Current peer-reviewed literature and reviews indicate that late-night or mistimed eating is associated with an increased risk of weight gain over time, though definitive direct causal proof remains limited by observational study designs.
The aim of this short review is to provide an updated commentary on the current literature examining the impact of meal timing on obesity and weight gain in adults. The potential mechanisms, including novel and emerging factors, behind timing of food intake across the 24-h period in the development of obesity, and dietary strategies manipulating meal timing to ameliorate weight gain are also explored. Dietary patterns that feature meal timing outside of the regular daytime hours can contribute to circadian disruption as food is metabolised in opposition to internal daily rhythms and can feedback on the timekeeping mechanisms setting these rhythms. Epidemiological evidence examining the impact of late meal timing patterns is beginning to suggest that eating at night increases the risk of weight gain over time. Mechanisms contributing to this include changes to the efficiency of metabolism across the day, and dysregulation of appetite hormone and gut microbiota by mis-timed meals. When meals are eaten, in relation to the time of day, is increasingly considered of importance when implementing dietary change in order to address the growing burden of obesity, although further research is required in order to determine optimal patterns.
The potential mechanisms, including novel and emerging factors, behind timing of food intake across the 24-h period in the development of obesity, and dietary strategies manipulating meal timing to ameliorate weight gain are also explored. Recent Findings Dietary patterns that feature meal timing outside of the regular daytime hours can contribute to circadian disruption as food is metabolised in opposition to internal daily rhythms and can feedback on the timekeeping mechanisms setting these rhythms. Epidemiological evidence examining the impact of late meal timing patterns is beginning to suggest that eating at night increases the risk of weight gain over time.
This is in part due to the increased propensity for weight gain observed in those with mis-timed eating patterns, i.e. eating occasions extending in to the night hours, when the body is usually primed for rest [ 3 ]. Night shift workers are a case in point, being frequently active and eating at night in the course of their employment, and experiencing higher rates of cardio-metabolic disease [ 4 ]. The human body is highly attuned to the cycling of day and night (circadian rhythm), with daily fluctuations in many physiological processes, including insulin sensitivity, occurring in anticipation of this routine environmental change [ 5 ].
earlier during the day, appeared to reduce the risk of weight gain at 3.5-year follow-up (OR = 0.62, 95% CI: 0.47; 0.80) [ 17 ]. Eating late into the day and the overnight period is common for 15–20% of the population employed in shift work roles, as such data from this unique population group can assist our understanding of associations between meal timing and body weight. A number of retrospective studies have reported a link between exposure to shift work and weight gain [ 18 – 20 ] and a recent meta-analysis found a significantly increased prevalence of overweight/obesity in shift workers from the 22 cross-sectional studies included as part of the review [ 21 ].
This would be important to examine in the future as night-time eating is more prevalent in short sleepers and can both be a consequence of, and effectuate, short sleep duration [ 25 ]. While there are clear limitations in methodological difference in dietary data collection and synthesis of findings due to heterogeneity in the classification of night eating exposure and outcomes measured, this evidence is starting to suggest that the time of day when meals are consumed can impact body weight and that night eating may lead to weight gain.
Future prospective cohort studies which comprehensively characterise the timing of meals, in addition to more traditional markers of diet quality, are needed before strong conclusions can be formed in regards to the contribution of meal timing patterns to obesity. The mechanisms behind the observed increase in risk of obesity and weight gain in populations frequently eating at night are likely to be multifaceted, and, as suggested in the epidemiological evidence, not explained by disturbances to energy intake alone.
There is evidence that both of these components fluctuate over the course of the day, which, given that RMR and TEF combined make up approximately 80% of TEE, could help explain the difficulties in achieving weight maintenance when meal timing
If circadian rhythms are constantly disrupted, as occurs with frequent late or night-time eating, this has been shown to uncouple peripheral circadian clocks in intestinal epithelial cells [ 54 ] which can then reduce fuel utilisation and lead to fuel storage in adipose tissue. Thus, the alteration in fuel utilisation has been proposed as a contributor to weight gain in shift workers who routinely face circadian misalignment. Time restricted feeding in rodent models partially restores this misalignment and in turn has been shown to influence the improve host metabolic efficiency [ 55 ].
Following a dietary pattern with frequent eating at night, in the long term, may increase risk of weight gain, although currently robust conclusions in relation to the effect of meal timing patterns on obesity risk cannot be arrived at as a predominance of cross-sectional studies in the epidemiological evidence pose inherent limitations in the assessment of causality, especially so in determining impact on weight change as reverse causality cannot be ruled out. It is thus important for future cohort studies examining the relationships between dietary patterns and disease outcomes to capture accurate information on the temporal timing of meals.
