The circadian rhythm diet is essentially time-restricted eating in which you eat within a certain time frame, generally during daylight hours, and fast the rest of the time.
Our circadian rhythms are influenced by light and dark, which tells our body when it’s time to wake and when it’s time to sleep.
It is said that nearly every tissue and organ in our body is regulated by a biological clock, with a master clock located in our brain called suprachiasmatic nucleus, or SCN, keeping all the other clocks in sync and on schedule.
There is, however, one interesting thing to note about this system.
“Food actually overrides the clocks in all of our peripheral tissues. It doesn’t affect the brain tissue. The brain keeps going with the sun, but the clocks in the body are actually more controlled by the food that we eat,” says Associate Professor Leonie Heilbronn, who leads the obesity and metabolism laboratory at the South Australian Health and Medical Research Institute.
“Food can unsynchronise the clock in your head from the clocks in your body and when they’re not talking well to each other, you don’t get optimal responses (from the body).”
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Circadian rhythms, metabolism, and nutrition are intimately linked [1, 2], although effects of meal timing on the human circadian system are poorly understood. We investigated the effect of a 5-hr delay in meals on markers of the human master clock and multiple peripheral circadian rhythms. Ten healthy young men undertook a 13-day laboratory protocol. Three meals (breakfast, lunch, dinner) were given at 5-hr intervals, beginning either 0.5 (early) or 5.5 (late) hr after wake. Participants were acclimated to early meals and then switched to late meals for 6 days. After each meal schedule, participants’ circadian rhythms were measured in a 37-hr constant routine that removes sleep and environmental rhythms while replacing meals with hourly isocaloric snacks. Meal timing did not alter actigraphic sleep parameters before circadian rhythm measurement. In constant routines, meal timing did not affect rhythms of subjective hunger and sleepiness, master clock markers (plasma melatonin and cortisol), plasma triglycerides, or clock gene expression in whole blood. Following late meals, however, plasma glucose rhythms were delayed by 5.69 ± 1.29 hr (p < 0.001), and average glucose concentration decreased by 0.27 ± 0.05 mM (p < 0.001). In adipose tissue, PER2 mRNA rhythms were delayed by 0.97 ± 0.29 hr (p < 0.01), indicating that human molecular clocks may be regulated by feeding time and could underpin plasma glucose changes. Timed meals therefore play a role in synchronizing peripheral circadian rhythms in humans and may have particular relevance for patients with circadian rhythm disorders, shift workers, and transmeridian travelers.
Light and dark cycles are the dominant zeitgeber of the master clock in the SCN, whereas the rhythm of feeding behavior is arguably the most powerful zeitgeber of the peripheral tissues. In a classic study, Damiola et al. (35) showed that restricting food access to the inactive phase in mice (i.e., the light phase) caused a phase shift in the peripheral tissue clocks of the liver, pancreas, heart, skeletal muscle, and kidney. In contrast, the central clock in the SCN was unaffected. This uncoupling between the central and peripheral clocks occurred equally when the animals lived with normal light–dark cycles or in constant darkness (35). Feeding is therefore an ineffective zeitgeber for the SCN even in the absence of light, its primary zeitgeber. At the same time, feeding is a potent zeitgeber for the periphery regardless of opposing cues from the light-entrained SCN clock. Further studies confirmed that the food exerts a dominant zeitgeber effect on peripheral clock phase without affecting the SCN (36–40). Furthermore, phase advancing the light–dark cycle does not alter the phase of the liver clock if accompanied by a fixed restricted feeding schedule, and restricted feeding entrains the liver even in SCN-lesioned mice (37).
Nevertheless, the peripheral clock phase is still indirectly controlled by the light-entrained SCN. This is demonstrated by the fact that when feeding rhythms and the light phase are inverted, peripheral clock resetting is slowed by opposing signaling from the SCN. In nocturnal rodents who normally consume most food during the dark phase, restricting the feeding schedule to the day produces slow phase resetting of the liver and kidney to match feeding rhythms, with comparatively rapid resetting when returning from day to nighttime eating; this effect of slowed switching in the ‘wrong direction’ does not occur in adrenalectomized or glucocorticoid insensitive mice (41). That the master clock acts to counteract discordant entrainment of peripheral clocks by light phase feeding was confirmed by in vivo recording of Bmal1-driven luciferase activity in the hepatocytes of SCN-lesioned mice. After only 6 days of daytime restricted feeding, the hepatocytes in the SCN-lesioned mice had undergone a steady and complete phase shift to match the food intake rhythm, in contrast to the sham-operated mice where the hepatocyte clock had only partially phase-shifted this short time (42).
The differential responsiveness of tissues to a particular zeitgeber makes evolutionary sense because the component of an endogenous clock presented to natural selection is its phase relationship with respect to the environmental events it anticipates. As tissues become specialized in their function, the relevance of environmental cues as zeitgebers would be aligned accordingly. For example, in a metabolically active organ such as the liver, regularly timed food intake is an important event with which metabolic processes are synchronized. Among the peripheral organs studied in the literature, the liver clock phase shifts the most rapidly in response to restricted feeding (35), corresponding to its primary metabolic function. It is interesting that while SCN is not sensitive to time-restricted feeding, it does respond to long-term fasting and caloric restriction. The SCN phase shifts in response to caloric restriction (43) and synchronizes to a single hypocaloric meal given at the same time each day in constant darkness (44). Whereas, acute differences in food intake timing are not relevant zeitgebers to the SCN, perceived starvation certainly is.
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