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      Daylight saving time transitions and hospital treatments due to accidents or manic episodes

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      1 , , 1 , 1 , 2 , 1
      BMC Public Health
      BioMed Central

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          Abstract

          Background

          Daylight saving time affects millions of people annually but its impacts are still widely unknown. Sleep deprivation and the change of circadian rhythm can trigger mental illness and cause higher accident rates. Transitions into and out of daylight saving time changes the circadian rhythm and may cause sleep deprivation. Thus it seems plausible that the prevalence of accidents and/or manic episodes may be higher after transition into and out of daylight saving time. The aim of this study was to explore the effects of transitions into and out of daylight saving time on the incidence of accidents and manic episodes in the Finnish population during the years of 1987 to 2003.

          Methods

          The nationwide data were derived from the Finnish Hospital Discharge Register. From the register we obtained the information about the hospital-treated accidents and manic episodes during two weeks before and two weeks after the transitions in 1987–2003.

          Results

          The results were negative, as the transitions into or out of daylight saving time had no significant effect on the incidence of accidents or manic episodes.

          Conclusion

          One-hour transitions do not increase the incidence of manic episodes or accidents which require hospital treatment.

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          Most cited references17

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          We are chronically sleep deprived.

          Data from recent laboratory studies indicate that nocturnal sleep periods reduced by as little as 1.3 to 1.5 hours for 1 night result in reduction of daytime alertness by as much as 32% as measured by the Multiple Sleep Latency Test (MSLT). Other data document that 1) 17%-57% of normal young adults have MSLT latencies of or = 10 minutes and 2) 28%-29% of young adults reported normally sleeping < or = 6.5 hours on each weeknight. More extensive reduction of daily sleep amount is seen in nightshift workers. A minimum of 2%-4% of middle-aged adults have hypersomnolence associated with sleep apnea. Together, these data show that significant sleep loss exists in one-third or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just 1 night in the laboratory. In light of the magnitude of this sleep debt, it is not surprising that fatigue is a factor in 57% of accidents leading to the death of a truck driver and in 10% of fatal car accidents and results in costs of up to 56 billion dollars per year. A recent sleep extension study suggests that the average underlying sleep tendency in young adults is about 8.5 hours per night. By comparison, the average reported sleep length of 7.2-7.4 hours is deficient, and common sleep lengths of < or = 6.5 hours can be disastrous. We must recognize the alertness function of sleep and the increasing consequences of sleepiness with the same vigor that we have come to recognize the societal impact of alcohol.
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            Circadian clocks - the fall and rise of physiology.

            Circadian clocks control the daily life of most light-sensitive organisms - from cyanobacteria to humans. Molecular processes generate cellular rhythmicity, and cellular clocks in animals coordinate rhythms through interaction (known as coupling). This hierarchy of clocks generates a complex, approximately 24-hour temporal programme that is synchronized with the rotation of the Earth. The circadian system ensures anticipation and adaptation to daily environmental changes, and functions on different levels - from gene expression to behaviour. Circadian research is a remarkable example of interdisciplinarity, unravelling the complex mechanisms that underlie a ubiquitous biological programme. Insights from this research will help to optimize medical diagnostics and therapy, as well as adjust social and biological timing on the individual level.
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              High concordance of bipolar I disorder in a nationwide sample of twins.

              The few studies of bipolar I disorder in twins have consistently emphasized the genetic contribution to disease liability. The authors report what appears to be the first twin study of bipolar I disorder involving a population-based twin sample, in which the diagnoses were made by using structured, personal interviews. All Finnish same-sex twins (N=19,124) born from 1940 to 1957 were screened for a diagnosis of bipolar I disorder as recorded in the National Hospital Discharge Register between 1969 and 1991 or self-reported in surveys of the Finnish Twin Cohort in 1975, 1981, and 1990. Thirty-eight pairs were thereby identified and invited to participate in the study; the participation rate was 68%. Lifetime diagnoses were made by using the Structured Clinical Interview for DSM-IV. The authors calculated probandwise and pairwise concordances and correlations in liability and applied biometrical model fitting. The probandwise concordance rates were 0.43 (95% CI=0.10 to 0.82) for monozygotic twins and 0.06 (95% CI=0.00 to 0.27) for dizygotic twins. The correlations in liability were 0.85 and 0.41, respectively. The model with no familial transmission was rejected. The best-fitting model was the one in which genetic and specific environmental factors explained the variance in liability, with a heritability estimate of 0.93 (95% CI=0.69 to 1.00). The high heritability of bipolar disorder was demonstrated in a nationwide population-based twin sample assessed with structured personal interviews.
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                Author and article information

                Journal
                BMC Public Health
                BMC Public Health
                BioMed Central
                1471-2458
                2008
                26 February 2008
                : 8
                : 74
                Affiliations
                [1 ]Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland
                [2 ]Department of Psychiatry, University of Helsinki, Helsinki, Finland
                Article
                1471-2458-8-74
                10.1186/1471-2458-8-74
                2266740
                18302734
                992800b8-fa76-4045-be55-f635138ed09d
                Copyright © 2008 Lahti et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 11 June 2007
                : 26 February 2008
                Categories
                Research Article

                Public health
                Public health

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