Objective

The current review focuses on two main topics: mechanistic pathways for the role of sleep deprivation in development of obesity and the current knowledge on the relationship between sleep deprivation and food and dietary choices. In more details: first of all, an overview on the description, causes, consequence and prevalence of sleep deprivation is presented. Then, scientific evidence for the link between sleep deprivation and obesity is reviewed, and mechanistic pathways for the effect of sleep deprivation in promoting obesity are discussed. Possible effects of sleep deprivation on energy intake, appetite regulation, physical activity and energy expenditure will be described. Also, the role of sex and weight status in the effect of sleep deprivation on appetite control and food selection will be stated. Impact of sleep deprivation on food selection, diet quality, consumption of snacks and desire for consumption of sweets are among issues that will be discussed in more details. At the end, the relationships are reversed and evidence for possible effects of eating habits, diet quality and dietary components on sleep health will be presented. Applying these diet considerations may help in reducing sleep problems in affected individuals.

Role of sleep deprivation in development of obesity

The relationship of sleep deprivation and weight gain has been highlighted in previous investigations^{(Reference Cooper, Neufeld, Dolezal and Martin41)}. Longitudinal cohort studies have shown the fastest weight gain in people who get the least amount of sleep^{(Reference Patel, Malhotra, White, Gottlieb and Hu42)}. Also, meta-analyses of cohort studies in both children^{(Reference Miller, Bates, Ji and Cappuccio43)} and adults^{(Reference Bacaro, Ballesio and Cerolini44)} have emphasised short sleep duration as a predisposing factor for obesity. For instance, a meta-analysis of 22 cohort studies on adults showed that <7 h sleep compared with 7–8 h sleep was associated with an odds ratio of 1·26 (95% confidence interval (CI): 1·17, 1·36) for obesity^{(Reference Guimarães, Silva, Latorraca, Oliveira and Crispim45)}. Also, a meta-analysis of 33 cohort studies on children and adolescents revealed an obesity risk of 1·57 (95% CI: 1·36, 1·81) for short sleep duration^{(Reference Deng, He, He, Zhu, Zhang and Niu46)}. Results of meta-analyses on cohort studies have been confirmed by meta-analysis of randomised controlled trials (RCT), in which strategies that improve duration and/or quality of sleep reduced body weight^{(Reference Capers, Fobian, Kaiser, Borah and Allison47)}.

Each hour sleep deprivation has been associated with 0·16 and 0·35 kg/m² increase in body mass index (BMI) in adolescents^{(Reference Wells, Hallal, Reichert, Menezes, Araújo and Victora48)} and adults^{(Reference Cappuccio, Taggart and Kandala49)}, respectively. Accumulation of fat occurs especially in central body areas even when total body fat does not change. As an example, in an RCT on healthy non-obese individuals, alterations in total body fat did not differ between sleep restriction (14 d sleep restriction with 4 h sleep opportunity) and control conditions, but total abdominal fat increased during sleep restriction, with significant increases evident in both subcutaneous and visceral abdominal fat masses^{(Reference Covassin, Singh and McCrady-Spitzer50)}. Also, in a study on resident physicians, those with poor sleep quality reported greater weight gain and higher frequency of abnormal waist circumference after beginning of residency compared with physicians with better sleep quality^{(Reference Mota, Waterhouse and De-Souza51)}.

In weight loss programmes, sleep disturbance during weight loss has been associated with an elevated risk of failure to lose weight^{(Reference Li, Li and Zhou52)}. Moreover, higher sleep fragmentation, which is determined by measuring the number of wake-ups, led to less weight reduction in those who participated in weight loss programmes^{(Reference Sawamoto, Nozaki and Furukawa53)}. Energy restriction programmes may have more adverse effects on sleep-restricted individuals. Nedeltcheva et al. reported that energy-restricted individuals under insufficient sleep had a higher loss of fat-free mass whereas those with adequate sleep showed higher loss of fat mass^{(Reference Nedeltcheva, Kilkus, Imperial, Schoeller and Penev54)}. Sleep curtailment decreased the proportion of weight lost as fat by 55% and increased loss of fat-free mass by 60%.

The association of short sleep duration and obesity seems to be stronger in younger ages. This has been clearly shown in a meta-analysis of observational data collected from 634,511 participants with ages ranging from 2 to 102 years^{(Reference Cappuccio, Taggart and Kandala49)}. The relationship of short sleep duration and obesity had odds ratios of 1·89 (95% CI: 1·46, 2·43) and 1·55 (95% CI: 1·43, 1·68) in children and adults, respectively. Short sleep duration in childhood may predict adulthood obesity. A 32 year prospective birth cohort study showed that shorter childhood sleep times were associated with higher adult BMI values, and the association remained after adjustment for adult sleep time and potential confounders such as early childhood BMI, parental BMI and adult physical activity^{(Reference Landhuis, Poulton, Welch and Hancox55)}.

It is worthwhile noting that it is not only sleep deprivation that acts as a risk factor for obesity but oversleeping may also function as a risk factor, suggesting a U-shaped relationship between sleep duration and BMI. However, there may be a sex-specific effect in this proposed U-shaped relationship^{(Reference Ren, Chang, Kang, Zhao, Chen and Pei56)}. In this regard, a 10 year cohort study in women showed that both habitual short and long sleep durations were risk factors for general obesity in women aged <40 years^{(Reference Theorell-Haglöw, Berglund, Berne and Lindberg57)}. Habitual long sleep duration was also a risk factor for central obesity in young women. But, this kind of association was not observed in a meta-analysis which included prospective studies of both sexes^{(Reference Wu, Zhai and Zhang58)}. Hence, long sleep duration may be the risk factor of obesity only in women. Since there is still controversy for the existence of such curvilinear association between sleep duration and BMI especially in men^{(Reference Ren, Chang, Kang, Zhao, Chen and Pei56)} more studies examining consequences of long sleep duration are needed. Consistent with what was mentioned for short sleep duration, long sleep duration is also associated with increased mortality risk^{(Reference Patel, Ayas and Malhotra39)}.

In the following sections, we will present some of the mechanisms by which sleep deprivation may contribute to obesity.

