SLEEP

doi: 10.1093/sleep/zsad008pmid: 36715175

doi: 10.1093/sleep/zsad006pmid: 36683293

This is a correction to: Do your troubles today seem further away than yesterday? On sleep’s role in mitigating the blushing response to a reactivated embarrassing episode, Sleep, Volume 45, Issue 11, November 2022, zsac220, https://doi.org/10.1093/sleep/zsac220 In the originally published version of this manuscript, Figures 2 and 3 were published with details lacking which indicated statistical comparisons and their outcomes. Figure 2 should appear thus: Instead of: And Figure 3 should appear thus: Instead of The emendations to these figures have been completed in the article. © Sleep Research Society 2023. Published by Oxford University Press on behalf of the Sleep Research Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact [email protected]

McCullough, Lindsay M; Mokhlesi, Babak

doi: 10.1093/sleep/zsad003pmid: 36610803

Accepted manuscripts Accepted manuscripts are PDF versions of the author’s final manuscript, as accepted for publication by the journal but prior to copyediting or typesetting. They can be cited using the author(s), article title, journal title, year of online publication, and DOI. They will be replaced by the final typeset articles, which may therefore contain changes. The DOI will remain the same throughout. Article PDF first page preview Close PDF This content is only available as a PDF. © The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected] This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/pages/standard-publication-reuse-rights)

