Photograph by Shizuo Kambayashi/AP

Since June, 1957, the Centers for Disease Control and Prevention has been monitoring America’s health habits, tabulating things like whether we smoke, drink, or sit around all day, and how many of us visit our doctors regularly and take our medications at the prescribed times. Until recently, though, one aspect of our behavior largely escaped note: the amount of time we spend sleeping. And so, in 2009, the C.D.C. decided to add a sleep dimension to its survey.

Average sleep length has been declining throughout the country, for all age groups, since the nineteen-eighties, and this shorter sleep duration is very likely making people less healthy. When the C.D.C. surveyed some seventy-five thousand American adults about their sleeping habits, more than thirty-five per cent reported that they regularly slept fewer than seven hours a night. It wasn’t just these individuals who were functioning poorer; even some of their longer-sleeping peers—those who slept more than seven hours, but still short of the recommended amount—were feeling the effects of sleep deprivation. Nearly forty per cent had fallen asleep unintentionally at least once in the prior month, while five per cent—more than fifteen and a half million people nationally—had fallen asleep behind the wheel at least once in the same time frame. When you narrowed the sample to people between twenty-four and thirty-four years old (the group reporting the least sleep), the rate rose to more than seven per cent.

Sleep deprivation can cause actual physical harm, like a car crash, or cause you to hit “reply all” when you don’t mean to—a crash of a different sort. It results in severe cognitive impairments: lower productivity and difficulty concentrating, memory issues, and motivational problems. It even makes you like your hobbies less. That’s not to mention the known increased health risks, like hypertension, heart disease, obesity, stroke, diabetes, cancer, and even neurodegenerative diseases, like Alzheimer’s. Sleep deprivation may be one of our greatest, and often invisible, public-health threats. And, as Ian Parker wrote in the magazine last year, it’s not a threat that’s very easily addressed through our usual approach of more—or better—drugs.

Allan Pack wasn’t always a sleep expert. He started his career as a pulmonologist and came to the University of Pennsylvania, in the late seventies, to study the neurophysiology of breathing. Though the work was interesting, Pack wanted to pursue something with a more direct, tangible impact on patients’ lives. “I realized that there’s not that much clinical significance to pulmonology,” he told me. Around the same time, the clinical community recognized a new disorder—sleep apnea, a chronic condition in which irregular breathing causes severe sleep disruption. This, it seemed, was the perfect application for Pack’s expertise: a breathing issue, but one with wide clinical implications. “I appreciated just how impactful it was on people’s lives and how effective the treatment could be. In the end, I gave up the pulmonary side altogether, and became a sleep person,” he says. In the early eighties, Pack decided to dedicate his lab to the basic questions about sleep: why we sleep; what genes determine sleeping habits, if any; and what happens when sleep is disrupted.

When Pack began studying the nature of sleep deprivation, one fact struck him: when deprived of sleep, some people responded much better than others. After thirty-six hours of sleep deprivation, some might do things like leave their house keys in the fridge or walk to work in slippers. Others would be basically fine. “We knew it was a stable trait: the same person would respond the same way to being sleep deprived on two separate occasions,” he said. “But what we really wanted to know was how much of that is genetic.” Was resistance something heritable that you could pin down—and then use to help better understand the mechanisms of sleep itself, to aid the chronic sleep sufferers who need it most?

After three decades of work, Pack is closing in on an answer. In 2012, he and his colleagues at the University of Pennsylvania’s Center for Sleep and Circadian Neurobiology published the results of an ongoing study of the sleep patterns of identical and fraternal twins. For thirty-eight hours, each twin was kept continuously awake while being carefully monitored by a team of sleep researchers. Every two hours, each one was given a Psychomotor Vigilance Test (P.V.T.), a task in which one must react quickly to a light or a dot that appears on a screen at random times, to determine his reaction time in different conditions. “If susceptibility to sleep deprivation is heritable, the identical twins should be close together on their performance, and the non-identical should be further apart,” Pack said. What the researchers found was that the reaction to sleep deprivation was largely heritable: eighty per cent of the variation among peoples’ susceptibility to the cognitive effects of sleep deprivation was explained by genetics. “The genes people had clearly affected how they responded to sleep deprivation,” Pack said.

But what, precisely, were those genes? And how was the difference actually playing out inside the twins’ bodies? Pack had half the answer—sleep deprivation had a genetic component—but he didn’t know what that other component was. In 2009, however, he got a hint, when Ying-Hui Fu’s laboratory, at the University of California, San Francisco, which is dedicated to the molecular study of human sleep behaviors, noted a curious anomaly in her sleep data. Among the hundreds of people Fu had studied over the years, two individuals stood out: a mother and a daughter in the same extended family who slept six hours a night—a level that is considered sleep-impaired for the overwhelming majority of the population—but who functioned perfectly well. Fu, a geneticist, analyzed their DNA and found one particular mutation in a gene known to regulate circadian rhythms that seemed to separate them from their sleep-deprived counterparts. She then inserted that mutation into mice genomes.The effect was clear: the animals with the mutation not only began to sleep less than their counterparts but continued functioning well even after six hours of sleep deprivation (a long time for a mouse). Those without the mutation showed the usual signs of deprivation.

For Pack, Fu’s work was monumental. If one mutation had such an effect on sleep duration and subsequent cognitive function, couldn’t there be more that did the same? He decided to test that theory with the twins whose sleep patterns he had been studying. His team proceeded to sequence the same gene that Fu had identified in the entire twin sample, to see if they could find the same, or a related, mutation that would replicate the sleep-deprivation effect. Luck was on their side. They found the perfect sample: twenty-seven-year-old male twins, only one of whom had a mutation. It wasn’t the precise variant that Fu had found, but it was related to the same circadian-regulating gene.

As it turns out, the twin who had the mutation slept, on average, two hours less per night than his brother. When Pack looked at how the pair had fared on the P.V.T.—the measure of sleep deprivation used in his earlier study—he found that the twin carrying the mutation significantly outperformed his brother. When the twins were allowed to catch up on the sleep that they had lost in the study, the carrier twin needed far less time to recover—almost a hundred minutes less. Here, then, was a genetic variant that appeared to allow its carriers to derive the same benefit from six hours of sleep as the vast majority of us gets from eight. Pack and his colleagues published the results last month.