This Research Article has been written by Nutritionist Anum Nazir).She is Senior Lecturer in School of Nutritional sciences At University of Faisalabad).She is active worker for fight against hunger.Her credible work  is mentioned.


The rising prevalence of obesity is now a global concern. Eating behavior and circadian rhythm are proving to be much important factors in the etiology of obesity. The night-eating syndrome is characterized by increased late-night eating, insomnia, a depression and distress. It is evident that the prevalence is higher among weight-related populations than general community. The exact relationship between this syndrome and obesity still remains unclear. The reasons for the discrepancies found in literature likely include varying diagnostic criteria and a wide range of study population characteristics. Night eating syndrome does not always lead to weight gain in thus certain individuals may be susceptible to night-eating-related weight gain. Weight loss through surgical and behavioral treatments has shown success in diminishing symptoms. The increasing literature associating obesity with circadian imbalances strengthens the link between the NES and obesity. Circadian genes may play a role in this syndrome. This review will examine different aspects of obesity in the context of the night eating syndrome.

The night-eating syndrome is a clinical representation of a circadian imbalance first reported among obese individuals resistant to weight loss. The first clinical definition was described as a triad of morning anorexia, evening hyper-phagia (25% of total energy intake after 7 pm) and insomnia. Since, the definition of night eating syndrome has varied over the years. Recently, however, standardized diagnostic criteria were proposed. The prevalence of night eating syndrome varies considerably depending on the study population and diagnostic criteria. Nonetheless, trends in the literature emerge revealing that certain populations are at greater risk for developing night eating syndrome. Among these are individuals with weight problems. The purpose of this article is to review the literature regarding night eating syndrome and obesity and to examine the different links between night eating syndrome, obesity and the circadian rhythm

Compared with the general community, it is evident that night eating syndrome is more prevalent in populations with weight-related issues. Although many studies observed a positive relationship between night eating syndrome and body weight, many others have not. Possible reasons for this discrepancy include inter-study differences in NES diagnostic criteria, i.e. extent of evening hyper-phagia, in methods of expressing night eating syndrome, i.e. dichotomous (present/absent) vs. continuous (night-eating questionnaire score), in study population characteristics, i.e. low body weight variability, and the possibility that night eating syndrome is not related to body weight in every individual. In non-clinical populations with large variations in body size, night eating syndrome symptom severity, measured by the continuous NEQ score, has been positively associated to body mass index (BMI) in dental patients and in a cohort of families with children at risk for obesity.

Night-eating syndrome and weight gain night eating syndrome could theoretically lead to weight gain as a result of excess calories consumed at night. Indeed, studies have shown that night eating leads to weight gain (4.3–4.5 kg over 3–6 years) and that obesity onset occurs earlier in life (6.0–7.5 years) in those with night eating syndrome. Additionally, (Zwaan et al., 2018) found that night eating syndrome preceded obesity in 40% of obese night eaters. Certain individuals or populations may be susceptible to night eating syndrome-related weight gain. In one population study, obese female night eaters gained significantly more weight than obese women who did not eat at night (5.2 kg vs. 0.9 kg over 6 years) (15). There was no significant difference in weight gain in male night eaters and non-night-eaters, regardless of body weight. Further evidence supporting the hypothesis that night eating syndrome contributes to obesity in certain individuals is found in the aforementioned study by (Zwaanet al., 2018) where only some normal weight individuals gained weight after night eating syndrome onset. The reasons for this selective weight gain are mostly unknown, and the retrospective nature of these data is a main limitation of this study. Behavioral factors may explain in part the lack of weight gain among some individuals with night eating syndrome. In a study among normal weight individuals, those with night eating syndrome were reported to have more days of intense exercise, greater cognitive restraint and a greater fear of weight gain than those without night eating syndrome. This type of behavior profile may have successfully controlled their body weight. Further evidence supporting the implication of in elevated body weight is seen in clinical trials of the pharmacological treatment of night eating syndrome. In one study, night eating syndrome symptoms significantly improved and were accompanied by a significant reduction in body weight (2.9 kg) in overweight individuals treated with sertraline for 18 weeks. This reduction in body weight was in the absence of weight loss advice or guidance. Taken together, not every individual with night eating syndrome exhibits weight problems, yet the syndrome may aggravate or maintain obesity, specifically in those susceptible to weight gain.

