Meal timing has witnessed changes in different cultures over time [20,21,22,23]. Moreover, religion may have an impact as well on mealtimes. The timing of meals during the Middle Ages was shaped by the presence of daylight. In a time without electricity, people would rise earlier to utilize natural light for a range of tasks, including meal preparation and eating [24]. Due to the absence of electricity, the option to cook dinner in the evening was not available. Peasants had their main meal around midday, although it was a considerably simpler and less extravagant event [24]. Ancient traditional Chinese Medicine, practiced for over 2500 years, suggests that the ideal time for carbohydrate-rich meals is between 0700 and 1100, with smaller meals recommended later in the day during the transition from an active phase (“yang”) to a resting phase (“yin”) [20,25]. This practice is rooted in the belief that consuming energy-dense meals in the evening can disrupt sleep and various bodily functions. In medieval England, dinner, the main meal of the day, was consumed around noon or 01:00 p.m., while supper, a smaller meal, was closer to sunset, typically between 04:00 p.m. and 06:00 p.m. [20,26]. Religion also impacts mealtime; for example, during Islamic fasting inside or outside the month of Ramadan, followers refrain from eating and drinking between dawn and sunset for a month and are requested to eat an early pre-dawn meal called Suhur before fasting, which has a religious dimension [27]. Also, during ordinary days, Muslims were historically required to wake up every day for the dawn prayer, where they eat a meal after the prayer and start their day [27]. The advent of artificial lighting, such as oil lamps, led to a shift in dinner and other activities to later times. By the late eighteenth century, dinner had moved to around 04:00 p.m. or 05:00 p.m., and the introduction of lunch was a response to extended fasting periods between breakfast and dinner. The Industrial Revolution also contributed to later dinner times among working-class men who split the workday with a quick noon meal [20,26]. In the USA, an examination of data derived from the National Health and Nutrition Examination Survey (NHANES) demonstrated that snacks consumed after dinner constituted the largest share of calories, providing nearly 45% of overall calorie consumption [28]. Over 40 years, from 1971–1974 to 2007–2010, the timing of breakfast and lunch generally shifted to later times, while dinner timing remained stable [28]. In the most recent NHANES analysis involving 15,341 adults from the 2009 to 2014 cycle, the average dinner time was 6:24 p.m., with the average time of the last eating episode being 8:18 p.m. [28]. In fact, contrary to the commonly held belief that humans follow a strict three-meal pattern, it is currently evident that calorie intake occurs sporadically and over an extensive timeframe throughout the 24-h cycle [29]. Hence, limiting food intake to predetermined time windows may present a readily implementable behavioral intervention with the potential to enhance outcomes in patients with metabolic syndrome.

Every organ, tissue, and cell in the body functions according to a biological clock that adheres to a circadian rhythm. Biological clocks can be classified into central and peripheral clocks depending on where they are located anatomically [30]. The primary biological clock is situated within the hypothalamus, precisely within the suprachiasmatic nucleus (SCN), while peripheral clocks exist in all cells throughout the body [31]. These clocks help maintain normal tissue function by regulating the activity of tissue-specific genes [31]. The body’s internal clocks, known as circadian rhythms, rely on independent oscillators within cells to regulate gene expression; circadian clocks are intrinsic biological oscillators that exhibit a periodicity of approximately 24 h [32], even without external cues [33]. To achieve external and internal synchrony, the body’s biological clocks must be entrained daily.

Circadian clocks are intrinsic biological oscillators that exhibit a periodicity of approximately 24 h [32]. Found in a wide range of light-sensitive organisms, these clocks play a vital role in coordinating rhythmic activities in accordance with the natural daily cycles [34]. In order to stay synchronized with the external environment, circadian clocks rely on external signals called zeitgebers or timing cues to undergo phase resetting [32,34]. The retinohypothalamic tract primarily entrains the SCN through exposure to external light, whereas neurohormonal factors exert an influence on peripheral clocks and mealtimes [35,36], and peripheral tissues can be moderately affected by nonphotic signals, such as food intake and glucocorticoids [37,38]. The nervous and endocrine systems both regulate the peripheral clocks in vivo. One example is the secretion pattern of glucocorticoids, which is regulated by the SCN and helps synchronize peripheral clocks [38,39]. Exposure to intense light during nighttime can disrupt the secondary clocks and rhythms that are controlled by the central clock situated in the SCN; similarly, eating meals during the night can also disrupt the peripheral clocks.

External or internal circadian system desynchrony has been associated with diverse metabolic dysfunctions, including compromised glucose tolerance and diminished insulin sensitivity, elevated susceptibility to complications related to reduced insulin sensitivity, such as non-alcoholic fatty liver disease (NAFLD), heightened levels of proinflammatory cytokines, elevated arterial blood pressure, and decreased energy expenditure, leading to obesity [40,41,42]. Moreover, epidemiological data support the connection between circadian misalignment and elevated susceptibility to metabolic disorders, diabetes, disorders affecting the cardiovascular system, and NAFLD [43,44,45,46].

