Sleep disruption has been shown to be associated with an increased risk of atherosclerosis, but the mechanism has been unclear. A new study in the open-access journal PLOS Biology reveals that fragmented sleep exacerbates atherosclerosis and may raise the risk of stroke via an effect on inflammatory pathways. 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 authors found that sleep fragmentation, as measured by actigraphy, predicted both higher neutrophil (but not monocyte) counts and higher coronary artery calcium, a measure of atherosclerosis pathology. They showed that the influence of sleep fragmentation on coronary artery calcium was mediated through the increase in neutrophils; in other words, poor sleep led to an increase in neutrophils, which in turn led to an increase in atherosclerosis.
Improving sleep may offer a novel way to reduce inflammation and thus reduce the risk of atherosclerosis. 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.