Observational research suggests that short sleep duration is an important risk factor for obesity. Previous research has linked each hour of sleep reduction, relative to 7 hours of sleep, to a 9% increase in obesity risk. One potential explanation for this association is that sleep restriction may lead to a higher energy intake. Indeed, according to a 2021 meta-analysis, restricting sleep to no more than 5 hours per night resulted in an average increase in energy intake of around 200 calories per day. That said, it remains unknown if, and to what extent, increasing sleep duration in a real-life setting reduces energy intake in people with overweight. The trial summarized here examined this possibility.
In this 2-week randomized controlled trial, 80 men and women ages 21–40 with a BMI between 25 and 29.9 (i.e., overweight) and habitual sleep duration of less than 6.5 hours per night were randomized to one of two groups:
Sleep extension group: Participants in this group were provided with individualized sleep hygiene recommendations to follow, with the aim of extending their bedtime duration to 8.5 hours.
Control group: Participants in this group continued with their usual sleep habits.
The participants in both groups were asked to continue their daily routine without any prescribed diet or physical activity. The researchers continuously monitored the participants’ sleep-wake patterns at home using wrist actigraphy.
The primary outcome was energy intake, which was calculated from the sum of total energy expenditure (measured using the doubly labeled water method, which involves tracking the excretion of hydrogen and oxygen isotopes from the body over time) and change in body energy stores (calculated from changes in body weight and body composition measured with dual-energy X-ray absorptiometry). Other outcomes of interest were body weight and body composition.
Compared to the participants in the control group, participants in the sleep extension group increased their sleep duration by an average of 1.2 hours per night. Energy intake decreased in the sleep extension group by 156 calories per day, and increased in the control group by 115 calories per day. Overall, there was an inverse association between sleep duration and energy intake, with every one-hour increase in sleep duration associated with a reduction in energy intake of approximately 162 calories per day. There were no changes in energy expenditure in either of the two groups.
In the sleep extension group, there were small reductions in body weight (−0.48 kilograms), fat free mass (−0.36 kilograms), and fat mass (−0.12 kilograms). In contrast, body weight, fat free mass, and fat mass increased in the control group by 0.39, 0.26, and 0.13 kilograms, respectively.
According to the study abstract, compared with the control group, the sleep extension group had a statistically significant reduction in energy intake of 270 calories per day. While this is technically true, it’s worth keeping in mind that this between-group difference was not entirely due to a reduction in energy intake in the sleep extension group. Instead, it was partly due to an increase in energy intake of 115 calories per day in the control group.
It’s also worth noting that there were some discrepancies between the preregistered outcomes and the outcomes specified in the published paper. Specifically, several primary outcomes were prespecified (insulin sensitivity, energy expenditure, energy intake, beta-cell function, and disposition index), while only one primary outcome (energy intake) was specified in the published paper. This is an issue because it means that the researchers could have tested all five of the preregistered outcomes, and then specified the primary outcome in the published paper as the one for which they discovered statistically significant results.
Preregistering a study forces researchers to clearly think through the ins and outs of their study design beforehand, and also helps reduce their ability to fish for a changed primary outcome after the data are collected, since any deviations from the preplanned protocol are public.
However, preregistration doesn’t guarantee that the study design is high quality. Sometimes, there are discrepancies between preregistration and the final study. More often, the preregistration is vague. Perhaps the outcomes aren’t specified, or there are many primary outcomes listed. Ideally, there should be one. And, even if the preregistered outcomes are specific, it’s very rare to see the study analysis in the preregistration. But preregistering the data analysis plan is very useful, as this is where a lot of data fishing can occur. Making the analysis plan public forces the researchers to think clearly about their data beforehand, while also making fishing for significant results more difficult.
The big picture
The findings of the study summarized here are supported by the results of a 2019 meta-analysis, which found that healthy individuals consumed an average of 253 calories more in a single meal during short-term sleep restriction of up to 14 days, compared to when they slept normally. The meta-analysis also found that sleep restriction resulted in an increase in body weight of 0.34 kilograms. However, keep in mind that the study under review did not explore the effects of sleep restriction, but, rather, of sleep extension.
Several potential explanations have been proposed for the reduced sleep–obesity link, some of which relate to how sleep may affect energy intake.
The first potential explanation is that short sleep duration may stimulate hunger through its effects on appetite-regulating hormones, and thus lead to higher energy intake. Specifically, short sleep duration may decrease the levels of leptin, a hormone that suppresses appetite, and increase the levels of ghrelin, a hormone that stimulates hunger. However, even though sleep restriction has previously been reported to increase subjective hunger levels, its purported effects on the levels of leptin and ghrelin have not been confirmed in meta-analyses. That said, it’s worth noting that hormones other than leptin and ghrelin, such as peptide YY, cholecystokinin, and glucagon-like peptide-1, are involved in appetite and hunger regulation and could play a role in the link between sleep and hunger.
The second potential explanation for the sleep–obesity link is that reduced sleep duration enhances the activity in neuronal centers of the brain associated with pleasure and reward, thereby promoting the consumption of “unhealthy,” energy-dense foods. On the other hand, sleep extension may reduce the desire for such foods, ultimately leading to a reduction in energy intake.
One more possible explanation is that more time awake provides more opportunity to eat. This means that more time spent in bed and/or sleeping reduces available time to eat, resulting in a reduction in energy intake.
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