Gool, Jari K; Schinkelshoek, Mink S; Fronczek, Rolf

doi: 10.1093/sleep/zsad005pmid: 36629301

The influenza A virus subtype H1N1 pandemic surfaced in the first month of 2009. Subsequently, a rigorous vaccination campaign began. With this came the first reports of a clearly increased incidence of narcolepsy in Scandinavian children [1]. The H1N1 vaccine named Pandemrix was suggested to be the culprit. Not long after, however, research groups from countries with a low vaccination grade (e.g. China, the United States, Taiwan, and several other European countries) reported a more modest increase in narcolepsy incidence [2–5]. A possible role for the H1N1 virus itself was thus emphasized. Increased incidences were mainly reported in children, and to a lesser extent in adults. More than 10 years later, Wang et al., now consolidate one major piece of this puzzle by collecting the incidence of narcolepsy on a large scale over a 20-year period in mainland China with data from multiple sleep centers [6]. The incidence of both narcolepsy types before the H1N1 pandemic was 0.8 per 100 000 person-years. This increased to 3.1 during the pandemic, remaining somewhat higher (1.0) after the pandemic. This remained true when only considering clearly defined type 1 narcolepsy (88% of the 2869 included cases), and when excluding cases that had received prior vaccination against H1N1. Of note, the vaccine used for this in mainland China was not Pandemrix and was also not adjuvanted. Interestingly, the patients during the pandemic were of younger age (5–9 years old) compared to before and after the pandemic. The efforts of Wang et al. clearly show that the chance for people to develop narcolepsy type 1 increases when the H1N1 flu virus is rampant and activating the immune system. This is independent of vaccination against H1N1. Yet, as is well established and now also again seen in the Chinese data, only occurs in people with the DQB1*06:02 HLA allele. Is the autoimmune hypothesis of narcolepsy thus proven? Hypocretin-deficient narcolepsy type 1 is assumed to be caused by the autoimmune destruction of hypothalamic hypocretin neurons [7]. Because the hypocretin peptides resemble parts of the H1N1 virus, cross-reactivity has been suggested [8]. Note that this theory does not explain narcolepsy type 2, in which hypocretin is not absent. People with this form of narcolepsy are thus mostly left out of studies involving the autoimmune hypothesis. In 2018, hypocretin-specific T-cells were identified in the blood of people with narcolepsy type 1 [9]. This was a fascinating and crucial finding. However, these cells were primarily restricted by HLA-DR and not by HLA DQB1*06:02. Furthermore, there was no cross-reactivity with influenza peptides. Finally, similar T-cells were also found in a low percentage of healthy controls. The question thus remains if these T-cells truly reflect the primary narcolepsy disease mechanism. They might also represent secondary effects of hypocretin neurons damaged by an—as of yet—unknown other processes. Therefore, the exact role of HLA-DQB1*06:02 and autoreactive T-cells is still a mystery. Is H1N1 still triggering narcolepsy across the globe? Since the 1918 Spanish flu pandemic, there has been almost a century in which the H1N1 virus has hardly been detected. The 2009–2010 pandemic changed this [10]. Yet, hypocretin-deficient narcolepsy also existed in the last century. This implies that (vaccination against) H1N1 is not the sole trigger. Multiple other candidates have been suggested. Most convincingly, streptococcal infections have been proposed [11, 12]. Whether there could be a role for non-H1N1 flu strains and other vaccinations in the development of narcolepsy has not been systematically studied. Yet, persistent circulation of the H1N1 virus most likely still contributes to the development of new narcolepsy cases. A study involving 22 sleep centers across the US reported a 1.6-fold increase in pediatric cases after the 2009 pandemic [4]. Within Europe, a new child-specific narcolepsy type 1 incidence peak was seen in 2013 in the Netherlands, Italy, and France [13]. Of note, the 2010 narcolepsy peak was relatively mild in these countries. This may suggest the existence of a “limited pool” of people susceptible to developing narcolepsy. Wang et al. have also reported varying narcolepsy incidence rates in mainland China after 2010, with other peaks in 2012, and 2014. They have deemed the “limited pool” hypothesis unlikely since Chinese post-pandemic narcolepsy incidence rates did not normalize and generally remained increased. Narcolepsy incidence generally peaked in spring in both mainland China and the United States, 4–8 months after the preceding H1N1 flu season intensity peak [4–6]. In contrast, two American cases have previously been identified in which narcolepsy symptoms directly started after H1N1 infection [4]. This would suggest that the presumed autoimmune process underlying narcolepsy could take between days–months to complete. In a large study in the United