18th March 2019

Genetically awake: Insomnia linked to genes

Researchers have linked 57 gene regions to insomnia, revealing new potential target areas for treatment to this increasingly prevalent condition
Genetically awake: Insomnia linked to genes
Photo: Seniju @ Flickr

Tired of being tired? 30% of the population regularly suffer from insomnia but little is understood about the condition. Genetics might provide an explanation, but this brings its own problems.

Insomnia is a sleep disorder characterised by an inability to fall asleep or stay asleep for long periods of time. It can leave sufferers exhausted, agitated, and accident prone as well as increase their risk of alcoholism. Clinically, its definition is vague as the amount of sleep each person requires varies, and periods of stress or uncomfortable sleeping environments can make falling asleep harder. Typically though, if a person is struggling or failing to fall asleep three nights a week for at least three months and they feel drained the next morning, then they are considered to be an insomniac.

Not much is understood about the causes of insomnia. It is often attributed to excess consumption of stimulants such as caffeine or mental health issues such as anxiety, stress, and depression. However, these can also arise as a result of insomnia itself.

Genetic factors are also involved. A study by Massachusetts General Hospital, University of Exeter Medical School, and the Universities of Bristol and Manchester identified 57 gene-regions that are associated with symptoms of insomnia, including the four regions that were known of previously. These gene sites studied were involved in regulating protein destruction and were expressed in multiple regions of the brain, adrenal gland, and skeletal muscle. They are also not known to be affected by risk factors for insomnia. Researchers are hopeful that they could therefore be used as new drug targets and tackle the route mechanisms of insomnia and other related sleep disorders.

Interestingly, the study also reported that insomnia can double a person’s risk of developing coronary artery disease and that it shares genetic factors with restless leg syndrome. This may explain why the gene sites studied were expressed in the skeletal muscle. Further study is required to understand the mechanisms behind these associations. However, with insomnia alone costing the American economy an estimated $107.5 billion a year, there is a dire need for more to be done.

Scientists and those in the medical profession should proceed with care though. There are inherit problems associated with linking genetics to a trait or disease. Whilst such knowledge can be useful for diagnostics, counselling, drug treatments, and preventative measures, it is important to stress that for most behaviours genetic associations are just that: associations. They are not always directly causative and often work in conjunction with environmental and social factors to determine the final effect.

If this is not stressed, biology can be perverted. That is not to say that knowledge about insomnia and coronary artery disease will lead to eugenics, but the overemphasis of genetic links can lead to a narrow focus on treatments such as gene therapy at the expense of solutions that target environmental factors.

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