The well-known bidirectional link between seizures and sleep may be most conspicuous in environments where the chief zeitgeber – sunlight – undergoes extreme but consistent changes over the course of a year. Routine circannual encounters with the midnight sun and midday darkness strategically position Earth’s polar regions as natural laboratories to study this effect. We reviewed 2337 studies that related status epilepticus (SE), light exposure, and sleep in people in the Arctic or Antarctic. Status epilepticus represented the most extreme – and arguably incontrovertible – expression of seizure. After applying filters and exclusion criteria, 5 studies were included for SE and 36 for sleep. Status epilepticus was correlated with increasing daylength going into summer (ie, brighter sunlight vector ) at high latitudes. Sunlight and chronotype demonstrated a linear relationship, with more sunlight going into summer (ie, brighter sunlight vector) advancing chronotype, less sunlight going into winter (ie, darker sunlight vector ) delaying chronotype, and extreme cases becoming free-running in either vector direction. U-shaped relationships were also surmised, with increased sleep fragmentation and decreased sleep duration for both brighter and darker sunlight vectors. A parsimonious synthesis is that a brighter sunlight vector advances chronotype to shorten and fragment sleep, thereby triggering more SE and seizures. Although these data are derived from Earth’s poles, they are not specific to polar regions; rather, they hold ramifications for everyone on planet Earth – 1 in 10 of whom will have a seizure in their lifetime.
Time-of-day variation in neuromuscular performance is well established, but the contribution of circadian phenotype remains unclear. This study examined whether maximal knee-extensor strength and fatigue resistance differ between morning and evening and whether chronotype and actigraphy-derived sleep-timing are associated with diurnal performance variation. Forty-four healthy young adults (21 males, 23 females) completed a randomised-crossover protocol consisting of neuromuscular testing in the morning (0700-0900) and evening (1700-1900). Participants completed 7 days of actigraphy monitoring and the Composite Morningness Questionnaire to characterise behavioural circadian phenotype. Sleep timing was assessed using habitual sleep midpoint (between sleep-onset and wake-time), with night-to-night variability in sleep midpoint used as an index of sleep-timing variability. Maximal voluntary isometric contraction (MVIC) torque, fatigue index, contractions completed, and time-to-exhaustion were assessed during each trial. Baseline MVIC torque was greater in the evening compared with the morning (2.96 ± 0.80 vs 2.85 ± 0.77 N m kg⁻ 1 ; P < .0001), with post-fatigue torque also remaining higher in the evening (2.00 ± 0.60 vs 1.84 ± 0.54 N m kg⁻ 1 ; P < .0001). Participants demonstrated a lower fatigue-index (32.57 ± 6.99 vs 35.58 ± 6.26%; P < .0001), completed more contractions (37.95 ± 8.29 vs 35.09 ± 7.58; P < .0001), and exhibited longer time-to-exhaustion (6.36 ± 1.51 vs 5.85 ± 1.26 minutes; P < .0001) during evening testing. Chronotype was strongly associated with the PM-AM difference in MVIC torque ( r = −.684, P < .0001), explaining 47% of the variance in diurnal performance responses. Neither habitual sleep midpoint ( r = −.029, P = .848) nor night-to-night variability in sleep midpoint ( r = −.055, P = .721) was associated with performance differences. No significant sex-related differences were observed. Maximal knee extensor strength and fatigue resistance were enhanced during evening compared with morning testing. The magnitude of this response was strongly associated with behavioural circadian phenotype, but not actigraphy-derived sleep-timing. Findings suggest that chronotype influences time-of-day differences in neuromuscular performance and should be considered when evaluating exercise performance.