Consideration should be given in these protocols to match the energy density of diets, so that effects of night and late eating, over and above increases to energy intake, can be elucidated.
This paper presents a review of the current literature in support of a model explaining the relationships between sleep health and risk for type 2 diabetes in adolescents. Short sleep duration is associated with risk of developing obesity in youth. Sleep restriction increases energy expenditure, but also increases hunger, appetite, and food intake, causing positive energy balance, impacting appetite-regulating hormones, and leading to increased eating late at night. Insufficient sleep may lead to reduced physical activity and greater sedentary behaviors. In addition, short sleep duration is associated with reduced insulin sensitivity. The cumulative negative consequences of insufficient sleep increase risk for type 2 diabetes. Applications to clinical care, public policy, and future research are discussed. Insufficient sleep in adolescence increases risk for type 2 diabetes directly through impact on insulin sensitivity and indirectly through increased dietary intake, sedentary activity, and weight gain.
These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. Purpose of Review This paper presents a review of the current literature in support of a model explaining the relationships between sleep health and risk for type 2 diabetes in adolescents. Recent Findings Short sleep duration is associated with risk of developing obesity in youth. Sleep restriction increases energy expenditure, but also increases hunger, appetite, and food intake, causing positive energy balance, impacting appetite-regulating hormones, and leading to increased eating late at night.
Insufficient sleep may lead to reduced physical activity and greater sedentary behaviors. In addition, short sleep duration is associated with reduced insulin sensitivity. The cumulative negative consequences of insufficient sleep increase risk for type 2 diabetes. Applications to clinical care, public policy, and future research are discussed. Summary Insufficient sleep in adolescence increases risk for type 2 diabetes directly through impact on insulin sensitivity and indirectly through increased dietary intake, sedentary activity, and weight gain.
Thus, we developed a model to explain the relationship between sleep health and risk for T2D in adolescents based on the current literature. Model of Sleep and Risk for Diabetes in Adolescents Our model (Fig. 1 ) posits that the pubertally related circadian delay that leads to a propensity for delayed bedtimes, combined with forced early morning school day rise times, results in insufficient sleep. Insufficient sleep may then lead to decreased physical activity, increased evening food intake, and increased weight gain and obesity risk.
Thus, in addition to pubertally induced IR, insufficient sleep both directly and indirectly, through its impact on activity, diet, and weight, results in IR, which in turn, increases future risk for developing T2D. Here, we discuss the evidence base to date in support of this model. Fig. 1 A model of sleep and risk for diabetes in adolescents Definition of Sleep Health in Adolescents Sleep health is a multidimensional construct, including sleep duration, continuity or efficiency, timing, sleepiness, and subjective satisfaction or quality [ 17 ].
These factors drive late sleep onset, which, when combined with imposed early school start times, result in high rates of insufficient sleep in adolescents [ 4 ]. Data from the 2019 Youth Risk Behavior Survey reveal that 83% of 12th grade students report obtaining < 8 h sleep per night, and as many as 43% of teens obtain < 6 h sleep per night [ 1 ]. Adolescence is a developmental stage during which youth have more autonomy over their bedtimes, which has been shown to result in later bedtimes and shorter sleep duration [ 18 ].
Additionally, age and sex may be important factors in this association: in a longitudinal assessment of adolescents biannually at six timepoints, shorter sleep at baseline was found to be associated with an increase in BMI over time for older adolescent females (16–18 years), whereas baseline sleep was associated only with baseline BMI, not weight gain over time, for males [ 26 ]. Finally, findings from a meta-analysis of prospective studies revealed a causal relationship between short sleep duration and subsequent weight gain and obesity in youth across development, including adolescence [ 27 •].
Timing of eating in relation to sleep may be another important factor. Adults with later timing of sleep (later bed and wake time) consumed more protein, fat, and carbohydrates in the evening (after 8 pm), and dietary intake after 8 pm was associated with higher BMI [ 38 ]. Evidence suggests that dietary intake during times of high circulating melatonin levels (late at night, or early in the morning) may contribute to weight and metabolic dysregulation [ 39 , 40 ].
The consequences of late eating timing have potential negative implications for adolescents, given the circadian phase delay that occurs in this developmental stage, and adolescents, particularly those with late chronotype (diurnal preference), demonstrate most eating occasions clustered late in the day [ 41 , 42 ]. Indeed, later chronotype was associated with greater evening caloric intake in one sample of adolescents [ 42 ].