Kingdom [14], people were identified who had developed narcolepsy symptoms up to 5 years after their Pandemrix vaccination. In people with a quick onset of narcolepsy symptoms after H1N1 flu infection or vaccination, a causal relationship seems plausible. However, the possibility of long delays between possible immunological triggers and the development of narcolepsy remains to be shown. To conclude, Wang et al. again show a clear relation between infection with the H1N1 flu virus and a relatively swift and severe development of narcolepsy type 1 in people with the DQB1*06:02 HLA allele. On top of this, data from Europe shows the adjuvanted H1N1 vaccine Pandemrix to play a role [2] and other infections (e.g. streptococcus) have also been implicated [11, 12]. This does not seem to leave a lot of room for doubt regarding the autoimmune nature of narcolepsy type 1. It is thus surprising that direct evidence for the suspected autoimmune process is still lacking. More than 20 years after the discovery of hypocretin deficiency in narcolepsy with cataplexy the ultimate question remains unsolved. What happens to the hypothalamic hypocretin neurons in narcolepsy type 1? Are the hypocretin neurons of genetically susceptible people indeed unrecoverably killed by T-cells that wrongly elicit an immune response to a self-antigen in hypocretin neurons after an immune trigger (or several triggers)? Or is the immune mechanism in reality aimed at another target outside hypocretin neurons? Are the hypocretin neurons really gone? Disclosure Statement Financial disclosure statement: The authors have no financial or nonfinancial disclosures. References 1. Partinen M , et al. . Increased incidence and clinical picture of childhood narcolepsy following the 2009 H1N1 Pandemic Vaccination Campaign in Finland . PLoS One. 2012 ; 7 ( 3 ): e33723 . doi:10.1371/journal.pone.0033723 Google Scholar Crossref Search ADS PubMed WorldCat 2. Wijnans L , et al. . The incidence of narcolepsy in Europe: before, during, and after the influenza A(H1N1)pdm09 pandemic and vaccination campaigns . Vaccine. 2013 ; 31 ( 8 ): 1246 – 1254 . doi:10.1016/j.vaccine.2012.12.015 Google Scholar Crossref Search ADS PubMed WorldCat 3. Huang W-T , et al. . Narcolepsy and 2009 H1N1 pandemic vaccination in Taiwan . Sleep Med. 2020 ; 66 : 276 – 281 . doi:10.1016/j.sleep.2018.10.036 Google Scholar Crossref Search ADS PubMed WorldCat 4. Simakajornboon N , et al. . Increased incidence of pediatric narcolepsy following the 2009 H1N1 pandemic: a report from the pediatric working group of the sleep research network . Sleep. 2022 ; 45 ( 9 ). doi:10.1093/sleep/zsac137 Google Scholar OpenURL Placeholder Text WorldCat 5. Han F , et al. . Narcolepsy onset is seasonal and increased following the 2009 H1N1 pandemic in china . Ann Neurol. 2011 ; 70 ( 3 ): 410 – 417 . doi:10.1002/ana.22587 Google Scholar Crossref Search ADS PubMed WorldCat 6. Wang X. Changed epidemiology of narcolepsy before, during, and after the 2009 H1N1 pandemic: a nationwide narcolepsy surveillance network study in mainland China, 1990–2017. Sleep. 2023 . Online ahead of print. doi:10.1093/sleep/zsac325 Google Scholar OpenURL Placeholder Text WorldCat 7. Kornum BR. Narcolepsy type 1: what have we learned from immunology? Sleep. 2020 ; 43 ( 10 ). doi:10.1093/sleep/zsaa055 Google Scholar OpenURL Placeholder Text WorldCat 8. Luo G , et al. . Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy. Proc Natl Acad Sci USA. 2018 ; 115 ( 52 ): 201818150 . doi:10.1073/pnas.1818150116 Google Scholar Crossref Search ADS WorldCat 9. Latorre D , et al. . T cells in patients with narcolepsy target self-antigens of hypocretin neurons . Nature. 2018 ; 562 ( 7725 ): 63 – 68 . doi:10.1038/s41586-018-0540-1 Google Scholar Crossref Search ADS PubMed WorldCat 10. Morens DM , et al. . The persistent legacy of the 1918 influenza virus . New Engl J Med. 2009 ; 361 ( 3 ): 225 – 229 . doi:10.1056/NEJMp0904819 Google Scholar Crossref Search ADS WorldCat 11. Aran A , et al. . Elevated anti-streptococcal antibodies in patients with recent narcolepsy onset . Sleep. 2009 ; 32 ( 8 ): 979 – 983 . doi:10.1093/sleep/32.8.979 Google Scholar Crossref Search ADS PubMed WorldCat 12. Ding Q , et al. . Anti-streptococcal antibodies in Chinese patients with type −1 narcolepsy . Sleep Med. 2020 ; 72 : 37 – 40 . doi:10.1016/j.sleep.2020.03.019 Google Scholar Crossref Search ADS PubMed WorldCat 13. Zhang Z , et al. . New 2013 incidence peak in childhood narcolepsy: more than vaccination? Sleep. 2020 ; 44 ( 2 ). doi:10.1093/sleep/zsaa172 Google Scholar OpenURL Placeholder Text WorldCat 14. Stowe J , et al. . Reassessment of the risk of narcolepsy in children in England 8 years after receipt of the AS03-adjuvanted H1N1 pandemic vaccine: a case-coverage study . PLoS Med. 2020 ; 17 ( 9 ): e1003225 . doi:10.1371/journal.pmed.1003225 Google Scholar Crossref Search ADS PubMed WorldCat © Sleep Research Society 2023. Published by Oxford University Press on behalf of the Sleep Research Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

