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RHYTHMS

At the New York Obesity Research Center of Columbia University, assistant professor Marie-Pierre St-Onge randomly assigned her research volunteers to one of two groups. For five consecutive nights, the first group was granted nine hours in bed per night, while the second group was condemned to only four (unfortunately for the former group, they had to swap interventions in the second phase of the study). Both groups slept and ate in the lab during that time so that researchers could closely monitor them. Each night, the volunteers were outfitted with a tangle of electrodes and wires that monitored brain waves and other indicators of sleep. The goal of this intensive study was to understand the impact of sleep restriction on food intake and brain activity, a topic that has captured the attention of many researchers in recent years—and which may help explain why we overeat in the modern world.

On the fifth day of St-Onge’s study, the volunteers were turned loose upon the world and allowed to eat whatever they wanted for a day. The only catch was that they had to let the research team weigh and record everything they chose. At the end of the study, St-Onge and her colleagues analyzed the data and came to a striking conclusion: Their volunteers ate nearly 300 more Calories per day when they were sleep-deprived than when they were well-rested. “In our experience,” explains St-Onge, “sleep restriction increases food intake. It’s as simple as that.” DYING TO SLEEP

To understand how sleep restriction causes us to overeat—and what we can do about it—we first need to understand the biological basis of sleep. The story begins in 1916, when the Viennese neurologist Constantin von Economo began seeing patients with a previously unknown brain disorder. People afflicted with the disorder would sleep excessively—up to twenty hours per day—scarcely leaving time for other activities. Encephalitis lethargica, as von Economo named the disorder, swept through Europe and North America in the early twentieth century, afflicting as many as one million people. Most patients were left either dead or permanently disabled by the brain damage it caused. By 1928, the disease vanished as suddenly as it had appeared, and few cases have been reported since. To this day, we still aren’t sure what caused it, although many believe it was triggered by an infectious agent.

Naturally, von Economo was interested in the biological basis of encephalitis lethargica, so he performed a series of brain autopsies on patients who had suffered from the disease. What he found was remarkable: patients with encephalitis lethargica invariably had brain damage at the junction between the upper brain stem and the lower forebrain, as illustrated in figure 40. These findings led him to propose that the region affected by encephalitis lethargica contains an arousal system that normally keeps the rest of the brain awake.

Over the course of the ensuing century, our understanding of sleep has grown considerably, yet von Economo’s observations have withstood the test of time. The brain does contain an arousal system that creates wakefulness and alertness, and part of this system lies precisely in the area he identified. We now know that the arousal system has multiple component brain regions, most of which are located in the brain stem and hypothalamus. These regions send a broad network of fibers throughout much of the brain, releasing chemicals like dopamine, serotonin, norepinephrine, and acetylcholine, which keep us awake and alert.

The brain also contains a complementary sleep center, located in a part of the hypothalamus called the ventrolateral preoptic area (VLPO). When it’s time to sleep, the VLPO sends signals to the various parts of the arousal system, shutting them down and allowing the brain to disengage from the outside world.

Cliff Saper, a sleep neuroscientist at Harvard University, has shown that the sleep center and the arousal system are the yin and yang of sleep and wakefulness. Each one inhibits the other, such that when one is active, the other is shut down. Saper’s former graduate student Thomas Chow, who happens to have an electrical engineering degree from the Massachusetts Institute of Technology, pointed out to Saper that engineers refer to this arrangement as a “flip-flop switch.” This is the kind of circuit you design when you want a system to fully occupy one of two states, such as wakefulness or sleep, but nothing in between. “It’s Electrical Engineering 101,” explains Saper. In our case, this flip-flop switch means we’re either awake or asleep, without much middle ground.

Since sleep and wakefulness are stable states, there has to be a signal that’s strong enough to kick one state into the other, or else we’d never fall asleep or wake up. We know that when we sleep too little, do hard physical or mental work, or stay up longer than usual, we feel sleepy and we’re more likely to doze off. This suggests that some sort of sleep-inducing signal accumulates in the brain, and the longer we’re awake, the harder we work, the more it builds up. We now have strong evidence that a chemical called adenosine is that signal. Adenosine builds up in the brain while we’re awake, and it builds up even faster when we exert ourselves. As it accumulates, it begins to inhibit the arousal system and activate the VLPO. Eventually, when adenosine builds up sufficiently, it triggers the flip-flop switch, and we fall asleep. During sleep, the brain clears excess adenosine, restoring our wakefulness by morning. Caffeine works by blocking adenosine’s actions.

