@article{nokey,

title = {Impact of one night of sleep restriction on sleepiness and cognitive function: A systematic review and meta-analysis},

author = {L. N. Wüst and N. C. Capdevila and L. T. Lane and C. F. Reichert and R Lasauskaite},

url = {https://www.sciencedirect.com/science/article/pii/S1087079224000443},

doi = {10.1016/j.smrv.2024.101940},

year  = {2024},

date = {2024-04-26},

urldate = {2024-04-26},

journal = {Sleep Medicine Reviews},

volume = {76},

number = {101940},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Brain activity during a working memory task after daily caffeine intake and caffeine withdrawal: a  randomized double-blind placebo-controlled trial.},

author = {Y.-S. Lin and J. Weibel and H.-P. Landolt and F. Santini and H. Slawik and S. Borgwardt and C. Cajochen and C. F. Reichert},

doi = {10.1038/s41598-022- 26808-5},

year  = {2023},

date = {2023-01-18},

urldate = {2023-01-18},

journal = {Scientific Reports},

volume = {13},

number = {1002},

issue = {1},

abstract = {Acute caffeine intake has been found to increase working memory (WM)-related brain activity in healthy adults without improving behavioral performances. The impact of daily caffeine intake-a ritual shared by 80% of the population worldwide-and of its discontinuation on working memory and its neural correlates remained unknown. In this double-blind, randomized, crossover study, we examined working memory functions in 20 young healthy non-smokers (age: 26.4 ± 4.0 years; body mass index: 22.7 ± 1.4 kg/m2; and habitual caffeine intake: 474.1 ± 107.5 mg/day) in a 10-day caffeine (150 mg × 3 times/day), a 10-day placebo (3 times/day), and a withdrawal condition (9-day caffeine followed by 1-day placebo). Throughout the 10th day of each condition, participants performed four times a working memory task (N-Back, comprising 3- and 0-back), and task-related blood-oxygen-level-dependent (BOLD) activity was measured in the last session with functional magnetic resonance imaging. Compared to placebo, participants showed a higher error rate and a longer reaction time in 3- against 0-back trials in the caffeine condition; also, in the withdrawal condition we observed a higher error rate compared to placebo. However, task-related BOLD activity, i.e., an increased attention network and decreased default mode network activity in 3- versus 0-back, did not show significant differences among three conditions. Interestingly, irrespective of 3- or 0-back, BOLD activity was reduced in the right hippocampus in the caffeine condition compared to placebo. Adding to the earlier evidence showing increasing cerebral metabolic demands for WM function after acute caffeine intake, our data suggest that such demands might be impeded over daily intake and therefore result in a worse performance. Finally, the reduced hippocampal activity may reflect caffeine-associated hippocampal grey matter plasticity reported in the previous analysis. The findings of this study reveal an adapted neurocognitive response to daily caffeine exposure and highlight the importance of classifying impacts of caffeine on clinical and healthy populations.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Reichert2022,

title = {Adenosine, caffeine, and sleep–wake regulation: state of the science and perspectives},

author = {C. F. Reichert and T. Deboer and H.-P. Landolt},

url = {http://www.chronobiology.ch/reichert-2022-adenosine-caffeine-sleep-review-2/},

doi = {10.1111/jsr.13597},

year  = {2022},

date = {2022-05-16},

journal = {Journal of Sleep Research},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lin2022,

title = {Time to recover from daily caffeine intake},

author = {Y.-S. Lin and J. Weibel and H.-P. Landolt and F Santini and C Garbazza and J Kistler and S Rehm and K Rentsch and S Borgwardt and C Cajochen and C. F. Reichert},

url = {https://www.frontiersin.org/articles/10.3389/fnut.2021.787225/full},

doi = {10.3389/fnut.2021.787225. },

year  = {2022},

date = {2022-02-02},

journal = {Front Nutr.},

volume = {8},

number = {787225},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Weibel2021b,

title = {Regular caffeine intake delays REM sleep promotion and attenuates sleep quality in healthy men},

