INTRODUCTION
Few health problems capture the dynamic interaction between human biology and the environment better than the current obesity epidemic. Although circadian and appetite biological systems were aligned well with the demands of the premodern world to promote survival in unstable food environments, these same systems are now misaligned with the modern food environment to instead promote obesity, metabolic diseases, and eating disorders.1 This article will provide an overview of ways in which this biology-environment interaction has shifted in the last half-century to predispose individuals to develop metabolic diseases related to overnutrition and unhealthy eating patterns and behaviors, and to highlight validated treatments to reverse these trends.
Consider some of the most important food environment changes occurring in recent decades. In the “leptogenic” food environment characterizing the Western world prior to the mid-20th century, food was unprocessed, high in fiber, nutrient dense, and available only at limited times.2 The premodern food environment was characterized by high energy demands for obtaining and preparing food and lighting constraints that limited eating to daytime and early evening hours. Culture played a complimentary role by encouraging social and family-oriented eating patterns that partly constrained both food choices and food quantities.
In just a few decades, however, centuries of biologically, socially, and culturally regulated aspects of eating and appetite were replaced by an “obesogenic” environment.2 Food became hyperpalatable, calorie dense, and fiber and nutrient poor. Advances in food technology further made these premade foods available ubiquitously. Combined with similar advances in commercial electricity and multimedia entertainment, these changes enabled eating across day and nighttime hours to become not only possible but desirable and even normative.3 With rapid changes in society, food and eating themselves assumed new meanings. Traditionally tied to family meals and cultural events, food evolved to become a form of self-expression, a source of entertainment, the focal point of holidays, and a means of coping with stress.4 The latter form of coping, described further in the subsections later in this discussion, became widespread as the type of stress we experienced in society gradually transformed from mostly acute stress to primarily chronic stress. These physical changes in the food environment, coupled with behavioral and psychological changes in eating patterns and preferences, may help explain both the rapid rise of obesity in recent decades and the difficulties sustaining weight loss with conventional behavioral treatments (Fig. 1).5 As a result of these interactive changes, our circadian and appetite regulatory systems are disrupted by the modern food environment, with the sobering result being that an estimated 88% of Americans were metabolically unhealthy in 2018.6
Fig. 1.
Psychophysiological mechanisms contributing to the obesity epidemic.
CLINICS CARE POINTS.
The modern food environment is contributing to the obesity epidemic and related metabolic diseases.
Food has become more processed, calorie-dense, and lacking in nutrients compared to the premodern environment.
Changes in food technology, commercial electricity, and multimedia entertainment have enabled eating at all hours of the day and night.
Food has also taken on new meanings, such as a form of self-expression and a means of coping with stress.
These changes in the food environment and eating patterns have disrupted circadian and appetite regulatory systems, leading to an estimated 88% of Americans being metabolically unhealthy in 2018.
STRESS EATING AND EMOTIONAL EATING
Stress eating or emotional eating is a maladaptive behavioral response to stress. While some people may undereat and/or lose weight under stressful conditions, approximately 70% of individuals tend to overeat and/or gain weight in response to stress.7 Stress eating also typically involves ingesting calorically dense and highly palatable foods, also known as “comfort foods.” In conjunction with the overabundance of food and a modern, sedentary lifestyle, stress eating behavior plays an important role in unintended weight gain, metabolic health, and the continuing obesity epidemic.
The traditional, physiological model of stress includes the “fight or flight” mode in response to acute (ie, life threatening) stress. In this model, acute stress triggers a cascade of sympathetic hormones that redirects bodily and organ functioning away from metabolic and appetitive mechanisms, such as food intake and digestion.8 Instead of the acute stress most often faced by our premodern ancestors, in the modern world individuals are more likely to face stressors that are long-term, cumulative, and psychosocial in nature – that is, chronic stress. Chronic stress instigates an HPA-axis-regulated endocrine response, in particular the release of cortisol, which induces overeating of energy-dense foods.9 Eating these “comfort foods”—those that are high in fat and carbohydrate content—may reduce the chronic-stress activation of the HPA-axis.10 Thus, stress eating or emotional eating can be fundamentally understood as a coping mechanism to chronic stress.