The biological rhythm ensures that human behavior is appropriately synchronized to the external environment. Individuals may experience negative physiological and psychological effects in a circumstance of circadian disruption. Neuroendocrine and behavioral studies have demonstrated a potential circadian AR rhythmicity among those with night eating syndrome, which manifests in late-night eating with a phase delay of 1.5 h (78). The cause for this disruption is unknown. Several physiological systems have been hypothesized to be involved in the mechanistic drive in night eating syndrome, such as the glucocorticoid and serotonergic systems. This circadian AR rhythmicity could be one of the links between night eating syndrome and obesity as emerging findings have linked Chrono disruption with increased body weight. The nature of this relationship is complex and the directionality remains unclear. Forcing circadian-regulated behavior, such as sleeping and eating, to be uncoupled from regular biological rhythm disrupts lipid and glucose metabolism, insulin regulation and may lead to obesity, such as seen in shift workers. In one experimental study, insulin sensitivity decreased, leptin secretion was suppressed and the rhythm of cortisol was completely inverted after 10 adults were subjected to a protocol in which their behavioral circadian rhythm (i.e. eating, sleeping) was uncoupled from their biological rhythm. Similarly, a crossover study revealed that late-night eating (50% of their total calories in the evening) and delayed sleep blunted the nocturnal peaks of melatonin and leptin, and impaired the glucose and insulin relationship. The hormonal milieu created by behavioral and circadian misalignment and late-night eating could lead to reduced energy expenditure, increased appetite sensations and weight gain. Epidemiological evidence of this is seen in a Swedish cohort where obesity was related to skipping breakfast and lunch and eating at night and in the high prevalence of obesity among shift workers. Animal models confirm the association between late-night eating, metabolic AR rhythmicity and obesity. Mice fed during the light phase had metabolic arrhythmic ties and gained more weight than mice fed the same diet during the dark phase. The fact that various appetite regulating hormones follow an exogenous circadian rhythm may indicate that timing of meals is important for proper metabolic and body weight regulation. In ‘late sleepers’, calories consumed after 8 pm were independent predictors of BMI after controlling for age, sleep duration and timing of sleep onset, and late-night eating was a stronger predictor of obesity than total energy intake. More human research is needed to verify if the timing of food intake promotes circadian AR rhythmicity and weight gain independent from energy expenditure and absolute energy intake

Review of literature

The circadian system orchestrates a daily cycle of 24-h behavior and physiological functions that is critical for maintaining metabolic health. The mammalian circadian clock comprises a central pacemaker in the suprachiasmatic nucleus and a series of peripheral clocks throughout the body. The rhythms of these clocks are produced by coordinated transcriptional–translational feedback loops involving clock genes and their downstream targets. The disruption of the circadian system, such as by chronic shift work or irregular eating habits, leads to the dysregulation of metabolic homeostasis, which is also related to an increased risk of obesity, cardiovascular diseases, and other metabolic diseases. Therefore, a growing body of evidence suggests that eating in synchronization with body clock rhythms might improve metabolic health. In contrast, eating at the times that disrupt these rhythms causes misalignment of the circadian system, thereby resulting in impaired cardio metabolic endpoints, which cause deleterious conditions that range from glucose tolerance, insulin sensitivity and ectopic fat accumulation to diabetes and stroke. Though the best timing for eating at is based on common sense, eating behaviors are increasingly varied due to the work and lifestyles of the current society. For example, the best times for a traditional breakfast, lunch and dinner have become more difficult to distinguish because skipping meals has become a more prevalent behavior. Additionally, epidemiological and interventional studies have found that skipping breakfast or eating a late night dinner result in a greater risk of obesity, diabetes and cardiovascular diseases. Furthermore, numerous animal studies were also designed to investigate the impacts of mealtime and unhealthy dietary habits, including skipping breakfast and late-night eating, on metabolic health.

For example, a recent study found that skipping breakfast under a normal 12 h/12 h light/dark cycle led to increased body weight accompanied by oscillation shifts in the hepatic clock and the expression of lipid metabolism-related genes in rats fed high-fat diets. Therefore, studies have now also focused on the manipulation of mealtime or dietary habits for the prevention and treatment of lifestyle-related metabolic disorders. Among these interventional approaches, time-restricted feeding, such as early time restricted feeding and intermittent fasting, has become a promising tool for inducing circadian and metabolic improvements. However, these studies in animals were primarily based on the typical 12 h/12 h light/dark cycle, which does not reflect the many real life situations, such as light use in the night and sleep times of fewer than 8 h, and the dietary habits mandated by TRF therapy counter many typical eating habits (Ni et al., 2019).