Energy intake in sleep deprivation

Most obesity cases result from positive energy balance due to extra energy intake^{(Reference Brondel, Quilliot, Mouillot, Khan, Bastable, Boggio, Leloup and Pénicaud59)}. Meta-analyses of RCT indicate that partial sleep deprivation increases total energy intake compared with habitual sleep^{(Reference González-Ortiz, López-Bautista, Valencia-Flores and Espinosa Cuevas60,Reference Soltanieh, Solgi, Ansari, Santos and Abbasi61)} . Cross-sectional studies have also shown the association of sleep deprivation and increased energy intake^{(Reference Zuraikat, Makarem, Liao, St-Onge and Aggarwal62–Reference Stelmach-Mardas, Iqbal and Mardas65)}. Most of this extra energy is consumed in the form of snacks especially after dinner^{(Reference Markwald, Melanson and Smith66)} as discussed later in this article. This increased energy intake is assumed to be a physiologic adaptation to compensate the augmented energy expenditure due to additional wake hours to prevent weight loss^{(Reference Markwald, Melanson and Smith66)}. However, easy access to snacks, increased desire for energy-dense snacks after sleep deprivation, and in some cases increased hunger, leads to overeating and weight gain^{(Reference García-García, Juárez-Aguilar, Santiago-García and Cardinali67)}, as will be discussed in the following sections.

Despite the above justifications, sleep deprivation has not increased energy intake in some trials with short but severe restriction, for example, after two nights of 4 h sleep^{(Reference Schmid, Hallschmid and Jauch-Chara68)} or one night of <5 h sleep^{(Reference Romney, Larson, Clark, Tucker, Bailey and LeCheminant69)}. It is likely that psychological stress caused by severe sleep deprivation reduces food intake while in prolonged sleep deprivations a sort of adaption occurs. The lack of the relationship of sleep deprivation with energy intake in some cross-sectional studies can also be justified. In an analysis of NHANES data, short sleepers had lower mean percentage of energy from main meals but higher energy intake from snacks^{(Reference Kant and Graubard70)}. Although energy intake did not associate with sleep duration, eating main meals and snacks at or after 20.00 in short-duration sleepers was suggestive of eating behaviours that may, in the long-term, lead to positive energy balance. Also, in a cross-sectional study on Japanese women, energy intake was lower in women with low sleep efficiency compared to participants with the middle and high sleep efficiency^{(Reference Hashimoto, Inoue and Kuwano71)}. Since the participants were young Japanese women, the authors justified this unexpected finding to participants’ desire to control their energy intake to prevent obesity, and thus attributed the observed low sleep efficiency a consequence of this eating control.

Appetite regulation in sleep deprivation

Increased food intake is driven by homoeostatic or hormonal and non-homoeostatic mechanisms. In the following sections, we describe these mechanisms in detail.

Non-homeostatic regulation of appetite, the role of food reward system

Brain reward system

The paradox of increased food and energy intake in the lack of change in appetite-regulating hormones, e.g.^{(Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97)} may be explained by the brain reward system, which in addition to homoeostatic factors regulate the eating. Brain reward system is responsible for stimulating behaviours that increase the likelihood of survival and reproduction^{(Reference Schultz105)}. Rewarding stimulus for such a system is any stimulus, object, activity or situation that elicits pleasure and is thus attractive and motivating. Food is one of these stimuli^{(Reference Jager and Witkamp106)}. Non-homoeostatic appetite regulation operates independently of homoeostatic regulation. Thus, the increased activity of the reward system and subjective food valuation could occur in the absence of hunger and alteration in appetite-related hormones (ghrelin, leptin, insulin and cortisol)^{(Reference Rihm, Menz and Schultz99)}. Food reward consists of two components: appetitive that refers to “wanting” or motivation to consume a food and consummatory which returns to the hedonic aspects of a food and leads to “liking” a food^{(Reference Jager and Witkamp106)}.

Neuroanatomy of the food reward system

Parts of cortical and subcortical areas of brain are known to evaluate food stimuli^{(Reference Greer, Goldstein and Walker107)}. At the cortical region, the anterior insula cortex, lateral orbital frontal cortex and anterior cingulate cortex have roles in governing appetitive choices and food preferences. Thus, the activity of cortical areas relates to the “liking” component of food reward. At subcortical regions, the amygdala and ventral striatum are engaged in managing motivation to eat, what is called “wanting”^{(Reference Greer, Goldstein and Walker107)}. In fact, the amygdala is involved in modulation of emotional feeding and reward processing^{(Reference Zhang, Li and Guo108,Reference Izadi and Radahmadi109)} . Reward information from the motivational and hedonic structures is sent to the nucleus accumbens and then to the lateral hypothalamic area to control feeding behaviours^{(Reference Uribe-Cerda, Morselli and Perez-Leighton110–Reference Morales and Berridge112)}. In abnormal conditions, the function of the reward system is impaired and leads to over- or under-eating. For instance, patients with anorexia or frail elderly lose weight because they suffer from loss of pleasure in eating and appetite^{(Reference Jager and Witkamp106)}. In contrast, in some obesity cases, hyper-sensitisation of motivational structures in brain leads to excessive food “wanting”^{(Reference Morales and Berridge112)}. Such condition also occurs in cases of drug addiction.

Sleep deprivation and food reward system

A large body of evidence indicates that sleep deprivation alters reward-driven eating behaviour^{(Reference Chaput113)}. Animal and human subject studies have shown that sleep deprivation increases motivation for reward^{(Reference Liu, Wang and Cai114)}. There are two hypotheses by which the reward system reacts to inadequate sleep. In the first hypothesis, the sensitivity of the reward system to food cues increases, thus individuals have augmented responsiveness to food rewards^{(Reference Demos, Sweet and Hart115,Reference St-Onge, McReynolds, Trivedi, Roberts, Sy and Hirsch116)} . In this regard, Demos et al. showed that compared to sufficient sleep (9 h/night), short sleep (6 h/night) caused greater activity to food images in brain regions of reward processing (e.g nucleus accumbens and putamen) and sensory/motor signalling (i.e. right paracentral lobule) effects that are mostly seen in individuals with obesity^{(Reference Demos, Sweet and Hart115)}. Also, St-Onge and colleagues reported an increased neuronal activity in response to food stimuli after restricted sleep (4 h/night) compared with habitual sleep (9 h/night)^{(Reference St-Onge, McReynolds, Trivedi, Roberts, Sy and Hirsch116)}. In the second hypothesis, insufficient or low-quality sleep causes weaker neuronal reactivity in reward-related regions in response to food intake, thus more inspiring food rewards (i.e. delicious high-energy foods) may need to induce neurons in the reward system or alternatively more foods need to be consumed to compensate for the reduced reward response and induce good pleasure^{(Reference Chaput113)}. Mechanisms involved in both of these hypotheses result in overeating.

