Scientists belonging to the Massachusetts General Hospital along with people belonging to other research centers have investigated the development of atherosclerosis in the mouse model.
The researchers have found that the mice who had disturbed sleep suffered from larger plaques in their vessels as compared to those who slept well. The sleep-deprived mice were also found to have higher quantities of inflammatory cells with low levels of hypocretin, a hormone that regulates wakefulness.
The researchers also observed a decrease in inflammatory cells as well as atherosclerosis in these mouse model after receiving hypocretin supplementation. The findings demonstrated that sleep can influence cardiovascular health by the regulation of hypocretin within the brain.
These findings have been published in the journal called Nature.
Health, Sleep, and Atherosclerosis
Sleep is an extremely important part of health. Insufficient or disturbed sleep is a prominent public health issue affecting millions of individuals. In the United States alone, almost 35 percent of the people were found to sleep for less than 7 hours per day in 2014.
Studies have also associated a lack of sleep with long-term health problems such as depression, obesity, type 2 diabetes, and heart disease. However, the underlying biological mechanism has not been highlighted.
Dr Swirski along with colleagues set out to investigate the effects of sleep on cardiovascular health by emphasizing on the development of atherosclerosis. The plaques arising as a result of atherosclerosis may take years and mainly consist of fat molecules, calcium, cholesterol, and other agents. As they gather, they reduce the flow of oxygen and nutrient-rich blood.
Atherosclerosis may lead to a variety of problems such as coronary heart diseases characterized by the buildup of plaque in the arteries supplying the heart.
Poor Sleep Patterns and Atherosclerosis
The researchers used mice that were genetically more predisposed to acquire atherosclerosis. Half of them were allowed to sleep properly while the other half underwent disturbances in sleep.
Comparing both groups, the researchers found that mice with disrupted sleep patterns were one-third more likely to develop arterial plaques.
The sleep disturbance was also found to double the production of a particular type of pro-inflammatory white blood cells in the bone marrow. Moreover, the lateral hypothalamus in these mice was found to secrete a reduced level of hypocretin.
Atherosclerosis was found to be of a slow onset in mice that were provided with hypocretin supplementation. The researchers also noticed that the hypocretin controlled the blood cell production in bone marrow by regulation of CSF1, a kind of signaling protein.
They concluded that a rise in the white blood cells and the consequent increase in atherosclerosis in sleep-deprived mice was mainly due to an increase in CSF1 and a decrease in hypocretin.
They also suggested that an intact sleep provides protection to the blood vessels from atherosclerosis by regulation of hypocretin levels.
Experts say that this research has helped provide a direct demonstration of the molecular connections that link the state of sleep with cardiovascular health.