To be human is to sleep. You spend roughly a third of your life in slumber—but your body doesn’t simply flip an “off” switch for all these hours. Your brain, in particular, carries out a long housekeeping list when the lights go out.
One of these tasks is known as “brainwashing,” in which your glymphatic system, an intricate network of vessels, clears toxic waste from the brain—including amyloid-beta and tau, proteins linked to Alzheimer’s disease and other forms of dementia.
Neuroscientist Maiken Nedergaard, co-director of the Center for Translational Neuromedicine and professor at the University of Rochester Medical Center, says she and her colleagues didn’t fully understand what powered this process back in 2012 when they first highlighted the significance of brainwashing.
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Now, they believe they’ve connected the dots in a new study published in the journal Cell—which also details their discovery that a common sleep aid may suppress your brain’s ability to carry out this important task.
Here’s why the new findings are renewing long-held questions about the effects of sleep medications—and what you should keep in mind if you’re one of the 8 percent of Americans who use one to drift off.
Discovering the ‘black hole’ of the glymphatic system
In the Cell study, the researchers’ goal was to find the “black hole”—or the missing mechanism—in how brainwashing works, says Natalie Hauglund, lead study author and postdoctoral fellow at the University of Oxford and the University of Copenhagen.
Specifically, they wanted to figure out how cerebrospinal fluid keeps flowing in the glymphatic system, facilitating a rinse cycle of sorts. The clear fluid glides alongside arteries and seeps into the crevices between small blood vessels that enter your brain, absorbing molecular trash and then funneling it to other areas of your body where it can be expelled
The process is thought to be a boon for brain health, Nedergaard says.
By tracking and measuring blood flow, fluid movement, chemical levels, and other markers in the brains of sleeping mice, the researchers found that it all began when the mice’s brains released norepinephrine, a neurotransmitter integral to the fight-or-flight response. This triggered “micro-arousals” that constricted the brain’s blood vessels. The subsequent drop in blood volume cleared the way for a flood of cerebrospinal fluid.
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When norepinephrine dropped, blood vessels relaxed and puffed up again, nudging the waste-laden fluid out of the brain. These expansions and contractions of blood vessels were measured as rhythmic oscillations (about every 50 seconds), producing a pump-like effect that moved fluid throughout the glymphatic system during non-REM sleep, or deep sleep.
“The brain is the only organ with a skull around it, meaning it has a defined volume,” Nedergaard explains. “So every time blood volume in the brain changes, cerebrospinal fluid has to move to compensate.”
This process has mostly beenobserved in mice, but the researchers say the observations could point to similar happenings in the human brain due to a likeness in certain structures. In fact, previous research had detected the ebb and flow of cerebrospinal fluid in the human brain, but Nedergaard and Hauglund’s paper is the first to pinpoint norepinephrine as a possible trigger.
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Identifying how the brain might clean itself led to an additional discovery: Compared to mice that dozed off naturally, those that were given zolpidem—a common sedative sold under the brand Ambien—experienced oscillations that were significantly suppressed, stunting the flow of cerebrospinal fluid, Nedergaard says.
Bryce Mander, an associate professor of psychiatry and human behavior at the UC Irvine Center for Neurobiology of Learning and Memory, says this finding is “impactful” because it’s early “evidence of the glymphatic system, a neurobiological function in sleep, being actively disrupted by a sedative.”
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Scientists need to examine zolpidem’s potential effect on brainwashing in humans before we draw sweeping conclusions about sleep meds, but that’s challenging to pull off: Rodent studies are the gold standard for measuring glymphatic function because analyzing it in human brains is difficult to do ethically with current technologies, Mander says.
However, it points to broader questions about what it means to get quality sleep. “We need to think about how we evaluate our sleep medications to make sure they aren’t disrupting the fundamental functions that sleep supports,” Mander says, adding that different classes of sleep medications could theoretically cause different types of brain disruptions that haven’t been identified yet. “The goal is not just to be knocked out,” he stresses. “The goal is to have restorative sleep.”
What this means for people who use sleep meds
Brainwashing is just one of your body’s many mysterious functions—and this is just one study that builds on ideas about how it might play a role in your health.
Experts agree you shouldn’t just stop taking your prescribed sleep meds (which is risky without the guidance of a doctor) based on these findings alone, but this new study adds another layer to a growing body of evidence that cautions against their long-term use.
On one end of the spectrum, these drugs can be a “lifeline” for people suffering from debilitating insomnia and other chronic sleep disturbances, says Rebecca Robbins, an assistant professor of medicine in the division of sleep and circadian disorders at Brigham and Women’s Hospital.
For the more than 50 million Americans who have a sleep disorder, medication can quickly offer short-term relief—and we know that getting enough sleep is vital.
However, experts don’t fully understand how these drugs might affect your brain health—and the science on sleep medications is complicated, says sleep researcher Adam Spira, a professor in the department of mental health at the Johns Hopkins Bloomberg School of Public Health.
Studies suggest that regularly popping a sleeping pill could be linked to an increased dementia risk—with caveats. It’s tricky for experts to pin down whether neurodegenerative changes are directly caused by sleep medications or the chronic sleep issues that sparked the need for a prescription in the first place. It’s also possible these meds may amplify symptoms of cognitive decline that were already in motion.
There are opposing theories as well: “Because different sleep aids work on different pharmacological and physiological mechanisms, it’s plausible that some of these drugs may be beneficial for brain health,” Spira explains.
He points to studies that explored how certain sleep medications could theoretically have protective effects against Alzheimer’s disease—but cautions that much more research is needed on this front too. So the jury’s still out.
That said, experts agree that sleep aids don’t replicate natural sleep. That’s why it’s crucial to consider the pros and cons of using one of these drugs with the help of a sleep medicine doctor, if you have that option.
There’s also a drug-free alternative that experts say is worth considering: Among sleep specialists, cognitive behavioral therapy for insomnia (CBT-I) is recommended as the first-line treatment for consistently bad shuteye because the practice is often more effective long-term and conducive to quality rest than sleep meds, without the murky cloud of possible side effects.
Despite the lingering questions, Nedergaard and Hauglund’s new findings underscore one clear thing: Not all sleep is created equal—and we’re slowly inching toward what that means for the brain.