Common sense suggests that sleep is an important restorative process for the brain and the body, and research is increasingly backing this up. During sleep, the brain clears waste products that accumulate during the day as a result of normal metabolism, including adenosine. It gently remodels itself, reinforcing important connections and pruning unimportant ones. And it mops up the protein amyloid-β, which is implicated in the development of Alzheimer’s disease, one of the most tragic scourges of aging.

The fundamental importance of sleep is highlighted by the fact that all animals with a nervous system sleep, or at least enter sleeplike states. Saper explains that “every species that we’ve looked at, even going back to simple invertebrates like sea slugs, tend to have rest-activity cycles.” He believes animals need sleep because neurons require periods of rest for the biochemical processes that support learning.

The restorative processes that happen during sleep are extremely important for the optimal functioning of the brain, and interfering with them leads inevitably to degraded performance of numerous brain functions—and worse. David Dinges, a sleep researcher at the University of Pennsylvania, has spent much of his career studying the effects of sleep restriction on brain function. In one particularly telling study, Dinges’s team assigned volunteers to eight hours, six hours, or four hours in bed per night, for two weeks. Every two hours of waking time throughout the study, volunteers had to complete a battery of tests designed to measure various aspects of cognitive performance, including reaction time, attention, working memory, and basic arithmetic abilities. Their conclusion should serve as a caution to people who think sleep is a waste of time: “Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks.” In other words, by a variety of measures, people who slept four or six hours per night showed substantially worse cognitive performance than people who slept eight hours per night. What’s more, these deficits grew with each additional night of short sleep. Importantly, volunteers felt sleepier for the first few days of sleep restriction, but after that, “subjects were largely unaware of these increasing cognitive deficits.” This suggests that people who short themselves on sleep may not even be aware of how poorly they’re performing.

In the extreme, sleep loss can be deadly. This is illustrated by a rare genetic disease called familial fatal insomnia. As the result of a neurodegenerative process, patients with fatal familial insomnia gradually lose the ability to sleep, descending into hallucinations, delirium, dementia, and after a period of months, death. Researchers aren’t sure to what extent death results from sleep loss rather than other aspects of the neurodegenerative process, but their condition does deteriorate rapidly after they develop insomnia. Older experiments in rats also back up the hypothesis that chronic sleep deprivation can kill. Yet even when sleep loss doesn’t kill us, insufficient or poor-quality sleep can have insidious effects on brain activity and metabolic processes that tend to favor weight gain.

SWEET DREAMS

Returning to St-Onge’s experiment from the beginning of the chapter, her team didn’t stop at measuring food intake in her sleep-restricted volunteers. They also performed fMRI to see how sleep restriction affects the brain’s response to food cues. The results of these brain scans suggest that sleep restriction increases the brain’s responsiveness to food—particularly calorie-dense junk food like pizza and doughnuts. The parts of the brain associated with food reward, including the ventral striatum, were more active in sleep-restricted volunteers, perhaps explaining why they ate more.

Interestingly, the pattern of brain activity St-Onge observed in her sleep-restricted volunteers is quite similar to the pattern Rudy Leibel observed in the brains of people who had previously lost weight—and also the pattern Ellen Schur observed in my own brain when I was looking at food images in a hungry state. This suggests that lack of sleep doesn’t just impair our cognitive functions; it may also impair the lipostat that senses the body’s energy status and sets our motivation for food. “The brain is basically telling you that you’re in a food-deprived state when you really are not,” explains St-Onge. “It primes you for overeating and trying to overcome negative energy balance that’s really not there.” Essentially, when you don’t sleep enough, your lipostat mistakenly thinks you need more energy, which activates your food reward system and causes you to eat more without intending to and often without even realizing it.

An aside: Astute readers may note that when you sleep less, it also increases your calorie expenditure, because your metabolic rate is higher during wakefulness than during sleep. St-Onge and her team have shown that limiting sleep to four hours a night does indeed increase calorie expenditure, but only by about 100 Calories per day. Since her sleep-deprived volunteers ate nearly 300 excess Calories daily, that still leaves 200 Calories to accumulate around their midsections at the end of the day—enough to turn a susceptible person overweight over time.