Wang, Xiling; Xiao, Fulong; Wang, Yiping; Deng, Xiaowei; Chen, Zhiyuan; Dong, Xiaosong; Wang, Wei; Li, Chenyang; Xu, Zhifei; Wu, Huijuan; Yu, Huan; Su, Changjun; Wang, Zan; Tang, Xiangdong; Lv, Yunhui; Li, Yun;

Malow, Beth A

doi: 10.1093/sleep/zsac323pmid: 36617183

Dear Editor, We appreciate the interest of Martin-Olalla and Mira in response to the Sleep Research Society (SRS) position statement supporting the abolition of the seasonal clock change and the adoption of permanent standard time (pST). Their criticism of two elements of the current practice of the seasonal clock change, namely the use of a 1-h interval and the choice of transition dates, are areas in which we agree, as we also recognize the detrimental health consequences of this abrupt shift. We do caution that while multistep adjustments may result in fewer health risks, these are likely not feasible for businesses and the transportation industry. Where we disagree is that Martin-Olalla and Mira wish to continue the current practice of moving our clocks ahead in the spring and back in the fall, while the SRS [1] and other sleep and circadian societies [2], national organizations [3], and the majority of Americans [4, 5], wish to abolish this practice. We also disagree with Martin-Olalla and Mira’s statement that the “deepest concern of the chronobiological and sleep community” is related to the acute 1-h clock change. The SRS and other organizations are also profoundly concerned about the almost eight months of the year spent under daylight saving time (DST) during which circadian misalignment and its detrimental effects on health exist [6]. While Martin-Ollalla and Mira correctly point out that “DST does not shift daylight”, the clock changes that DST imposes result in daylight being present 1 h later in the morning and 1 h later in the evening according to clock time. They then argue that “DST changes the phase of human activity… it is advanced in the spring and delayed in the winter… and that DST regulations result in the population waking earlier in the summer and later in the winter”. In fact, independent of school or work schedules, DST’s later sunrises and later sunsets result in delays in wake times and bedtimes in the spring and summer. When early morning school or work times force early morning awakenings, DST results in sleep loss (due to delayed bedtimes) and chronic misalignment between human activity (defined by clock time) and circadian time (aligned to solar time). Those populations most vulnerable to sleep loss and circadian misalignment resulting from DST are students who cannot control their early school start times, and adults with early morning work times. As evidence gathers on the detrimental health consequences of both the abrupt shift and the circadian misalignment resulting from seasonal clock changes, a growing number of organizations [most recently the American Medical Association [7] have advocated for permanent standard time (pST)]. Notably, Mexico has also recently adopted pST, stating that “This new law seeks to guarantee the human right to health and increase safety in the mornings, procure the well-being and productivity of the population, and contribute to saving electric energy” [8]. Disclosure Statement Financial Disclosure: None. Non-financial Disclosure: None. References 1. Malow BA. It is time to abolish the clock change and adopt permanent standard time in the United States: a Sleep Research Society position statement . Sleep. 2022 ; 45 ( 12 ): zsac236 . doi:10.1093/sleep/zsac236. PMID: 36156090 Google Scholar Crossref Search ADS PubMed WorldCat 2. Rishi MA , et al. . Daylight saving time: an American Academy of Sleep Medicine position statement . J Clin Sleep Med. 2020 ; 16 ( 10 ): 1781 – 1784 . doi:10.5664/jcsm.8780 Google Scholar Crossref Search ADS PubMed WorldCat 3. Save Standard Time . https://savestandardtime.com/endorsements/. Accessed August 27, 2022 . 4. Frankovic K. Daylight saving time: Americans want to stay permanently “sprung forward” and not “fall back” . YouGovAmerica, 2021 . https://today.yougov.com/topics/politics/articles-reports/2021/11/04/daylight-saving-time-americans-want-stay-permanent. Accessed August 27, 2022. 5. AP-NORC Center for Public Affairs Research . “Dislike for changing the clocks persists . https://apnorc.org/projects/dislike-for-changing-the-clocks-persists/. Accessed August 27, 2022 . 6. Giuntella O , et al. . Sunset time and the economic effects of social jetlag: evidence from US time zone borders . J Health Econ. 2019 ; 65 : 210 – 226 . doi:10.1016/j.jhealeco.2019.03.007 Google Scholar Crossref Search ADS PubMed WorldCat 7. American Medical Association . AMA calls for permanent standard time . https://www.ama-assn.org/press-center/press-releases/ama-calls-permanent-standard-time. Accessed December 11, 2022 . 8. The New York Times . Mexico’s senate votes to eliminate daylight saving time . https://www.nytimes.com/2022/10/27/world/americas/mexico-daylight-saving-time.html. Accessed December 11, 2022 . © The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected] This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/pages/standard-publication-reuse-rights)