Laboratory-controlled studies suggest that acute circadian rhythm misalignment increases the risk of developing metabolic disorders [11]. However, more research is needed in the general population as well as long-term studies to investigate the potential for adaptation to long-term disruption of the circadian rhythm [47].

Clock genes are central to circadian rhythms, profoundly influencing behavior and human physiology [48]. These genes, discovered in fruit flies and mammals like mice, form networks that display a 24-h oscillation [49,50]. These networks not only govern physiological and behavioral rhythms but extend their influence to other cellular functions [51]. Mammalian circadian rhythms arise from a feedback loop involving transcriptional activators and repressors [52]. Key proteins, BMAL1 and CLOCK, stimulate the transcription of Cry and Per genes. When repressor proteins CRY and PER reach a specific concentration, they interfere with the CLOCK-BMAL1, starting a new transcription cycle [33]. Current studies underline the significance of circadian rhythm in health disorders and its synchronization for optimal cellular functioning [53]. Moreover, there is a documented interplay between clock genes and feeding times, with feeding rapidly impacting circadian clock gene expression in animals [54,55]. For nocturnal rodents, daylight feeding alters circadian clock phases in peripheral tissues but not in the central timekeeper [56]. The relationship between human feeding times and clocks is an emerging field, suggesting that timed feeding could have clinical benefits [57].

Emerging evidence highlights the significant role of mealtime in controlling metabolic processes and its close interaction with the biological clock [11,58]. Chrononutrition, a new discipline, addresses the interplay between mealtime, circadian rhythm, and metabolic regulation [59]. Current research indicates that meal timing influences the circadian cycle, metabolic regulation, and body weight [60]. Consuming meals during inappropriate time periods can cause misalignment between peripheral biological clocks and the central biological clock in the SCN, increasing the potential for developing metabolic disorders [7,36,58]. Studies in both nocturnal species and humans have shown comparable results, wherein consuming meals at inappropriate hours (dark hours, “inactive phase” for humans) is linked to an increased likelihood of experiencing metabolic impairment [61]. In shift workers, night eating has been linked to metabolic disturbances [62,63]. Research has also shown that confining the timing of food intake to either daytime or nighttime can influence the risk of metabolic disorders [29,64,65,66]. However, it is essential to acknowledge that studying the intricate interplay between mealtime, circadian rhythm, and metabolism poses challenges due to the influence of multiple interacting factors. Factors including individual chronotype, lifestyle elements like shift work, sleep disruptions and sleep patterns, dietary composition and portion sizes, physical activity levels, environmental factors including nighttime light exposure, age, and genetic factors can interact with these rhythms, with some evidence suggesting that high-fat meals eaten late at night may be particularly disruptive [58,67,68].

In addition to caloric intake control, maintaining a consistent meal schedule is crucial as it aids in the effective management of energy balance. Consuming meals at set times from sunrise to sunset (between dawn and dusk rather than continuously throughout the day) enhances circadian rhythmicity and promotes a beneficial cycle for optimal metabolic health [20]. In experiments conducted on Wistar rats, it was observed that providing a daily serving of chocolate during the period of activity (breakfast) facilitated the adjustment of the SCN activity to the new schedule in a model of jet lag, leading to faster re-entrainment [69]. Additionally, in a model using rats simulating shift work, having a daily serving of chocolate coinciding with the start of the active phase (breakfast time) prevented disruption of the body’s internal clock by increasing the strength of the day–night activation in the SCN, specifically involving c-Fos (c-Fos is a helpful physiological marker of neural activation, which proved to be successfully utilized in the SCN) [69,70]. In contrast, chocolate consumed during dinner hindered re-synchronization in the jet lag condition and fostered disruption of circadian coordination in shift work models [69]. Furthermore, rats consuming chocolate during breakfast showed lower weight gain, while those having chocolate during dinner exhibited increased body weight [69]. These findings emphasize the importance of meal timing in regulating circadian synchrony and metabolic function, particularly for a high-calorie and appetizing meal like chocolate.

The favorable impacts of morning meal (breakfast) consumption on body weight and cardiometabolic well-being have not been consistently reported in all studies [71,72]. A consensus statement from the American Heart Association concluded that while epidemiological evidence indicates a potential adverse impact of consuming meals late in the day on cardiometabolic hazard, the scope of clinical intervention studies addressing this issue has been scant and lacks the specific focus to draw definitive conclusions or formulate recommendations [36]. The statement also emphasized that mealtime and frequency are not the sole determining factors; the length of time between meals and caloric intake are also crucial considerations [36].

6. The Interaction between Mealtime and Circadian Hormones

6.1. Cortisol

6.2. Melatonin

6.3. Other Mechanisms