Time for another reality check: Although many studies have shown that sleep restriction increases the brain’s response to food, increases calorie intake, and sometimes increases body weight, these studies haven’t lasted longer than two weeks. To get an idea of whether this effect persists over the long term and results in gradual weight gain, we must turn to long-term observational studies that measure habitual sleep duration and see how it correlates with weight changes over time. At this point, researchers have conducted many such studies, and they overwhelmingly show that adults who sleep six or fewer hours per night do tend to gain more weight over time than those who sleep seven to nine hours per night. It’s also worth noting that the association between short sleep and weight gain is particularly strong in children. Although these studies by themselves can’t establish a cause-and-effect relationship between sleep duration and weight gain, when considered alongside the controlled studies we’ve just discussed, they make quite a compelling case that part of the reason why we eat too much and gain weight is that we don’t sleep enough.

This conclusion has disturbing implications for those of us who live in affluent, modern societies, because many of us don’t get enough sleep. Twenty-nine percent of American adults get six hours of sleep or fewer per night, up from 22 percent in 1985. Researchers have reported similar trends among adolescents. Short sleepers are not only more likely to have obesity than people who sleep more; they’re also more likely to develop chronic diseases, such as cardiovascular disease and diabetes, and more likely to die overall. Contrary to the claims we often encounter in the media and even sometimes in the scientific literature, our average time in bed in the United States hasn’t changed drastically over the last two decades, but it has declined slightly. I suspect this small decline is due to the meteoric rise of mentally stimulating digital media, such as video games and the Internet. We also have access to bright electric light at night and stimulating media at any time of day. Compare that to our distant ancestors, whose only source of light at night was a campfire or perhaps a candle and whose only source of evening entertainment was one another.

HOW MUCH SLEEP DO YOU NEED?

Different people need different amounts of sleep to feel rested. Although this remains to be tested scientifically, it’s possible that naturally short sleepers get the same amount of benefit in, say, six hours, that long sleepers get in nine hours. If true, this would suggest that what harms us isn’t necessarily short sleep itself, but rather sleeping less than each of us needs as an individual. For example, a person who sleeps six hours per night but feels fully rested when she wakes up may not have anything to gain from attempting to sleep more, while another person who sleeps six hours per night but wakes up feeling miserable may benefit from more shut-eye. For now, the best advice is probably to sleep as much as you need to feel fully restored, rather than following rigid sleep guidelines that are based on averages from population studies.

Although our average time in bed may not have changed much over the years, the amount of time in bed we actually spend getting high-quality sleep has dropped more substantially due to the sharp increase in the prevalence of sleep-disordered breathing conditions such as sleep apnea. Researchers attribute this problem to our expanding waistlines over the last forty years, which increases the volume of soft tissues around the airway that can interfere with breathing at night. This may create a vicious cycle in which fat gain leads to sleep-disordered breathing, which leads to sleep loss, which further exacerbates overeating and fat gain.

Yet sleep loss doesn’t just affect the lipostat—it also undermines our ability to control the very impulses it activates.

A PRISONER OF YOUR IMPULSES

Sleep loss also favors overeating by affecting how we perceive risks and rewards. In 2011, Duke sleep researcher Michael Chee published a paper suggesting that sleep loss has far-reaching impacts on our economic decision-making behavior. Chee and his team had twenty-nine young adult volunteers either sleep normally or skip one night of sleep, and then he asked them to perform a series of experimental gambling sessions while lying in an fMRI machine.

Chee’s results showed that pulling an all-nighter causes people to become less concerned about potential losses and more attracted to potential gains—basically, they become risk takers. Furthermore, this effect correlated with measurable differences in brain activity. People who hadn’t slept showed greater activation of reward-related regions of the brain such as the ventral striatum in response to gambling gains, while also showing diminished brain responses to losses.

“Generally, with sleep loss you have a shifting of your economic preferences,” explains Dan Pardi, a graduate student in the lab of Stanford sleep researcher Jamie Zeitzer. Researchers call this effect an optimism bias, and Pardi wondered if it might also apply to eating behavior. As we discussed in chapter 5, the brain weighs the potential costs and benefits of eating as it decides what and how much to eat. To revisit an earlier example, the brain may have to decide between keeping three dollars in your wallet and putting a pastry in your belly. Often, when we’re faced with unhealthy food, the benefit is the immediate reward we get from eating something tasty, while the cost is the long-term impact on our adiposity and health. So Pardi hypothesized that if he added insufficient sleep to the mix—and consequently, optimism bias—people might also be more attuned to the benefits of eating than the costs. And this might nudge them toward unhealthy food choices.

