Researchers Identify New Gene Regions Associated with Insomnia

Insomnia is a common disorder linked with adverse long-term medical and psychiatric outcomes. It affects 10-20% of adults, and several twin and family studies suggested that about a third of the risk of insomnia is inherited. Now a team of scientists from the University of Exeter and Massachusetts General Hospital has identified 57 new gene regions associated with symptoms of insomnia.

Lane et al identified 57 loci for self-reported insomnia symptoms in the UK Biobank (n = 453,379) and confirmed their effects on self-reported insomnia symptoms in the HUNT Study (n = 14,923 cases and 47,610 controls), physician-diagnosed insomnia in the Partners Biobank (n = 2,217 cases and 14,240 controls), and accelerometer-derived measures of sleep efficiency and sleep duration in the UK Biobank (n = 83,726). Image credit: Medical Gallery of Mikael Häggström, 2014 / WikiJournal of Medicine, doi: 10.15347/wjm/2014.008.

Lane et al identified 57 loci for self-reported insomnia symptoms in the UK Biobank (n = 453,379) and confirmed their effects on self-reported insomnia symptoms in the HUNT Study (n = 14,923 cases and 47,610 controls), physician-diagnosed insomnia in the Partners Biobank (n = 2,217 cases and 14,240 controls), and accelerometer-derived measures of sleep efficiency and sleep duration in the UK Biobank (n = 83,726). Image credit: Medical Gallery of Mikael Häggström, 2014 / WikiJournal of Medicine, doi: 10.15347/wjm/2014.008.

“Insomnia has a really significant impact on millions of people worldwide. We’ve long known there’s a link between insomnia and chronic disease. Now our findings suggest that depression and heart disease are actually a result of persistent insomnia,” said study co-author Dr. Samuel Jones, a researcher at the University of Exeter Medical School.

“All of these identified regions are possible new therapeutic targets for insomnia, and 16 of these regions contain known drug targets. The new causal relationships indicate the potential usefulness of insomnia therapeutics as possible treatments for coronary artery disease and depression,” said study lead author Dr. Jacqueline Lane, from Massachusetts General Hospital.

Dr. Lane, Dr. Jones and their colleagues analyzed data from more than 450,000 UK Biobank participants, 29% of whom reported frequent insomnia symptoms.

The analysis associated 57 gene sites with self-reported insomnia, associations that were not affected by known risk factors such as lifestyle, caffeine consumption, depression or recent stress.

The genomic regions identified include genes involved in ubiquitin-mediated proteolysis — a process by which proteins are tagged for destruction — and those expressed in several brain regions, skeletal muscles and the adrenal gland.

While some of these genes imply connections between insomnia symptoms, restless leg syndrome and coronary artery disease, the identified regions did not include neurotransmission genes known to be involved in sleep regulation.

To test whether the UK Biobank results generalize to other populations, the team analyzed data from the HUNT study and from the Partners HealthCare Biobank.

The comparisons of 15,000 HUNT study participants who reported insomnia symptoms with more than 47,600 controls, and of 2,200 Partners HealthCare Biobank participants with clinical diagnoses of insomnia with 14,240 controls confirmed the findings.

Data from a subset of almost 85,000 UK Biobank participants who had worn motion-detecting devices called accelerometers for up to seven days suggested that the insomnia-associated gene regions lowered sleep efficiency, a measure of the quality of sleep, and the duration of sleep and increased day-to-day variations in sleep duration.

An analysis technique called Mendelian randomization, which can reveal whether one of two traits present in individuals may cause the other, indicated that increased insomnia symptoms were causative of coronary artery disease (almost doubling the risk), symptoms of depression and a reduced sense of well-being.

“There are problems with current treatments for insomnia — including issues with accessibility, addiction and side effects,” said co-author Dr. Michael Weedon, a researcher at the University of Exeter.

“We hope that understanding more about the underlying processes involved in insomnia will pave the way for better and more personalized treatments, which in turn could reduce the number of people suffering from insomnia and improve the long-term health of those that do.”

“Next comes the hard work of figuring out how we get from genetic changes to insomnia,” added study senior author Dr. Richa Saxena, from Massachusetts General Hospital.

The results were published in the journal Nature Genetics.

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Jacqueline M. Lane et al. 2019. Biological and clinical insights from genetics of insomnia symptoms. Nature Genetics 51: 387-393; doi: 10.1038/s41588-019-0361-7

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