Areas of the brain that are affected by sleep deprivation and the manner of changes are subject to controversy in neuroimaging investigations. For instance, Greer et al. reported that one night sleep deprivation suppressed activity in the cortical regions involved in hedonic evaluation and augmented that in the amygdala, leading to increased desire for consumption of high-energy foods^{(Reference Greer, Goldstein and Walker107)}. In contrast, Katsunuma et al. found that one night sleep deprivation (39 h wakefulness) activated the right anterior insula in response to food images but the activity of the amygdala remained unchanged although in optimal sleep condition both amygdala and anterior insula had low activity^{(Reference Katsunuma, Oba and Kitamura117)}. Likewise, six nights of sleep restriction increased neural activity in response to food stimuli in brain regions associated with reward^{(Reference St-Onge, McReynolds, Trivedi, Roberts, Sy and Hirsch116)}. Also, Benedict et al. reported that one night sleep deprivation increased neural activation in the right anterior cingulate cortex in response to food images^{(Reference Benedict, Brooks and O’Daly118)}. Although these studies seem contradictory at the first glance, an overview of their results suggests that sleep loss may modulate neural activity in at least one of cortical or subcortical regions. In the majority of the above examples, it was the cortical region (involved in liking) that increased its activity following sleep loss^{(Reference St-Onge, McReynolds, Trivedi, Roberts, Sy and Hirsch116–Reference Benedict, Brooks and O’Daly118)}, but suppression of cortical neurons when accompanied with heightened subcortical neuron activity also associated with augmented food desirability^{(Reference Greer, Goldstein and Walker107)}.

Inhibitory control

In addition to homoeostatic and reward-driven regulation, as a third mechanism, sleep deprivation impairs inhibitory control over eating. Inhibitory control or dietary restraint is defined as the ability to resist a potent stimulus, such as a palatable food^{(Reference de Klerk, Smeets and la Fleur119)}. The interaction between food reward system and inhibitory control predicts food intake^{(Reference Appelhans, Woolf, Pagoto, Schneider, Whited and Liebman120)}. Hence, a strong food reward perception along with low levels of inhibitory control may lead to overeating. Acute sleep deprivation reduces the ability to exert cognitive inhibition toward food stimuli^{(Reference Cedernaes, Brandell and Ros121)}. This low inhibitory control along with hormonal signals for hunger from the gut and/or increased motivation towards food stimuli from the reward system intensifies the risk of obesity. An overview of the possible mechanisms of sleep deprivation in the development of obesity has been given in Fig. 2.

Fig. 2. Possible mechanisms by which sleep deprivation lead to overweight and obesity. CCK, cholecystokinin; GLP-1, glucagon-like peptide-1.

Interaction of different systems

The hormonal, cognitive, emotional and behavioural systems that control feeding behaviour influence and interact with one another^{(Reference Lundahl and Nelson122,Reference Liu and Kanoski123)} . For instance, specific areas of the brain reward system, such as the hypothalamic arcuate nucleus, have receptors for ghrelin and leptin. Moreover, ghrelin levels have been positively correlated with increased sensitivity to dairy odour and higher intensity ratings to food odors including dairy and vanilla^{(Reference Ginieis, Abeywickrema, Oey and Peng124)}. In addition, the homoeostatic regulation has a strong control overeating under normal circumstances, but in abnormal conditions like adiposity, depression or sleep deprivation, particularly when the person lives in an obesogenic environment with easy access to highly energetic and palatable foods, the homoeostatic control may be weakened^{(Reference Berthoud125)}. Thus, the outcome of the interaction of these systems will finally determine the eating behaviour.

Physical activity in sleep deprivation

Weight gain in sleep deprivation seems to be partly due to decreased exercise and physical activity as a result of fatigue and tiredness^{(Reference Schmid, Hallschmid and Jauch-Chara68)}. In contrast, good sleep quality may predict increased physical activity through its positive effect on emotion regulation^{(Reference Semplonius and Willoughby126)}. On the opposite side of exercise, sedentary activities may be increased during sleep deprivation^{(Reference Romney, Larson, Clark, Tucker, Bailey and LeCheminant69,Reference Bromley, Booth, Kilkus, Imperial and Penev127–Reference Jindal, Puyau, Adolph, Butte, Musaad and Bacha129)} . Sedentary activities not only have low energy requirements but they may also promote consumption of high-energy snacks, further predisposing individuals to overweight. A hypothetical scheme for the possible effect of sleep deprivation on physical activity has been depicted in Fig. 3.

Fig. 3. Hypothetical scheme for the possible effect of poor sleep quality on physical activity.

Nonetheless, controlled trials for the effect of sleep deprivation on physical activity are inconsistent and all cases of increased^{(Reference Brondel, Romer, Nougues, Touyarou and Davenne73,Reference Hursel, Rutters, Gonnissen, Martens and Westerterp-Plantenga130,Reference McNeil, Doucet and Brunet131)} , decreased^{(Reference Schmid, Hallschmid and Jauch-Chara68,Reference Bromley, Booth, Kilkus, Imperial and Penev127,Reference Lee132)} or of no effect^{(Reference Romney, Larson, Clark, Tucker, Bailey and LeCheminant69,Reference Porter, Pettit-Mee and Emerson133,Reference Bosy-Westphal, Hinrichs and Jauch-Chara134)} in the amount and/or intensity of physical activity have been reported. These controversies may have resulted from diversity in study protocols. For instance, the observation of increased physical activity has been mostly in trials with one night of sleep deprivation^{(Reference Brondel, Romer, Nougues, Touyarou and Davenne73,Reference McNeil, Doucet and Brunet131)} or two nights of fragmented sleep^{(Reference Hursel, Rutters, Gonnissen, Martens and Westerterp-Plantenga130)} where the severity of sleep deprivation was mild. Decreased physical activity has been reported during prolonged (14 d) sleep deprivation^{(Reference Bromley, Booth, Kilkus, Imperial and Penev127)} or in studies where participants were not allowed to exercise and perform brisk physical activities^{(Reference Schmid, Hallschmid and Jauch-Chara68)}. Under normal living conditions (not laboratory) and ad libitum eating and free exercise, a moderated sleep curtailment may not largely affect physical activity^{(Reference Porter, Pettit-Mee and Emerson133,Reference Bosy-Westphal, Hinrichs and Jauch-Chara134)} . The time of sleep restriction also seems to matter. For instance, in a trial on normal-weight men sleep restriction during the second half of night reduced physical activity more than sleep restriction during the first half^{(Reference Wilms, Kuhr and Chamorro135)}, indicating that sleep during the second half of the night has a more important effect on feeling freshness during the next day. In agreement, McNeil et al. reported that participants with delayed sleep had more moderate-intensity physical activity than those with advanced wakeup time, although vigorous-intensity physical activity was greater following advanced wakeup^{(Reference McNeil, Doucet and Brunet131)}.

