods, indicating poor CV functioning in recently detoxified alcohol-dependent men and women.

Respiratory and auditory cortical processing in children with obstructive sleep apnea syndrome.

RATIONALE: Children with obstructive sleep apnea syndrome (OSAS) have impaired cortical processing of respiratory afferent stimuli, manifested by blunted sleep respiratory-related evoked potentials (RREP). However, whether this impairment is limited to respiratory stimuli, or reversible after successful treatment, is unknown. We hypothesized that, during sleep, children with OSAS have (1) abnormal RREP, (2) normal cortical processing of nonrespiratory stimuli, and (3) persistence of abnormal RREP after treatment. OBJECTIVES: To measure sleep RREP and auditory evoked potentials in normal control subjects and children with OSAS before and after treatment. METHODS: Twenty-four children with OSAS and 24 control subjects were tested during N3 sleep. Thirteen children with OSAS repeated testing 4-6 months after adenotonsillectomy. MEASUREMENTS AND MAIN RESULTS: RREP were blunted in OSAS compared with control subjects (N350 at Cz -27 ± 15.5 vs. -47.4 ± 28.5 µV; P = 0.019), and did not improve after OSAS treatment (N350 at Cz pretreatment -25.1 ± 7.4 vs. -29.8 ± 8.1 post-treatment). Auditory evoked potentials were similar in OSAS and control subjects at baseline (N350 at Cz -58 ± 33.1 vs. -66 ± 31.1 µV), and did not change after treatment (N350 at Cz -67.5 ± 36.8 vs. -65.5 ± 20.3). CONCLUSIONS: Children with OSAS have persistent primary or irreversible respiratory afferent cortical processing deficits during sleep that could put them at risk of OSAS recurrence. OSAS does not seem to affect the cortical processing of nonrespiratory (auditory) afferent stimuli during sleep.

Variation in longitudinal trajectories of regional brain volumes of healthy men and women (ages 10 to 85 years) measured with atlas-based parcellation of MRI.

Numerous cross-sectional MRI studies have characterized age-related differences in regional brain volumes that differ with structure and tissue type. The extent to which cross-sectional assumptions about change are accurate depictions of actual longitudinal measurement remains controversial. Even longitudinal studies can be limited by the age range of participants, sex distribution of the samples, and scan intervals. To address these issues, we calculated trajectories of regional brain volume changes from T1-weighted (SPGR) MRI data, quantified with our automated, unsupervised SRI24 atlas-based registration and parcellation method. Longitudinal MRIs were acquired at 3T in 17 boys and 12 girls, age 10 to 14 years, and 41 men and 41 women, age 20 to 85 years at first scan. Application of a regression-based correction function permitted merging of data acquired at 3T field strength with data acquired at 1.5T from additional subjects, thereby expanding the sample to a total of 55 men and 67 women, age 20 to 85 years at first scan. Adjustment for individual supratentorial volume removed regional volume differences between men and women due to sex-related differences in head size. Individual trajectories were computed from data collected on 2 to 6 MRIs at a single field strength over a ~1 to 8 year interval. Using linear mixed-effects models, the pattern of trajectories over age indicated: rises in ventricular and Sylvian fissure volumes, with older individuals showing faster increases than younger ones; declines in selective cortical volumes with faster tissue shrinkage in older than younger individuals; little effect of aging on volume of the corpus callosum; more rapid expansion of CSF-filled spaces in men than women after age 60 years; and evidence for continued growth in central white matter through early adulthood with accelerated decline in senescence greater in men than women.

The acute effects of alcohol on sleep architecture in late adolescence.

BACKGROUND: Alcohol consumption is prevalent in late adolescence; however, little is known about its effect on sleep in this group. In mature adults, alcohol decreases sleep onset latency (SOL) and sleep efficiency (SE) and increases wake after sleep onset (WASO). It also increases slow wave sleep (SWS) and decreases rapid eye movement (REM) sleep in the first half of the night, with the inverse occurring in the second half. Alcohol's effect on sleep during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption and significant developmental changes in the central nervous system. This study examined the effect of alcohol on sleep architecture in women and men aged 18 to 21 years and whether previously reported sleep architecture effects may have been as an artificial result of changes to sleep cycle length. METHODS: Twenty-four (12 women) healthy 18- to 21-year-old light social drinkers (19.1 ± 1.0 years) underwent 2 conditions: presleep alcohol (target breath alcohol concentration [BAC] 0.10%) and placebo-administered under controlled conditions, followed by standard polysomnography. RESULTS: In the alcohol condition, mean BAC at lights out was 0.084 ± 0.016%. Time in bed, total sleep time, and SOL (all p > 0.05) did not differ between conditions. However, there was less REM (p = 0.011) and more stage-2 sleep (p = 0.035) in the alcohol condition. Further, alcohol increased SWS (p = 0.02) and decreased REM sleep (p < 0.001) in the first half of the night and disrupted sleep in the second half, with increased WASO (interaction: p = 0.034), and decreased SE (p = 0.04) and SWS (p = 0.01) and no REM sleep rebound in the second half of the night (p = 0.262). Additionally, alcohol had no effect on sleep cycle length (p = 0.598). CONCLUSIONS: The results were broadly consistent with the adult literature with the novel extension that half night sleep architecture effects could not be attributed to changes in sleep cycle length. However, alcohol did not reduce SOL, or result in a REM rebound following reduced REM in the first half of the night. The results suggest that the effects of alcohol on sleep are modified by sleep's prevailing developmental stage.

