Although researchers discovered a correlative relationship between poor sleep and cardiovascular disease some time ago, the literature is still rife with obscurities.
A new study published in the journal, PLOS Biology nudges research a little further into the light. More discreetly, the authors explore the mechanisms of staffing broken sleep’s association with atherosclerosis—a disease that describes the deposition of plaques of fatty material on the inner walls of the arteries.
“In a diverse sample of over 1,600 individuals, we describe a pathway wherein sleep fragmentation raises inflammatory-related white blood cell counts (neutrophils and monocytes), thereby increasing atherosclerosis severity, even when other common risk factors have been accounted for,” the researchers write in the study’s abstract. “Improving sleep quality may thus represent one preventive strategy for lowering inflammatory status and thus atherosclerosis risk, reinforcing public health policies focused on sleep health.”
Broken sleep as a predictor of the development of hardened blood vessels
The activities of the 1,600 adults featured in the new paper were monitored nightly.
In order to measure fragmented sleep and assess the degree of movement in the participants, the authors used lab-based polysomnography and an actigraph.
Upon further inspection, with the combined help of the tools indexed above, the research team was able to determine how sleep disruptions affect the levels of white blood cells that contribute to the inflammatory response of the body.
Neutrophils, monocytes, and levels of plaque-causing-calcium deposits in the coronary arteries proved to be of particular relevance.
Poor sleep quality caused by frequent movements yielded a decisive correlation with an increase in both neutrophil, inflammation, and calcium measurements. Alone, these biological changes make individuals more susceptible to serious metabolic and cardiovascular diseases.
Over time, increased neutrophil counts and calcium deposits that occur on behalf of chronic fragmented sleep produces several adverse effects on the cardiovascular system. All possible outcomes are compounded by the development of atherosclerosis.“Improving sleep may offer a novel way to reduce inflammation and thus reduce the risk of
atherosclerosis,” explained lead author Matthew Walker, a Professor of Psychology at Berkeley, in a media release.
“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,” he concluded.
CW Headley is a reporter for the Ladders and can be reached at email@example.com