Energy expenditure

Like physical activity, the effect of sleep deprivation on daily energy expenditure has not been completely elucidated and all modes of increased^{(Reference Markwald, Melanson and Smith66,Reference Shechter, Rising, Albu and St-Onge136–Reference Jung, Melanson, Frydendall, Perreault, Eckel and Wright138)} , decreased^{(Reference Benedict, Hallschmid and Lassen139)} and no effect^{(Reference Covassin, Singh and McCrady-Spitzer50,Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97,Reference Hibi, Kubota and Mizuno140–Reference Calvin, Carter and Adachi142)} have been reported. There are many reasons for the controversies such as the difference in sleep deprivation protocol, very low sample size of some trials, the type of activities that were allowed during waking hours, and age, sex and BMI of participants. Studies largely differ in sleep deprivation protocol, such as total v. partial, moderate v. severe, and acute v. chronic sleep deprivation as well as the time of sleep deprivation. For the last item, depriving from deep or slow-wave sleep may have a different impact on energy expenditure than depriving from REM^{(Reference Kayaba, Park and Iwayama143)}.

A positive effect of sleep deprivation on energy expenditure was mostly seen in investigations where subjects had to spend at least 3 d inside calorimetric units. Staying for several days inside these units may cause a sort of psychological stress in participants because of limitations that such units impose, for instance, in eating, exercise, daily routine activities and communication with people as desired^{(Reference Vitale and Smith144)}. Such kind of stress may have also occurred by prolonged (40 h) sleep deprivation^{(Reference Jung, Melanson, Frydendall, Perreault, Eckel and Wright138)}. Stressful conditions may increase cortisol and/or norepinephrine levels, augment heart rate^{(Reference Benedict, Hallschmid and Lassen139)} and subsequently increase metabolic rate^{(Reference Haase, Long and Gillooly145)}. However, investigations that give participants some sort of freedom for eating, physical activity, and doing daily activities did not find a significant increase in energy expenditure^{(Reference Covassin, Singh and McCrady-Spitzer50,Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97,Reference St-Onge, Roberts and Chen141,Reference Calvin, Carter and Adachi142)} . The extent of the increase is estimated to be ∼ 4–5% equal to ∼ 377–460 kJ/day^{(Reference St-Onge and Shechter146)}. This amount is not large enough to compensate the increased energy intake during waking hours. For this increased energy expenditure, carbohydrates have shown to be oxidised more than fats, thereby promoting fat accumulation and weight gain^{(Reference Hursel, Rutters, Gonnissen, Martens and Westerterp-Plantenga130,Reference de Jonge, Zhao and Mattingly147)} .

Basal metabolic rate

Few studies have examined the association of sleep deprivation with metabolic rate, and again findings are with controversy. In a cross-sectional study on obese individuals with short sleep duration, poor sleep quality was associated with increased resting energy expenditure^{(Reference de Jonge, Zhao and Mattingly147)}. The authors reasoned that secretion of cortisol and epinephrine during short sleep stress may be the cause of this increase. In contrast, in a cross-sectional study on children and adolescents, suboptimal sleep was associated with lower basal metabolic rate and physical activity and higher sedentary behaviours^{(Reference Jindal, Puyau, Adolph, Butte, Musaad and Bacha129)}. There are also cross-sectional studies that did not find a relationship between sleep deprivation and basal metabolic rate^{(Reference Jurado-Fasoli, Mochon-Benguigui, Castillo and Amaro-Gahete148,Reference Shechter, Rising, Wolfe, Albu and St-Onge149)} . On the other hand, two RCT reported decreased metabolic rate following sleep deprivation. In one study, Nedeltcheva et al. reported that energy restriction with 5·5 h sleep/night for 14 d decreased resting metabolic rate and 24 h plasma epinephrine concentrations compared with energetic restriction with 8·5 h sleep/night^{(Reference Nedeltcheva, Kilkus, Imperial, Schoeller and Penev54)}. In agreement, Spaeth et al. reported that 4 h sleep/night for five nights reduced resting metabolic rate and 12 h recovery sleep returned it to baseline levels^{(Reference Spaeth, Dinges and Goel150)}.

According to what was stated in this and the previous two sections, there is still much work to be done to complete our understanding of the effect of sleep deprivation on physical activity, total and resting energy expenditure and thermic effect of food; for the latter, evidence is scarce.

Sex-specific effects

There is a large difference in the sleep and metabolic consequences of sleep deprivation between men and women. A global sleep dataset of 11·14 million nights from 69 650 non-shift workers aged 19–67 years from forty-seven countries showed that men tended to sleep less than women across the lifespan, but nighttime awakening was more prevalent in women, which was coincided with early to middle adulthood, i.e. a life stage associated with child-rearing^{(Reference Jonasdottir, Minor and Lehmann151)}. The prevalence of evening chronotype is higher in men than women, meaning that men generally wake up later in the morning and go to sleep later at night than women^{(Reference Adan and Natale152)}. This could be because the timing of the circadian rhythm of core body temperature and pineal melatonin secretion occurs earlier in women than men^{(Reference Cain, Dennison and Zeitzer153)}. A study of intrinsic circadian rhythm in a group of men and women aged 18–74 years revealed that the intrinsic circadian period is shorter in women (24 h 5 min in women v. 24 h 11 min in men) and that a greater proportion of women have intrinsic circadian periods shorter than 24·0 h (35% v. 14%)^{(Reference Duffy, Cain and Chang154)}.

