Eating and sleeping
are two of the most basic human functions, both essential to survival. They are also two biological processes that are deeply entwined, as science is increasingly discovering. There are foods that promote
sleep (including potassium-rich fruits and dark leafy greens) and foods that can interfere
with sleep (think high-fat snacks). Too much or too little sleep alters appetite
and wreaks havoc with hunger-related hormones
. Going without enough sleep makes junk food look more tempting
, and increases desire for fatty and high-calorie foods. Staying up late at night often leads to greater overall calorie consumption
and makes us more prone to putting on weight. On the other hand, high-quality, restful sleep in moderate amounts (not too little, not too much) has a positive influence
on long-term weight control.
New research gives us a glimpse of just how deeply connected sleeping and eating may be. Scientists have discovered in fruit flies that a brain molecule already known to regulate appetite may also play an important role in sleep regulation. Researchers at Brandeis University found that a neuropeptide in the fruit fly brain, already recognized as a regulator of eating, also can dramatically influence sleep and activity levels. Neuropeptides are molecules that enable communication among cells in the brain, and are involved in regulating a number of important physiological processes, including appetite and metabolism. Researchers examined the possible role in sleep regulation of a particular neuropeptide, known as sNPF, that is already known to regulate food intake and metabolic function. Researchers manipulated the sNPF neuropeptide in fruit flies to see what effects this had on sleep and activity levels. They found that altering the activity of sNPF had a dramatic, sleep-inducing effect on the flies:
- When sNPF was activated above normal levels, fruit flies fell asleep almost immediately.
- Flies slept excessively and activity levels dropped dramatically after sNPF activation. The flies woke from sleep in order to eat or to locate a new food source and then fell back asleep.
- When sNPF levels were returned to normal, the fruit flies’ sleep habits changed and the flies returned to normal sleeping patterns and activity levels.
- The activation of sNPF that changed sleep patterns and activity levels in the fruit flies did not alter feeding behavior in the short term.
What does this discovery mean? It provides new window into the neurological connection between sleeping and eating. These findings on their own don’t explain how the physiological mechanisms behind sleeping and eating are related or influenced by one another. But the identification of a shared signal that regulates both eating and sleeping establishes an important and very tangible neurological connection between the two functions. Other recent research also has explored the brain-based connections between sleeping and eating, and the possible implications for weight control:
Researchers at University of California, Berkeley investigated the effects of sleep deprivation on brain functions related to food choices. Using MRI scans, scientists observed the neurological activity of sleep-deprived and well-rested people as they viewed pictures of a range of healthful and unhealthful foods. The scans revealed that the reward center of the brain responded more strongly to images of high-calorie foods among the sleep-deprived group than the well-rested group. The MRI scans also showed that sleep deprivation decreased activity in the area of the brain that regulates behavior control. This study suggests that insufficient sleep has a two-fold effect on eating—not sleeping enough makes us more inclined to eat poorly, and at the same time less able to exert control over our impulses to eat those not-good-for-us foods.
Scientists at St. Luke’s-Roosevelt Hospital Center and Columbia University also examined the effects of sleep deprivation on neurological responses to food. Researchers used MRI scans to observe brain activity among two groups of healthy-weight adults—one group had received several full nights’ of sleep, and the other group had been limited to no more than 4 hours of sleep per night for 5 nights. The sleep-restricted group demonstrated greater activity in the reward center of the brain when looking at pictures of junk food. MRI scans showed the reward centers of sleep-restricted subjects did not react to the sight of healthful foods this way. The well-rested group did not display this heightened reward-center response to images of junk food.
Both sleep problems and metabolic problems associated with overeating pose significant challenges to long-term health. Disrupted and insufficient sleep has become an increasingly common problem over the past several decades, contributing to the risk of a number of serious diseases, including cardiovascular disease, some types of cancer, and diabetes. Obesity is a significant public health problem in the United States. The rise in the rate of obesity is slowing somewhat after decades of sharp growth. Still, by 2030, projections suggest that more than 40% of U.S. adults will be obese.
Understanding the relationship of sleep to food consumption, weight regulation, and metabolism is critical work. Identifying a single neurological molecule that helps regulate both sleeping and eating is a significant development in that understanding. There is much more to learn about the relationship between sleeping and eating—and how we can use that relationship to foster weight loss and improve overall health. But this latest discovery could be one important piece of the sleep-weight puzzle.
Michael J. Breus, PhD
The Sleep Doctor®
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