author = {J. Weibel and Y.-S. Lin and H.-P. Landolt and C. Berthomier and M. Brandenwinder and J. Kistler and S. Rehm and K. Rentsch and M. Meyer and S. Borgwardt and C. Cajochen and C. F. Reichert },

url = {https://journals.sagepub.com/doi/pdf/10.1177/07487304211013995},

doi = {10.1177/07487304211013995},

year  = {2021},

date = {2021-05-23},

journal = {Journal of Biological Rhythms},

abstract = {Acute  caffeine  intake  can  attenuate  homeostatic  sleep  pressure  and  worsen  sleep  quality.  Caffeine  intake—particularly  in  high  doses  and  close  to  bedtime—may  also  affect  circadian-regulated  rapid  eye  movement  (REM)  sleep  promotion,  an  important  determinant  of  subjective  sleep  quality.  However,  it  is  not  known  whether  such  changes  persist  under  chronic  caffeine  consumption  during  daytime.  Twenty  male  caffeine  consumers  (26.4  ±  4  years  old,  habitual  caffeine  intake  478.1  ±  102.8  mg/day)  participated  in  a  double-blind  crossover  study. Each volunteer completed a caffeine (3 × 150 mg caffeine daily for 10 days), a withdrawal (3 × 150 mg caffeine for 8 days then placebo), and a placebo condition. After 10 days of controlled intake and a fixed sleep-wake cycle, we recorded electroencephalography  for  8  h  starting  5  h  after  habitual  bedtime  (i.e.,  start  on  average at 04:22 h which is around the peak of circadian REM sleep promotion). A 60-min evening nap preceded each sleep episode and reduced high sleep pres-sure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM sleep latency was longer after daily caffeine intake compared with both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was delayed, and volunteers reported more difficulties with awakening after sleep and feeling more tired upon wake-up in the caffeine condition  compared  with  placebo.  Our  data  indicate  that  besides  acute  intake,  also  regular  daytime  caffeine  intake  affects  REM  sleep  regulation  in  men,  such  that  it  delays  circadian  REM  sleep  promotion  when  compared  with  placebo.  Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lin2021,

title = {Daily Caffeine Intake Induces Concentration-Dependent Medial Temporal Plasticity in Humans: A Multimodal Double-Blind Randomized Controlled Trial },

author = { Y.-S. Lin and J. Weibel and H. Landolt and F. Santini and M. Meyer and J. Brunmair and S. Meyer-Menches and C. gerner and S. Borgwardt and C. Cajochen and C. F. Reichert},

url = {http://www.chronobiology.ch/wp-content/uploads/2021/02/Lin_2021_CC_acc_uncorrect.pdf},

doi = {doi.org/10.1093/cercor/bhab005},

year  = {2021},

date = {2021-02-15},

journal = {Cerebral Cortex},

abstract = {Caffeine is commonly used to combat high sleep pressure on a daily basis. However, interference with sleep–wake regulation could disturb neural homeostasis and insufficient sleep could lead to alterations in human gray matter. Hence, in this double-blind, randomized, cross-over study, we examined the impact of 10-day caffeine (3 × 150 mg/day) on human gray matter volumes (GMVs) and cerebral blood flow (CBF) by fMRI MP-RAGE and arterial spin-labeling sequences in 20 habitual caffeine consumers, compared with 10-day placebo (3 × 150 mg/day). Sleep pressure was quantified by electroencephalographic slow-wave activity (SWA) in the previous nighttime sleep. Nonparametric voxel-based analyses revealed a significant reduction in GMV in the medial temporal lobe (mTL) after 10 days of caffeine intake compared with 10 days of placebo, voxel-wisely adjusted for CBF considering the decreased perfusion after caffeine intake compared with placebo. Larger GMV reductions were associated with higher individual concentrations of caffeine and paraxanthine. Sleep SWA was, however, neither different between conditions nor associated with caffeine-induced GMV reductions. Therefore, the data do not suggest a link between sleep depth during daily caffeine intake and changes in brain morphology. In conclusion, daily caffeine intake might induce neural plasticity in the mTL depending on individual metabolic processes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Reichert2020,

