Homeostatic and circadian processes control the quality of sleep, and awake periods [34]. The main role of the circadian clock is to promote awakening during the internal biological day and to favor sleep during the internal biological night [34]. However, today, due to unlimited access to artificial light, people exhibit undesirable behaviors regarding their endogenous circadian rhythm [35]. This temporal misalignment, called circadian misalignment, occurs when the internal circadian system is not correctly aligned with the external environment [36] and can lead to chronic sleep deprivation, very common in modern societies [37]. This deprivation can be attributed to quantitative factors, such as insufficient sleep duration, or to qualitative factors, such as fragmented sleep periods [9]. Circadian misalignment is often associated with numerous health problems [35]. One of the effects of circadian misalignment is a reduction in total sleep time, which may also affect sleep architecture since human sleep is composed of rapid eye movement (REM) sleep and non-REM sleep [2,34]. Several factors are responsible for circadian misalignment: the increase in the number of individuals who work in shifts or at night, the increase in the number of working hours, commute times, jet lag, psychosocial stress and engagement with television, radio, and the Internet [9,34,36,38]. Shift work is an essential system in society, being very present in industry as well as in medical institutions [39]. However, shift work is associated with adverse health outcomes, including gastrointestinal disorders, metabolic syndrome, diabetes, reproductive difficulties, and breast and prostate cancer, as well as glucose intolerance and cardiovascular function [40,41]. Caffeine has been shown to have both positive and negative effects on behavior, cognition, and health, depending on the amount consumed. When consumed in excess, it can cause sleep disturbances, since its consumption significantly reduces sleep time and causes disturbances in sleep quality [42]. In recent years, electronic devices, including computers and mobile phones, game consoles and tablets, have been associated with poor sleep among young people [43,44]. Some studies [13,45,46] have linked the mere presence of these devices in the bedroom with the tendency to sleep later, and consequently, shorten sleep duration and increase daytime sleepiness [43,44]. This idea was further reinforced as the use of these devices became the subject of great clinical interest: it was not only shown to increase sedentary behavior but also impoverish the quality of subjective sleep, even leading to falling asleep during school hours and increasing daytime sleepiness [43,44]. In the case of children, among the many factors that affect their sleep time are television viewing and the presence of a television in the bedroom [24]. Television-related behaviors can directly disturb sleep time or increase emotional/mental arousal and light exposure, which can be determinants of sleep duration and quality [24]. These inadequate hours of sleep are associated with poor mental and physical health, which include impaired academic performance, depression, injuries, and an increased risk of obesity [24].