Effects of emerging alcohol use on developmental trajectories of functional sleep measures in adolescents.

STUDY OBJECTIVES: Adolescence is characterized by significant brain development, accompanied by changes in sleep timing and architecture. It also is a period of profound psychosocial changes, including the initiation of alcohol use; however, it is unknown how alcohol use affects sleep architecture in the context of adolescent development. We tracked developmental changes in polysomnographic (PSG) and electroencephalographic (EEG) sleep measures and their relationship with emergent alcohol use in adolescents considering confounding effects (e.g. cannabis use). METHODS: Adolescents (n = 94, 43% female, age: 12-21 years) in the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) study had annual laboratory PSG recordings across 4-years. Participants were no/low drinkers at baseline. RESULTS: Linear mixed effect models showed developmental changes in sleep macrostructure and EEG, including a decrease in slow wave sleep and slow wave (delta) EEG activity with advancing age. Emergent moderate/heavy alcohol use across three follow-up years was associated with a decline in percentage rapid eye movement (REM) sleep over time, a longer sleep onset latency (SOL) and shorter total sleep time (TST) in older adolescents, and lower non-REM delta and theta power in males. CONCLUSIONS: These longitudinal data show substantial developmental changes in sleep architecture. Emergent alcohol use during this period was associated with altered sleep continuity, architecture, and EEG measures, with some effects dependent on age and sex. These effects, in part, could be attributed to the effects of alcohol on underlying brain maturation processes involved in sleep-wake regulation.

Perceived poor sleep quality in the absence of polysomnographic sleep disturbance in women with severe premenstrual syndrome.

Women with severe premenstrual syndrome report sleep-related complaints in the late-luteal phase, but few studies have characterized sleep disturbances prospectively. This study evaluated sleep quality subjectively and objectively using polysomnographic and quantitative electroencephalographic measures in women with severe premenstrual syndrome. Eighteen women with severe premenstrual syndrome (30.5 ± 7.6 years) and 18 women with minimal symptoms (controls, 29.2 ± 7.3 years) had polysomnographic recordings on one night in each of the follicular and late-luteal phases of the menstrual cycle. Women with premenstrual syndrome reported poorer subjective sleep quality when symptomatic in the late-luteal phase compared with the follicular phase (P < 0.05). However, there were no corresponding changes in objective sleep quality. Women with premenstrual syndrome had more slow-wave sleep and slow-wave activity than controls at both menstrual phases (P < 0.05). They also had higher trait-anxiety, depression, fatigue and perceived stress levels than controls at both phases (P < 0.05) and mood worsened in the late-luteal phase. Both groups showed similar menstrual-phase effects on sleep, with increased spindle frequency activity and shorter rapid eye movement sleep episodes in the late-luteal phase. In women with premenstrual syndrome, a poorer subjective sleep quality correlated with higher anxiety (r = -0.64, P = 0.005) and more perceived nighttime awakenings (r = -0.50, P = 0.03). Our findings show that women with premenstrual syndrome perceive their sleep quality to be poorer in the absence of polysomnographically defined poor sleep. Anxiety has a strong impact on sleep quality ratings, suggesting that better control of mood symptoms in women with severe premenstrual syndrome may lead to better subjective sleep quality.

Growth trajectories of cognitive and motor control in adolescence: How much is development and how much is practice?

OBJECTIVE: Executive control continues to develop throughout adolescence and is vulnerable to alcohol use. Although longitudinal assessment is ideal for tracking executive function development and onset of alcohol use, prior testing experience must be distinguished from developmental trajectories. METHOD: We used the Stroop Match-to-Sample task to examine the improvement of processing speed and specific cognitive and motor control over 4 years in 445 adolescents. The twice-minus-once-tested method was used and expanded to four test sessions to delineate prior experience (i.e., learning) from development. A General Additive Model evaluated the predictive value of age and sex on executive function development and potential influences of alcohol use on development. RESULTS: Results revealed strong learning between the first two assessments. Adolescents significantly improved their speed processing over 4 years. Compared with boys, girls enhanced ability to control cognitive interference and motor reactions. Finally, the influence of alcohol use initiation was tested over 4 years for development in 110 no/low, 110 moderate/heavy age- and sex-matched drinkers; alcohol effects were not detected in the matched groups. CONCLUSIONS: Estimation of learning effects is crucial for examining developmental changes longitudinally. (PsycInfo Database Record (c) 2022 APA, all rights reserved).