Circadian rhythms in intensive care unit (ICU) patients are vulnerable to disruption, which may contribute to adverse clinical outcomes. Continuously monitored vital signs offer a unique opportunity to assess 24-hour rhythms in real-world ICU settings. The aim of this scoping review is to systematically map methodological approaches used to characterize 24-hour rhythms in vital signs in ICU populations and to summarize reported associations with patient characteristics, clinical outcomes, or interventions. A systematic literature search was conducted to identify studies that assessed 24-hour rhythms in routinely collected vital signs in adult, pediatric and neonatal ICU patients published between January 2015 and December 2025. Thirty-five studies comprising nearly 288 000 patients were included, with most studies conducted in adult ICUs (n = 32), 3 in neonatal ICUs, and none in pediatric ICUs. Substantial heterogeneity existed in preprocessing strategies, assessment windows, analytical methods, and derived rhythmicity metrics that were used to determine 24-hour variation, as well as in the level of detail with which these were reported. Cosinor analysis was the most frequently used method to characterize rhythmicity, followed by day-night comparisons, and max-min approaches. Across studies, rhythmicity analyses revealed that 24-hour rhythms in vital signs were detectable in ICU patients, although methodological heterogeneity and lack of detail on analytical decisions limit evidence synthesis. In addition, the direction and magnitude of associations between rhythmic properties (such as amplitude or acrophase) and mortality and other clinically relevant outcomes varied considerably among studies. While most, though not all, studies reported that higher amplitudes were associated with mortality, it remains unclear whether this reflects circadian physiology rather than clinical instability. Harmonization of reporting practices and the development of a core outcome set on circadian parameters derived from vital signs in critical care contexts will help to guide future research in this burgeoning field.
Chronic kidney disease (CKD) affects roughly 10% of the world’s population, and growing evidence suggests that disruption of the circadian system—now recognized as an important regulator of numerous physiological pathways, may contribute to impaired kidney function and increased CKD risk. This narrative review aims to synthesize the existing literature on the association between determinants of circadian rhythm (shift work, artificial light at night [ALAN], melatonin) as well as sleep health and CKD risk. Three databases (PubMed, Web of Science, and Embase) were searched for original articles published from 1966 through 28 February 2026. A total of 34 studies examined the association between circadian factors and CKD risk: 7 on shift work, 2 on ALAN, 4 on melatonin, 4 on chronotype, 2 on social jetlag, 2 on insomnia, and 18 on sleep duration. Taken together, these studies offer consistent evidence that shift work, evening chronotype, prolonged social jetlag, and both short and long sleep duration are associated with elevated CKD risk. Given the potential implications for early detection, risk stratification, and targeted behavioral interventions, future research should employ standardized approaches and improved measures using, for example, actigraphy, to clarify causal pathways and strengthen the evidence base.
A 12-h (12-h) periodicity in a transcriptomic series is routinely reported as a "12-h rhythm," yet a single 12-h spectral peak can arise from 3 mechanistically distinct processes: the second harmonic of a non-sinusoidal 24-h waveform (a harmonic), an autonomous 12-h oscillator with its own phase (such as the IRE1α-XBP1s ER-stress cycle), or the apparent 12-h when 2 anti-phase 24-h processes combine as synthesis minus degradation (an intersection). These origins carry opposite biological meanings but are indistinguishable to standard detectors such as JTK_CYCLE, RAIN, and Cosinor. To resolve the origin of 12-h rhythms, Circadian Harmonic Oscillation Resolution and Disentanglement (CHORD) detects 12-h periodicity and resolves it into this ternary taxonomy. Detection fuses 4 tests through the Cauchy Combination Test; disentanglement rests on 4 complementary statistics, each tied to one identifiable model feature and combined by a calibrated multinomial classifier. On a held-out benchmark, CHORD separates autonomous from driven 12 h at area under the curve (AUC) 0.83 and a genuine oscillator from an intersection at 0.93. An interventional test anchors the classifier to biology: in a liver-specific XBP1 knockout, the hepatic 12-h program collapses when the IRE1-XBP1 clock is ablated (knockout/wild-type ratio 0.27) while the 24-h circadian clock is preserved (0.91). The canonical autonomous genes are 12-h dominant with little 24 h, which a single series cannot resolve, so CHORD abstains and the intervention resolves them; the confidently classified autonomous set also collapses more than the driven set (0.47 vs. 0.62). Because the program is strongly coregulated, a correlation-adjusted test keeps the program-versus-driven collapse significant (p=00.045); this validation covers the autonomous arm in liver only. An identifiability budget shows that 12-h signal-to-noise, not sampling density, bounds classification. CHORD reframes ultradian transcriptomics from whether a 12-h rhythm exists to what kind it is.