Men and women respond differently to stress. Women are more likely to use food as a coping mechanism, whereas men tend to use nicotine or alcohol.11,12 The association between stress-related eating and obesity is also stronger among women than men.13 Women also are more likely than men to engage in dietary restraint, which can be defined as the self-regulatory behavior of restraining caloric intake to lose or maintain weight, due to societal pressures to be thin.14 Dietary restraint, especially among those who have a tendency to overeat, may trigger compensatory eating, and thus beget a cycle of overeating.15 Being overweight may also increase the risk of stress-eating behavior, as the stress related to weight stigma may be a trigger.16 Additionally, in the absence of adaptive stress coping mechanisms, such as physical exercise, one may be more likely to engage in stress eating.17
Since chronic stress is a key factor in stress-eating, stress reduction strategies are essential for successful treatment. Mindfulness, both a key component of Acceptance Commitment Therapy (ACT) and Dialectical Behavior Therapy (DBT), encourages regulating eating habits by increasing awareness to internal hunger and satiety cues and to sensory responses while eating.18 Guided meditations to increase awareness and identify eating triggers is also a key element in mindfulness-based interventions. Mindfulness-based approaches are effective in addressing dysregulated eating in both subclinical and clinical populations.19
CLINICS CARE POINTS.
Stress eating or emotional eating is a coping mechanism for chronic stress and is characterized by the ingestion of calorically dense and highly palatable foods.
Stress eating behavior plays a role in unintended weight gain and the obesity epidemic.
Chronic stress can trigger the release of cortisol, which can induce overeating of energy-dense foods.
Women are more likely than men to use food as a coping mechanism for stress and to engage in dietary restraint.
Being overweight may increase the risk of stress-eating behavior due to weight stigma.
Stress reduction strategies, such as mindfulness-based approaches, can be effective in addressing dysregulated eating in both subclinical and clinical populations.
PATHOLOGICAL EATING AND EATING DISORDERS
In some cases, stress or emotional eating can lead to binge eating disorder (BED). BED is characterized by recurrent episodes of binge eating (BE; ie, occurring once per week over a 3-month period) during which individuals consume large amounts of food within a distinct period of time (ie, 2 hours) and experience a sense of loss of control over their eating. Those with BED are markedly distressed by BE episodes but refrain from using extreme compensatory behaviors (ie, self-induced vomiting, laxative misuse) between episodes.20 Though not central to the diagnosis, BE episodes tend to occur during the evening hours.21,22 BED is the most commonly diagnosed eating disorder, with lifetime prevalence rates of 3.5% for women and 2.0% for men.23 Most individuals with BED are either overweight (BMI: 25–29.9) or obese (BMI: 301).24 The diagnosis is associated with numerous psychological and medical comorbidities, including overweight and obesity.23
Though the eating pattern exhibited by individuals with BED is distinct from those of anorexia and bulimia nervosa, the three major eating disorders share the same underlying psychopathology: an over-evaluation of the importance of shape and weight—and an individual’s corresponding ability to control these factors—when determining one’s self-worth. Across presentations, this emphasis leads to attempts to restrain or reduce one’s eating, the severity of which differs by diagnosis.25 The front-line treatment of eating disorders, including BED, is cognitive-behavioral therapy-enhanced (CBT-E),24 a time-limited, transdiagnostic, yet individualized treatment of eating disorder psychopathology. When used to treat BED, CBT-E consists of 20 treatment sessions across 20 weeks and can be administered in either an individual or group format.
BED treatment consists of 4 distinct stages.25 Stage one involves intensive twice-weekly sessions during which the provider constructs an individualized client case conceptualization, provides psychoeducation about treatment, and introduces the client to the main tenets of CBT-E: weekly in-session weight assessments and the establishment and ongoing self-monitoring of a regular eating pattern (ie, 3 meals and 3 snacks per day) to disrupt attempts at dietary restraint. Within the CBT-E framework, these attempts—and subjective “failures” to maintain this restraint—are posited as the practice that perpetuates binge eating episodes. Stage 2 is a transitionary stage during which the provider assesses client momentum and self-monitoring records in order to detect any barriers to weekly weighing and/or adherence to a regular eating pattern. Stage 3 consists of 8 weekly sessions of individualized treatment during which the provider and client work collaboratively to evaluate the negative consequences of the overemphasis on shape and weight, bolster the relative importance of other domains when assessing self-worth (eg, relationships, school, work, hobbies) and address other potential BED maintenance factors, including self-imposed dietary rules, event or mood-related changes in eating, negative body image, low self-esteem, clinical perfectionism, and interpersonal problems. The fourth and final stage of treatment consists of 2 biweekly sessions that prepare the client for future success by reviewing the maintenance of treatment gains, identifying realistic goals for continued improvement, and developing a plan for any anticipated obstacles. Typically, a follow-up session occurs approximately 20 weeks after treatment completion to review the client progress. CBT for BEDs yields transdiagnostic remission rates of no more than 50%, rendering it only marginally more efficacious than, if not equal to, other treatments for eating disorders.26,27 However, it remains the most extensively studied and evidence-informed treatment of EDs to date.28
CLINICS CARE POINTS.
