Recent research highlights sleep as a crucial factor in maintaining cardiovascular health. Studies have demonstrated connections between adequate sleep and improved blood pressure, lower cholesterol levels, and reduced risks of heart attack and stroke. However, new findings now suggest that sleep may also aid in repairing damage after a heart attack.
A study published in Nature on October 30 observed that sleep is essential for recovery in mice that had suffered heart attacks. This research also presents evidence that sleep may serve a similar restorative function in humans, based on a related sleep restriction study conducted at Columbia University. Marie-Pierre St-Onge, a Columbia University nutritional medicine associate professor and a co-author of the study, provided insights into this research.
St-Onge’s research was designed to explore whether sleep deprivation directly contributes to heart disease. Participants, who initially had adequate sleep, were instructed to reduce their sleep by 90 minutes each night over six weeks. The study revealed that even a mild reduction in sleep duration—common among many Americans—triggers physiological changes associated with a higher risk of cardiovascular disease, marking one of the first demonstrations of a causal link between sustained mild sleep deprivation and heart disease.
In the Nature study, scientists from Mount Sinai discovered that, after a heart attack, the brain releases signals that encourage sleep, which then facilitates cardiac recovery. Mice deprived of sleep after a heart attack showed elevated levels of inflammatory cells in the heart, worsened heart function, and higher mortality rates. Notably, blood samples from sleep-deprived participants in St-Onge’s study indicated similar inflammatory activity as observed in the sleep-restricted mice, suggesting a comparable process in humans, even though these participants had not suffered heart attacks.
Further supporting the study’s findings, researchers observed immune responses in the brain following a heart attack. In mice, immune cells called monocytes accumulated in the brain, releasing a protein known as tumor necrosis factor (TNF), which promotes sleep. By blocking monocyte accumulation, the scientists found that the mice no longer experienced an increase in slow-wave sleep following a heart attack, emphasizing the role of monocytes and TNF in inducing restorative sleep.
Additionally, when researchers disrupted this stage of sleep, mice showed heightened inflammation in both the heart and brain and exhibited worse outcomes, underlining the healing role of sleep post-heart attack.