All animals, including humans, evolved over millions of years in a stable, seasonal light–dark environment, in which the intervals between light and dark moments could be distinguished within a 24 h period [31,38,47,48,49]. Because of this repetitive and extremely regulated 24 h cycle, an internal circadian clock developed that allows day–night adjustments of metabolic activities, which are at the base of circadian rhythms [44,50]. The internal clock in humans is in the suprachiasmatic nucleus of the anterobasal hypothalamus, functioning as a stopwatch and regulating gene/protein expression, and thus the flow of all the functions of the organism, such as the use and storage of energy, feeding, sleep–wake cycle, electrical activity and concentration of ions and substances, cyclic changes in metabolism and energy homeostasis [31,38,47,48,49]. It is apparent that the basis of the circadian clock is the light–dark cycle. Therefore, the most important external signal is light, which makes individual and physiological behavior correspond to the external day–night cycle, influencing several hormones with metabolic relevance since they present a circadian oscillation with different daily patterns [38,48,50]. Thus, it is believed that changes in the pattern of light–dark exposure or inappropriate exposure to light can affect the circadian rhythm, causing the internal rhythm to become out of sync with the external environment, damaging sleeping behavior and compromising metabolic processes [48]. A metabolic process that is clearly dependent on the light–dark cycle and the function of the suprachiasmatic nucleus is the melatonin cycle [49]. Falling asleep with the television on or sleeping with the light on has been associated with a change in the brain’s natural sleep cycle and melatonin production [51]. The production and secretion of melatonin by the pineal gland occurs in a nocturnal circadian pattern, with the peak being reached 3–5 h after dark, declining precipitously after waking up [49,52,53]). Since melatonin is rapidly released by the pineal gland soon after its production, it can be said that the concentration of melatonin in the blood reflects its synthesis, and fluctuations in melatonin concentration play an important role in the transmission of essential information to the various organs [49]. In addition to its role in transmitting information, melatonin secretion, and the location of its receptors throughout the body, which include the β cells of the pancreatic islets, mean that, according to some authors, melatonin can play an important role in glucose metabolism [54,55]. In fact, performed in vitro tests [54,55] have verified that prolonged exposure of the β islets of the pancreas to melatonin, with the purpose of simulating the period of sleep, increases the sensitivity of the β receptors to glucose [53]. Sleep loss not only affects the melatonin cycle but has also been linked to disturbances in other metabolic functions, specifically an increase in the appetite-stimulating hormone ghrelin [14,16,52,56]. A sleep restriction of 4 h per night for two consecutive days, as well as one night of total sleep restriction, have been shown to increase daytime plasma ghrelin concentrations in young men, mainly in the early hours of the day [6]. However, sleep deprivation also causes a decrease in leptin, the appetite-suppressing hormone, thus favoring food intake by increasing appetite [14,16,52]. Leptin is an amino acid essentially produced by adipocytes, which is secreted in a circadian manner, suggesting that it is influenced by the circadian clock through its sympathetic input in adipocytes [15,57]. However, leptin can also be expressed by non-adipose tissues, such as stomach tissue, and, to this extent, gastric leptin levels show oscillations, being elevated during the night, leading to a reduction in appetite and promoting satiety and night rest, but low during the day, increasing appetite [15,56,57]. Thus, it is suggested that gastric leptin may be involved in appetite regulation by inducing satiety [15,56,57]. Some authors [58] have associated leptin with increased insulin sensitivity as it promotes fat oxidation and reduces fat accumulation in non-adipose tissues. This effect can be directly mediated by leptin due to AMPK activation in certain skeletal muscles and indirectly through the sympathetic hypothalamic axial nervous system [57]. The activation of AMPK, activated protein kinase, leads to the inhibition of acetyl-coenzyme A (CoA) carboxylase [57,59], which leads to a reduction in the intracellular levels of the malonyl CoA metabolite. The entry of fatty acids into the mitochondria decreases and the oxidation of fatty acids is favored [57]. There are published results [60] which indicate that leptin-dependent sleep disturbances may result in an alteration in leptin-sensitive axial hormones. In addition to leptin, adipocytes are also the main producers of adiponectin, which has anti-diabetic, anti-atherogenic and anti-inflammatory properties [57]. Like leptin, adiponectin improves insulin sensitivity thanks to the activation of AMPK and is also responsible for the decrease in hepatic glucose production due to the decrease in mRNA expression of two essential enzymes involved in gluconeogenesis, namely phosphoenolpyruvate carboxylase and glucose-6-phosphatase [57]. Ghrelin, on the other hand, is an anorexigenic peptide produced in the stomach and other organs, such as the pancreas and hypothalamus, but it is mostly released by the stomach and its levels fluctuate based on food intake [15], with a rapid decrease in ghrelin after eating and an increase immediately before a meal [8,15,56]. It has been shown that ghrelin levels increase by 20% before breakfast, 45% before lunch and 51% at dinner [20]. Despite the absence of food intake, it is possible to find high levels of ghrelin during the first hours of the night, with a peak between midnight and two in the morning, which progressively decreases with food intake [15,20,56]. Sleep deprivation causes an increase in circulating ghrelin levels, and this phenomenon is accompanied by an increased feeling of hunger [15]. The way ghrelin stimulates appetite is through the activation of neuropeptide Y, located in the lateral part of the hypothalamus [15]. Ghrelin is responsible for the feeling of appetite and for weight gain and is also responsible for stimulating the release of growth hormones. This hormone is a hypothalamic neuropeptide that regulates eating, energy metabolism, reproduction, and sleep [61]. Regarding the latter, it stimulates the neurons that promote the wake-to-eat cycle, thus modulating arousal and appetite [8]. There are several studies that describe how the growth hormone is controlled through the homeostasis of the wake–sleep cycle, with an increase in its production during sleep being verified in men, namely in stages three and four of slow-wave sleep (SWS). When the sleep period is interrupted, there is a change in the release of growth hormones, the impact being particularly evident in men, but also detectable in women [56]. Another cycle that is influenced by the circadian rhythm is the cortisol profile, which oscillates over the 24 h, since the decrease in its secretion occurs in the early hours of the night and the peak of its secretion occurs at the time of awakening, decreasing progressively throughout the day [50]. Manipulations of the sleep cycle have minimal effects on the cortisol profile, as it is very difficult to detect changes when sleep is interrupted in the morning, coinciding with the peak of corticotropic activity [56]. Sleep deprivation has also been shown to have a negative influence on the response of adrenocorticotropic hormones, adrenaline and on the sensitivity of serotonin (5-HT) receptors, which over time can lead to changes in the system’s response to stress, seen in changes in humor [52]. Serotonin (5′hydroxyptitanin) has been implicated not only in the regulation of emotions, attention and memory, but also in the regulation of appetite and sleep, and its synthesis in the brain is considered critical since for this to occur, the availability of its precursor, the essential amino acid tryptophan, is necessary, and it can only be obtained by humans from the diet [10,62,63].

