New Study Unveils Link Between Heart Disease and Sleep Problems
Scientists have made a groundbreaking discovery that links heart disease to sleep problems for the first time. In a study conducted on mice and human tissues, researchers have identified a direct connection between heart disease and the production of the sleep hormone melatonin.
Published in the journal Science, the study reveals that heart disease can disrupt the production of melatonin in the brain due to damage to a group of nerves known as the superior cervical ganglion (SCG). These nerves, located in the neck, are part of the autonomic nervous system, which controls involuntary bodily functions such as breathing and heart rate. Nerves from the SCG connect to both the heart and the pineal gland, the brain structure responsible for melatonin production. Hence, issues with the heart can cause disturbances in melatonin production.
Lead author Stefan Engelhardt, a professor of pharmacology and toxicology at the Technical University of Munich, likened the ganglion to an electrical switchbox, where a problem with one wire can lead to a fire breaking out and affecting other wires. This analogy illustrates how heart disease can impact melatonin production.
The study is being hailed as “important and timely” by Brooke Aggarwal, an assistant professor at Columbia University. Aggarwal noted that the findings provide a novel mechanism explaining why individuals with heart disease often experience sleep disturbances. However, she also stressed the need for future studies and clinical trials to confirm these findings and explore potential treatments stemming from this mechanism.
Insomnia is a common side effect of heart disease, with up to 73% of heart failure patients experiencing sleep problems. Past studies have shown that individuals with heart disease have lower levels of melatonin, but the reasons behind this were previously unknown.
To unravel the mystery, researchers analyzed brain tissue samples from deceased individuals with and without heart disease. The analysis revealed a diminished number of axons, or nerve fibers, in the SCG of those with heart disease. Moreover, the SCG in these individuals exhibited scarring and enlargement.
Further experiments conducted on mice with heart disease confirmed these findings. The mice had immune cells called macrophages present in their cervical ganglia, and their nerves showed signs of inflammation and scarring. Additionally, the mice had fewer axons in their pineal glands and lower levels of melatonin in their blood compared to healthy mice. The disrupted melatonin production affected the mice’s circadian rhythms and led to changes in their metabolic rates and activity levels.
Notably, administering melatonin to the mice completely reversed the disruptions in their circadian rhythms. Destroying the macrophages in the mice’s SCGs also restored their melatonin levels.
While the study’s findings are significant, the researchers emphasize the need for further investigations. They suggest studying the nerve cells linking the heart and spinal cord, as well as the messenger proteins called cytokines that attract macrophages, to fully understand the mechanisms involved.
Looking ahead, the researchers believe that this study could lead to the development of new drugs to treat sleep disturbances caused by heart disease. Professor Engelhardt emphasizes the importance of conducting randomized clinical trials to determine the effectiveness of therapeutic melatonin in treating sleep disorders in individuals with chronic heart disease. If successful, this could spare patients from the unnecessary side effects associated with standard sleeping pills.