Moreover, for the past decade, it has been argued that breakfast skipping may result from conditions in the preceding night, such as late-night dinner eating, eating snacks after dinner, or drinking alcohol until immediately before going to bed. Simultaneously, the quality and quantity of sleep, which usually manifest as short or long duration of sleep, may affect conditions in the early morning such as appetite for the breakfast meal. Of note, short duration of sleep has been robustly associated with similar cardio metabolic conditions to those associated with breakfast skipping and late night eating, such as obesity, diabetes, and metabolic syndrome, as well as increased mortality. Taken together, the effect of short sleep on the above health risks may include the effect of breakfast skipping, and vice versa. However, short sleep and breakfast skipping syndromehas rarely been considered together. Circadian misalignment may be prevalent in individuals with late night eating, breakfast skipping, and short sleep. Because late night eating and short sleep can be closely related and can aggravate each other, these three factors should not be considered separately in terms of health and cardio metabolic conditions. In this context, late night eating and breakfast skipping may be representative unhealthy eating habits around sleep (Nakajima et al., 2019).

Taken together, specific features can form when UEHAS and short sleep are combined because of the relationships between them, whereas sleep and UEHAS are sufficiently independent in individuals with good sleep and healthy eating-habits around sleep. It is reasonable to assume that BS prolongs the fasting state and results in a lack of energy in the morning, which can result in hampered physical and intellectual activities and possibly in larger meal consumption later in the day, though conflicting outcomes have been reported. However, this theory may be exclusively applicable to healthy people without late night eating, i.e., those who do not take dinner late at night. Of note, late night eating may be associated with hyperglycemia, which remains until early morning. A time period of less than 6 h from late night eating to the end of a short sleep falls short of the 8-10 h criteria commonly used for overnight fasting, although the definition of overnight fasting has not been definitively established. Theoretically, therefore, late night eating within 2 h of going to bed combined with a short (< 6 h) sleep does not yield a fasting state in the early morning. If people with late night eating sleep for a normal length of time, the opportunity for breakfast consumption may be missed because they do not have enough time to take a breakfast meal. It is important to take energy in the early morning for healthy physical activity, whereas attaining a fasting state for a certain period in the day, usually during sleep because sleep involves equal or lower energy expenditure than resting energy expenditure, is essential for metabolic homeostasis. Adequate fasting especially during sleep can enable plasma glucose to return to the pre-prandial level and plasma insulin to decline to baseline level, which prevents over-secretion of insulin and has a protective action for β-cell function in the pancreas. Having an appetite, i.e., a feeling of hunger, for breakfast may be inappropriate if the body is not in a fasting state. Consumption of breakfast without adequate fasting may lead to an absence of the fasting state throughout the day, which results in sustained hyperglycemia and elevated insulin secretion. Meanwhile, in view of the time course, late night eating can affect the quantity and the quality of the following sleep, which may in turn affect the conditions of the next morning, i.e., eating breakfast. Studies concerning the effect of late night dinner eating on sleep are limited and the underlying mechanisms remain poorly understood (Nakajima et al.,2019).

Late night dinner eating can deteriorate circadian rhythms and the secretion of leptin, peptide-YY, melatonin, orexins, and ghrelin. Late night dinner eating, which can result in sleep with a full stomach, may cause gastroesophageal reflux disease and reduced diet-induced thermogenesis, both of which reduce the quality of sleep. Additionally, higher circulation volumes consisting of a large volume of water and high concentrations of sodium and glucose in the trunk circulation may burden the heart, vessels, and kidney, possibly resulting in arrhythmia and incidents of proteinuria, as observed in our previous studies.

Shorter time periods between dinner and sleep, and between sleep and breakfast, can intensify the plausible effect of the postprandial condition after late night dinner eating on sleep and the effect of poor sleep on breakfast, respectively. In addition, late night dinner of sleep is shorter. Therefore, it is best to refrain from late night dinner eating for a healthy sleep and for optimal conditions in early morning. However, if it is impossible to prevent late night dinner eating because of compulsory shift work or family or individual reasons, the dinner should have less energy and consist of a small amount of easy-to-digest ingredients. Alternatively, instead of completely skipping breakfast, consumption of a very low-calorie meal of less than 200 kcal including water, minimum minerals, and vitamins may be an effective option for avoiding potential fasting and adverse reactions such as hypoglycemia and dehydration. Simultaneously, healthy sleep habits may be necessary for conditions the next morning

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