Additional data on sleep timing, physical activity, sedentary behaviors, and dietary habits during the COVID-19 time period are also needed. Conclusions Our model proposes that insufficient sleep in adolescence increases risk for T2D both directly through its impact on IR and indirectly through increased dietary intake, sedentary behavior, and weight gain. This is alarming given that a majority of adolescents are not achieving the recommended sleep duration, particularly on school nights [ 98 – 101 ]. Moreover, adolescents are already at increased risk for abnormal glucose metabolism as puberty is strongly associated with IR [ 6 ].
ABSTRACT Inappropriate eating habits such as skipping breakfast and eating late at night are associated with risk for abnormal weight-gain and adiposity. We previously reported that time-imposed feeding during the daytime (inactive phase) induces obesity and metabolic disorders accompanied by physical inactivity in mice. The present study compares metabolic changes induced in mice by time-imposed feeding under voluntary wheel-running (RW) and sedentary (SED) conditions to determine the effects of voluntary wheel-running activity on obesity induced in mice by feeding at inappropriate times. Mice were individually housed in cages with or without running-wheels. We compared food consumption, core body temperature, hormonal and metabolic variables in the blood, lipid accumulation in the liver, circadian expression of clock and metabolic genes in peripheral tissues, and gains in body weight between mice allowed access to food only during the sleep phase (daytime feeding; DF) or only during the active phase (nighttime feeding; NF) under SED or RW conditions. Only a high-fat high-sucrose diet was available to the mice throughout restricted feeding. Nocturnal activity was maintained in both NF and DF mice under RW conditions, but significantly suppressed during the latter half of the dark phase in DF mice. Nocturnal fluctuations in core body temperature were maintained in DF and NF mice under both SED and RW conditions, although DF attenuated the day–night amplitude more under SED, than RW conditions. The degrees of DF-induced increases in body weight gain, food efficiency, adipose tissue mass, lipogenic gene expression in metabolic tissues, and hepatic lipid accumulation were essentially identical between SED and RW conditions. Daytime feeding also induced hyperinsulinemia and hyperleptinemia under both SED and RW conditions, although DF-induced hyperleptinemia was slightly attenuated by wheel-running. The temporal expression of circadian clock genes became synchronized to feeding cycles in the liver but not in the skeletal muscle of mice under both SED and RW conditions. Chronic voluntary exercise on running-wheels minimally affected obesity and adiposity in mice caused by daily feeding at unusual times. The timing of food intake might be more important than physical exercise for preventing metabolic disorders. Abbreviations: ANOVA: analysis of variance; DF: daytime feeding; FFA: free fatty acid; GLP-1: glucagon-like peptide-1; HOMA-IR: homeostasis model assessment of insulin resistance; NEAT: non-exercise activity thermogenesis; NF: nighttime feeding; RF: restricted feeding; RW: running-wheel; SCN: suprachiasmatic nucleus; SE: standard error of the mean; SED: sedentary; SPA: spontaneous physical activity; T-Cho: total cholesterol; TG: triglyceride; WAT: white adipose tissues
Abstract Studies have suggested that meal timing plays a role in nutritional health, but this subject has not been sufficiently studied in pregnant women. We analysed the effect that timing of food intake has on eating patterns, diet quality and weight gain in a prospective cohort study with 100 pregnant women. Data were collected once per trimester: 4th–12th, 20th–26th and 30th–37th weeks. Food intake was evaluated using three 24-h dietary recalls, which were used to assess eating patterns and diet quality. Distribution of energy and macronutrient intake throughout the day was considered eating patterns. Diet quality was assessed using the Brazilian Healthy Eating Index-Revised. Weight gain was evaluated during each trimester. Women were classified as early or late timing of the first and last eating episodes if these values were below or above the median of the population, respectively (first eating episode = 08.38 hours; last eating episode = 20.20 hours). Generalised estimating equation models adjusted for confounders were used to determine the effects of timing of the first and last eating episodes (groups) and gestational trimesters (time) (independent variable) on eating patterns, diet quality and weight gain (dependent variables). Early eaters of the first eating episode have a higher percentage of energy and carbohydrate intake in morning and a lower at evening meals. They also have a better diet quality for fruit components when compared with late eaters of the first eating episode. Our results emphasise the importance of considering meal timing in the nutritional antenatal guidelines to promote maternal–fetal health.
