Regulation of Adolescent Sleep: Implications for Behavior

Adolescent development is accompanied by profound changes in the timing and amounts of sleep and wakefulness. Many aspects of these changes result from altered psychosocial and life-style circumstances that accompany adolescence. The maturation of biological processes regulating sleep/wake systems, however, may be strongly related to the sleep timing and amount during adolescence-either as "compelling" or "permissive" factors. The two-process model of sleep regulation posits a fundamental sleep-wake homeostatic process (process S) working in concert with the circadian biological timing system (process C) as the primary intrinsic regulatory factors. How do these systems change during adolescence? We present data from adolescent participants examining EEG markers of sleep homeostasis to evaluate whether process S shows maturational changes permissive of altered sleep patterns across puberty. Our data indicate that certain aspects of the homeostatic system are unchanged from late childhood to young adulthood, while other features change in a manner that is permissive of later bedtimes in older adolescents. We also show alterations of the circadian timing system indicating a possible circadian substrate for later adolescent sleep timing. The circadian parameters we have assessed include phase, period, melatonin secretory pattern, light sensitivity, and phase relationships, all of which show evidence of changes during pubertal development with potential to alter sleep patterns substantially. However the changes are mediated-whether through process S, process C, or by a combination-many adolescents have too little sleep at the wrong circadian phase. This pattern is associated with increased risks for excessive sleepiness, difficulty with mood regulation, impaired academic performance, learning difficulties, school tardiness and absenteeism, and accidents and injuries

Sleep patterns are associated with common illness in adolescents

This prospective, field-based study examined the association between actigraphically-measured total sleep time and incident illness including cold, flu, gastroenteritis, and other common infectious diseases (e.g., strep throat) in adolescents over the course of a school semester. Participants were 56 adolescents ages 14–19 years (mean = 16.6 (standard deviation = 1.2), 39% male) from 5 high schools in Rhode Island. Beginning in late January, adolescents wore actigraphs (mean 91 (19) days, range 16 – 112 days) and were assigned post-hoc to Longer or Shorter sleep groups based on median splits. Adolescents were interviewed weekly across as many as 16 weeks (modal number of interviews = 13) using a structured protocol that included 14 health event questions. Illness events and illness-related school absences were coded for 710 completed interviews, with 681 illness events and 90 school absences reported. Outcomes (illness bouts, illness duration, and absences) were compared among sex, sleep, and academic year groups using non-parametric regression. In a subset of 18 subjects, mean actigraphically estimated total sleep time 6 nights before matched illness/wellness events was compared using MANOVA. Longer sleepers and males reported fewer illness bouts; total sleep time effects were more apparent in males than females. A trend was found for shorter total sleep time before ill events. The present findings in this small naturalistic sample indicate that acute illnesses were more frequent in otherwise healthy adolescents with shorter sleep, and illness events were associated with less sleep during the prior week than comparable matched periods without illness

Adolescence and parental history of alcoholism: insights from the sleep EEG

BACKGROUND Disrupted sleep is a common complaint of individuals with alcohol use disorder and in abstinent alcoholics. Furthermore, among recovering alcoholics, poor sleep predicts relapse to drinking. Whether disrupted sleep in these populations results from prolonged alcohol use or precedes the onset of drinking is not known. The aim of this study was to examine the sleep electroencephalogram (EEG) in alcohol-naïve, parental history positive (PH+), and negative (PH-) boys and girls. METHODS All-night sleep EEG recordings in 2 longitudinal cohorts (child and teen) followed at 1.5 to 3 year intervals were analyzed. The child and teen participants were 9/10 and 15/16 years old at the initial assessment, respectively. Parental history status was classified by Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria applied to structured interviews (DIS-IV) resulting in 14 PH- and 10 PH+ children and 14 PH- and 10 PH+ teens. Sleep data were visually scored in 30-second epochs using standard criteria. Power spectra were calculated for EEG derivations C3/A2, C4/A1, O2/A1, O1/A2 for nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. RESULTS We found no difference between PH+ and PH- individuals in either cohort for any visually scored sleep stage variable. Spectral power declined in both cohorts across assessments for NREM and REM sleep in all derivations and across frequencies independent of parental history status. With regard to parental history, NREM sleep EEG power was lower for the delta band in PH+ teens at both assessments for the central derivations. Furthermore, power in the sigma band for the right occipital derivation in both NREM and REM sleep was lower in PH+ children only at the initial assessment. CONCLUSIONS We found no gross signs of sleep disruption as a function of parental history. Modest differences in spectral EEG power between PH+ and PH- children and teens indicate that a marker of parental alcohol history may be detectable in teens at risk for problem drinking

