A scientific study published in the journal Science revealed that heart diseases may disrupt the production of the sleep hormone melatonin in the brain due to damage to a group of nerves connected to both the heart and the superior cervical ganglion. These nerves are located in the neck and are part of the autonomic nervous system, which regulates involuntary processes in the body such as breathing and heart rate.
Since the nerves originating from the superior cervical ganglion are connected to both the heart and the pineal gland, heart-related problems can explain why melatonin production in the body may deviate from the correct pathway. Stefan Engelhardt, a professor of pharmacology and toxicology at the Technical University of Munich, stated in the study: "Imagine the ganglion as an electrical switchboard. In a patient experiencing sleep disorders following a heart condition, you might think of a problem in one of the wires that causes a fire in the switchboard and then spreads to another wire."
Assistant professor of medical sciences at Columbia University, Brooke Agrawal, emphasized that "the research is significant and timely," noting that it "proposes a new mechanism that may help explain why individuals with heart diseases are more prone to sleep disorders." She stated, "Further studies and clinical trials for any potential treatments arising from this mechanism should be conducted."
Approximately 73% of those with heart failure experience symptoms of insomnia. Previous studies have shown that melatonin levels drop among individuals with heart diseases, but scientists did not know the reason.
In the new study, researchers analyzed samples of human brain tissue taken from deceased heart patients and from individuals without heart diseases. This post-mortem analysis revealed a reduced number of nerve fibers, or axons, in the superior cervical ganglion of individuals with heart diseases compared to the "healthy heart" control group. The superior cervical ganglion of individuals with heart diseases was significantly enlarged.
In experiments with mice, the team found immune cells called macrophages, which consume sick and damaged cells, were present in the ganglia of mice with heart diseases, and the nerves exhibited signs of inflammation and scarring. The mice also had fewer axons in their pineal glands and lower melatonin levels in their blood compared to healthy mice. Additionally, the mice's circadian rhythms—internal processes that regulate how the body responds during day and night—were also disrupted, as evidenced by changes in metabolic rates and activity levels, for example.
The team discovered that administering melatonin to the mice completely reversed this disruption. Furthermore, when drugs were used to destroy the macrophages in the superior cervical ganglion of the rodents, their melatonin levels were restored.
Since these analyses were conducted on mice and only 16 individuals, the findings "require further studies" to uncover the mechanisms driving immune cells to the superior cervical ganglion, as the researchers noted in the paper. This may involve examining the neurons connecting the heart and spinal cord, as well as messenger proteins called cytokines that summon macrophages.
The study paves the way for the development of new drugs to treat sleep disorders caused by heart diseases.
