Sleep is that golden chain that ties health and our bodies together. Thus wrote the English playwright Thomas Dekker in the 16th century, reflecting a view that has persisted through the centuries. Sleep is crucial to our wellbeing. Disturb it and you will find your constitution troubled and twisted out of joint.
It is a view supported by science. Experiments in which men and women have endured periods of up to 11 days without shut-eye have shown that if we cannot sleep we develop increasingly severe symptoms: progressive decreases in concentration, perception and other higher mental processes. Intriguingly, these problems vanish once subjects are allowed a couple of nights curled up in their beds in a state of blissful unconsciousness.
Just why we need sleep has been more difficult to answer. Freud argued that sleep allows us to have dreams in which we can act out wishes that are too disturbing to contemplate while awake. Others have maintained that sleep is a leftover from our stone age past, when it would have been dangerous to blunder around in the night at the mercy of nocturnal carnivores. So we evolved the habit of sleep to keep us safe, sound and unconscious in our caves. More recently, scientists have argued that sleep is involved in helping our bodies to recover from the vicissitudes of the day and for our brains to process the experiences of the previous 12 hours.
All these theories have their proponents and opponents – for scientists are certainly far from reaching an agreement about the biological causes of sleep. However, a couple of papers published last week suggest there may be new avenues for researchers to explore so that they can learn how sleep works and why animals need it so badly.
The first, by researchers at Washington State University and several other institutions, is published in the open-access journal Science Advances, and highlights how one particular gene is involved in the quality of sleep that is experienced by different animals, including humans – and raises hopes that it could be involved in sleep regulation.
The second paper, published in the journal Cell, is the work of a team led by Alina Patke, of the laboratory of genetics at Rockefeller University. It focuses on the phenomenon of night owls – those of us who are happy to go on carousing late at night, but who find it difficult to rise in the morning, even the late morning – and indicates it is linked to a gene mutation that causes our internal clocks to run slowly.
In the case of the Washington State research, the project was led by Jason Gerstner, at the university’s College of Medicine. He has found that the expression of the gene FABP7 changes over the day inside the brains of mice. In addition, his team discovered that mice that have had their FABP7 gene knocked out – ie, disabled – slept more fitfully compared to normal mice, which had an intact gene.
This discovery raised the question of how humans might be affected by mutations in the FABP7 gene. So the team turned to a sleep study of 300 Japanese men that included analysis of their DNA. Crucially, a total of 29 of these men were found to have a special variant of the FABP7 gene: one that was correlated with their sleep patterns. Those with the variant slept more fitfully and woke up more often than other people with the “normal” variant of the gene.
Further research showed a similar effect could be induced in fruit flies. “This suggests there is some underlying mechanism throughout all these species that regulates consolidated sleep,” says Gerstner. “It suggests we have found an ancient mechanism that [has] persisted over evolutionary time.”
Although the team stress that other genes are almost certainly involved in sleep regulation, the discover of the link with the FABP7 – which is involved in controlling other genes involved in growth and metabolism – is highly encouraging for sleep research.
The second paper, in Cell, concerns a different mutation, this time in the CRY1 gene. Scientists led by Patke have found that one variant alters the human circadian clock, which dictates our sleep-wake cycles. It was found that carriers of the variant experience night-time sleep delays of more than two hours. “It’s as if these people have perpetual jet lag, moving eastward every day,” said Michael Young, another researcher at the genetics laboratory. “In the morning, they are not ready for the next day to arrive.”
The condition – known as delayed sleep phase disorder – can cause people to struggle to sleep at night and is associated with raised risk of diabetes, cardiovascular disease and Alzheimer’s. Again, the discovery of a link between this vulnerability to a specific piece of DNA suggests a new understanding of the control mechanisms involved in sleep could be obtained in the near future.
One day, in the near future, we may at last gain a true understanding of how “nature’s sweet restorer” affects our lives – and use that knowledge to make our lives a little better.
