Genomic Analysis Suggests That "Morning People" Have Better Mental Health
News Jan 30, 2019 | Original Press Release from the University of Exeter
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The study, published in Nature Communications, suggests that being genetically programmed to rise early may lead to greater well-being and a lower risk of schizophrenia and depression. However, despite much previous speculation, the results did not reveal any strong links to diseases such as diabetes or obesity.
The study was conducted by an international collaboration, led by the University of Exeter and Massachusetts General Hospital and funded by the Medical Research Council. It highlights the key role of the retina in the eye in helping the body to keep time. It also increases the number of areas of the genome known to influence whether someone is an early riser from 24 to 351.
Professor Mike Weedon, of the University of Exeter Medical School, who led the research, said: “This study highlights a large number of genes which can be studied in more detail to work out how different people can have different body clocks. The large number of people in our study means we have provided the strongest evidence to date that ‘night owls’ are at higher risk of mental health problems, such as schizophrenia and lower mental well-being, although further studies are needed to fully understand this link.”
The work was conducted in 250,000 US-based research participants from 23andMe, a company that provides private genomic analyses, and 450,000 people in the UK Biobank study. All participants were asked if they were a “morning person” or an “evening person”, and their genomes were analysed to look at which genes they had in common which may influence their sleep patterns.
The researchers confirmed their results using information from wrist-worn activity trackers worn by more than 85,000 individuals in the UK Biobank. This information showed that the genetic variants the researchers identified could shift a person’s natural waking time by up to 25 mins - changing some people’s waking time from 8am to 8.25am, for example. The researchers found that the genetic areas influence sleep timing, but not the quality or duration of sleep.
The genomic regions identified include those central to our body clocks, also referred to as circadian rhythms, as well as genes expressed in the brain and in retinal tissue in the eye. The body clock cycle is slightly longer than the 24-hour daily cycle. The eye tissue connection may help explain how the brain detects light to “reset” the body clock each day and to align with the 24-hour cycle.
Our body clocks are influenced by genes and lifestyle factors including diet, exposure to artificial light and our jobs and activities. Our body clock affects a wide range of molecular processes, including hormone levels and core body temperature, as well as our waking and sleeping patterns.
Lead author Dr Samuel E. Jones, of the University of Exeter Medical School, said: “The discovery of this fundamental body clock mechanism in the brain recently won the Nobel prize for medicine in 2017. However, we still know very little about whether or not your body clock influences your risk of disease
“Our work indicates that part of the reason why some people are up with the lark while others are night owls is because of differences in both the way our brains react to external light signals and the normal functioning of our internal clocks. These small differences may have potentially significant effects on the ability of our body clocks to keep time effectively, potentially altering risk of both disease and mental health disorders.”
This article has been republished from materials provided by the University of Exeter. Note: material may have been edited for length and content. For further information, please contact the cited source.
Reference: Jones, S. E., Lane, J. M., Wood, A. R., Hees, V. T. van, Tyrrell, J., Beaumont, R. N., … Weedon, M. N. (2019). Genome-wide association analyses of chronotype in 697,828 individuals provides insights into circadian rhythms. Nature Communications, 10(1), 343. https://doi.org/10.1038/s41467-018-08259-7