Martín-Olalla, José María; Mira, Jorge

doi: 10.1093/sleep/zsac309pmid: 36630300

Dear Editor, Sleep recently published a position statement by the Sleep Research Society supporting the abolition of the seasonal clock change, and the adoption of permanent standard time in the United States after “a thorough review of the existing literature” [1]. The beginning section of the statement, devoted to the history of daylight saving time (DST) regulations, shows a key misunderstanding which often occurs within the chronobiological and sleep community. We bring here this letter in an attempt to clarify what is and what is not DST. Malow [1] attributes to Benjamin Franklin the concept of changing the hours of human activity to “save daylight” and ends saying: “In contrast to what Franklin proposed, where a population wakes earlier to make the best use of daylight, DST changes the clock time. DST shifts daylight into the early evening in exchange for less daylight in the early morning.” There are two things of the utmost importance to note. First, DST does not shift daylight, which is a natural phenomenon alien to human conventions. All else equal, DST changes the phase of human activity: it is advanced in spring and delayed in autumn. As a result of this, the second point to note is: DST regulations exactly achieve what Franklin demanded; the population wakes earlier in summer, and later in winter. In other words: there is no “in contrast” that opposes the current, annoying, DST regulations to Franklin’s prior proposal. Both bring the same main effect: “make the best use of daylight,” meaning people wakes up earlier in summer and later in winter or, only metaphorically, both shift “daylight into the early evening in exchange for less daylight in the early morning.” There are issues to criticize in connection with the seasonal clock regulations (the stroke of 1 h and the choice of the transition dates, chiefly), but their main effect is not one of those issues because it goes in line with the ancient seasonal practice, and in line with the role of daylight (sunrise) as a synchronizer for the onset of human activity. Therefore, we find interesting that position papers [1] and review papers [2] demand the canceling of the regulation, the adoption of permanent standard time, but, at the same time, they acknowledge the propensity of the population for advancing the activity during the summer (and delaying it back in winter). The thing to note is that since the 20th-century Daylight Saving Time regulations are successfully easing this propensity in modern, Extratropical societies. Else, people would have already delayed their morning times in summer, playing against the regulations [3] or, simply, they would have been deprecated. In this line, we hypothesize that the abolition of the practice will not improve the current scenario in the ranges of latitudes where the contiguous United States locate [4]. Roenneberg et al.’s [2] “potential solution” to daylight saving time consists in the adoption of seasonal start times. In 1810 (only 20 years after Franklin’s death), the Spanish National Assembly already regulated their opening and closing times seasonally (10 am–2 pm from October to April; 9 am–1 pm from May to September) [3], imperfectly mimicing the natural, ancient seasonal adaptation at their circle of latitude, bringing early activity in summer and late activity in winter to representatives. This seasonal behavior has been superseded by the current clock regulations. Both solutions are identical on an individual basis and bring the same hazards. In addition, we must note that during the past 100 years people in the United States, the United Kingdom, and elsewhere, have had every opportunity to offset the clock regulations by moving their start times in opposition (as an example 9 am during the standard time (ST) period and 10 am during the DST period). Nearly nobody behaved like that. Nonetheless, DST is flagged as an “artificial” setting [2, 5]. We do acknowledge that the transition dates should be altered for the benefit of the population. The spring transition date should come after the Equinox so that larger shares of the population do not experience a dark rise time after clocks are changed. An early April transition date, as occurred until 2007 in the United States, would help to mitigate this. Accordingly, if the autumn transition were set to early October, as occurred until 1954, many working population and children would cease to be subjected to the stressing dark hours in the October mornings. See Figure 1 for a graphical sketch of this idea. Figure 1. Open in new tabDownload slide The yearly evolution of the solar altitude at the hour of the winter sunrise (top thick black line, designated 07:22 ST); at 1 h ahead (medium thick black line, designated 07:22 DST or 06:22 ST); and at the summer sunrise (bottom thin blueish line, designated 05:31 DST) for the 40 °N circle of latitude (the latitude of New York and Madrid). The winter sunrise is a synchronizer for the onset of human activity [6, 7]. When DST is set from early April to early October, the onset of the human activity occurs in daylight and delays at most 01 h 51 min from the sunrise. This proposition is noted by solid lines. The vertical arrows annotate the current transition dates in the United States. Numbers inside the graph annotate solar altitude at the beginning of calendar months. The orange zigzag line sketches a four-stroke circadian preadaptation to