Scientists have been trying to solve the mysteries of sleep for as long as we’ve been tossing and turning. There are plenty of suggested cures for sleeplessness — avoiding caffeine, alcohol, and computer screens before bedtime; ramping up your exercise; skipping midday naps; and the like. But there’s little consensus on what might be happening physiologically to make us more or less likely to snooze.
Researchers at Harvard Medical School recently entered the debate with a study suggesting it may be connected to the body’s immune response, specifically certain types of brain-based immune proteins known as NLRP3 inflammasome. When the brain detects inflammation in the body, it releases a sleep-inducing immune molecule called interleukin-1 beta.
Lead study author Mark Zielinski, PhD, and his team subjected two groups of mice to sleep deprivation and bacterial exposure. They found it triggered an immune response that led to better sleep in the control group with the NLRP3 inflammasome genes than in a group of mice without them.
“Our research points, for the first time, to the inflammasome acting as a universal sensing mechanism that regulates sleep,” says Zielinski. Those who lack the genes necessary to trigger this molecular action may be more prone to sleep disorders.
But DNA is not destiny. When researchers gave interleukin-1 beta to the mice without the gene, they found they enjoyed better sleep quality.
More research is needed, Zielinski says, but the study could lead to future treatment options for folks hoping for more shuteye.