Sleep and meal timing influence food intake and its hormonal regulation in healthy adults with overweight/obesity

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Abstract

Studies associate sleeping and eating late in the day with poor dietary quality and higher obesity risk but differences in sleep duration confound this association. We aimed to determine whether sleep and meal timing, independent of sleep duration, influenced food intake in healthy adults. This was a controlled, 2×2 inpatient crossover study with normal (0000–0800h) or late (0330–1130h) sleep and normal (1, 5, 11, and 12.5h after awakening) or late (4.5, 8.5, 14.5, and 16h after awakening) meals. Food intake was controlled while blood samples were obtained for determination of appetite-regulating hormones on days 3–4. Self-selected food intake was assessed on day 5. Data were analyzed using linear mixed model analysis with sleep, meal, and sleep × meal interaction as dependent variables. Five participants completed all phases (mean age 25.1 ± [SD] 3.9y, body mass index 29.2 ± 2.7kg/m 2 ). There was a significant sleep × meal interaction on energy intake (P=0.035) and trends on fat and sodium intakes (P<0.10). Overnight ghrelin concentrations were higher under normal sleep and meal conditions relative to late (P<0.005) but lower when both were combined (P<0.001). Overnight leptin concentrations were higher under normal meal conditions (P=0.012). There was a significant sleep × meal interaction on ghrelin (P=0.032) and glucagon-like peptide 1 (P=0.041) concentrations, but not leptin (P=0.83), in response to a test meal. Our results suggest that alignment of sleep and meals may influence food choice and energy balance. Additional research is necessary to expand and confirm our findings.

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Circadian timing of food intake contributes to weight gain.

Deanna Arble, Joseph Bass, Aaron D. Laposky … (2009)

Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. The present study focused on the role of the circadian phase of food consumption in weight gain. We provide evidence that nocturnal mice fed a high-fat diet only during the 12-h light phase gain significantly more weight than mice fed only during the 12-h dark phase. A better understanding of the role of the circadian system for weight gain could have important implications for developing new therapeutic strategies for combating the obesity epidemic facing the human population today.

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Light at night increases body mass by shifting the time of food intake.

L. K. Fonken, J. L. Workman, J C Walton … (2010)

The global increase in the prevalence of obesity and metabolic disorders coincides with the increase of exposure to light at night (LAN) and shift work. Circadian regulation of energy homeostasis is controlled by an endogenous biological clock that is synchronized by light information. To promote optimal adaptive functioning, the circadian clock prepares individuals for predictable events such as food availability and sleep, and disruption of clock function causes circadian and metabolic disturbances. To determine whether a causal relationship exists between nighttime light exposure and obesity, we examined the effects of LAN on body mass in male mice. Mice housed in either bright (LL) or dim (DM) LAN have significantly increased body mass and reduced glucose tolerance compared with mice in a standard (LD) light/dark cycle, despite equivalent levels of caloric intake and total daily activity output. Furthermore, the timing of food consumption by DM and LL mice differs from that in LD mice. Nocturnal rodents typically eat substantially more food at night; however, DM mice consume 55.5% of their food during the light phase, as compared with 36.5% in LD mice. Restricting food consumption to the active phase in DM mice prevents body mass gain. These results suggest that low levels of light at night disrupt the timing of food intake and other metabolic signals, leading to excess weight gain. These data are relevant to the coincidence between increasing use of light at night and obesity in humans.

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Sleep curtailment is accompanied by increased intake of calories from snacks.

Arlet Nedeltcheva, Jennifer Kilkus, Jacqueline Imperial … (2009)

Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite. We tested the hypothesis that the curtailment of human sleep could promote excessive energy intake. Eleven healthy volunteers [5 women, 6 men; mean +/- SD age: 39 +/- 5 y; mean +/- SD body mass index (in kg/m(2)): 26.5 +/- 1.5] completed in random order two 14-d stays in a sleep laboratory with ad libitum access to palatable food and 5.5-h or 8.5-h bedtimes. The primary endpoints were calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-h profiles of serum leptin and ghrelin. Sleep was reduced by 122 +/- 25 min per night during the 5.5-h bedtime condition. Although meal intake remained similar (P = 0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 +/- 541 compared with 866 +/- 365 kcal/d; P = 0.026), with higher carbohydrate content (65% compared with 61%; P = 0.04), particularly during the period from 1900 to 0700. These changes were not associated with a significant increase in energy expenditure (2526 +/- 537 and 2390 +/- 369 kcal/d during the 5.5-h and 8.5-h bedtime periods, respectively; P = 0.58), and we found no significant differences in serum leptin and ghrelin between the 2 sleep conditions. Recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks but not meals.