the spring transition (from the standard clock to the daylight saving clock) achieved by an alarm clock. The deepest concern of the chronobiological and sleep community lies on the hazards that the stroke of 1 h brings [8–10]. Yet, this is unavoidable after clock time gained significance in modern societies (see the preceding example in Spain): assemblies, schools, companies, and universities can only regulate their start times by whole hours, and not smoothly. Again, DST regulations have provided a simple, effective, socially synchronized mechanism to do so. Notwithstanding this, individuals can adapt their phase preemptively by altering their alarm clock in the weeks preceding the spring transition. The zigzag line in Figure 1 shows the idea for a four 15-min stroke adaptation. Similar settings for three (20 min) or two (30 min) strokes are possible. Malow [1] alerts that evening light “extended too close to bedtime can also disrupt sleep patterns.” However, this observation is mainly associated with the shortening of the scotoperiod that the summer brings to Extratropical latitudes. We must note that the winter sunrise time and the summer sunset time are separated by roughly 12 h, irrespective of latitude. If the onset of human activity is determined by the winter sunrise time and clock regulations apply, then the onset of human activity in summer is separated by 11 h from the sunset time, which likely suffices for proper sleep. For those individuals with an onset time earlier than the winter sunrise time, the clock regulations come less handy in summer. Noteworthy, the regulations have also played a role in preventing human activity from starting before the winter sunrise, thus minimizing the size of this group [4]. Disclosure Statement None declared. Data Availability The authors confirm that the data supporting this study are available within the manuscript. Sunrise times and solar altitudes in figure 1 were computed with the help of the software ‘xplanet’ by Hari Nair (https://xplanet.sourceforge.net/) to compute the solar declination during the year 2022; and the script ‘Equation of Time’ by Darin C. Koblick (available at MATLAB Central File Exchange https://www.mathworks.com/matlabcentral/fileexchange/32793-equation-of-time) to compute the equation of time. References 1. Malow BA. It is time to abolish the clock change and adopt permanent Standard Time in the United States: a sleep research society position statement. Sleep. 2022 ; 45 ( 12 ): zsac236 . doi:10.1093/sleep/zsac236 Google Scholar Crossref Search ADS PubMed WorldCat 2. Roenneberg T , et al. . Daylight saving time and artificial time zones—a battle between biological and social times . Front Physiol. 2019 ; 10 : 944 . doi:10.3389/fphys.2019.00944 Google Scholar Crossref Search ADS PubMed WorldCat 3. Martín-Olalla JM. The long term impact of daylight saving time regulations in daily life at several circles of latitude . Sci Rep. 2019 ; 9 : 18466 . doi:10.1038/s41598-019-54990-6 Google Scholar Crossref Search ADS PubMed WorldCat 4. Martín-Olalla JM. A chronobiological evaluation of the risks of canceling daylight saving time . Chronobiol Int. 2022 ; 39 ( 1 ): 1 – 4 . doi:10.1080/07420528.2021.1963760 Google Scholar Crossref Search ADS PubMed WorldCat 5. Johnson KG , et al. . Daylight saving time: neurological and neuropsychological implications . Curr Sleep Med Rep. 2022 ; 8 : 86 – 96 . doi:10.1007/S40675-022-00229-2 Google Scholar Crossref Search ADS WorldCat 6. Martín-Olalla JM. Latitudinal trends in human primary activities: characterizing the winter day as a synchronizer . Sci Rep. 2018 ; 8 : 5350 . doi:10.1038/s41598-018-23546-5 Google Scholar Crossref Search ADS PubMed WorldCat 7. Martín-Olalla JM. Seasonal synchronization of sleep timing in industrial and pre-industrial societies . Sci Rep. 2019 ; 9 : 6772 . doi:10.1038/s41598-019-43220-8 Google Scholar Crossref Search ADS PubMed WorldCat 8. Janszky I , et al. . Shifts to and from daylight saving time and incidence of myocardial infarction. N Engl J Med. 2009 ; 359 ( 18 ): 1966 – 1968 . doi:10.1056/NEJMC0807104 Google Scholar Crossref Search ADS WorldCat 9. Meira e Cruz M , et al. . Impact of daylight saving time on circadian timing system: an expert statement . Eur J Intern Med. 2019 ; 60 : 1 – 3 . doi:10.1016/j.ejim.2019.01.001 Google Scholar Crossref Search ADS PubMed WorldCat 10. Fritz J , et al. . A chronobiological evaluation of the acute effects of daylight saving time on traffic accident risk . Curr Biol. 2020 ; 30 ( 4 ): 729 – 735 . doi:10.1016/j.cub.2019.12.045 Google Scholar Crossref Search ADS PubMed WorldCat © Sleep Research Society 2023. Published by Oxford University Press on behalf of the Sleep Research Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

Liu, Yue; Wen, Hongwei; Peng, Yun

doi: 10.1093/sleep/zsad002pmid: 36611279

Accepted manuscripts Accepted manuscripts are PDF versions of the author’s final manuscript, as accepted for publication by the journal but prior to copyediting or typesetting. They can be cited using the author(s), article title, journal title, year of online publication, and DOI. They will be replaced by the final typeset articles, which may therefore contain changes. The DOI will remain the same throughout. Article PDF first page preview Close PDF This content is only available as a PDF. © The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected] This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/pages/standard-publication-reuse-rights)