A night of missed sleep could leave you weaker and more at risk of obesity, according to research which aims to understand how our bodies respond to the increasingly common shift working pattern s well as jet lag and fatigue.
Several studies have shown nurses, pilots and manual workers who have worked years night shifts for years are at higher risk of heart disease, diabetes and cancer, but how the change occurs is less well documented.
Now a team of Swedish researchers has shown how a single night of poor sleep switches on genes in fatty – adipose – tissue which increase the body’s ability to store fat and are implicated in type 2 diabetes.
They also recorded the opposite effect in muscle tissue as complex proteins – the building blocks of muscle – began to break down into simpler forms. This could be an adaptation to help the body hold on to fat stores it is building up, the researchers suggest.
Britain’s night shift workforce has increased by more than 260,000 to 3.2 million people in the past five years.
“Shift working and sleep loss are very common these days, that’s why it’s important to investigate this,” said Dr Jonathan Cedernaes from Uppsala University in Sweden, lead author of the research findings.
“We believe our new study findings provide evidence for how chronic sleep loss and shift work may increase risk of obesity and type 2 diabetes, while at the same time decreasing your muscle mass.”
“We also found evidence this could be linked to changes in the circadian clock, which is known to regulate [the] 24 hour rhythms of how these key tissues utilise metabolic fuel and respond to stimuli.”
Previous studies have only been able to point to an association between muscle loss, diabetes and weight gain in people working shifts, and couldn’t rule out lifestyle factors such as bad diet or lack of exercise as contributory causes.
The study, published in Science Advances on Wednesday, provides some of the first evidence interrupting sleep cycles can directly affect the body’s metabolic processes and lead to long term health risks, though the findings still need replicating in future studies.
To test their theory, the researchers recruited 15 healthy volunteers and took blood, muscle and adipose tissue samples from them after a night of normal sleep and following a night where they were kept awake, to mimic a night shift.
Meal times, exercise patterns and lighting were kept the same on both days to control other factors that could affect metabolism.
One of the tests the researchers ran looked at DNA methylation in tissues – the process which switches on sections of the genetic code which programme certain cellular tasks.
The analysis showed, after sleep disruption methylation increased in sections of the adipose tissue cells DNA that are known to be linked to fat storage.
In muscle tissue there was a decrease in activity in the genes linked to the maintenance of the large, energy intensive muscles, leading the structures to break down – a process known as catabolism.
Both factors could be a response to environmental stress to ensure the body puts on energy reserves, like fat, and consumes less in the day, via muscle wasting. The authors note other studies have shown sleep loss is linked to a reduction in testosterone, and other growth factors which might support their theory.
However it is not known how long lasting the changes are, or how much they are counteracted by activities such as exercise.
“These observations are thus the first to offer an explanation at the tissue level for two seemingly contrasting clinical phenotypes seen following experimental sleep loss in humans: gain of fat mass, occurring concomitantly with loss of lean mass,” the authors wrote.
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