Changes in food choices and eating behaviors are associated with short sleep time [33]. Sleep disturbances have been associated with increased sleepiness and changes in thermoregulatory functions and secretion of the growth hormone by the hypothalamic–pituitary–adrenal gland axis during SWS, which leads to a decrease in energy expenditure [64,65]. This factor was confirmed by Jung et al. (2011), who reported a 7% increase in energy expenditure over 24 h during a day of total elimination of sleep compared to a normal day, which supports the importance of sleep for energy conservation [66], due to a decrease in the practice of physical activity [6,64,65]. However, sleep deprivation also increases the appetite for food intake, and the food choices made at these times result in meals rich in sweet and high-density energy foods, and these phenomena are associated with changes in neuroendocrine control of appetite. Sleep disturbances cause an increase in circulating ghrelin levels and a decrease in leptin levels, which favors an increase in the sensation of appetite and hunger, affecting the energy balance [3,11,28,36,64,65,67,68,69]. The feeling of hunger and appetite due to sleep disturbances makes people choose foods with a high caloric density and rich in carbohydrates, such as sweets, salty snacks, and starchy foods [4,6,33,70,71], verified in girls, with increased intake of sweets and/or fast food and soft drinks in boys [71]. Sleep disorders in children and sleeping less than 7 h/night in adults have been associated with reduced consumption of fruit and vegetables and increased consumption of energy-rich foods with low nutritional value [33]. Adolescents who report sleeping less than 8 h/night tend to consume more total calories from fat than from carbohydrates and protein when compared to those who sleep for 8 or more hours/night [33,36]. In adults, acute sleep deprivation increases caloric intake, mainly due to increased consumption of carbohydrates and fat, as well as increased consumption of snacks [4,70].

Children aged 8–11 years change their energy intake because of changes in their sleep duration [36]. However, sleep deprivation is also responsible for causing physiological stress, which can itself alter energy balance regulators [36]. In a prospective study [76], it was shown that physical and social stress related to family and/or work matters was associated with an increased risk of incidence and persistence of insomnia. Insomnia is characterized by difficulty initiating and/or maintaining sleep, waking up in the early hours of the day and, in general, dissatisfaction with both the quality and quantity of sleep [73].

Night eating syndrome (NES) is characterized by morning anorexia, hyperphagia in the afternoon and insomnia, and is often due to periods of stress, such as unsuccessful attempts to lose weight [77]. Research demonstrates that patients with NES experience high levels of insomnia and poor sleep quality [78,79,80]. Expanding on this research, when comparing patients with NES with evening hyperphagia to patients with nocturnal ingestions, Loddo et al. found differences in sleep features across NES subgroups. The researchers observed a higher total duration of eating episodes, eating latency following wakening and sleep latency following eating episodes in the evening hyperphagia group [81]. It may be that sleep disturbance is heightened in patients with evening hyperphagia [82]. Zwaan et al. [83] found that across studies, the prevalence of NES in pre-operative bariatric patients ranged from 6 to 64% [83]. The overall prevalence of NES ranges from 2.8 to 8.2% across the eating disorder, obese and bariatric surgery populations [84].

Currently, there is increasing evidence of a relationship between sleep and the risk of cardiovascular disease [85]. Recently, literature reviews [86,87] have demonstrated the link between dysfunctional sleep patterns and their contribution to the increased risk of cardiovascular disease in shift workers. Evidence supports the existence of a relationship between poor quality and duration of sleep, on the one hand, and the activation of the sympathetic nervous system and increased levels of inflammation, on the other, which are believed to be responsible for inducing endothelial dysfunction, a key factor in the onset of atherosclerosis and consequent increases in the risk of cardiovascular diseases [32,40,85].

Scientific evidence [88,89] has shown that acute sleep loss increases food intake, with damage to glucose tolerance and insulin sensitivity, the latter of which increases in the body to maintain glucose homeostasis [75]. Just as important in this whole process is the intestinal hormone glucagon-like peptide 1, GLP-1, secreted after ingesting nutrients by mouth. GLP-1 can improve insulin resistance and reduce food intake; when there is a deterioration of sleep, GLP-1 signaling may be compromised [5]. It was found that in young males, plasma GLP-1 concentrations in the afternoon were reduced after a night of fragmented sleep compared to a regular night of sleep. However, the general concentration of GLP-1 during the 24 h was not affected, which may be due to the subtlety of the intervention, characterized by a small variation in the time spent in REM sleep relative to the time spent in stage two [5]. In other studies [90,91], SWS duration was correlated with insulin sensitivity, although no relationship with arousal was reported. The exact effect that reduced sleep exerts on insulin sensitivity is not yet known, but hormonal mechanisms, particularly changes in hormones responsible for promoting appetite, are increasingly evident [75].