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Unsleeping genes | Harvard Medical School



An international research team led by researchers at the Harvard Medical School based at the Massachusetts General Hospital and colleagues at the Medical School at the University of Exeter identified 57 genetic regions associated with symptoms of insomnia.

The report of the team, which also indicates a causal link between insomnia and coronary artery disease, is receiving an advanced online publication in Genetics of nature.

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"Our discoveries confirm a role for genetics in the symptoms of insomnia and expand on the four loci genes found above for this condition," said the lead author of the study Jacqueline Lane, HMS instructor in anesthesia at the General Mass.

"All these identified regions help us understand why some people get insomnia, what paths and systems are affected and point to possible new therapeutic goals," he said.

Insomnia affects 10 to 20 percent of adults and twin and family studies suggest that about a third of the risk of insomnia is inherited. Although the evidence suggested that insomnia increases the risk of anxiety disorders, alcohol use disorder, major depression and cardiometabolic diseases, little was learned about the mechanisms involved.

By 2017 Genetics of nature study conducted by Lane e Richa SaxenaHMS, Associate Professor of Anesthesia at the General Mass, main author of the current report, identified three genetic sites associated with self-reported symptoms of insomnia among more than 112,500 participants in the Biobanc study in the United Kingdom.

Shared connections

For the current study, the team analyzed data from more than 450,000 Biobank participants in the United Kingdom, 29 percent of which reported frequent symptoms of insomnia.

The analysis associated 57 genetic sites with self-reported insomnia, associations that were not affected by risk factors known as lifestyle, caffeine consumption, depression or recent stress. Genomic regions identified include genes involved in ubiquitin-mediated proteolysis, a process by which proteins are marked for destruction and those expressed in various brain regions, skeletal muscles and adrenal glands.

Although some of these genes involve connections between symptoms of insomnia, 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 results of the Biobank of the United Kingdom generalized to other populations, the researchers analyzed data from the HUNT study – a Norwegian-based epidemiological study – and Boston-based HealthCare Biobank partners. Comparisons of 15,000 participants from the HUNT study that reported symptoms of insomnia with more than 47,600 controls and 2,200 partners The Biobank participants at HealthCare with clinical diagnosis of insomnia with 14,240 controls confirmed the results of the Biobanc in the United Kingdom.

The data from a subset of almost 85,000 Biobank participants in the United Kingdom that used motion detection devices called accelerometers for up to seven days suggested that genetic regions associated with insomnia have reduced sleep efficiency, a measure of sleep quality and the duration of sleep and increased daily variations in the duration of the dream.

Shared genetic factors associated with insomnia and restless leg syndrome support previous research team work and suggest that undiagnosed restless leg syndrome may undergo insomnia in some patients.

New goals

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

"Insomnia has a very important impact on millions of people around the world. Many know that there is a relationship between insomnia and chronic diseases," said co-author Samuel Jones of the University of Exeter School of Medicine. "Now our results suggest that depression and heart disease are in fact the result of persistent insomnia."

"All of these regions identified are possible new therapeutic goals for insomnia and 16 of these regions contain well-known drug goals," said Lane, a member of the Center for Genomic Medicine and the Department of Anesthesia, Critical Medicine and Pain at the General Mass.

"New causal relationships indicate the possible utility of therapeutic insomnia as possible treatments for coronary artery disease and depression," he said.

Co-senior author Michael Weedon of the University of Exeter added: "There are problems with current treatments for insomnia, including problems with accessibility, addiction and side effects. We hope that understanding more about the underlying processes involved in insomnia will open the way for better treatment and more personalized, which in turn can reduce the amount of insomnia and improve the long-term health of people who do it ".

The main author, Saxena, said: "Next comes the arduous work of discovering how genetic changes to insomnia are obtained. This requires studies in human cells, mice, fruit flies, zebrafish and other model organisms. Essential detailed studies that define more precisely the links causing insomnia to clinical results. None of this work is possible without major collaborative studies in several institutes and countries. Biobank of the United Kingdom is a transformational study in scope and scale, and we need more studies like this, particularly in groups that are poorly represented in genetic studies. "

Support for the study includes the National Institutes of Health (grants R01 DK107859, R21 HL121728, F32 DK102323, R01 HL113338, R01 DK102696, R35 HL135818, R01 DK105072, T32 HL007567 and K01HL136884), the Medical Research Council of the United Kingdom (MR concession / M005070 / 1) and the Wellcome Trust Strategic Support Fund (WT097835MF).

A complete list of authors can be found online with the study.

Image: IStockPhoto

Adapted from a General Mass news liberation


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