Responsible for a staggering 31 percent of all deaths worldwide, cardiovascular disease is the number one killer in the world, according to the World Health Organization. The main risk factors are lifestyle choices like a bad diet, smoking, lack of exercise – and poor sleep. That last point has gone relatively unstudied, but new research out of Harvard has found the chemical chain reaction that links disrupted sleep and cardiovascular disease.
It might not be that surprising then that poor sleepers seem more likely to develop cardiovascular disease, but exactly how it happens was the focus of the new study.
"The research showing a link between sleep and cardiovascular disease in humans is abundant," says Filip Swirski, corresponding author of the study. "We wanted to know the 'how.' In this study we uncovered one small piece of what is surely a much larger puzzle."
The team focused on one aspect of cardiovascular disease in particular – atherosclerosis, where the arteries become harder and inflamed in response to the build up of fatty plaques. Things only get worse when the immune system sends white blood cells to the rescue, which get caught up in the plaques and end up making them bigger. As the plaques grow blood flow is reduced, and there's a chance that they can cause blood clots that clog arteries, leading to heart attacks or strokes.
To investigate the connection between sleep and atherosclerosis, the Harvard researchers experimented with mice that were fed a high-fat diet and had been genetically altered to develop the condition. One group was then deprived of sleep, and the team found that these mice developed larger plaques than a control group. More white blood cells were also found in the plaques and bloodstreams of the experimental group compared to the control group.
Through further experiments, the researchers found the mechanism that seems to cause the problem. Poor sleep appears to reduce the levels of a protein called hypocretin, which is produced in the hypothalamus – the brain region responsible for regulating sleeping patterns.
Low levels of hypocretin, in turn, leads to higher levels of a protein called colony-stimulating factor 1 (CSF-1), which ramps up white blood cell production. Interestingly, when the team gave the sleep-deprived mice supplements of hypocretin, the athersclerosis declined.
"The role of hypocretin was certainly very, very shocking and unexpected to us," says Cameron McAlpine, first author of the study. "We really didn't know what to make of it initially. We had no idea we would find increasing white blood cells and this production could actually be regulated by sleep."
Of course, as a mouse study there's no guarantee the same mechanism is at work in humans, but finding out is the next step for the team. If it is, it might also help uncover new treatment options for other inflammatory conditions.
The research was published in the journal Nature.
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