The reason why individuals with heart disease experience sleep problems can be attributed to the impact on the production of the sleep hormone melatonin in the brain, according to research.
Around one-third of people with heart disease face various sleep issues, including sleep apnea, insomnia, frequent awakenings during the night, and restless legs syndrome.
Heart diseases affect the production of melatonin in the pineal gland
The study, led by a team from the University of Munich (TUM) in Germany, revealed that heart diseases affect the production of melatonin in the pineal gland, located inside the brain, with a critical link between these two organs being a ganglion situated in the neck region.
Melatonin, the sleep hormone, is synthesized in the pineal gland, and like the heart, it is regulated through the autonomic nervous system, which controls involuntary bodily processes. The nerves related to both the heart and pineal gland originate in the ganglia, particularly the superior cervical ganglion, which holds significant importance for these functions.
To illustrate the findings, the ganglion was compared to an electrical switch box. In heart disease patients experiencing sleep disturbances, it can be likened to a problem with one wire causing a fire in the switchbox, subsequently affecting other wires.
The research team observed that mice with heart disease had an accumulation of macrophages, cells responsible for engulfing dead cells, in the cervical ganglion. These macrophages led to inflammation, scarring, and the destruction of nerve cells within the ganglion. Long fibers, known as axons, connected to the nerve cells and extended to the pineal gland in both mice and humans.
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As the disease progressed, there was a significant reduction in the number of axons connecting the gland to the nervous system, resulting in decreased melatonin levels and disruptions to the animals’ day/night rhythm.
A similar effect was observed in humans. Pineal glands from nine heart patients showed significantly fewer axons compared to the control group. Additionally, the superior cervical ganglion in these patients displayed scarring and noticeable enlargement.
The researchers believe that the negative effects of the damaged axons become irreversible at an advanced stage of the disease.
In a positive development, the team managed to restore melatonin production to its original level in mice during the early stages of the disease by using drugs to eliminate the macrophages in the superior cervical ganglion. This finding not only underscores the role of the ganglion in this phenomenon but also offers hope that drugs could be developed to prevent irreparable sleep disturbances in individuals with heart disease.
The study brings new hope for heart patients, potentially leading to effective treatments for sleep disturbances, and highlights the significance of ganglia from a diagnostic perspective.