Hormonal regulation of appetite in sleep restriction may also differ between sexes. Nymo et al. reported that while in men shorter habitual sleep duration and worse sleep quality was associated with increased basal and postprandial ghrelin, in women lower sleep quality was associated with decreased postprandial ghrelin^{(Reference Nymo, Kleppe, Coutinho, Rehfeld, Kulseng and Martins87)}. Also, in a study by St-Onge et al., sleep deprivation led to an increase in ghrelin in men and a decrease in glucagon-like peptide-1 in women without significant change in leptin levels^{(Reference St-Onge, O’Keeffe, Roberts, RoyChoudhury and Laferrère155)}. In the same line, a cohort study on 655 children showed an association between chronic curtailed sleep and lower leptin levels at age 7 years in girls, but not boys^{(Reference Boeke, Storfer-Isser, Redline and Taveras91)}. In contrast, in another cohort of 502 adolescents shorter sleep was associated with lower leptin in males^{(Reference Boeke, Storfer-Isser, Redline and Taveras91)}. Although somehow contradictory, the current findings mostly support the notion that the increased food consumption after sleep restriction may be caused by increased feeling of hunger in men and weakened satiety in women. Circadian misalignment has proved to reduce fullness in women and increase cravings for energy-dense and savory foods in men, suggesting that men may be more sensitive to hedonic regulation of food intake^{(Reference Qian, Morris, Caputo, Wang, Garaulet and Scheer156)}. This diverse and sex-specific hormonal response to sleep restriction may partly justify the lack of sleep deprivation effect on appetite hormones in studies that have not separated their results by sex.

Men and women also show a different weight response to sleep deprivation; i.e. men appear more susceptibility to weight gain than women. For instance, in RCT with sleep restriction for five nights men gained more weight than females^{(Reference Markwald, Melanson and Smith66,Reference Spaeth, Dinges and Goel157)} . Also, a cross-sectional study in elderly aged 67–96 years showed that the risk of increased BMI in sleep durations <5 h was greater in men than women^{(Reference Patel, Blackwell and Redline158)}. Cross-sectional investigations on children and adolescents have also shown an inverse correlation between sleep duration and BMI in boys but not girls^{(Reference Larsen, Sleddens, Vink, van den Broek and Kremers159,Reference Skidmore, Howe and Polak160)} . The reason of this sex-specific effect of sleep deprivation on weight is not clear but hormonal fluctuations in women^{(Reference Herzog, Jauch-Chara, Oltmanns and Benedict161)} and the dominant hedonic aspects of food selection in men^{(Reference Qian, Morris, Caputo, Wang, Garaulet and Scheer156)} may partially explain it. For the latter, a large cross-sectional study on school-aged children in China showed that short sleep duration was associated with increased risk of more sugar-sweetened beverage intake among younger children and boys and less vegetable and fruit intake among older children and girls^{(Reference Cao, Zhu, Sun, Luo and Jing162)}. Also, in a trial after chronic sleep restriction, men showed a trend towards decreased implicit positive attitude for low-energy foods whereas women did not show a significant change^{(Reference Alkozei, Killgore and Smith163)}. A summary of the sex-specific effect of sleep deprivation is depicted in Fig. 4.

Fig. 4. The effect of sleep deprivation on males and females. GLP-1, glucagon like peptide-1.

Influence of weight status

Neural response to sleep deprivation depends on weight status. Jensen et al. found that in sleep restriction, both normal-weight and overweight/obese adolescents showed higher activity in reward regions irrespective of their weight status^{(Reference Jensen, Duraccio and Barnett164)}. However, while adolescents with normal-weight demonstrated concomitant increases in neural activity in brain regions associated with food reward and inhibitory control, adolescents who were overweight/obese showed only increases in brain areas related to food reward without a change in inhibition-related brain processing^{(Reference Jensen, Duraccio and Barnett164)}. This suggests that in sleep restriction, individuals who are overweight/obese may be at a higher risk of food overconsumption compared with their normal-weight counterparts. Interestingly, in sufficient sleep conditions, adolescents with overweight/obesity had higher level of activity in inhibition-related regions than their normal-weight counterparts but in sleep restriction they showed a considerable decrease in neural activity of such regions^{(Reference Jensen, Duraccio and Barnett164)}. Contrary to the results observed by Jensen et al. ^{(Reference Jensen, Duraccio and Barnett164)}, Duraccio and colleagues^{(Reference Duraccio, Zaugg and Jensen165)} found that adolescents with normal weight demonstrated increased perception of food appeal following sleep restriction but adolescents with overweight/obesity consistently indicated high scores of food reward, which did not differ between habitual and restricted sleep conditions^{(Reference Duraccio, Zaugg and Jensen165)}. However, both groups showed poor scores of food-related inhibitory control task following sleep restriction^{(Reference Duraccio, Zaugg and Jensen165)}. These results suggest that sleep restriction increases the risk of weight gain in both normal-weight and overweight/obese adolescents but adolescents who were overweight/obese are at greater risk. A summary of the possible influence of weight status in homoeostatic regulation of appetite has been depicted in Fig. 5.

Fig. 5. Differential response to sleep restriction according to body weight. Both normal-weight individuals and individuals who are overweight/obese are assumed to stimulate the food reward system more strongly during sleep deprivation, but individuals who are overweight/obese indicate a weaker inhibitory control over eating compared with normal-weight individuals.

Impact of sleep deprivation on food selection

As stated above, a part of eating behaviours following sleep restriction is driven by reward-driven food intake, which results in “eating in the absence of hunger”. Available evidence indicates that contribution of this reward-driven eating in the increased food intake is larger than hormonal factors even in adequate sleep but more importantly in sleep deprivation^{(Reference Rihm, Menz and Schultz99,Reference Benedict, Brooks and O’Daly118)} , reviewed in Alonso-Alonso et al.^{(Reference Alonso-Alonso, Woods and Pelchat166)}. In this regard, a systematic review showed that insufficient sleep leads to increments in energy and fat intake, body weight, appetite, hunger, eating occasions and portion size without affecting leptin, ghrelin and cortisol concentrations, suggesting the dominance of non-homoeostatic mechanisms over the hormonal or homeostatic factors^{(Reference Soltanieh, Solgi, Ansari, Santos and Abbasi61)}. Also, in a cross-sectional study on normal-weight young women, scores of emotional eating (i.e. eating in response to aroused emotional states) and external eating (i.e. eating in the presence of food irrespective of hunger) were higher in women who had poor sleep quality (but not short sleep duration)^{(Reference Dweck, Jenkins and Nolan167)}. Upon administration of snacks, participants who scored high on emotional eating and reported short sleep consumed higher amounts of snacks. Similarly, an RCT on normal-weight young men showed that in sated state (i.e. following breakfast), men who experienced one night total sleep deprivation chose larger snack portions, further indicating the predominance of reward-driven eating over homoeostatic signals^{(Reference Hogenkamp, Nilsson and Nilsson168)}. Also, five nights of sleep restriction (6·5 h sleep/night) in adolescents did not affect their self-reported hunger or desire for non-sweet foods but pictures of sweet/dessert foods were more appealing for them^{(Reference Simon, Field, Miller, DiFrancesco and Beebe169)}.

