Night sleep loss and desire for food

 

Nutrients. 2023 Apr 23;15(9):2035. doi: 10.3390/nu15092035

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

Svenja Meyhöfer 1,2,3,4,†, Rodrigo Chamorro 1,5,†, Manfred Hallschmid 2,6,7, Denisa Spyra 1, Nelli Klinsmann 1, Bernd Schultes 1, Hendrik Lehnert 4,8, Sebastian M Meyhöfer 1,2,4,*, Britta Wilms 1,2,4

Editors: Albert Lecube, David J Mela

 Introduction

Sleep loss has become common in modern societies [1] 

and has been reported in different populations and age groups during the past decades [2].

 In parallel, the prevalence of obesity and metabolic comorbidities, such as type 2 diabetes (T2D), are rising worldwide [3].

 A meta-analysis, including more than 600,000 adults and 30,000 children, showed a strong association between reduced sleep duration of less than 5 h/day and obesity [4].

 Large epidemiological studies indicate that reduced quantity and decreased sleep quality are associated with adverse metabolic conditions, such as obesity and impaired glucose tolerance, and several meta-analyses confirmed an association between short, but also long, sleep and the prevalence of the metabolic syndrome [5,6]. 

An important mediator for these metabolic changes seems to be changes in the central nervous control of energy homeostasis, including an increase in appetite, sensitivity to food stimuli, and energy intake. Thus, sleep loss seems to be a relevant risk factor for metabolic diseases, such as obesity and T2D [7].

 As sleep is a process regulated by the circadian clock, being related to the suprachiasmatic nucleus of the hypothalamus as the main zeitgeber and also feedback to the clock [8],

 the consequences of impaired sleep duration and timing can lead to acute, but also chronic, circadian disruption. In fact, the detrimental health effects of mistimed sleep have been shown by adverse health effects of shift work and social jetlag, two widespread conditions in current societies [9,10,11]. 

A meta-analysis, including 13 studies, revealed that night shift work is associated with a 57% increased risk of the metabolic syndrome. Data further showed a dose–response relationship with years of night shift work, with 77% increased risk of metabolic syndrome in those with longer exposure to shift work than in those with shorter work in rotating shift (12%) [12].

Most experimental studies have shown that acute sleep loss increases ghrelin and decreases leptin concentrations, as relevant orexigenic and anorexigenic hormonal mediators of hunger and appetite, respectively. In line, short sleep was accompanied by increased feelings of hunger and appetite, as well as caloric intake [13,14],

 which could promote weight gain and obesity in long term. However, there are also data on unchanged hunger, appetite, and food intake after acute sleep loss [15].

 This, at first glance, seems to be a contradictory result, but it may be able to be explained—at least in part—by overeating after both short and regular sleep, since subjects had unlimited access to different foods, including tasty and high caloric items in this last study with ingested energy exceeding the calculated 24 h energy requirement by approximately 60% [15].

The mechanisms linking short sleep to acute changes in feelings of hunger and, thus, shift in the energy balance are under investigation. Elevated ghrelin concentrations might mediate increased food intake, and some, but not all, studies report increased ghrelin concentrations after shortened sleep [16,17,18,19].

 In addition, dampened leptin concentrations trigger increased food intake after sleep restriction in some studies [20,21]. 

However, others have reported unchanged or elevated leptin concentrations after varying degrees of shortened sleep [16,22,23].

 Different study protocols could partly explain these contradictory results regarding the degree and duration of sleep restriction, access to food (e.g., unlimited vs. served according to subject’s energy requirement), type of foods (e.g., palatable vs. standard), participants’ characteristics, and physical activity level.

Regarding the desire to eat after short sleep, some studies report no changes in perceived pleasantness of food or the desire to eat after one night with reduced sleep of 4 h and after five consecutive days of insufficient sleep, mimicking a work week, respectively [14,24].

 In contrast, others have shown increased hunger and prospective food consumption after three nights of sleep restriction with a sleep duration of 3.5 h per night [25].

 Since most studies did not synchronize sleeping and waking periods under experimental conditions, it has been speculated [15] that the waking time is a prerequisite for the orexigenic effect of sleep loss [14,26,27].

The impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. Alterations in the timing of sleep during restricted sleep could result in dissimilar sleep and metabolic impairments, given the notorious influence of sleep on metabolic processes [7]. 

Early evidence on this issue showed that mistimed sleep (i.e., early night and late-night sleep loss) during restricted sleep led to changes in sleep architecture in young adults, even without differences in the anorectic hormone leptin levels between sleep restriction-timing conditions [28]. Others have reported that changes in sleep stages after sleep restriction (4 h sleep, from 01:00–05:00 h) was related to changes in hunger feelings [29]. McNeil et al. also showed increased appetite before and after breakfast after short sleep with advanced wake time (i.e., 4 h of sleep with advanced wake up time) in young adults [30]. The same group showed that short sleep with delayed wake-up time increased energy intake from carbohydrates [31]. Additionally, short sleep with both delayed bedtime and advanced wake-up time affected physical activity pattern.

We have previously shown that the timing of sleep loss is relevant for glucose homeostasis and physical activity patterns in healthy humans. Sleep loss, with advanced awakening time, led to reduced glucagon and altered cortisol levels [32] toand also led to reduced physical activity and intensity the day after [33].

 Thus, besides its consequences on sleep and metabolic outcomes, impairment in the control of appetite regulation can be expected after mistimed sleep loss.

The present study investigated the impact of the specific timing of sleep loss compared to regular sleep on appetite regulation and desire for foods. We hypothesized that both short sleep duration per se and the timing of sleep loss, i.e., early night sleep loss vs. late night sleep loss, may modulate the adverse effects of sleep loss on humans’ appetite regulation, feelings of hunger, and desire for food.