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

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

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 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

Circadian gene variants influence sleep and the sleep electroencephalogram in humans

<p>The sleep electroencephalogram (EEG) is highly heritable in humans and yet little is known about the genetic basis of inter-individual differences in sleep architecture. The aim of this study was to identify associations between candidate circadian gene variants and the polysomnogram, recorded under highly controlled laboratory conditions during a baseline, overnight, 8 h sleep opportunity. A candidate gene approach was employed to analyze single-nucleotide polymorphisms from five circadian-related genes in a two-phase analysis of 84 healthy young adults (28 F; 23.21 ± 2.97 years) of European ancestry. A common variant in <i>Period2</i> (<i>PER2</i>) was associated with 20 min less slow-wave sleep (SWS) in carriers of the minor allele than in noncarriers, representing a 22% reduction in SWS duration. Moreover, spectral analysis in a subset of participants (<i>n</i> = 37) showed the same <i>PER2</i> polymorphism was associated with reduced EEG power density in the low delta range (0.25–1.0 Hz) during non-REM sleep and lower slow-wave activity (0.75–4.5 Hz) in the early part of the sleep episode. These results indicate the involvement of <i>PER2</i> in the homeostatic process of sleep. Additionally, a rare variant in <i>Melatonin Receptor 1B</i> was associated with longer REM sleep latency, with minor allele carriers exhibiting an average of 65 min (87%) longer latency from sleep onset to REM sleep, compared to noncarriers. These findings suggest that circadian-related genes can modulate sleep architecture and the sleep EEG, including specific parameters previously implicated in the homeostatic regulation of sleep.</p