February 18, 2019Cardiology
Poor or insufficient sleep is a major public health problem affecting millions of people of all ages. Studies show that getting enough quality sleep at the right times is vital for health, but fewer than half of adults in the United States get the recommended seven to eight hours per day. Recent research has linked sleep deficiency and certain sleep disorders, such as sleep apnea, to an increased risk of obesity, diabetes, cancer, as well as heart disease. But little is known about the cellular and molecular underpinnings that could help explain the link between sleep and cardiovascular health.
According to an article published in Nature (13 February 2019), based on studies in mice, a previously unknown mechanism between the brain, bone marrow, and blood vessels was discovered that appears to protect against the development of atherosclerosis (hardening of the arteries), but only when sleep is healthy and sound. According to the NIH, the discovery of this pathway underscores the importance of getting enough, quality sleep to maintain cardiovascular health and could provide new targets for fighting heart disease, the leading cause of death among women and men in the United States.
According to the authors, the study identified a mechanism by which a brain hormone controls production of inflammatory cells in the bone marrow in a way that helps protect the blood vessels from damage. The authors added that this anti-inflammatory mechanism is regulated by sleep, and it breaks down when one frequently disrupts sleep or experience poor sleep quality. To learn more about the impact of this deficiency on cardiovascular disease, the authors focused on a group of mice that were genetically engineered to develop atherosclerosis. For the experiment, the sleep patterns were disrupted for half of the mice and allowed the other half to sleep normally. Results showed that over time, the mice with disrupted sleep developed progressively larger arterial lesions compared to the other mice. Specifically, the sleep-disrupted mice developed arterial plaques, or fatty deposits, that were up to one-third larger than the mice with normal sleep patterns. The sleep-disrupted mice also produced twice the level of certain inflammatory cells in their circulatory system than the control mice, and also lower amounts of a hypocretin, a hormone made by the brain that is thought to play a key role in regulating sleep and wake states. The authors also showed that sleep-deficient, atherosclerotic mice that received hypocretin supplementation tended to produce fewer inflammatory cells and develop smaller atherosclerotic lesions when compared to mice that did not get the supplementation. These results, according to the authors, demonstrate that hypocretin loss during disrupted sleep contributes to inflammation and atherosclerosis. However, the authors cautioned that more studies are needed, particularly in humans, to validate these findings and especially before experimenting with hypocretin therapeutically.
Still, health experts say, targeting the newly discovered biological mechanism -- a so-called neuro-immune axis -- could be a breakthrough that one day leads to new treatments for heart disease, sleep, and other disorders.