Sleep_December.indd

Study Objectives: This analysis examined associations between the salivary dim light melatonin onset (DLMO) phase and self-selected sleep/ wake schedules in groups of children and adolescents during summer vacation and during the school year to determine the degree to which sleep/wake patterns can estimate salivary DLMO phase. Design And Setting: Participants slept at home on self-selected schedules for 5 consecutive nights and reported their bedtime and wake-up time via daily telephone messages. Salivary melatonin was sampled in the laboratory on one evening every 30 minutes in dim light (<50 lux) to determine DLMO phase. Within group bivariate regressions between sleep pattern measures (bedtime, wake-up time, and midsleep time) and DLMO phase were computed. Participants: One group, ages 9 to 17 years (mean age=12.5, SD=2.3 years, 74 males, 75 females) contributed 149 DLMO phase and sleep/ wake pattern measures while on a school year schedule ("school group"). A separate group, ages 9 to 16 years (mean age=13.1, SD=1.3 years, 30 males, 29 females) contributed 59 DLMO phase and sleep/wake pattern measures while on a summer schedule ("summer group"). Results: Bedtime, midsleep time, and wake-up time were positively correlated with DLMO phase in both groups. Although all correlation coefficients for the summer group were statistically greater compared to the school group, the regression equations predicted DLMO phase within ±1 hour of the measured DLMO phase in ~80% for both groups. Conclusions: DLMO phase can be estimated using self-selected sleep/ wake patterns during the school year or summer vacation in healthy children and adolescents

A Longitudinal Assessment of Sleep Timing, Circadian Phase, and Phase Angle of Entrainment across Human Adolescence

The aim of this descriptive analysis was to examine sleep timing, circadian phase, and phase angle of entrainment across adolescence in a longitudinal study design. Ninety-four adolescents participated; 38 (21 boys) were 9-10 years ("younger cohort") and 56 (30 boys) were 15-16 years ("older cohort") at the baseline assessment. Participants completed a baseline and then follow-up assessments approximately every six months for 2.5 years. At each assessment, participants wore a wrist actigraph for at least one week at home to measure self-selected sleep timing before salivary dim light melatonin onset (DLMO) phase - a marker of the circadian timing system - was measured in the laboratory. Weekday and weekend sleep onset and offset and weekend-weekday differences were derived from actigraphy. Phase angles were the time durations from DLMO to weekday sleep onset and offset times. Each cohort showed later sleep onset (weekend and weekday), later weekend sleep offset, and later DLMO with age. Weekday sleep offset shifted earlier with age in the younger cohort and later in the older cohort after age 17. Weekend-weekday sleep offset differences increased with age in the younger cohort and decreased in the older cohort after age 17. DLMO to sleep offset phase angle narrowed with age in the younger cohort and became broader in the older cohort. The older cohort had a wider sleep onset phase angle compared to the younger cohort; however, an age-related phase angle increase was seen in the younger cohort only. Individual differences were seen in these developmental trajectories. This descriptive study indicated that circadian phase and self-selected sleep delayed across adolescence, though school-day sleep offset advanced until no longer in high school, whereupon offset was later. Phase angle changes are described as an interaction of developmental changes in sleep regulation interacting with psychosocial factors (e.g., bedtime autonomy

Demographics by individual at each age in the younger and older cohorts.

a<p>Participants transitioned from Tanner 1 to 2 at 10 years (n = 5), 11 years (n = 6), and 12 years (n = 5).</p>b<p>Participants transitioned from Tanner 1 to 3 at 11 years (n = 1).</p>c<p>Participants transitioned from Tanner 2 to 3 at 12 years (n = 1) and 13 years (n = 1).</p>d<p>Participants transitioned from Tanner 3 to 4 at 11 years (n = 2), 13 years (n = 1), and 15 years (n = 1).</p>e<p>Participants transitioned from Tanner 3 to 5 at 11 years (n = 2).</p>f<p>Participants transitioned from Tanner 4 to 5 at 15 years (n = 3) and 16 years (n = 1).</p><p>Notes: if more than one Morningness/Eveningness score was collected at each age, then the mean score was used; Tanner stage was unavailable for 1 participant at ages 9, 11, and 13 years, and for 2 participants at age 15 years.</p><p>Demographics by individual at each age in the younger and older cohorts.</p

Means (SDs) for actigraphic sleep and circadian outcomes by age in the younger and older cohorts.

<p>Notes: These data are from 94 participants (N = 38 in the younger cohort; N = 56 in the older cohort) who contributed on average 4.29 assessments range (1 to 6). Three observations at age 19 were included in the 18+ category.</p><p>Means (SDs) for actigraphic sleep and circadian outcomes by age in the younger and older cohorts.</p

Modeled developmental trajectories (bold line) and individual trajectories (thin lines) for actigraphically estimated sleep onset and offset on weekdays (A and D) and weekends (B and E) in the proximal 7 days before DLMO phase was measured in both cohorts.

<p>Sleep onset and offset differences between weekends and weekdays (C and F) illustrate when participants slept earlier (<0) or later (>0) on weekends compared to weekdays. The younger cohort (9–13 years) is on the left and the older cohort (15–19 years) is on the right of each plot.</p

Modeled developmental trajectories (bold line) and individual trajectories (thin lines) for DLMO phase (A), DLMO phase angle to sleep onset (B), and DLMO phase angle to sleep offset (C).

<p>A negative DLMO phase angle to sleep onset indicates when the DLMO occurred after weekday sleep onset.</p