To test his hypothesis, Pardi’s team recruited fifty volunteers who believed they had signed up for a study on how sleep loss affects cognitive function. They were divided into seven groups, and each group was told to spend a different amount of time in bed the night preceding the experiment. These prescribed sleep times ranged from 60 to 130 percent of each person’s usual time in bed. (A key advantage of Pardi’s study is that it modeled a realistic range of sleep times that we commonly see in the general population, as opposed to many other sleep restriction studies, which allowed subjects as little as four hours of sleep, or none at all.) Seven days before the change in sleep time, Pardi’s team gave each person a battery of tests to assess their typical level of alertness and feelings of sleepiness. On the day following the change in sleep time, they repeated the same tests.

Yet Pardi had a trick up his sleeve, on which the whole experiment hinged. While the volunteers took a break between tests, he had them watch two forty-minute movies that were unrelated to food. And during that time, Pardi put out bowls of foods like gummy bears, toffee peanuts, apple rings, and almonds that the volunteers could graze on. Pardi’s team covertly measured each person’s food intake by weighing the bowls before and after the movie break. At the end of the study, volunteers filled out a questionnaire rating how much they liked each food and how healthy they thought each item was.

Consistent with St-Onge’s findings, sleepier participants munched more calories during the movie break. Yet they weren’t just more likely to eat food in general—they were specifically more likely to eat food they themselves rated as both delicious and unhealthy. Just as Chee’s results had predicted, Pardi’s sleep-deprived volunteers seemed to be more compelled by the immediate reward of eating tempting foods than by the long-term costs. “When you have inadequate sleep,” explains Pardi, “you’re probably less likely to live in accordance with your own health goals. You’re less likely to get into bed on time, you’re less likely to go to the gym, and you’re less likely to have your eating behaviors align with your long-term health goals.” fMRI research supports Pardi’s interpretation, showing that one night of total sleep deprivation reduces the food cue responsiveness of brain regions that support planning, reasoning, and long-term goals, while at the same time enhancing the responsiveness of brain regions that drive food reward. Together, this suggests that when you don’t sleep enough, you’re a prisoner of your own impulses—and those impulses will tell most of us to overeat unhealthy food.

But we know that not all sleep is the same. Why is sleep more restorative when it happens at the time we’re used to sleeping? To answer this question, we’ll have to return to the brain, exploring a system that may be able to make us fatter without even increasing our calorie intake.

THE DARKEST NIGHT

So far, we’ve covered some of the key brain regions that regulate sleep and wakefulness, ultimately impacting eating behavior—yet there’s more to the story. Why do we feel compelled to sleep at night and not during the day? Why do we feel awful and perform poorly if we have to undertake a task when we would normally be sleeping?

In 1962, a French geologist and cave explorer named Michel Siffre conducted an unusual experiment that paved the way to answering these questions. It was the height of the Space Race, and scientists were eager to understand how the human body and mind would react to the absence of time cues that we might experience during space travel.

To find out, Siffre lowered himself into the Abyss of Scarasson, an inky black cave below the surface of the French-Italian Maritime Alps. He made his camp on a small subterranean glacier 427 feet below the surface, where the temperature hovered just below freezing and the relative humidity was 98 percent. There he stayed, cold, wet, and alone, for sixty-three days.

Siffre didn’t bring a watch or anything else that could possibly reveal what time of day it was. He phoned his research colleagues on the surface to indicate each time he went to sleep, awoke, and ate.

When Siffre emerged from the Abyss of Scarasson and analyzed his results, he realized something remarkable: the length of his wake-sleep cycle had remained close to twenty-four hours for his entire two-month séjour in the cave. Yet because his cycle was slightly longer than twenty-four hours, it gradually desynchronized from the day-night cycle of the sun.

This suggested that the human body must quite literally contain a twenty-four-hour(ish) clock. Research over the ensuing half century has confirmed this, although we now know there is more than one clock. In fact, there are thirty-seven trillion of them: a tiny molecular timepiece in nearly every one of your cells. Together, these clocks synchronize many of the body’s functions with the twenty-four-hour cycle of the sun—creating what is called a circadian rhythm. Our sleeping and waking cycle tends to follow a circadian rhythm, and so do our cognitive performance, eating behaviors, digestive functions, metabolic processes, and many other aspects of our behavior and physiology. If you’ve ever experienced the brain fog, lack of hunger, and digestive discomfort of jet lag, you understand the importance of circadian rhythms in regulating cognition, eating behavior, and digestion.

