Sleep curtailment is accompanied by increased intake of calories from snacks

Arlet V Nedeltcheva, Jennifer M Kilkus, Jacqueline Imperial, Kristen Kasza, Dale A Schoeller, Plamen D Penev, Arlet V Nedeltcheva, Jennifer M Kilkus, Jacqueline Imperial, Kristen Kasza, Dale A Schoeller, Plamen D Penev

Abstract

Background: Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite.

Objective: We tested the hypothesis that the curtailment of human sleep could promote excessive energy intake.

Design: 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.

Results: 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.

Conclusions: 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.

Figures

FIGURE 1
FIGURE 1
Average daily energy intake from meals (top panels), snacks (middle panels), and meals plus snacks (bottom panels) as a function of the initial body weight of the 11 subjects during the 8.5-h (left) and 5.5-h bedtime (right) conditions. Each panel shows a corresponding best-fit line along with the Spearman's correlation coefficient (r) and its P value.
FIGURE 2
FIGURE 2
A: Mean (±SE) daily energy balance of 11 subjects during the 8.5-h (open bars) and 5.5-h (solid bars) bedtime conditions. B: Individual variability in weight gain during each 14-d study period. Data points connected with a line reflect the change in body weight of the same individual during the 8.5-h (left) and 5.5-h (right) bedtime conditions. Triangles represent female and circles male subjects. Solid symbols: subjects who completed the 8.5-h bedtime intervention first; open symbols: subjects who started with the 5.5-h bedtime condition first. C: Mean (±SE) 24-h serum leptin concentrations before the start of the 8.5-h (open circles) and 5.5-h (solid circles) bedtime conditions (n = 11). D: Mean (±SE) 24-h leptin concentrations at the end of the 8.5-h (open circles) and 5.5-h (solid circles) bedtime conditions (n = 11). E: Mean (±SE) 24-h serum ghrelin concentrations before the start of the 8.5-h (open circles) and 5.5-h (solid circles) bedtime conditions (n = 9). F: Mean (±SE) 24-h ghrelin concentrations at the end of the 8.5-h (open circles) and 5.5-h (solid circles) bedtime conditions (n = 9).

Source: PubMed

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