title = {Wide awake at bedtime? The effects of caffeine on sleep and circadian timing in teenagers - a randomized crossover trial.},

author = {C. F. Reichert and S. Veitz and M. Bühler and G. Gruber and G. Deuring and S. S. Rehm, K. Rentsch and C. Garbazza and M. Meyer and H. Slawik and Y.-S. Lin and J. Weibel},

url = {http://www.chronobiology.ch/wp-content/uploads/2021/09/1-s2.0-S0006295220305190-main.pdf},

doi = {https://doi.org/10.1016/j.bcp.2020.114283},

year  = {2020},

date = {2020-10-15},

journal = {Biochemical Pharmacology},

abstract = {Adolescents often suffer from short and mistimed sleep. To counteract the resulting daytime sleepiness they frequently consume caffeine. However, caffeine intake may exaggerate sleep problems by disturbing sleep and circadian timing. In a 28-hour double-blind randomized crossover study, we investigated to what extent caffeine disturbs slow-wave sleep (SWS) and delays circadian timing in teenagers. Following a 6-day ambulatory phase of caffeine abstinence and fixed sleep-wake cycles, 18 male teenagers (14–17 years old) ingested 80 mg caffeine vs. placebo in the laboratory four hours prior to an electro-encephalographically (EEG) recorded nighttime sleep episode. Data were analyzed using both frequentist and Bayesian statistics. The analyses suggest that subjective sleepiness is reduced after caffeine compared to placebo. However, we did not observe a strong caffeine-induced reduction in subjective sleep quality or SWS, but rather a high inter-individual variability in caffeine-induced SWS changes. Exploratory analyses suggest that particularly those individuals with a higher level of SWS during placebo reduced SWS in response to caffeine. Regarding salivary melatonin onsets, caffeine-induced delays were not evident at group level, and only observed in participants exposed to a higher caffeine dose relative to individual bodyweight (i.e., a dose > 1.3 mg/kg). Together, the results suggest that 80 mg caffeine are sufficient to induce alertness at a subjective level. However, particularly teenagers with a strong need for deep sleep might pay for these subjective benefits by a loss of SWS during the night. Thus, caffeine-induced sleep-disruptions might change along with the maturation of sleep need.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Weibel2020,

title = {Caffeine-dependent changes of sleep-wake regulation: Evidence foradaptation after repeated intake},

author = {J. Weibel and Y.-S. Lin and H.-P. Landolt and C. Garbazza and V. Kolodyazhniy and J. Kistler and S. Rehm and K. Rentsch and S. Borgwardt and C. Cajochen and C. F. Reichert },

url = {http://www.chronobiology.ch/1-s2-0-s0278584619304798-main-2/},

doi = {10.1016/j.pnpbp.2019.109851 },

year  = {2020},

date = {2020-04-20},

journal = {Progress in Neuro-Psychopharmacology and Biological Psychiatry},

abstract = {Background: Circadian and sleep-homeostatic mechanisms regulate timing and quality of wakefulness. To enhance wakefulness, daily consumption of caffeine in the morning and afternoon is highly common. However, the effects of such a regular intake pattern on circadian sleep-wake regulation are unknown. Thus, we investigated if daily daytime caffeine intake and caffeine withdrawal affect circadian rhythms and wake-promotion in habitual consumers.

Methods: Twenty male young volunteers participated in a randomised, double-blind, within-subject study with three conditions: i) caffeine (150 mg 3 x daily for 10 days), ii) placebo (3 x daily for 10 days) and iii) withdrawal (150 mg caffeine 3 x daily for eight days, followed by a switch to placebo for two days). Starting on day nine of treatment, salivary melatonin and cortisol, evening nap sleep as well as sleepiness and vigilance performance throughout day and night were quantified during 43 h in an in-laboratory, light and posture-controlled protocol.

