Poor sleep quality linked to heart disease
Researchers at UC Berkeley have identified a link between poor sleep quality and cardiovascular disease. The experts are describing how fragmented nightly sleep can lead to chronic inflammation and atherosclerosis, a disease characterized by the buildup of fatty materials in the arteries.
“We’ve discovered that fragmented sleep is associated with a unique pathway – chronic circulating inflammation throughout the bloodstream — which, in turn, is linked to higher amounts of plaques in coronary arteries,” said study senior author Professor Matthew Walker.
Fatty plaque buildup can harden over time, narrowing the arteries and potentially causing a fatal heart attack or stroke.
The new study indicates that poor sleep quality should be added as a key risk factor for cardiovascular disease, the leading cause of death in America.
Known risk factors for cardiovascular disease include poor diet, lack of exercise, obesity, high blood pressure, and smoking.
Study lead author Raphael Vallat is a postdoctoral researcher in the Center for Human Sleep Science at UC Berkeley.
“To the best of our knowledge, these data are the first to associate sleep fragmentation, inflammation and atherosclerosis in humans,” said Vallat.
The research was focused on data from the Multi-Ethnic Study of Atherosclerosis, which involved more than 1,600 middle-aged and older adults.
The Berkeley team used statistical modeling to analyze the data, controlling for known risk factors in order to isolate the effect of sleep quality on heart health.
Next, the researchers tracked the health outcomes of the study participants by looking at blood tests, calcium scores related to plaque buildup, and several different measures of sleep. The individuals had worn sleep trackers for a week and engaged in an overnight sleep study that measured electrical brainwave signals.
The results of the analysis revealed a clear connection between disrupted sleep patterns and higher levels of inflammatory factors in circulating blood.
In particular, the experts found that poor sleep quality was linked to higher concentrations of white blood cells known as monocytes and neutrophils, which are key indicators of atherosclerotic plaques.
“In revealing this link with chronic inflammation, the findings suggest a missing middleman that is brokering the bad deal between fragmented sleep and the hardening of blood vessels,” said Professor Walker.
“Indeed, these associational results in humans mirror recent data in which experimentally manipulated sleep disruption in mice led to higher levels of circulating inflammation that caused atherosclerotic lesions in the rodents,” said Vallat.
According to the researchers, the findings linking poor sleep to atherosclerosis through chronic inflammation have major public health implications. For example, atherosclerosis often begins in early adulthood.
“Unfortunately, this process goes largely unnoticed until the plaque buildup, in middle or old age, suddenly blocks arterial blood flow to the heart, lungs, brain and/or other organs, hence its moniker, ‘silent killer,'” said Vallat.
The experts recommend monitoring sleep quality with the use of clinical grade tracking device.
“The insidious nature of the disease requires that we pay attention to our sleep hygiene, even starting in early to midlife,” said study co-lead author Vyoma Shah.
“If you track your sleep patterns using objective measures, the same way you track your weight, blood pressure or cholesterol, you can make modifications to your sleep habits, which could make a tangible difference to later life health outcomes.”
The study is published in the journal PLOS Biology.