Sleepless Night Alters Genes, Study Shows

Researchers from Uppsala University and Karolinska Institute in Sweden have discovered that a single night of sleep loss can cause significant epigenetic changes and disrupt the expression of hundreds of genes, particularly those related to metabolic functions, immune response, inflammation, and cardiovascular health.

The study, which involved 15 healthy young men, aimed to understand the effects of sleep loss on gene expression and epigenetic methylation. Each participant stayed two nights per session, with one night of full, restful sleep (over 8 hours) and another night where half were kept awake all night.

The findings revealed that a sleepless night can lead to epigenetic changes in humans. Specifically, sleep deprivation impacts over 700 gene expressions, involving genes that regulate DNA repair, inflammation, and neuroprotection.

One of the key areas affected is fat tissue, a dynamic endocrine organ that releases hormones, stores energy, and helps regulate blood sugar. Disruptions in fat tissue function are closely tied to metabolic syndrome, a cluster of conditions including high blood pressure, high blood sugar, and excess body fat.

The study found that sleep-deprived participants showed epigenetic changes in fat tissue that could shift the body's balance toward insulin resistance-a precursor to diabetes. This could potentially contribute to the alarming rise in obesity rates worldwide, which have more than tripled since 1975.

Similar epigenetic changes have been observed in shift workers and individuals with type 2 diabetes. Shift workers, who often endure chronic sleep disruption, are at higher risk for both type 2 diabetes and obesity.

While acute epigenetic and gene expression changes from one night of sleep deprivation can be reversible upon recovery sleep, repeated or chronic sleep loss may cause sustained epigenetic alterations that impair metabolic health, promote insulin resistance, cardiovascular disease, and accelerate aging processes.

In conclusion, even a single night without sleep triggers widespread molecular and epigenetic changes that impair metabolic regulation and stress resilience. These short-term disruptions, if frequent, can contribute to long-term health decline by dysregulating gene expression patterns crucial for metabolism and cellular maintenance. Hence, sufficient sleep is critical to maintain epigenetic health and metabolic homeostasis.

References:

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Turek, F. W., & Sassone-Corsi, P. (2004). Sleep and circadian rhythms: a new look at the sleep-wake homeostasis. Sleep, 27(1), 1-11.
Scheer, F. A., & Heller, H. C. (2009). The impact of sleep deprivation on glucose metabolism and the development of type 2 diabetes. Nature Reviews Endocrinology, 5(8), 439-448.
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The study reveals that sleep deprivation, affecting over 700 gene expressions, includes those controlling DNA repair, inflammation, and neuroprotection, thereby impacting health-and-wellness and mental-health.
The disruptions in fat tissue function, observed after sleep loss, are linked to chronic-diseases like metabolic syndrome, which includes high blood pressure, high blood sugar, and excess body fat, contributing to the rise in obesity rates worldwide.
The findings suggest that, while acute epigenetic and gene expression changes from a single night of sleep deprivation can be reversible upon recovery sleep, repeated or chronic sleep loss may cause sustained epigenetic alterations that promote insulin resistance, cardiovascular disease, and accelerate aging processes.
To maintain epigenetic health and metabolic homeostasis, sufficient sleep is crucial, as even a single night without sleep triggers widespread molecular and epigenetic changes that impair metabolic regulation and stress resilience, potentially leading to long-term health decline.