The nationwide experiment will initially include around 100,000 volunteers.
The eating schedule—and not the amount of calories—can make the difference between an obese, diabetic, sick mouse and one with a healthy metabolism.
February 1, 2013|
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M. Hatori et al., “Time-restricted feeding without reducing caloric intake prevents metabolic diseases in mice fed a high-fat diet,” Cell Metab, 15:848-60, 2012.
Circadian disruptions can prime animals toward obesity, but does the maintenance of diurnal eating rhythms prevent excess weight gain? Satchidananda Panda at the Salk Institute and his colleagues found that mice fed a high-fat diet only during normal waking hours staved off obesity, metabolic dysfunction, and liver damage—all of which plagued animals with access to food around the clock.
Both groups ate the same number of calories, but after 18 weeks, the free-feeding mice weighed about 45 grams, compared to about 33 grams for the time-restricted mice. In addition, liver function and circadian control fell out of whack in mice that ate whenever they wanted. For instance, Panda’s group showed that the circadian oscillator genes Per2, Bmal1, and Rev-erbα were expressed in their normal diurnal peaks and troughs in mice fed only at night—the most active time for a mouse—while the free-fed group had less-pronounced diurnal variation.
Why it happens “is the billion-dollar question,” says Panda. He pointed out that certain genes need a period of fasting in order to be activated. Perhaps the constant stream of food never gives them the opportunity to switch on properly, he speculated. For example, coordinating the timing of gene activation is important to maintain proper glucose levels in the liver.
Joseph Bass, at Northwestern University, who was not part of this study, said that Panda’s work suggests that proper eating schedules may prevent metabolic diseases in humans, by extending the period of time we fast during each 24-hour day. “If you correct the timing abnormalities, you may correct the defects.”