Sleep Patterns, Diet Quality and Energy Balance.
ABSTRACT There is increasing evidence showing that sleep has an influence on eating behaviors. Short sleep duration, poor sleep quality, and later bedtimes are all associated with increased food intake, poor diet quality, and excess body weight. Insufficient sleep seems to facilitate the ingestion of calories when exposed to the modern obesogenic environment of readily accessible food. Lack of sleep has been shown to increase snacking, the number of meals consumed per day, and the preference for energy-rich foods. Proposed mechanisms by which insufficient sleep may increase caloric consumption include: (1) more time and opportunities for eating, (2) psychological distress, (3) greater sensitivity to food reward, (4) disinhibited eating, (5) more energy needed to sustain extended wakefulness, and (6) changes in appetite hormones. Globally, excess energy intake associated with not getting adequate sleep seems to be preferentially driven by hedonic rather than homeostatic factors. Moreover, the consumption of certain types of foods which impact the availability of tryptophan as well as the synthesis of serotonin and melatonin may aid in promoting sleep. In summary, multiple connections exist between sleep patterns, eating behavior and energy balance. Sleep should not be overlooked in obesity research and should be included as part of the lifestyle package that traditionally has focused on diet and physical activity.
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ABSTRACT: Habitual short sleep duration appears to increase the risk of obesity. The objective of this paper is to investigate the association of habitual sleep duration with objective measures of energy balance. One hundred twelve African-American and 111 non-Hispanic whites aged 21-69 y participated in a cross-sectional study of dietary assessment and biomarkers. Participants reported the mean number of hours per day spent sleeping over the past year. Short sleep duration was defined as ≤6 h/d of sleep. Energy intake (kilocalories) was objectively assessed using the 2-point doubly labeled water technique to determine total energy expenditure, which is approximately equal to energy intake. Physical activity energy expenditure (kilocalories) was estimated as total energy expenditure minus each participant's calculated basal metabolic rate and the thermogenic effect of food. Compared with participants who slept ≤6 h, individuals who slept 8 h were significantly less likely to be obese (OR: 0.33; 95% CI: 0.14, 0.79). However, this association was not linear across 6-9 h of sleep (P-trend = 0.16). There was an inverse association between sleep and energy intake (P-trend = 0.07): compared with ≤6 h/d, adults who reported ≥9 h sleep consumed 178 fewer kcal/d. There was also an inverse association between sleep and physical activity (P-trend = 0.05): compared with ≤6 h/d of sleep, adults who reported 9 h of usual sleep expended 113 fewer kcal/d in physical activity. These data indicate that, compared with longer sleep duration, adults who report habitual short sleep duration have somewhat higher physical activity energy expenditure but considerably higher energy intake. Habitual short sleep duration appears to be 1 of the facets of modern life leading to a mismatch between energy intake and physical activity.Journal of Nutrition 02/2014; 144(4). DOI:10.3945/jn.113.186890 · 3.88 Impact Factor
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ABSTRACT: Background & Objectives Shorter sleep is associated with higher weight in children, but little is known about the mechanisms. The aim of this study was to test the hypothesis that shorter sleep was associated with higher energy intake in early childhood.Methods Participants were 1303 families from the Gemini twin birth cohort. Sleep duration was measured using the Brief Infant Sleep Questionnaire (BISQ) when the children were 16 months old. Total energy intake (kcal/day) and grams/day of fat, carbohydrate and protein were derived from 3-day diet diaries completed by parents when children were 21 months old.ResultsShorter nighttime sleep was associated with higher total energy intake (p for linear trend=0.005). Children sleeping <10 h consumed around 50 kcals/day more than those sleeping 11 to <12 h a night (the optimal sleep duration for children of this age). Differences in energy intake were maintained after adjustment for confounders. As a percentage of total energy intake, there were no significant differences in macronutrient intake by sleep duration. The association between sleep and weight was not significant at this age (P=0.13).Conclusions This study provides the first evidence that shorter nighttime sleep duration has a linear association with higher energy intake early in life. That the effect is observed before emergence of associations between sleep and weight indicates that differences in energy intake may be a mechanism through which sleep influences weight gain.International Journal of Obesity accepted article preview online, 26 March 2014; doi:10.1038/ijo.2014.50.International journal of obesity (2005) 03/2014; 38(7). DOI:10.1038/ijo.2014.50 · 5.00 Impact Factor
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ABSTRACT: Background: Three-month-old neuron-specific lipoprotein lipase (LPL)-depleted mice (NEXLP(-/-)) mice are preobese and have normal body weight before developing obesity by 4.5 months. This series of experiments investigated responses to novel environment stimuli and acute sleep deprivation in preobese NEXLPL(-/-)) mice to test the hypothesis that neuron-specific LPL deletion alters normal adaptive metabolic responses to environmental challenges. Methods: Three-month-old, age- and weight-matched, male NEXLPL(-/-)) (n=10) and wild-type (WT) (n=10) mice were housed in individual metabolic chambers with a 12-hr dark cycle. Food and water intake, locomotor activity, and calorimetry data were recorded in 12-min intervals. Novel environmental responses were elicited by first-time introduction to chambers at dark onset, followed by acclimation, baseline recording, and 6-hr of sleep deprivation on subsequent experimental days. Results: NEXLPL(-/-)) mice displayed a 1.5-fold greater increase in activity in response to a novel environment than seen in WT controls (P=0.0308), and a two-fold greater increase in food intake following acute sleep deprivation (P=0.0117). NEXLPL(-/-)) mice averaged a 27% higher metabolic rate than WT mice throughout the experiments (P<0.0001). Body weight, composition, and temperature did not differ between murine groups throughout the experiments. Levels of free fatty acid, insulin, glucose, and triglycerides were similar between groups at the terminus. Conclusions: A deficiency in neuronal LPL signaling disrupts normal responses to novel environmental exposure and acute sleep deprivation, a maladaptive response that may contribute to weight gain in genetically predisposed mice, and perhaps humans.Metabolic syndrome and related disorders 04/2014; 12(6). DOI:10.1089/met.2013.0141 · 1.98 Impact Factor