We’ve seen evidence in recent years, though, that running up a sleep deficit and attempting to catch up at a later date meets with limited success. Recent research has indicated that the effects of insufficient sleep can’t be fully remedied by "recovery sleep." And for people who work especially long hours, or irregular and nighttime hours in shift work—and for others who suffer from chronic sleep deficiencies because of sleep disorders—sleep loss can become too large and too frequent a debt to surmount.
Worse Than We Thought
New research suggests that the consequences of chronic insufficient sleep are less reversible than previously understood and may involve lasting damage to the brain. Researchers at the University of Pennsylvania’s Perelman School of Medicine and China’s Peking University studied neural activity in mice under different levels of sleep loss. They found that prolonged periods without sleep led to impaired neurological cell function—and the death of brain cells.
This is some of the first evidence to indicate irreversible damage to the brain linked to insufficient sleep.
Scientists put the mice on a rotating sleep routine, including periods of normal rest, short periods of wakefulness, and extended periods without sleep. The sleep model was designed to mimic a human shift worker’s sleep routine. After each sleep period, researchers conducted neurological examinations to seek evidence of damage and altered function. Researchers were particularly interested in the area of the brain known as the locus coeruleus (LC). LC neurons participate in a wide range of important neurological functions, including regulation of arousal, attention and wakefulness, as well as memory, emotional responses, and cognitive function. Examining the mice after different degrees of sleeplessness, researchers found significant changes to the health and function of this area of the brain. They discovered that while LC neurons in the mice were able to cope effectively through short-term periods of sleep deprivation, periods of extended wakefulness brought diminished function and the eventual loss of brain cells:
We don’t know yet if these effects of recurring or chronic sleep deprivation observed in mice will present themselves similarly in humans. That’s a next step for researchers to explore, along with establishing more precisely the degree of sleep loss that might expose the brain to the risk of this type of lasting damage. But these results are troubling, and strongly caution against the idea that chronic sleep loss can be recouped—that we can continually repay ourselves a sleep debt in full and without harm or negative consequence.
Signs of Hope?
Other recent research has also highlighted the damaging effects of insufficient and poor-quality sleep on the brain:
This research delivers sobering news, but also opens some important pathways for future inquiry that may lead to new and better treatments for sleep problems and perhaps other neurodegenerative diseases. This research provides important new insight into how at least one part of the brain works to protect itself against short-term sleep loss—and that knowledge may be helpful in creating new treatments for people who struggle with chronic sleep insufficiency, including the 15 million shift workers in the United States and millions more around the world.
Researchers also intend to further examine the sleep-related damage to LC neurons, and a possible relationship to neurodegenerative diseases including Alzheimer’s disease and Parkinson’s disease, as there is evidence that damage to this area of the brain may speed the development of these conditions. Further study of the effects to this area of the brain as a result of sleep loss may help scientists identify people who—by age, health, or lifestyle—are at elevated risk for this type of neural damage.
This is yet another powerful reason to establish a routine of high-quality, plentiful sleep—and to avoid the cycle of sleep debt. You may protect your brain from damage that can’t be undone.
Michael J. Breus, Ph.D.
The Sleep Doctor™