Binge eating disorder (BED) is characterized by recurrent episodes of binge eating and a sense of loss of control over eating, occurring at least once per week over a 3-month period.
BED is the most commonly diagnosed eating disorder, with a lifetime prevalence of 3.5% for women and 2.0% for men.
Most individuals with BED are either overweight or obese.
The underlying psychopathology of BED, as well as other eating disorders, is an over-evaluation of the importance of shape and weight in determining self-worth.
The front-line treatment of BED is cognitive-behavioral therapy-enhanced (CBT-E), which consists of 4 stages and 20 treatment sessions over 20 weeks.
CBT-E can be administered in either an individual or group format and aims to disrupt attempts at dietary restraint, evaluate the negative consequences of an overemphasis on shape and weight, bolster the relative importance of other domains in assessing self-worth and address other potential BED maintenance factors.
CBT-E yields transdiagnostic remission rates of no more than 50% and is the most extensively studied and evidence-informed treatment of eating disorders.
CIRCADIAN CLOCK AND METABOLISM
A particularly modern source of chronic stress is the increase in light at night, shift work, and the availability of high-caloric foods in abnormal feeding times. These sources of chronic stress can lead to circadian dyssynchrony which has particularly dire metabolic consequences.29 The human body functions with an endogenous time-keeping system driven by internal molecular clock mechanisms and environmental entrainment cues such as light and feeding. The term circadian, derived from Latin “circa” (about) and “diem” (day), was first introduced in the 1950s as a means of defining this system. Mammalian innate physiology is influenced by rhythms organized with near 24-h periodicity.30–32 This circadian clock is an integral component of human function, with about 80% of all protein-coding genes displaying circadian expression,33 including the majority of genes encoding pharmaceutical drug targets.34 Alterations in the circadian clock can lead to states of disequilibrium with implications for aging and disease risk on a molecular level.35 Indeed, specific polymorphisms in circadian clock genes (eg, CRYPTOCHROME genes, PERIOD genes, CLOCK) are associated with obesity and poor weight loss in response to various therapies including bariatric surgery.36,37
The influence of circadian rhythms on metabolism has been an area of extensive investigation. Animal models with disruptions in circadian rhythms lead to metabolic pathophysiology.32 Various environmental cues can augment endogenous time-keeping. The most significant modulator is light,38 but others such as food intake independently alter peripheral body circadian rhythms, particularly of metabolically important organs such as the intestines, liver, and muscles.39 When behaviors (sleeping, physical activity, eating/drinking) are mistimed within the normal 24-h day cycle this can lead to circadian misalignment. One way which the interplay between metabolism and circadian misalignment has been studied is by examining the impact of shift work on body metabolism.
CLINICS CARE POINTS.
Chronic stress, such as that caused by light at night, shift work, and abnormal feeding times, can lead to circadian dyssynchrony, which has negative consequences for metabolism.
The human body has an endogenous timekeeping system (circadian clock) that is influenced by internal molecular mechanisms and external cues such as light and feeding.
Alterations in the circadian clock can contribute to the development of aging and disease.
Specific genetic variations in circadian clock genes have been linked to obesity and poor weight loss in response to various therapies, including bariatric surgery.
The influence of circadian rhythms on metabolism has been widely studied, and disruptions in these rhythms can lead to metabolic pathophysiology.
Environmental cues, including light and food intake, can alter the circadian rhythms of metabolically important organs such as the intestines, liver, and muscles.
Mistiming behaviors such as sleeping, physical activity, and eating can lead to circadian misalignment, which has been studied in the context of shift work and its impact on body metabolism.