Your body’s thirty-seven trillion cellular clocks are all kept more or less in synchrony by a master clock residing in a part of the hypothalamus called the suprachiasmatic nucleus (SCN). If we think of the cellular clocks in the body as a giant orchestra, the SCN is the conductor. The master clock, in turn, takes its cues from the retina, the light-sensitive film of cells in the back of the eye, which detects the day-night cycle of the sun. But due to the characteristics of the retinal cells that transmit this information, the SCN only responds to blue light, which happens to be most abundant at midday.

The SCN master clock uses its connections to other brain regions to set all the other clocks in the body. One of these connections is to the pineal gland, which secretes the sleep hormone melatonin. Melatonin levels increase at night, and this is an important signal that helps synchronize the body’s clocks by telling them when the sun has set. Connections from the SCN to other brain regions—including the arousal system and the VLPO sleep center—influence the circadian rhythms of sleep, physical activity, metabolism, and eating. These connections explain why we tend to sleep at night and not during the day.

Since blue light controls melatonin secretion, melatonin levels at night are exquisitely light sensitive. Artificial blue light, such as that emitted by the lightbulbs, computers, tablets, televisions, and cell phones in your house, suppresses melatonin levels at the time of night when it should be increasing. Your body’s thirty-seven trillion cells don’t get the message that it’s nighttime until you turn out the lights—several hours after the sun goes down. This pushes your biological wake-sleep cycle back by a few hours relative to the day-night cycle of the sun, desynchronizing the two. When it’s time to go to sleep, your body isn’t ready yet, and it also isn’t ready when it’s time to get up. This undermines your sleep quality and next-morning wakefulness. The system that evolved over billions of years to synchronize the body’s daily rhythms to the cycle of the sun is easily fooled by modern technology.

SYNCHRONIZING SLEEP

Technology such as lightbulbs undermines our sleep quality and perhaps our health, but technology can also provide solutions. There are two keys to keeping the circadian rhythm properly synchronized. The first is to reduce light intensity and blue-spectrum light at night. There are many ways to accomplish this. One easy fix is to get rid of night-lights and other sources of nighttime light in the bedroom, ensuring that it’s completely dark while you sleep. Another easy way is to get rid of “full-spectrum,” “daylight,” and “cool white” lightbulbs in your house, replacing them with “warm white” bulbs that emit less blue light (or limit full-spectrum bulb use to daytime). Look for a color temperature of 3000 K or lower on the box. Dimmer switches can help by allowing you to match light intensity to the time of day. Turning down the brightness of your light-emitting devices, such as televisions, tablets, and smartphones, after sundown can also help. On your computer, you can download a neat utility called f.lux that automatically changes the color spectrum of your monitor to a warmer hue at sundown. Similar apps, such as Twilight, are available for smartphones and tablets. And finally, you can buy glasses that specifically block blue-spectrum light without blocking other wavelengths. These are available from a variety of online retailers, but one popular and inexpensive option is the blue-blocking SCT-Orange safety glasses manufactured by Uvex. Studies have shown that blue-blocking glasses completely eliminate the effects of artificial light on melatonin levels, suggesting that they help the SCN master clock understand that it’s nighttime. Blue-blocking glasses let you use your lightbulbs and electronic devices as usual, while reducing their impact on your circadian rhythm. And you get to wear sunglasses at night.

The second key is exposing yourself to bright, blue-spectrum light early in the day so the SCN gets a clear message that it’s daytime. In conjunction with limiting blue-spectrum light at night, this helps keep the circadian clock in the proper phase relative to the sun. The best way to get bright, blue-spectrum light is to do what our ancestors did: go outside. Even on a cloudy day, sunlight is much brighter than indoor light, and it tends to contain more blue-wavelength light than most lightbulbs. If you can’t go outside, bright, full-spectrum indoor lighting is a good alternative.

Circadian disruption can do more than just interfere with our sleep, however. Research is increasingly suggesting that it’s one of the lesser-known reasons why many of us grow fat and sick.

