Sleep is something that nearly all species need to survive. On a daily basis, humans need about 8 hours, dogs and cats recharge with around 12 hours, and the koala takes nearly the entire day — napping a whopping 22 hours. But unlike dogs, koalas, or most other animals, we humans don’t always get enough of our required Zzz’s.
Our lives are either too busy or filled with too many distractions that keep us up at night. Sometimes sleep is difficult because of an illness or changing work schedule. No matter the cause, consistent sleep deprivation is harmful to our health and numerous studies have linked it to impairments in cognitive performance as well as numerous physiological health problems like obesity, diabetes, and hypertension.
So exactly why is sleep, especially getting the right amount, so crucial to our health? The answer to this isn’t fully understood. However, it is known that sleep is essential for cellular repair and for the rejuvenation processes in the body, such as muscle repair and hormone regulation. Because many of these functions are regulated via the metabolic system, scientists are interested in researching this area to better understand how sleep deprivation affects the body on a molecular level.
One such study recently conducted at Nova Southeastern University in Fort Lauderdale, Florida investigated the impact of sleep deprivation on systemic metabolism, including major redox metabolites as well as DNA methylation levels. Their results were published in the July issue of PLoS ONE.
Sleep is essential for cellular repair and for the rejuvenation processes in the body, such as muscle repair and hormone regulation.
Cellular redox status can influence the regulation of DNA methylation, or the process by which methyl groups are added to the DNA molecule. Prior studies have found that sleep deprivation can increase DNA methylation levels in circadian clock genes of adipose and muscle tissues which have greater metabolic activity. The epigenetic mark 5-methylcytosine (5-mC) oxidizes to 5-hydroxymethylcytosine (5-hmC) during states of oxidative stress. It’s also been reported that certain sleep disorders, like insomnia, can affect DNA methylation and epigenetically speed up the aging process.
Although several studies have assessed oxidative stress caused by sleep deprivation in animals, this was the first to measure the effects of sleep deprivation on the plasma levels of certain antioxidant metabolites and their epigenetic status in human subjects.
The study included 19 adult participants who each underwent total overnight sleep deprivation. The subjects were instructed to sleep 8 hours the night before their non-sleep session and each wore activity monitoring devices to objectively verify their behavior. In the morning before and after their sessions, saliva and plasma from blood samples were collected and analyzed. After just one night without sleep, the data revealed significantly reduced levels of antioxidant glutathione (GSH), ATP, cysteine, and homocysteine — all important elements of redox metabolism.
Using a popular commercial ELISA-based assay, the team further assessed global DNA methylation levels from genomic DNA that was isolated from plasma samples at different time-points. The results indicated altered levels of both 5-mC and 5-hmC following sleep deprivation.
“Specifically, we found that the levels of plasma antioxidant GSH are decreased with a concomitant elevation in oxidative damage,” the researchers reported. “Additionally, we also observed depleted levels of ATP which can indicate altered mitochondrial functioning.”
These changes are of great importance as previous studies have shown that altered redox and epigenetic status, mitochondrial function, and depleted ATP levels are strong contributors to neurological disorders, including many neurodegenerative diseases.
Interestingly, metabolic biomarkers were not found to correlate with sleep patterns. Therefore the research team ruled out prior sleep behavior as a contributor to the results. Their report stated, “It was the isolated consequences of overnight total sleep deprivation that influenced the above metabolic and molecular changes, not a combination of accumulated prior sleep behavior and sleep deprivation.”
Cortisol levels measured the next morning were also found to be diminished. The team took note that, while cortisol and ATP levels were correlated at baseline, they were not associated, however, after total overnight sleep deprivation.
Further investigation, preferably from a larger cohort, would be needed to validate these results. However, this paper does strongly suggest that sleep loss may induce oxidative stress and ATP loss. In addition, altered antioxidant status may be connected to downstream epigenetic modifications as was represented by the global DNA hypomethylation in the study.
As scientists continue to learn more about the function and regulation of sleep, one key focus has been to understand the risks associated with being chronically sleep deprived and the relationship between sleep loss and illness. Considering these preliminary results, future studies may want to take an epigenetic look at altered redox homeostasis caused by chronic sleep loss and how it predisposes a person to certain diseases and neurological damage. Moreover, these studies could eventually lead to therapies that counteract any damage caused by sleep deprivation, benefiting a large percentage of the population who struggle regularly to get a good night’s sleep.
Source: Trivedi, M.S., Holger D., Bui A.T., Craddock, T.J.A., Tartar, J.L. (2017). Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status. PLoS ONE, 12(7): e0181978.