SHIFT WORK AND OBESITY AND OBESITY-RELATED DISEASES
Shift work is a particularly modern source of chronic stress that can disrupt the body’s natural circadian rhythms. Shift-based workers often engage in atypical sleep/wake cycles based on the scheduling needs of their occupation. The misalignment caused by shift-work has been linked to negative consequences for metabolism and disease risk. This form of circadian disruption has been associated with adverse health events, including cardiovascular disease, and metabolic syndrome.29 There is a strong association between shift work and risk of overweight and obesity.40 Night shift work in particular is associated with the increased risk of obesity/overweight and shift workers had a higher frequency of developing abdominal obesity rather than other obesity types.41 Having ever worked a night shift is associated with increased risk for metabolic syndrome; higher cumulative years of night shifts was associated with progressively higher risk.42
Studies evaluating the association between sleep/duration and obesity-related disorders, in particular nonalcoholic fatty liver disease (NAFLD), have yielded varying results. Studies have shown that sleep duration <5 hours43,44 and <6 hours45 increased the risk of NAFLD among women; sleep duration <5 hours increased the risk of NAFLD and obesity in men compared to >7 hours which was associated with lower risk for NAFLD/obesity.46 However, long sleep duration (>9 hours) was associated with a modestly increased risk of NAFLD in both men and women.47 Poor sleep quality was associated with increased risk for NAFLD among both men and women44; and poor sleep quality predicted up to 20% of variability in liver stiffness among obese men and women with NAFLD.48 Overall, although there are associations between sleep variability and increased risk for metabolic derangements, the specifics of this interplay require further investigation. Still, these relationships between shift work and sleep variability with obesity exemplifies the impact circadian dysregulation can have on metabolism.
CLINICS CARE POINTS.
Shift work is a modern source of chronic stress that can disrupt the body’s natural circadian rhythms and lead to negative consequences for metabolism and disease risk.
Shift work has been associated with an increased risk of overweight and obesity, particularly among those working night shifts.
Shift work has also been linked to an increased risk of metabolic syndrome.
The relationship between sleep variability and increased risk for metabolic derangements, including obesity and NAFLD, is not fully understood but requires further investigation.
It is important to consider the role of circadian rhythms in the development and management of chronic stress, especially among shift workers, in order to minimize negative health outcomes.
THERAPEUTIC APPROACH: TIME-RESTRICTED EATING
The impact of shift work on metabolism and the risk of obesity and related disorders highlights the importance of addressing circadian dysregulation. One approach that has shown promise in this regard is time-restricted eating (TRE), which involves restricting food intake to specific periods of the day in order to synchronize the body’s internal clock with the external environment. TRE refers to the dietary intervention of limiting food consumption to a specific time window each day. The goal of TRE is the correction of circadian dyssynchrony by aligning feeding times to more active periods of central circadian rhythms. TRE is one of the many modalities of intermittent fasting, which encompasses dietary interventions that limit the timing, rather than content, of food intake.30,49
Early studies investigating the timing of food intake have shown that many individuals do not eat 3 discrete meals a day but rather are constantly grazing with an expanded window of caloric consumption.3 Several studies have investigated the effects of TRE on metabolism-related health outcomes. Some key findings from extended duration (>4 weeks) randomized-controlled trials are summarized in Table 1. In all, the weight loss outcomes from TRE tend to be modest with only 2% to 3% TBWL in long-term clinical trials.30 However, these clinical trials demonstrate that TRE can lead to improvements in insulin sensitivity, blood pressure, and oxidative stress in men with prediabetes50; improved blood glucose and insulin sensitivity in overweight adults with type 2 diabetes mellitus51; weight loss in overweight women52; weight loss and improved fasting blood glucose in obese men and women when combined with a commercial weight loss program53; weight loss with improved diastolic blood pressure and improved mood54; and significantly greater loss of fat in overweight/obese individuals when combined with concurrent exercise training.55 Yet, some studies have found that TRE does not improve metabolic outcomes despite causing weight loss. For example, one study noted that TRE led to a reduction in fat mass in patients with NAFLD, but did not alter liver stiffness, insulin sensitivity, or LDL/HDL.56 Another study showed that TRE reduced weight and frequency of eating but did not improve metabolic endpoints such as A1C, insulin sensitivity, or lipid measures.57 One RCT of middle-aged women found that TRE increased fasting glucose and insulin resistance despite causing weight loss.58
Table 1.
