Limiting late night eating can ward off negative effects of sleep deprivation

A study indicates that eating less late at night may help curb negative effects of sleep deprivation such as concentration and alertness deficits.

Eating less late at night may help curb the concentration and alertness deficits that accompany sleep deprivation, according to results of a new study from researchers at the Perelman School of Medicine at the University of Pennsylvania that will be presented at SLEEP 2015, the 29th annual meeting of the Associated Professional Sleep Societies LLC.

"Adults consume approximately 500 additional calories during late-night hours when they are sleep restricted," said the study's senior author David F. Dinges, PhD, director of the Unit for Experimental Psychiatry and chief of the division of Sleep and Chronobiology. "Our research found that refraining from late-night calories helps prevent some of the decline those individuals may otherwise experience in neurobehavioral performance during sleep restriction."

The study gave 44 subjects, ages 21 to 50, unlimited access to food and drink during the day, followed by only four hours of sleep each night for three nights. On the fourth night, 20 participants received continued access to food and drinks, while the 24 others were allowed only to consume water from 10:00 p.m. until they went to sleep at 4:00 a.m.

At 2 a.m. each night, all subjects completed a variety of tests to measure their working memory, cognitive skills, sleepiness, stress level and mood.

During the fourth night, subjects who fasted performed better on reaction time and attention lapses than subjects who had eaten during those late-night hours. In addition, subjects who ate showed significantly slower reaction times and more attention lapses on the fourth night of sleep restriction compared to the first three nights whereas study subjects who had fasted did not show this performance decline.

While countless studies associate numerous physical and mental health benefits with a healthy night's sleep, the Centers for Disease Control Prevention reports that "insufficient sleep is a public health epidemic" in the United States, including the estimated 50 to 70 million U.S. adults suffering from sleep and wakefulness disorders.

The new study results serve as a book end to other research on the links between eating and sleep deprivation. A 2013 study from the same Penn team found that individuals with late bedtimes and chronic sleep restriction may be more susceptible to weight gain due to the increased consumption of calories during late-night hours.

The research team also includes Andrea Spaeth, PhD, and Namni Goel, PhD.

The study was supported by the National Institutes of Health (R01 NR004281, F31 AG044102); the Penn Clinical and Translational Research Center (UL1RR024134); and the Department of the Navy, Office of Naval Research (Award No. N00014-11-1-0361).

In a related study (Abstract #0332), the same team of Goel, Spaeth and Dinges, found that adults who are chronically sleep restricted may need to compensate for decreased morning resting metabolic rate by reducing caloric intake or increasing physical activity to prevent weight gain. That research was led by senior author Namni Goel, PhD, a research associate professor of psychology in Psychiatry and the Unit for Experimental Psychiatry.

"Short sleep duration is a significant risk factor for weight gain and obesity, particularly in African Americans and men," Goel said. "This research suggests that reducing the number of calories consumed can help prevent that weight gain and some of the health issues associated with obesity in Caucasians and particularly in African Americans."

The NIH reports that 69 percent of U.S. adults are overweight or obese. Being overweight or obese increases your risk of coronary heart disease, high blood pressure, stroke, type 2 diabetes, cancer, sleep apnea, and other health problems.

In the study, 36 healthy adults, ages 21 to 50, slept for their usual amount for two nights. Next, they spent four hours in bed each night for five nights, followed by one night of 12 hours of recovery sleep. The control group of 11 subjects received 10 hours in bed each night for six nights. Resting metabolic rate, or measure of the amount of energy used in a relaxed condition, and respiratory quotient, or the ratio of the volume of carbon dioxide to oxygen used in a time period, were measured after overnight fasting.

In the experimental group, resting metabolic rate decreased after five nights of sleep restriction and returned to baseline levels after recovery sleep. No changes in resting metabolic rate were observed in control subjects. In the experimental group, African Americans exhibited comparable daily caloric intake relative to Caucasians, but a lower resting metabolic rate and higher respiratory quotient.

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Study: Genes link circadian clock to eating schedule

A study found that specific genes link a person's circadian clock to their eating schedule.

For most people, the urge to eat a meal or snack comes at a few, predictable times during the waking part of the day. But for those with a rare syndrome, hunger comes at unwanted hours, interrupts sleep and causes overeating.

Now, Salk scientists have discovered a pair of genes that normally keeps eating schedules in sync with daily sleep rhythms, and, when mutated, may play a role in so-called night eating syndrome. In mice with mutations in one of the genes, eating patterns are shifted, leading to unusual mealtimes and weight gain. The results were published in this month's Cell Reports.

"We really never expected that we would be able to decouple the sleep-wake cycle and the eating cycle, especially with a simple mutation," says senior study author Satchidananda Panda, an associate professor in Salk's Regulatory Biology Laboratory. "It opens up a whole lot of future questions about how these cycles are regulated."

More than a decade ago, researchers discovered that individuals with an inherited sleep disorder often carry a particular mutation in a protein called PER2. The mutation is in an area of the protein that can be phosphorylated -- the ability to bond with a phosphate chemical that changes the protein's function. Humans have three PER, or period, genes, all thought to play a role in the daily circadian clock and all containing the same phosphorylation spot.

The Salk scientists joined forces with a Chinese team led by Ying Xu of Nanjing University to test whether mutations in the equivalent area of PER1 would have the same effect as those in PER2 that caused the sleep disorder. So they bred mice to lack the mouse period genes, and added in a human PER1 or PER2 with a mutation in the phosphorylation site. As expected, mice with a mutated PER2 had sleep defects, dozing off earlier than usual. The same wasn't true for PER1 mutations though.

"In the mice without PER1, there was no obvious defect in their sleep-wake cycles," says Panda. "Instead, when we looked at their metabolism, we suddenly saw drastic changes."

Mice with the PER1 phosphorylation defects ate earlier than other mice -- causing them to wake up and snack before their sleep cycle was over -- and ate more food throughout their normal waking period. When the researchers looked at the molecular details of the PER1 protein, they found that the mutated PER1 led to lower protein levels during the sleeping period, higher levels during the waking period, and a faster degradation of protein whenever it was produced by cells.

Panda and his colleagues hypothesize that normally, PER1 and PER2 are kept synchronized since they have identical phosphorylation sites -- they are turned on and off at the same times, keeping sleep and eating cycles aligned. But a mutation in one of the genes could break this link, and cause off-cycle eating or sleeping.

"For a long time, people discounted night eating syndrome as not real," says Panda. "These results in mice suggest that it could actually be a genetic basis for the syndrome." The researchers haven't yet tested, however, whether any humans with night eating syndrome have mutations in PER1.

When Panda and Xu's team restricted access to food, providing it only at the mice's normal meal times, they found that even with a genetic mutation in PER1, mice could maintain a normal weight. Over a 10-week follow-up, these mice -- with a PER1 mutation but timed access to food -- showed no differences to control animals. This tells the researchers that the weight gain caused by PER1 is entirely caused by meal mistiming, not other metabolic defects.

Next, they hope to study exactly how PER1 controls appetite and eating behavior -- whether its molecular actions work through the liver, fat cells, brain or other organs.

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