Sleep deprived individuals usually look for and consume palatable foods, foods that are mostly unhealthy, i.e. energy-dense with high fat and/or high sugar content^{(Reference Kant and Graubard70,Reference Khan and Uddin170–Reference Cerolini, Rodgers and Lombardo173)} . Craving for unhealthy foods may be due to alteration in taste function including sweet, salt and even umami or sour tastes^{(Reference Lv, Finlayson and Dando174)}. Extended use of such unhealthy foods may disrupt appetite regulation by inducing addiction-like deficits in brain regions involved in the reward system, including the lateral hypothalamus, nucleus accumbens, ventral tegmental area, prefrontal cortex and amygdala^{(Reference Alonso-Alonso, Woods and Pelchat166,Reference de Macedo, de Freitas and da Silva Torres175)} . In an RCT in normal-weight individuals, after five nights sleep restriction with 4 h sleep/night, greater activation in parts of the brain reward system was seen upon viewing unhealthy foods (pepperoni pizza, doughnuts, chocolate bars and candy) compared with healthy foods (carrots, yogurt, oatmeal and grapes) whereas such increased activity did not occur after normal sleep^{(Reference St-Onge, Wolfe, Sy, Shechter and Hirsch176)}. In another RCT, the increased brain connectivity from the dorsal anterior cingulate cortex to the bilateral anterior insula after one night total sleep deprivation correlated with increased fat and decreased carbohydrate intake in healthy adults^{(Reference Fang, Spaeth and Ma177)}. A summary of the effect of sleep deprivation on food selection and eating behaviours is presented in Fig. 6.

Fig. 6. Effect of sleep deprivation on eating behaviours and food selection.

Effect of sleep deprivation on diet quality

Compelling evidence from cross-sectional investigations indicates an inverse relationship between sleep deprivation and diet quality. This inverse association has been reported, for instance, in adolescents aged 10–16 years^{(Reference Kracht, Chaput, Martin, Champagne, Katzmarzyk and Staiano178)}, postmenopausal women^{(Reference Stern, Grant and Thomson64)} and women with diverse age, race, and ethnicity^{(Reference Zuraikat, Makarem, Liao, St-Onge and Aggarwal62)} although postmenopausal women with ≥8 h sleep have also shown poor diet quality^{(Reference Stern, Grant and Thomson64)}. Furthermore, social jetlag, which is the difference in the average sleep duration between weekdays and weekends, has been associated with negative food choices even in cases of adequate weekly sleep duration^{(Reference Al Khatib, Dikariyanto, Bermingham, Gibson and Hall179)}. Interestingly, weekend catch-up sleep did not prevent the adverse effect of short weekday sleep on unhealthy dietary choices^{(Reference Al Khatib, Dikariyanto, Bermingham, Gibson and Hall179,Reference LeMay-Russell, Tanofsky-Kraff and Schvey180)} .

Sleep deprivation usually induces cravings for consumption of carbohydrates/starches, fast foods and sweets^{(Reference Li, Li and Zhou52)}. A cross-sectional study on resident physicians indicated that additional work was associated with higher intake of cereals, bread and pasta, and lower intake of fruits and beans, along with lower score of adapted healthy eating index^{(Reference Mota, Waterhouse and De-Souza51)}. Consistently, in motor freight workers, adequate sleep was associated with more healthful food choices^{(Reference Buxton, Quintiliani and Yang181)}. In agreement, a systematic review of interventions that used sleep extension as a strategy to improve cardiometabolic health suggested that sleep extension may be associated with reductions in overall appetite, desire for sweets and salty foods, and increased percentage of daily energy intake from protein^{(Reference Henst, Pienaar, Roden and Rae182)}. Although there are RCT denying the selection of high v. low energy foods under sleep deprivation states^{(Reference Chapman, Nilsson and Nilsson86,Reference Duraccio, Krietsch and Zhang183)} , most of trials agree with the effect of insufficient sleep on activation of the reward system and selection of high energy foods ^{(Reference Li, Li and Zhou52,Reference Spaeth, Dinges and Goel157, Reference Dweck, Jenkins and Nolan167,Reference Simon, Field, Miller, DiFrancesco and Beebe169,Reference St-Onge, Wolfe, Sy, Shechter and Hirsch176,Reference Fang, Spaeth and Ma177,Reference Brunet, McNeil, Jaeger Hintze, Doucet and Forest184)} . Unhealthy habits such as skipping breakfast^{(Reference Tambalis, Panagiotakos, Psarra and Sidossis171)}, skipping main meals^{(Reference Kant and Graubard70)}, and higher ingestion of snacks^{(Reference Kant and Graubard70)} have been reported in individuals with insufficient sleep.

Sleep insufficiency has also been associated with low diet quality in children and adolescents. Lower rate of fruit and vegetable consumption has been reported in sleep-deprived school-aged children in China^{(Reference Cao, Zhu, Sun, Luo and Jing162)}, children and adolescents of Australia^{(Reference Golley, Maher, Matricciani and Olds185)}, Spanish children^{(Reference Pérez-Farinós, Villar-Villalba and López Sobaler186)} and US adolescents^{(Reference Kruger, Reither, Peppard, Krueger and Hale172)}. In the same line, an analysis of data from 10 453 children from five European countries revealed that one additional hour of sleep was associated with increased consumption of fruits and vegetables^{(Reference Börnhorst, Wijnhoven and Kunešová187)}. Also, in a group of Danish 2–6-year-old children, those with more variable sleep duration consumed less fruit and vegetables and a higher amounts of added sugars and sugary beverages^{(Reference Rangan, Zheng, Olsen, Rohde and Heitmann63)}. Also, in a cross-sectional study on 118 462 Korean adolescents, short sleep duration of <6 h was associated with higher intake of soft drinks and confectionaries, and poor sleep quality with 7–8 h sleep was associated with lower intake of fruits, vegetables and milk, and higher intake of soda, soft drinks, fast-food, instant noodle and confectionaries^{(Reference Min, Kim and Park188)}. Given the importance of childhood habits in the formation of adulthood eating habits, results of these investigations remind the importance of childhood sleep in adulthood health status. Sleeping at earlier bedtimes may result in healthier eating behaviours such as eating low glycemic index foods, fruits and dairy in adolescents^{(Reference Asarnow, Greer, Walker and Harvey189)}.

