A lack of quality sleep may lead to a higher risk of atherosclerosis through the up-regulation of inflammatory-associated white blood cells, a new study published in PLOS Biology determined.
For the study, researchers used sleep lab-based polysomnography and a simple movement detector implemented on one’s wrist to measure sleep disruption in a group of participants. Their levels of neutrophils and monocytes were measured using standard blood cell counts. These two types of white blood cells correlate with inflammatory pathways.
According to the study’s co-authors, “Our findings confirm recent seminal work in mice demonstrating that experimentally induced sleep fragmentation, associated with increases in blood levels of monocytes and neutrophils, results in larger atherosclerotic lesions.”
“Advancing this research, we establish a sleep fragmentation—white blood cell—atherosclerosis association in a population-based sample of human adults and demonstrate that these effects remained robust when accounting for multiple other common atherosclerosis risk factors present in humans: age, sex, ethnicity, BMI, smoking status, blood pressure, and use of antihypertensive medication, as well as sleep apnea and insomnia diagnoses,” the study, led by co-author Raphael Vallat, states.
“Finally, we show that this indirect pathway can be quantified with objective sleep metrics, either using 1 week of wristwatch actigraphy or a single night of PSG recording.”
The study, titled Broken sleep predicts hardened blood vessels, was supported by MESA and the NIH.
