The pace of life has increased in the United States over the years, and every second counts. Every second counts in sleep as well, however, sleep may be taken for granted. The Centers for Disease Control and Prevention (CDC) reports approximately 70 million Americans suffer from chronic sleep problems. Sleep deprivation is associated with physical injuries, mental illnesses, poor quality of life and well-being, obesity, depression, and decreased work productivity.
A new study published in the journal Sleep found another reason to get a good night’s rest. Researchers from Uppsala University found that a night with no sleep can increase biomarkers responsible for brain damage.
Lead author and investigator Christian Benedict told Medical News Today, “We observed that a night of total sleep loss was followed by increased blood concentrations of [neuron-specific enolase (NSE)] and [S100 calcium-binding protein B (S-100B)]. These brain molecules typically rise in blood under conditions of brain damage. Thus, our results indicate that a lack of sleep may promote neurodegenerative processes.”
15 healthy young Swedish men participated in two conditions of the study. The first group received eight hours of sleep, while the second group participated in total sleep deprivation. Fasting blood samples were drawn before and after the sleep periods.
Participants who were under total sleep deprivation showed to have increased serum levels of the proteins NSE and S-100B by approximately 20 percent compared to the individuals who received eight hours of sleep. Increasing concentrations of these proteins in blood may reveal either neuronal damage, impaired blood brain barrier function, or both takes place in sleep deprivation. The ratio of beta-amyloid peptides 1-42 and 1-40 did not differ between sleep periods. A reduced ratio is considered an indirect measure of increased removal of beta-amyloid 1-42 peptide in the brain.
More studies need to be completed in order to prove that lack of sleep demonstrate neuronal damage. The researchers suggest that future studies which both serum and cerebrospinal fluid are sampled after sleep loss can clarify whether increased serum neuron-specific enolase and S100 calcium binding protein B is primarily caused by brain damage, impaired blood-brain barrier function, or is just a consequence of increased gene expression in non-neuronal cells.