Randomized control trials on time-restricted eating
Article | Intervention | Control | Population | Key Findings |
---|---|---|---|---|
Jamshed et al,54 2022 | TRE (7:00–15:00) with energy restriction diet and exercise counseling for 14 wk | Energy restriction diet and exercise counseling | Men and women aged 25–75 y with obesity following in weight management clinic at the University of Alabama at Birmingham hospital (N = 90) | TRE was more effective for losing weight and improving diastolic blood pressure and mood than eating over a window of 12 or more hours at 14 wk. |
Sutton et al,50 2018 | TRE (6-h eating window, dinner before 15:00) for 5 wk followed by 7 wk washout and crossover | 12-h eating period with matched food intake | Men with prediabetes (N = 12) | TRE did not improve weight loss but improved insulin sensitivity, β cell responsiveness, blood pressure, oxidative stress, and appetite. |
Che et al,51 2021 | TRE (8:00–18:00) for 12 wk | Unrestricted eating | Overweight men and women with type 2 diabetes (N = 60) | TRE led to significant decreases in body weight, A1C, and in hyperlipidemia |
Domaszewski et al,52 2022 | TRE (12:00–20:00) for 6 wk | Unrestricted eating | Overweight or obese women over age 60 (N = 45) | TRE led to weight loss (approximately 2 kg) with decreases in BMI and weight, with 88% of participants adherent to the TRE diet |
Peeke, et al,53 2021 | TRE (10 h) starting after dinner between 17:00 and 20:00) on a commercial weight loss program diet with a snack at fasting hour 12 for 8 wk | TRE (12 h) starting after dinner between 17:00 and 20:00 on a commercial weight loss program diet | Obese men and women (N = 60) | Those on 10 h TRE diet + fasting snack had slightly more weight loss (11 kg compared to 9 kg), with a significant reduction in fasting blood glucose only in the 10 hr TRE study arm |
Kotarsky et al,55 2021 | TRE (12:00–20:00) for 8 wk combined with aerobic and resistance training | Normal diet combined with aerobic and resistance training | Overweight and obese men and women (N = 21) | TRE led to more weight loss, specifically greater loss of fat mass |
Cai et al,56 2019 | TRE (8 h eating window) for 12 wk | 80% of energy needs consumed via otherwise unrestricted diet | Men and women aged 18–65 y with NAFLD (N = 271) | TRE led to a reduction in body weight and fat mass and serum triglycerides |
Chow et al,57 2020 | TRE (8 h eating window) for 12 wk | Unrestricted eating | Obese men and women (N = 20) | TRE led to reduced weight and fat mass, without impact on metabolic markers |
Isenmann et al,62 2021 | TRE (12:00–20:00) for 14 wk | Macronutrient-based diet | Overweight or obese (class I) adults aged 20–40 years old exercising at least twice per week (N = 35) | Both TRE and macronutrient-based diet led to weight loss, with higher adherence in the TRE group |
Liu et al,59 2022 | TRE (8:00–16:00) with calorie restriction for 12 mo | Calorie-restricted diet alone | Men and women with obesity (N = 118) | TRE with calorie restriction did not lead to significant changes in body weight, fat, or metabolic risk factors compared to calorie restriction alone |
Lowe et al,60 2002 | TRE (12:00–20:00) for 12 wk | 3 structured meals per day without time restriction | Overweight or obese men and women aged 18–64 (N = 116) | TRE did not lead to greater weight loss or improvement in secondary metabolic endpoints compared to structured meal intake |
Lin et al,58 2022 | TRE (8 h eating window) with low-calorie diet for 8 wk | Low-calorie diet | Overweight or obese women aged 40–65 (N = 63) | TRE with low-calorie diet led to more weight loss and decease in diastolic blood pressure compared to low-calorie diet alone, but higher fasting glucose and insulin resistance were noted in the TRE arm |
Phillips et al,63 2021 | TRE (12 h eating window) for 6 mo | Standard dietary advice with unrestricted eating | Adults with eating duration >14 h and one component of metabolic syndrome | TRE did not lead to a significant difference in weight loss achieved with standard dietary advice |
Thomas et al,61 2022 | TRE (10 h eating window) starting within 3 h of waking with daily caloric restriction for 12 wk | Daily caloric restriction | Overweight or obese men and women (N = 81) | TRE did not lead to any difference in weight loss at 12 or 39 wk or metabolic markers |
In contrast to some studies that have found TRE to have modest benefits on metabolic outcomes, other RCTs have observed no such effects. A recent trial found no difference between groups in the primary outcome of weight change from baseline, nor in secondary outcomes such as waist circumference, insulin sensitivity, and serum lipids.59 However, it is worth noting that this study did not adequately track food intake and the authors reported that the control group voluntarily restricted their food intake, which may complicate the interpretation of the results. Another RCT found no significant difference in weight change or secondary metabolic outcomes between the TRE group and the control group, which followed a consistent-meal timed diet with 3 structured meals and allowed for light snacking in between.60
Like other dietary and behavioral interventions, the success of patients using TRE will likely depend heavily on their adherence to the prescribed eating schedule. Moreover, it is not clear whether these benefits are due to the change in eating schedule itself or to the resulting caloric restriction that occurs when people adhere to this schedule,61–63 or whether they are particularly beneficial to shift workers. Only a single study has investigated the effects of TRE on shift workers.64 Early results from a study of firefighters who work 24-h shifts concluded that a 10-h TRE protocol significantly increased quality of life metrics, and in patients with cardiometabolic risk factors, decreased VLDL, and improved hemoglobin A1c and diastolic blood pressure.
