This study examined whether the curtailment of human sleep in an environment that promotes overeating and inactivity will be accompanied by an increased intake of energy from meals and snacks. Using a protocol of recurrent bedtime restriction, we were able to change the sleep duration of the study participants from over 7 hours/day, which in epidemiological studies corresponds to the sleep category with lowest prevalence of excess adiposity, to fewer than 5.5 hours/day, which falls in a category associated with an increased risk of obesity (5
). As intended, the physical activity levels of the participants during both sleep conditions were well within the range of sedentary humans (19
). Our results show that recurrent bedtime restriction in the setting of ad lib
access to palatable food is accompanied by an increased consumption of excess calories from snacks without a statistically significant change in the intake of energy from meals.
The concomitant monitoring of energy expenditure and peripheral leptin and ghrelin levels allowed us to assess the role of several factors that have been hypothesized to link the lack of sufficient sleep to increased energy intake. Previous studies in rodents have shown that partial sleep deprivation is associated with hyperphagia accompanied by markedly increased energy expenditure and weight loss (11
). In contrast, the direct measurements of energy expenditure during the short sleep condition of our study indicate that the increased consumption of snacks by the subjects was not related to a comparable rise in their energy needs (). The differences in the resting metabolic rate and the thermic effect of food between the two sleep conditions of this experiment were small and did not reach statistical significance. The existing studies of total sleep deprivation in humans further indicate that compared to relaxed wakefulness, a night of restful sleep saves relatively little energy (20
). The possibility that daily exposure to 3 extra hours of wakefulness may be accompanied by increased out-of-bed physical activity (22
) also did not have a large impact on the energy budget of our sedentary subjects (). Overall, the small changes in energy expenditure during the 5.5-hour bedtime condition were not sufficient to offset the observed rise in consumption of excess calories derived mostly from snacks (). Clearly, such changes in the energy balance of susceptible individuals could exacerbate their risk of weight gain and obesity (3
), however, the apparent modest size of any such effect indicates that much larger and longer studies will be needed to define the impact of sleep restriction on these clinical endpoints.
Cross-sectional observations of lower leptin and higher ghrelin levels in people with short sleep duration (8
) have led to the hypothesis that such hormone changes are likely to promote overeating and lead to increased risk of obesity. However, a recent clinical trial provided conflicting results (23
), raising the possibility that single measurements of leptin and ghrelin in epidemiological studies (8
) may be influenced by systemic differences in the diurnal profiles of food intake and peripheral metabolic hormones in short sleepers (24
). The finding of increased energy intake from snacks, but not meals, and the lack of significant changes in ghrelin (26
) during the short sleep condition of our study () are also at odds with the existing hypothesis. Likewise, in the setting of ad lib
energy intake, we did not find differences in the 24-hour leptin levels between the two bedtime conditions: final leptin concentrations increased along with the accumulation of a positive energy balance and reflected the adiposity of the subjects equally well irrespective of the presence or absence of sleep loss (). Two laboratory studies, designed to provide energy intake near weight maintenance levels, indicate that total sleep deprivation does not lower 24-hour leptin levels (25
). In contrast, lower leptin, higher ghrelin, and increased hunger and appetite were found in lean men exposed to short-term sleep curtailment and mild caloric restriction in the form of intravenous glucose (10
). When combined, these observations raise the possibility that acute sleep loss may amplify the human neuroendocrine response to caloric restriction and enhance the defense of affected individuals against disruptions in their food supply.
What then are the factors that underlie the increased intake of energy from snacks in our experiment? The results of the study support the concept that the control of human energy balance can be easily compromised by the propensity of many individuals to overeat in the setting of sedentary living with unlimited food availability (28
). Under these circumstances, the excessive consumption of calories from meals and snacks was augmented by the novelty of the experimental environment and emerged as an important predictor of individual weight gain (). These observations support the concept that “non-homeostatic” factors could play a considerable role in determining human feeding behavior (30
). Since bedtime curtailment resulted in more extended exposure (by 3 hours/day) to palatable food, this factor may have contributed to the observed increase in energy consumption. Such possibility is supported by the larger 54% relative increase in snack intake during the nighttime period of the 5.5-hour bedtime condition, which included most of the extra waking hours, compared to the 18% relative increase during the day, when the exposure to food between the two sleep conditions was more similar (). While these changes may share some similarity with certain aspects of the night eating syndrome (31
), our subjects exhibited a much more consolidated pattern of sleep during the 5.5-hour compared to the 8.5-hour bedtime intervention () and did not wake up to eat during the periods of restricted sleep.
Finally, the increase in the carbohydrate content of ingested snacks during the 5.5- hour bedtime condition suggests that sleep loss, itself, may have an effect on human energy intake. Enhanced carbohydrate consumption and preference for sweets have already been reported in psychologically demanding circumstances (32
). More recently, the discovery of a new group of orexin-containing neurons in the hypothalamus has led to the description of an integrated network of pathways that regulate mammalian arousal, waking, and feeding behavior (33
). These neurons respond to sleep loss and metabolic signals such as glucose, and can modulate the control of reward and motivation (34
). Some animal data already raise the possibility that changes in this system may contribute to the association between chronic metabolic disorders and insufficient sleep (35
). Our findings indicate that alterations in the balance between sleep and wakefulness can modify the amount, composition, and distribution of human food intake, and suggest that sleeping short hours in modern societies may aggravate the problem of excessive energy consumption.
In summary, bedtime restriction in an environment that promotes overeating and inactivity was accompanied by increased intake of calories from snacks with higher carbohydrate content without a statistically significant change in the consumption of energy from meals. In the absence of comparable changes in energy expenditure and differences in serum leptin and ghrelin, alternative mechanisms, such as more prolonged exposure to palatable food and sleep-loss-related changes in reward seeking and motivation, may underlie these changes in feeding behavior. The presence of considerable individual differences in the propensity to consume excess calories from snacks also raises the possibility that chronic bedtime curtailment may have more deleterious metabolic consequences in people with such preexisting susceptibility. While this hypothesis is consistent with epidemiological reports showing an association of self-reported short sleep with more frequent snacking and increased risk of obesity (36
), our discussion is based on the detailed evaluation of a small number of subjects over a limited period of time in the laboratory. Additional studies will be needed to examine the impact of habitual sleep curtailment on human food intake and energy metabolism under free-living conditions.