Results: Neither the time course of melatonin (i.e. onset, amplitude or area under the curve) nor the time course of cortisol was significantly affected by caffeine or withdrawal. During withdrawal, however, volunteers reported increased sleepiness, showed more attentional lapses as well as polysomnography-derived markers of elevated sleep propensity in the late evening compared to both the placebo and caffeine condition.

Conclusions: The typical pattern of caffeine intake with consumption in both the morning and afternoon hours may not necessarily result in a circadian phase shift in the evening nor lead to clear-cut benefits in alertness. The time-of-day independent effects of caffeine withdrawal on evening nap sleep, sleepiness and performance suggest an adaptation to the substance, presumably in the homeostatic aspect of sleep-wake regulation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Chellappa2020,

title = {Intraocular cataract lens replacement and light exposure potentially impact procedural learning in older adults},

author = {S. L. Chellappa and V. Bromundt and S. Frey and T. Schlote and

D. Goldblum and C. Cajochen and C. F. Reichert},

url = {http://www.chronobiology.ch/wp-content/uploads/2020/04/Chellappa-et-al.-JSR_2020.pdf},

doi = {10.1111/jsr.13043},

year  = {2020},

date = {2020-04-14},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Caviezel2020,

title = {The Neural Mechanisms of Associative Memory Revisited: fMRI Evidence from Implicit Contingency Learning},

author = {M. P. Caviezel and C. F. Reichert and D. S. Bahmani and C. Linnemann and C. Liechti and O. Bieri and S. Borgwardt and T. Leyhe and T. Melcher},

url = {http://www.chronobiology.ch/wp-content/uploads/2020/03/fpsyt-10-01002.pdf},

doi = {10.3389/fpsyt.2019.01002},

year  = {2020},

date = {2020-02-03},

journal = {Front. Psychiatry},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Differential impact in young and older individuals of blue-enriched white light on circadian physiology and alertness during sustained wakefulness},

author = {V. Gabel and C. F. Reichert and M. Maire and C. Schmidt and L. J. M. Schlangen and V. Kolodyazhniy and C. Garbazza and C. Cajochen and A. U. Viola},

url = {https://www.nature.com/articles/s41598-017-07060-8.pdf},

year  = {2017},

date = {2017-08-08},

journal = {Scientific Reports},

volume = {7},

number = {7620},

pages = {doi:doi:10.1038/s41598-017-07060-8},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{644,

title = {Cognitive brain responses during circadian wake-promotion: evidence for sleep-pressure-dependent hypothalamic activations},

author = {C. F. Reichert and M. Maire and V. Gabel and A. U. Viola and T. Götz and K. Scheffler and M. Klarhöfer and C. Berthomier and W. Strobel and C. Phillips and E. Salmon and C. Cajochen and C. Schmidt},

url = {http://www.chronobiology.ch/wp-content/uploads/2019/03/Reichert_et_al-2017-Scientific_Reports_Cognitive-brain-responses.pdf},

year  = {2017},

date = {2017-07-17},

journal = {Scientific Reports},

volume = {7},

pages = {doi:10.1038/s41598-017-05695-1},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Sleep-wake regulation and its impact on working memory performance: the role of adenosine},

author = {C. F. Reichert and M. Maire and C. Schmidt and C. Cajochen},

url = {http://www.chronobiology.ch/wp-content/uploads/2016/06/Reichert_2016.pdf},

year  = {2016},

date = {2016-06-27},

journal = {Biology},

volume = {5},

number = {1},

pages = {E11. doi:10.3390/biology5010011.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Pushing the limits: chronotype and time of day modulate working memory-dependent cerebral activity},

author = {C. Schmidt and F. Collette and C. F. Reichert and M. Maire and G. Vandewalle and P. Peigneux and C. Cajochen},

url = {http://www.chronobiology.ch/wp-content/uploads/2015/10/Schmidt_etal_fneur-06-00199_15.pdf},