CIRCADIAN CACOPHONY

Many researchers become interested in a subject because it affects them personally, and Deanna Arble, a postdoctoral researcher at the University of Michigan, is no exception. “When I was in high school,” she recalls, “I could sleep twelve hours a day, every day, and still take naps. I was an outlier.” As an undergraduate neuroscience major at the University of Virginia, she was drawn to sleep research because there was still so much that wasn’t known about sleep. She approached an established circadian rhythm researcher named Michael Menaker and interviewed for a position in his lab. During the interview, Menaker noted that his research often involves working with mice in the dark. When Arble asked how they do research in the dark, he explained that they use night-vision goggles. Arble was sold. “I got into circadian research for the night-vision goggles,” she jokes, “but I stayed for the science.” Arble’s subsequent Ph.D. work with Fred Turek at Northwestern University provided critical evidence that a disrupted circadian rhythm might contribute to our expanding waistlines.

To understand the importance of Arble’s work, first we have to consider studies that have examined the health effects of rotating shift work in humans. In rotating shift work, people work at different times on different days, including at night, and they are typically unable to maintain a regular sleep schedule. Their bodies’ circadian rhythm is perpetually misaligned with their cycle of activity and light exposure, and so they often sleep, eat, and perform physical tasks during times of day that their master clock isn’t anticipating.

If circadian biology plays an important role in adiposity and health, then rotating shift workers should be heavier and less healthy than people who consistently work during the day. Many studies have shown that this is the case. Rotating shift work is associated with an alarming array of health problems, including obesity, type 2 diabetes, cancer, and cardiovascular disease. The longer a person works a rotating shift, the more likely they are to gain weight and become ill. Why?

This brings us back to Deanna Arble and her mentor Fred Turek. They were familiar with the growing body of research on rotating shift work, and they knew that digestive and metabolic functions follow a circadian pattern. Yet they also knew an additional critical detail: Not only can the master clock desynchronize from the day-night cycle of the sun, but individual organ clocks can desynchronize from one another. For example, the SCN master clock can become desynchronized from the clocks in the intestine, the liver, the pancreas, and other organs that regulate digestion and metabolism. That’s because the latter group of clocks can be set by meal timing, and as far as they’re concerned, the meal signal is stronger than the one coming from the SCN. Usually, this isn’t a problem because the meal signal and the SCN signal are more or less aligned when we eat during the day. The conductor is in charge, and the orchestra is playing in harmonious synchrony. Yet when we disrupt the circadian rhythm by eating late at night, traveling to a faraway time zone, or doing shift work, some of our organ clocks can fall out of sync with others. What would normally be a harmonious performance is reduced to a disorganized cacophony. Researchers call this circadian desynchrony and hypothesize that it leads to metabolic problems and weight gain.

To test this idea, Arble studied two groups of mice, both eating the same fattening diet. One group had access to food only during the twelve hours of the day when they would normally be awake and active, while the other only had access to food during the twelve hours of the day when they would normally be asleep. Under normal, unrestricted conditions, mice eat about two-thirds of their food during the wake cycle and one-third during the sleep cycle. In Arble’s experiment, however, they could only eat during one period or the other, leading to two circadian conditions: one in which digestive and metabolic clocks were synchronized with the master clock in the brain, and one in which they were desynchronized.

Surprisingly, mice in both groups ate the same amount of food. Yet after two weeks, a striking trend began to emerge: the synchronized mice were hardly gaining weight, while the desynchronized mice were gaining fast. By the end of the six-week experiment, the desynchronized mice had gained nearly two and a half times more weight than the synchronized mice, and they tended to have more body fat as well. They were eating the same number of calories but metabolizing them differently. Subsequent rodent studies from other research groups have generally confirmed and extended Arble and Turek’s findings. Together, they lead us to two surprising conclusions: The first is that circadian desynchrony accelerates weight gain when rodents are fed a fattening diet. The second, even more striking conclusion is that fattening rodent diets aren’t particularly fattening when they’re only available during the appropriate time of day! This suggests that what is really fattening in these experiments is not simply fattening food but the combination of fattening food and circadian desynchrony.

OK, this is interesting, but how relevant is it to humans, since most of us don’t get up in the middle of the night to eat? Well, first of all, some of us do eat in the middle of the night. The most extreme example of this is a disorder called night eating syndrome, in which people eat the most of their calories at night, including in the middle of their sleep period. These people tend to be somewhat heavier than average. But we don’t necessarily have to eat in the middle of the night to experience the negative effects of circadian disruption. Remember that most people living in affluent nations already have shifted, desynchronized, or otherwise disrupted circadian rhythms due to artificial light at night, an insufficiently dark bedroom during sleep, a lack of morning sun, jet lag, and/or shift work. It’s likely that we could stay slimmer and healthier with less effort if we took better care of our circadian clocks.