Sleep disruption has been shown to be linked to an increased risk of atherosclerosis, but the mechanism has been unclear.
In a new study, researchers found that fragmented sleep boosts atherosclerosis and may raise the risk of stroke via an effect on inflammation.
Atherosclerosis is the buildup of fats, cholesterol, and other substances in and on the artery walls (plaque), which can restrict blood flow. The plaque can burst, triggering a blood clot.
These results provide a mechanism to explain the long-standing observation that poor sleep increases the risk of heart disease and stroke, and suggest simple and direct ways to reduce such risk.
The research was conducted by a team at the University of California at Berkeley.
To test whether the effect may be due in part to increased inflammation, the team measured sleep disruption through both sleep lab-based polysomnography and a simple movement detector worn on the wrist over multiple nights (actigraphy).
They found that sleep fragmentation predicted both higher neutrophil counts, a type of white blood cells responsible for driving inflammatory pathways, and higher coronary artery calcium, a measure of atherosclerosis.
They showed that the influence of sleep fragmentation on coronary artery calcium was mediated through the increase in inflammation.
In other words, poor sleep led to an increase in inflammation, which in turn led to an increase in atherosclerosis.
The influence of sleep disruption on neutrophils and atherosclerosis remained significant after accounting for multiple known contributors to artery disease.
The team says improving sleep may offer a novel way to reduce inflammation and thus reduce the risk of blood clots.
These findings may help inform public health guidelines that seek to increase the continuity of sleep as a way to improve health and decrease the burden of heart disease on society.
The study is published in PLOS Biology.
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