The timing and nutritional composition of food intake are important zeitgebers for the biological clocks in humans. Thus, eating at an inappropriate time (e.g., during the night) may have a desynchronizing effect on the biological clocks and, in the long term, may result in adverse health outcomes (e.g., weight gain, obesity, and poor metabolic function). Being a very late or early chronotype not only determines preferred sleep and wake times but may also influence subsequent mealtimes, which may affect the circadian timing system. In recent years, an increased number of studies have examined the relation between chronotype and health outcomes, with a main focus on absolute food intake and metabolic markers and, to a lesser extent, on dietary intake distribution and eating behavior. Therefore, this review aimed to systematically determine whether chronotype indirectly affects eating behaviors, dietary intake (timing, choice, nutrients), and biomarkers leading to body composition outcomes in healthy adults. A systematic literature search on electronic databases (PubMed, CINAHL, MEDLINE, SCOPUS, Cochrane library) was performed (International Prospective Register of Systematic Reviews number: CRD42020219754). Only studies that included healthy adults (aged >18 y), classified according to chronotype and body composition profiles, using outcomes of dietary intake, eating behavior, and/or biomarkers, were considered. Of 4404 articles, 24 met the inclusion criteria. The results revealed that late [evening type (ET)] compared with early [morning type (MT)] chronotypes were more likely to be overweight/obese with poorer metabolic health. Both MT and ET had similar energy and macronutrient intakes, consuming food during their preferred sleep-wake timing: later for ET than MT. Most of the energy and macronutrient intakes were distributed toward nighttime for ET and exacerbated by unhealthy eating behaviors and unfavorable dietary intakes. These findings from our systematic rev
Thus, eating at an inappropriate time (e.g., during the night) may have a desynchronizing effect on the biological clocks and, in the long term, may result in adverse health outcomes (e.g., weight gain, obesity, and poor metabolic function). Being a very late or early chronotype not only determines preferred sleep and wake times but may also influence subsequent mealtimes, which may affect the circadian timing system. In recent years, an increased number of studies have examined the relation between chronotype and health outcomes, with a main focus on absolute food intake and metabolic markers and, to a lesser extent, on dietary intake distribution and eating behavior.
Humans are physiologically suited to spend about two-thirds of their 24-h day awake, being active and eating and storing energy. They usually spend one-third of their time asleep, being in a fasting state at nighttime ( 13 ). During the day, ingested food provides energy to support metabolic processes, whereas during the night, when sleep usually occurs, stored energy is mobilized to maintain homeostasis ( 14 , 15 ). Thus, eating at an inappropriate time can have a desynchronizing effect on the biological circadian clocks, resulting in adverse health outcomes, including weight gain, obesity, and poor metabolic health outcomes ( 16–18 ).
An eating pattern that is high in energy-dense foods, such as sugar-sweetened beverages, fast foods, and fatty foods, and low in micronutrient-rich foods, such as fruit, vegetables, and fiber, is associated with weight gain ( 30 ) and an increased risk of metabolic syndrome and diabetes ( 31 , 32 ). Furthermore, disinhibited or restrained eating behaviors are known to affect energy intake by influencing the types and amounts of foods eaten, the timing of food intake, and the eating occasion or where food intake occurs ( 33 ).
Most of the studies that explored meal timing found that individuals tend to consume food based on preferences according to their chronotype ( 48 , 49 , 51 , 71 ). In ETs, most of their energy and macronutrient intake were distributed toward the biological night ( 82 ), and clock times for meals were later than those of MTs. The mechanisms of this chronotype–body composition relation are yet to be fully explained; however, it may be hypothesized and in part supported from data of this systematic review that several interconnected mechanisms, including mistimed food intake, lower diet quality, and eating behaviors that favor weight gain and metabolic alterations, have an influence.
Consequently, the overnight fasting period is prolonged and an increase in postprandial insulin concentrations and fat oxidation is seen ( 91 ). Ultimately, low-grade inflammation and impaired glucose metabolism may result in the development of metabolic inflexibility and weight gain ( 91
This reinforced previous studies that showed the detrimental effect of late eating ( 103 ). Generally, it seems that the timing of eating in alignment with one's chronotype could be an important and beneficial factor when considering body composition outcomes ( 57 ). When participants of the latter study were following chronotype-adjusted diets, they had greater weight-loss success compared with the traditional, hypocaloric control diet. The weight loss between MTs and ETs was similar, suggesting that this may be an effective approach for any chronotype ( 57 ).
Such data could inform strategies (e.g., eating in alignment with internal body clocks, improvement of sleep timing and quality, adjusting mealtimes to improve the eating and fasting windows, e.g., TRE) around healthy weight management in the future. This systematic review supports the assumptions that chronotype have an impact on body composition through interconnected mechanisms, including mistimed food intake, eating behaviors and food choices that favor weight gain, and metabolic alterations. Supplementary Material nmac093_Supplemental_File Click here for additional data file.
Everything we examined (5)
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