Eating When One Should be Resting is a Cause of Weight Gain
I have written several posts that discuss the negative effects of meal timing on weight control and the development of obesity and type 2 diabetes:
TIME RESTRICTED FEEDING AS A MEANS TO CONTROL OBESITY?
TIME RESTRICTED FEEDING ALSO BENEFITS HEALTHY INDIVIDUALS
BENEFITS OF TIME RESTRICTED EATING IN PATIENTS WITH METABOLIC SYNDROME
Now a new study, published in the journal, Molecular Metabolism, utilizing laboratory mice, with relevance to observations in humans, demonstrates that consuming food during a normal period of rest results in weight gain due to disruptions in normal circadian rhythms:
Rest phase snacking increases energy resorption and weight gain in male mice
As a point of fact, and for comparison purposes to humans, mice are nocturnal meaning they rest during the light phase and are active during the dark phase.
In this study male mice were fed a chocolate snack daily during the period when they would normally be resting (light phase) and compared to the situation where the chocolate snack was given to the mice during the normal active period (dark phase). Experiments were also carried out where the snacking was during continuous darkness as well as in mice in which one of the major circadian rhythm regulating genes was eliminated. The eliminated gene is known as CLOCK which stands for Circadian Locomotor Output Cycles Kaput. The protein encoded by the CLOCK gene is a transcription factor that controls the expression of several genes that regulate normal circadian rhythms. The reason for the latter experiments was to determine the influence of external and internal time cues in mediating the metabolic effects of snacking.
Before delving into the findings of this study it is important to understand that the circadian rhythm regulating genes in mice are identical in humans. Circadian clocks are the endogenous timekeepers that synchronize internal functions to daily light-dark rhythms that influence environmental demands of an organism. At the level of the genes, the mammalian circadian clocks are composed of feed-back loops of transcription (RNA synthesis) and translation (protein synthesis). The CLOCK gene encoded transcription factor turns on the expression of other genes in the circadian rhythm circuitry during daylight hours. Then at night the proteins whose synthesis is induced by CLOCK exert negative feed-back inhibition on their own expression. When light-dark cycles are aligned with feed-fast cycles, a master circadian pacemaker in the suprachiasmatic nucleus (SCN) of the hypothalamus in the brain synchronizes the circadian clocks of the peripheral tissue clocks. If food intake is shifted into the inactive phase of a normal circadian rhythm the circadian clock network becomes desynchronized. Demonstration of the role of the SCN in peripheral circadian rhythm control has been demonstrated in mice where this brain region has been lesioned. In these mice there is weight gain and impaired glucose homeostasis under constant environmental conditions.
Under normal circumstances mice do not eat during the rest-phase of the circadian clock. However, if they only receive food during this period there is a demonstrable reduction in energy expenditure and a consequent increase in body weight gain when compared to mice provided ad libitum (as desired) food intake. Correlation to the effects in humans has been demonstrated in numerous studies, some of which I have reported on in my blog, showing that not only excess caloric consumption itself, but also the timing of food intake results in disturbances in body weight regulation with resultant weight gain. One study demonstrated that when postmenopausal women consumed milk chocolate in the morning (representative active phase) or the evening (representative rest phase) there were distinct differences in appetite and energy expenditure.
Numerous parameters were analyzed in this rest phase snacking study and included serum levels of glucose, insulin, triglycerides, total cholesterol, and cholesterol in various lipoprotein fractions (i.e. LDL and HDL), examination of energy expenditure, as well as determination of the level of expression of numerous genes, primarily those encoding circadian rhythm-regulating proteins.
At the outset of the experiment all test animals were comparable with respect to body weight. During the initial period of daytime (rest phase for mice) versus nighttime (active phase for mice) chocolate snacking versus regular chow feeding there were no detectable differences in energy consumption. Chocolate snacking during the active phase eventually led to increased energy expenditure whereas, rest phase chocolate snacking eventually resulted in increased energy expenditure during rest phase and reducing it during the active phase. Active phase chocolate snacking reduced the respiratory exchange ratio (RER) during this phase. RER is a measure of metabolic activity related to oxygen consumption and carbon dioxide. In contrast, rest phase chocolate snacking increased the RER during this phase. The net effect is that snacking during the normal resting phase results in reduced energy expenditure throughout the active phase indicating a disruption of daily energy metabolism.
Of potential significance to the development of cardiovascular disease in humans the results of this study found that snacking during rest phases results in increased blood lipids when compared to snacking during an active phase. The increased blood lipids consisted of triglycerides and LDL cholesterol but not free fatty acid. Snacking during the normal rest phase also resulted in reduced activity of the mice during the active phase.
As for the effects of snack time on circadian rhythm regulation and circadian regulation of body weight regulation this study found that the effects of chronic rest phase snacking requires the functionality of the circadian clock.
TAKE HOME: Although this is a complex study to interpret it clearly establishes that snacking when one should be resting, say in the period following the evening meal and before bedtime, significantly contributes to disturbances in body weight regulation.
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