year  = {2015},

date = {2015-10-07},

journal = {Frontiers in Neurology},

volume = {25},

number = {6:199},

pages = {1-9},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Dawn simulation light impacts on different cognitive domains under sleep restriction},

author = {V. Gabel and M. Maire and C. F. Reichert and S. L. Chellappa and C. Schmidt and V. Hommes and C. Cajochen and A. U. Viola},

url = {http://www.chronobiology.ch/wp-content/uploads/2015/08/7.pdf},

year  = {2015},

date = {2015-08-20},

journal = {Behav Brain Res., doi: 10.1016/j.bbr.2014.12.043},

volume = {15},

pages = {281: 258-266},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Fighting Sleep at Night: Brain Correlates and Vulnerability to Sleep Loss},

author = {M. Maire and C. F. Reichert and V. Gabel and A. U. Viola and C. Phillips and J. Krebs and K. Scheffler and M. Klarhöfer and W. Strobel and C. Cajochen and C. Schmidt },

url = {http://www.chronobiology.ch/wp-content/uploads/2015/08/4.pdf},

year  = {2015},

date = {2015-08-20},

journal = {Ann Neurol., doi: 10.1002/ana.24434.},

volume = {78(2)},

pages = {235-247},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {The Circadian Regulation of Sleep: Impact of a Functional ADA-Polymorphism and Ist Association to Working Memory},

author = {C. F. Reichert and M. Maire and V. Gabel and M. Hofstetter and A.U. Viola and V. Kolodyazhniy and W. Strobel and T. Goetz and V.

Bachmann and H.-P. Landolt and C. Cajochen and C. Schmidt

},

url = {http://www.chronobiology.ch/wp-content/uploads/2014/12/Reichert-2014-napsleep-nback.pdf},

year  = {2014},

date = {2014-12-01},

journal = {PLoS ONE},

volume = {9},

number = {12},

pages = {1-23},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Light modulation of human sleep depends on a polymorphism in the clock gene Period3},

author = {S.L. Chellappa and A.U. Viola and C. Schmidt and V. Bachmann and V. Gabel and M. Maire and C. F. Reichert and A. Valomon and H.P. Landolt and C. Cajochen},

url = {http://www.chronobiology.ch/wp-content/uploads/2014/06/BBR_Chellappa_141.pdf},

year  = {2014},

date = {2014-06-06},

journal = {Behavioural Brain Research},

volume = {271},

pages = {23-29},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Insights into Behavioral Vulnerability to Differential Sleep Pressure and Circadian Phase from a Functional ADA Polymorphism},

author = {C. F. Reichert and M. Maire and V. Gabel and A.U. Viola and V. Kolodyazhniy and W. Strobel and T. Götz and V. Bachmann and H.P. Landolt and C. Cajochen and C. Schmidt},

url = {http://www.chronobiology.ch/wp-content/uploads/2014/04/Reichert-2014-behavioral-vulnerability1.pdf},

year  = {2014},

date = {2014-04-02},

journal = {Journal of Biological Rhythms},

volume = {29},

number = {2},

pages = {119-130},

abstract = {Sleep loss affects human behavior in a nonuniform manner, depending

on the cognitive domain and also the circadian phase. Besides, evidence

exists about stable interindividual variations in sleep loss–related performance

impairments. Despite this evidence, only a few studies have considered both

circadian phase and neurobehavioral domain when investigating trait-like

vulnerability to sleep manipulation. By applying a randomized, crossover

design with 2 sleep pressure conditions (40 h sleep deprivation vs. 40 h multiple

naps), we investigated the influence of a human adenosine deaminase

(ADA) polymorphism (rs73598374) on several behavioral measures throughout

nearly 2 circadian cycles. Confirming earlier studies, we observed that

under sleep deprivation the previously reported vulnerable G/A-allele carriers

felt overall sleepier than G/G-allele carriers. As expected, this difference

was no longer present when sleep pressure was reduced by the application of

multiple naps. Concomitantly, well-being was worse in the G/A genotype

under sleep loss when compared to the nap protocol, and n-back working

memory performance appeared to be specifically susceptible to sleep-wake

manipulation in this genotype. When considering psychomotor vigilance performance, however, a higher sensitivity to sleep-wake manipulation was detected in homozygous participants, but specifically at the end of the night

