The Mysterious Link Between COVID-19 and Sleep

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The Mysterious Link Between COVID-19 and Sleep

JAMES HAMBLIN DECEMBER 21, 2020

Close up of a woman sleeping

PETER CADE / GETTY

The newly discovered coronavirus had killed only a few dozen people when Feixiong Cheng started looking for a treatment. He knew time was of the essence: Cheng, a data analyst at the Cleveland Clinic, had seen similar coronaviruses tear through China and Saudi Arabia before, sickening thousands and shaking the global economy. So, in January, his lab used artificial intelligence to search for hidden clues in the structure of the virus to predict how it invaded human cells, and what might stop it. One observation stood out: The virus could potentially be blocked by melatonin.

Melatonin, best known as the sleep hormone, wasn’t an obvious factor in halting a pandemic. Its most familiar role is in the regulation of our circadian rhythms. Each night, as darkness falls, it shoots out of our brain’s pineal glands and into our blood, inducing sleep. Cheng took the finding as a curiosity. “It was very preliminary,” he told me recently—a small study in the early days before COVID-19 even had a name, when anything that might help was deemed worth sharing.

After he published his research, though, Cheng heard from scientists around the world who thought there might be something to it. They noted that, in addition to melatonin’s well-known effects on sleep, it plays a part in calibrating the immune system. Essentially, it acts as a moderator to help keep our self-protective responses from going haywire—which happens to be the basic problem that can quickly turn a mild case of COVID-19 into a life-threatening scenario.

Cheng decided to dig deeper. For months, he and colleagues pieced together the data from thousands of patients who were seen at his medical center. In results published last month, melatonin continued to stand out. People taking it had significantly lower odds of developing COVID-19, much less dying of it. Other researchers noticed similar patterns. In October, a study at Columbia University found that intubated patients had better rates of survival if they received melatonin. When President Donald Trump was flown to Walter Reed National Military Medical Center for COVID-19 treatment, his doctors prescribed—in addition to a plethora of other experimental therapies—melatonin.

Eight clinical trials are currently ongoing, around the world, to see if these melatonin correlations bear out. Few other treatments are receiving so much research attention. If melatonin actually proves to help people, it would be the cheapest and most readily accessible medicine to counter COVID-19. Unlike experimental drugs such as remdesivir and antibody cocktails, melatonin is widely available in the United States as an over-the-counter dietary supplement. People could start taking it immediately.

Yet Cheng emphasizes that he’s not recommending that. Like any substance capable of slowing the central nervous system, melatonin is not a trifling addition to the body’s chemistry. Its apparent benefit to COVID-19 patients could simply be a spurious correlation—or, perhaps, a signal alerting us to something else that is actually improving people’s outcomes. Cheng thinks that might be the case. He and others suggest that the real issue at play may not be melatonin at all, but the function it most famously controls: sleep.

In fact, several mysteries of how COVID-19 works converge on the question of how the disease affects our sleep, and how our sleep affects the disease. The virus is capable of altering the delicate processes within our nervous system, in many cases in unpredictable ways, sometimes creating long-term symptoms. Better appreciating the ties between immunity and the nervous system could be central to understanding COVID-19—and to preventing it.

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