Desire for consumption of snacks

Both epidemiological and interventional investigations have shown increased consumption of snacks in sleep deprivation conditions. A large cross-sectional study showed that adults with habitual short sleep duration reported a lower mean percentage of energy intake from main meals but higher energy from snacks^{(Reference Kant and Graubard70)}. Likewise, a survey on high school students revealed an association between shorter sleep and more frequent cracker consumption^{(Reference Lee132)}. In another cross-sectional study, university students with habitual short sleep ate more often, i.e. more than three meals per day and more frequent snacking, than those with long and sufficient sleep^{(Reference Hicks, McTighe and Juarez190)}. RCT have indicated the same line of evidence. For instance, two groups of investigators reported that during sleep curtailment in healthy volunteers, meal intake did not change but the amount or energy from snacks increased^{(Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97,Reference Hogenkamp, Nilsson and Nilsson168)} . These findings have been confirmed by other investigators^{(Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97,Reference Cerolini, Rodgers and Lombardo173,Reference Weiss, Xu, Storfer-Isser, Thomas, Ievers-Landis and Redline191)} .

Craving for sweetness

Increased consumption of sugar-sweetened beverages and snacks after sleep deprivation may result from the preference for sweet taste under such conditions. Cross-sectional investigations have shown inverse associations between sugar intake and sleep duration^{(Reference Kant and Graubard70,Reference Kjeldsen, Hjorth and Andersen192)} , and an inverse association between sleep efficiency and sweet cravings^{(Reference Kracht, Chaput, Martin, Champagne, Katzmarzyk and Staiano178)}. RCT have also reported sweet craving in normal-weight young adults after three nights of sleep restriction (5 h sleep/night)^{(Reference Tajiri, Yoshimura, Hatamoto, Shiratsuchi, Tanaka and Shimoda193)} or non-obese adults after one night of sleep curtailment with 33% reduction in habitual sleep duration^{(Reference Szczygiel, Cho and Tucker194)}. But, such alteration in sweet taste pleasantness or intensity was not observed after one night total sleep deprivation although feeling of hunger and ghrelin concentration increased^{(Reference Hogenkamp, Nilsson and Chapman75)}. It is likely that stress caused by total sleep deprivation decreases sensitivity to sweet taste^{(Reference Hogenkamp, Nilsson and Chapman75)} as animals with mild stress have shown attenuated sensitivity to food rewards^{(Reference Papp, Willner and Muscat195)}.

Sweet liking leads to increased consumption of energy from sugar-sweetened snacks and beverages by sleep-deprived individuals^{(Reference Broussard, Kilkus and Delebecque95,Reference Yang, Schnepp and Tucker196)} , augments glycaemic load of the consumed diets^{(Reference Beebe, Simon, Summer, Hemmer, Strotman and Dolan197,Reference Duraccio, Whitacre and Krietsch198)} , and enhances risk of obesity^{(Reference Hajhashemy, Mirzaei, Asadi, Akhlaghi and Saneei199)}. Moreover, sweetness sensitivity is associated with higher preference for sweets and other carbohydrate-dominated foods but lower preference for foods with high content of protein^{(Reference Han, Mohebbi, Seo and Hummel200)}. The low preference for protein is particularly important because proteins alter appetite regulating hormones in a direction that leads to increase satiety and decreased hunger^{(Reference Kohanmoo, Faghih and Akhlaghi201)}. Sweet sensitivity may also bring along a higher interest in high-fat food odours such as chocolate and peanuts^{(Reference Han, Mohebbi, Seo and Hummel200)}, consumption of which may further intensify risk of weight gain.

Appealing macronutrients

The extra energy consumed during sleep deprivation is provided from carbohydrate and fat rather than protein^{(Reference Tasali, Chapotot, Wroblewski and Schoeller76)}. Numerous cross-sectional and interventional investigations have shown increased fat^{(Reference St-Onge, Roberts and Chen141,Reference Fang, Spaeth and Ma177,Reference Weiss, Xu, Storfer-Isser, Thomas, Ievers-Landis and Redline191,Reference Saleh-Ghadimi, Dehghan, Abbasalizad Farhangi, Asghari-Jafarabadi and Jafari-Vayghan202–Reference McNeil, Forest and Hintze204)} and carbohydrate^{(Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97,Reference Mi, Kelly and Brychta205)} intake in sleep-deprived individuals. Consistently, increased sleep duration and quality following an exercise regimen in adolescent girls with obesity led to significant decreases in food energy density, fat, and sugar consumption^{(Reference Saidi, Rochette, Bovet, Merlin and Duché206)}. Likewise, transitioning from an insufficient to adequate/recovery sleep schedule decreased energy intake, especially that from fats and carbohydrates^{(Reference Markwald, Melanson and Smith66)}. However, there are also documents indicating the increase in fat intake and a decrease in carbohydrate consumption^{(Reference Fang, Spaeth and Ma177,Reference Weiss, Xu, Storfer-Isser, Thomas, Ievers-Landis and Redline191)} , suggesting that sleep deprivation may cause a greater desire for consumption of fats compared with non-sweet carbohydrates. In this regard, a cross-sectional study on adults with obesity showed associations between sleep apnea, as a sleep disorder, and a shift from carbohydrate to fat intake^{(Reference Galli, Piaggi and Mattingly207)}. Accordingly, a systematic review of RCT showed increased consumption of fat without a change in protein and carbohydrate intake in sleep deprived conditions^{(Reference Soltanieh, Solgi, Ansari, Santos and Abbasi61)}. It seems that the type of fat is also important. A meta-analysis of nine cohort studies with 14 906 participants of European descent showed associations between sleep duration and lower saturated fatty acid intake in adults aged 20–64 years old and higher total fat and polyunsaturated fatty acids (PUFA), as well as lower carbohydrate intake in women aged 65–80 years^{(Reference Dashti, Follis and Smith208)}. Similarly, a cross-sectional study on Mexican American children showed associations between longer sleep duration and higher percentage of energy obtained from fats, especially from PUFA^{(Reference Martinez, Tschann and Butte209)}. On the contrary, in an RCT on adults, sleep deprivation (4 h sleep for five nights) caused increases in the consumption of fats, notably saturated fats^{(Reference St-Onge, Roberts and Chen141)}. Based on these reports, in sleep deprivation, individuals crave foods high in fat, particularly saturated fats, while in sufficient sleep consumption of food sources of saturated fats seems less appealing.