and only for optimal task performance. Although these data are based on a

small sample size and hence require replication (12 G/A- and 12 G/G-allele

carriers), they confirm the assumption that interindividual differences regarding

the effect of sleep manipulation highly depend on the cognitive task and

circadian phase, and thus emphasize the necessity of a multimethodological

approach. Moreover, they indicate that napping might be suitable to counteract endogenously heightened sleep pressure depending on the neurobehavioral

domain.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Time-on-task decrement in vigilance is modulated by inter-individual vulnerability to homeostatic sleep pressure manipulation},

author = {M. Maire and C. F. Reichert and V. Gabel and A.U. Viola and J. Krebs and W. Strobel and H.P. Landolt and V. Bachmann and C. Cajochen and C. Schmidt},

url = {http://www.chronobiology.ch/wp-content/uploads/2014/03/Timeontask_MAIREetal2014.pdf},

issn = {1662-5153},

year  = {2014},

date = {2014-03-06},

journal = {Frontiers in Behavioral Neuroscience},

volume = {8},

number = {59},

abstract = {Under sleep loss, vigilance is reduced and attentional failures emerge progressively. It becomes difficult to maintain stable performance over time, leading to growing performance variability (i.e., state instability) in an individual and among subjects. Task duration plays a major role in the maintenance of stable vigilance levels, such that the longer the task, the more likely state instability will be observed. Vulnerability to sleep-loss-dependent performance decrements is highly individual and is also modulated by a polymorphism in the human clock gene PERIOD3 (PER3). By combining two different protocols, we manipulated sleep-wake history by once extending wakefulness for 40 h (high sleep pressure condition) and once by imposing a short sleep-wake cycle by alternating 160 min of wakefulness and 80 min naps (low sleep pressure condition) in a within-subject design. We observed that homozygous carriers of the long repeat allele of PER3 (PER35/5) experienced a greater time-on-task dependent performance decrement (i.e., a steeper increase in the number of lapses) in the Psychomotor Vigilance Task compared to the carriers of the short repeat allele (PER34/4). These genotype-dependent effects disappeared under low sleep pressure conditions, and neither motivation, nor perceived effort accounted for these differences. Our data thus suggest that greater sleep-loss related attentional vulnerability based on the PER3 polymorphism is mirrored by a greater state instability under extended wakefulness in the short compared to the long allele carriers. Our results undermine the importance of time-on-task related aspects when investigating inter-individual differences in sleep loss-induced behavioral vulnerability.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Sleep ability mediates individual differences in the vulnerability to sleep loss: Evidence from a PER3 polymorphism},

author = {M. Maire and C. F. Reichert and V. Gabel and A.U. Viola and W. Strobel and J. Krebs and H.P. Landolt and V. Bachmann and C. Cajochen and C. Schmidt},

url = {http://www.chronobiology.ch/wp-content/uploads/2014/01/Maire_Cortex_2013.pdf},

year  = {2014},

date = {2014-01-21},

journal = {Cortex},

volume = {http://dx.doi.org/10.1016/j.cortex.2013.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Sleep-Wake Rhythms and Cognition},

author = {M. Maire and C. F. Reichert and C. Schmidt},

url = {http://www.chronobiology.ch/wp-content/uploads/publications/Maire_2013.pdf},