Time of eating

Although, short-duration sleepers are reported to eat from the earliest time in the morning to the latest time of night^{(Reference Kant and Graubard70)}, extra energy is mostly consumed during evening hours^{(Reference McHill and Wright31,Reference Herzog, Friedrich and Fujita35,Reference Nedeltcheva, Kilkus, Imperial, Kasza, Schoeller and Penev97,Reference Spaeth, Dinges and Goel157,Reference Duraccio, Whitacre and Krietsch198,Reference Spaeth, Goel and Dinges210)} . For instance, adolescents who experienced five nights with 6·5 h sleep indicated increases in the intake of energy, fat and carbohydrates after 9 pm but not earlier in the afternoon or morning^{(Reference Duraccio, Whitacre and Krietsch198)}. Also, participants who experienced 4 h sleep/night for 5 d consumed additional energy between 10 pm and 4 am and consumed less energy the next morning^{(Reference Spaeth, Dinges and Goel157)}. Similarly, participants who had 5 h sleep/night for 5 d consumed a smaller breakfast but 42% more energy after dinner as snacks^{(Reference McHill and Wright31)}. Interestingly, the energy consumed after dinner have been more than that consumed at individual meals^{(Reference McHill and Wright31,Reference Spaeth, Goel and Dinges210)} . The cause of tendency to late-night food intake is not known, but it is likely that changes in circadian sleep and awakening time affect eating patterns. For instance, the reduced desire to consume breakfast may be due to short sleep and waking up at a time when the internal circadian clock is still promoting sleep. Also, staying awake during the night may stimulate food consumption because melatonin levels are high during the night and promote sleep, and the pleasure of eating helps to better tolerate a stressful insomnia condition^{(Reference McHill and Wright31)}. The additional energy consumed during late-night waking hours compensates for the extra energy needed to stay awake for the extra hours^{(Reference Spaeth, Goel and Dinges210)}. However, this additional energy may exceed energy needs and thus contribute to weight gain and obesity. In this regard, night eating syndrome is more frequently seen in individuals with obesity^{(Reference McCuen-Wurst, Ruggieri and Allison211,Reference Sutcu, Pamuk and Ongel212)} . Animal studies have shown that when mice eat food at times when they normally sleep, they gain weight even though they have their regular energy intake^{(Reference Fonken, Workman, Walton, Weil, Morris, Haim and Nelson213)}.

The effect of diet on sleep

In previous sections the effect of sleep on dietary intakes was discussed but the literature also contains documents claiming the influence of diet and eating behaviours on sleep health.

Other effective components

Numerous components in healthy diets may render sleep-promoting properties. An RCT on adults with obesity demonstrated that adults who are obese and poor sleepers may become good sleepers when they consume either the recommended or a higher protein energy-restricted healthy eating pattern^{(Reference Hudson, Zhou and Campbell246)}. Animal and plant protein in healthy diets provides tryptophan which is an essential amino acid and the precursor of serotonin and melatonin, both are known to play roles in sleep-wake cycle^{(Reference Bhat, Pires, Tan, Babu Chidambaram and Guillemin247)}. Evening consumption of tryptophan caused a 130% increase in plasma tryptophan to large neutral amino acids ratio and reduced sleepiness and improved brain-sustained attention processes the following morning^{(Reference Markus, Jonkman, Lammers, Deutz, Messer and Rigtering248)}. In agreement, a recent meta-analysis of 18 RCT showed that tryptophan supplementation, especially at ≥1 g, can help improve sleep quality^{(Reference Sutanto, Loh, Toh, Lee and Kim249)}.

Food sources of protein are good sources of zinc. Numerous studies in both cross-sectional and interventional designs have indicated the effect of zinc on improving the duration and quality of sleep and possible mechanisms of action have been suggested^{(Reference Cherasse and Urade250)}. Fruit and vegetables provide great quantities of magnesium. Observational studies have suggested an association between higher magnesium intake and sleep quality and RCT have shown a positive effect of magnesium supplementation on sleep quality, sleep efficiency and sleep time^{(Reference Arab, Rafie, Amani and Shirani251)}. Fibre also reduces stage 1 (the first 1–5 min of sleep) and increases slow wave sleep (deep sleep) in individuals with habitually normal sleep^{(Reference St-Onge, Roberts, Shechter and Choudhury220)}. Trials have also documented benefits of pro-, pre- and post-biotics on sleep length and quality^{(Reference Haarhuis, Kardinaal and Kortman252)}. Animal studies have shown that short-chain fatty acids, particularly butyrate, promote sleep^{(Reference Szentirmai, Millican, Massie and Kapás253)}.

In national surveys in the USA, short (<6 h) and long (>9 h) sleepers indicated lower variety in their diet compared to normal sleepers^{(Reference Grandner, Jackson, Gerstner and Knutson254)}. Also, short sleepers consumed less vitamin C, lutein, zeaxanthin and selenium^{(Reference Grandner, Jackson, Gerstner and Knutson254)}. Whether low consumption of antioxidants impairs sleep is not known but sleep deprivation has been associated with increased oxidative stress and reduced serum antioxidant capacity^{(Reference Atrooz and Salim255,Reference Jówko, Różański and Tomczak256)} and sleep is supposed to restore antioxidant potential of the body^{(Reference Jówko, Różański and Tomczak256,Reference Reimund257)} . Cross-sectional investigations have also shown inverse associations between serum folate, vitamin D and sleep disturbance and a positive association between total carotenoids concentrations and short sleep duration, although an inverse association was also observed between serum vitamin B₁₂ levels and sleep duration^{(Reference Beydoun, Gamaldo and Canas258)}. Regarding vitamin B₁₂, a cross-sectional study on Chinese patients with type 2 diabetes showed associations between elevated serum vitamin B₁₂ level and incidence of insomnia^{(Reference Xiong, Liu, Yao, Zhang and Ge259)}. However, evidence also suggests improvement in daytime alertness, concentration and in shortening and improving sleep following vitamin B₁₂ supplementation, likely through its effect on melatonin^{(Reference Mayer, Kröger and Meier-Ewert260)}. The literature for the effects of nutrients on sleep is largely incomplete and somehow contradictory, and many more investigations aimed at exploring the potential of food components on sleep duration and quality should be conducted in the future. A brief overview of the current findings is given in Fig. 7.

Fig. 7. Nutrients with possible influence on sleep health. GI, glycemic index; PUFA, polyunsaturated fatty acids; SFA, saturated fatty acids; Trp, tryptophan.