year  = {2013},

date = {2013-07-24},

journal = {Journal of Cognitive and Behavioral Psychotherapies},

volume = {13},

number = {1},

pages = {133-170},

abstract = {In human beings, homeostatic and circadian sleep-wake regulatory

processes are working together for the maintenance of sleep and

wakefulness at appropriate times within the 24-hour light-dark cycle. The

interaction between these processes also determines time-of-day

modulations in sleepiness and alertness levels, and affects performance in a

series of cognitive tasks. Besides, individuals differ in the synchronization

of a great number of behaviors, ranging from preferred timing for sleep and

wakefulness to habitual sleep duration or differences in sleep depth and

sleep structure. Genetic factors have been shown to contribute substantially

to inter-individual differences in most of these variables. Trait-like

variability has also been suggested in the cerebral bases underlying

cognitive effort under adverse circadian phase and sleep deprivation. The

field of human sleep and chronobiology research has been shown suitable

for translational research such that a multitude of therapeutic tools have

been derived, which start to be recognized in sleep medicine and

psychiatry. Regarding the presence of prominent inter-individual variability

in sleep-wake behaviors and its impact on cognition and subjective wellbeing,

individually tailored schemes might be more accurate, also for the

prediction of treatment efficiency at the clinical level.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{180,

title = {Effects of Artificial Dawn and Morning Blue Light on Daytime Cognitive Performance, Well-being, Cortisol and Melatonin Levels},

author = {V. Gabel and M. Maire and C. F. Reichert and S.L. Chellappa and C. Schmidt and V. Hommes and A.U. Viola and C. Cajochen},

url = {http://www.chronobiology.ch/wp-content/uploads/publications/Gabel_2013.pdf},

year  = {2013},

date = {2013-07-10},

journal = {Chronobiology International},

volume = {30},

pages = {988-97},

abstract = {Light exposure elicits numerous effects on human physiology and behavior, such as better cognitive performance and

mood. Here we investigated the role of morning light exposure as a countermeasure for impaired cognitive

performance and mood under sleep restriction (SR). Seventeen participants took part of a 48h laboratory protocol,

during which three different light settings (separated by 2 wks) were administered each morning after two 6-h sleep

restriction nights: a blue monochromatic LED (light-emitting diode) light condition (BL; 100 lux at 470 nm for 20 min)

starting 2 h after scheduled wake-up time, a dawn-simulating light (DsL) starting 30 min before and ending 20 min

after scheduled wake-up time (polychromatic light gradually increasing from 0 to 250 lux), and a dim light (DL)

condition for 2 h beginning upon scheduled wake time (58 lux). Cognitive tasks were performed every 2 h during

scheduled wakefulness, and questionnaires were administered hourly to assess subjective sleepiness, mood, and wellbeing. Salivary melatonin and cortisol were collected throughout scheduled wakefulness in regular intervals, and the

effects on melatonin were measured after only one light pulse. Following the first SR, analysis of the time course of

cognitive performance during scheduled wakefulness indicated a decrease following DL, whereas it remained stable

following BL and significantly improved after DsL. Cognitive performance levels during the second day after SR were

not significantly affected by the different light conditions. However, after both SR nights, mood and well-being were

significantly enhanced after exposure to morning DsL compared with DL and BL. Melatonin onset occurred earlier

after morning BL exposure, than after morning DsL and DL, whereas salivary cortisol levels were higher at wake-up

time after DsL compared with BL and DL. Our data indicate that exposure to an artificial morning dawn simulation

light improves subjective well-being, mood, and cognitive performance, as compared with DL and BL, with minimal

impact on circadian phase. Thus, DsL may provide an effective strategy for enhancing cognitive performance, wellbeing, and mood under mild sleep restriction.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{161,

title = {Human melatonin and alerting response to blue-enriched light depend on a polymorphism in the clock gene PER3},

author = { S.L. Chellappa and A.U. Viola and C. Schmidt and V. Bachmann and V. Gabel and M. Maire and C. F. Reichert and A. Valomon and T. Götz and H.P. Landolt and C. Cajochen},

url = {http://www.chronobiology.ch/wp-content/uploads/publications/Chellappa_et_al_2011_4.pdf},

year  = {2011},

date = {2011-01-01},

journal = {J Clin Endocrinol Metab 97(3)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}