More studies are needed to determine the optimal duration and timing of TRE that would increase the chances of desired metabolic outcomes and to better understand its effects on metabolism-related health outcomes. Mouse studies suggest that changes in the gut microbiome may play a role in the metabolic effects of time-restricted diets.65,66 For example, certain methods that mimic the changes in the microbiome caused by TRE improve glucose tolerance without affecting mouse weights.67 However, our understanding of the relationship between chronic stress, circadian disruption, and metabolism is incomplete, and further research may identify new therapeutic targets for reversing the negative metabolic effects of chronic stress.
CLINICS CARE POINTS.
Time-restricted eating (TRE) involves limiting food intake to specific periods of the day to synchronize the body’s internal clock with the external environment.
TRE is a form of intermittent fasting that limits the timing of food intake rather than the content.
TRE has been shown to have modest weight loss effects in long-term clinical trials, with a 2% to 3% reduction in total body weight loss (TBWL).
TRE has been linked to improvements in insulin sensitivity, blood pressure, and oxidative stress in men with prediabetes; improved blood glucose and insulin sensitivity in overweight adults with type 2 diabetes mellitus; weight loss in overweight women; weight loss and improved fasting blood glucose in obese men and women when combined with a commercial weight loss program; and significant fat loss in overweight/obese individuals when combined with concurrent exercise training.
TRE may be of particular benefit to those who are shift workers.
More research is needed to determine the optimal duration and timing of TRE, its effects on metabolism-related health outcomes, and whether it is particularly beneficial for shift workers.
Further research is needed to understand the relationship between chronic stress, circadian disruption, and metabolism and to identify potential therapeutic targets for reversing the negative metabolic effects of chronic stress.
SUMMARY
Environmental factors, including diet and stress, can contribute to the development of obesity. Stress-related eating patterns, such as consuming high-calorie foods in excess and eating late at night, may contribute to weight gain. Disruptions to the body’s natural circadian rhythms, such as those experienced by shift workers, may also contribute to obesity and metabolic syndrome. While more research is needed to determine the effectiveness of time-restricted eating for obesity management, stress reduction and mindfulness techniques, as well as cognitive-behavioral therapy, have been found to be helpful in addressing disordered eating behaviors, including Binge Eating Disorder.
KEY POINTS.
The current obesity epidemic is the result of the misalignment between human biology and the modern food environment, which has led to unhealthy eating patterns and behaviors and an increase in metabolic diseases.
This has been caused by the shift from a “leptogenic” to an “obesogenic” food environment, characterized by the availability of unhealthy food and the ability to eat at any time of day due to advances in technology.
Stress eating is a common response to chronic stress that can contribute to weight gain and obesity and can be addressed through stress reduction strategies such as mindfulness-based interventions.
The increase in light at night, shift work, and the availability of high-caloric foods at abnormal times can lead to chronic stress and circadian dyssynchrony, which has negative impacts on metabolism and can increase the risk of obesity and other diseases.
One dietary approach to address circadian dysregulation is time-restricted eating (TRE), which involves restricting food intake to specific periods of the day to synchronize the body’s internal clock with the external environment.
DISCLOSURES
A. Zarrinpar is a co-founder, acting chief medical officer, and equity-holder in Endure Biotherapeutics. He is supported by the VA Merit BLR&D Award I01 BX005707, and NIH R21 MH117780, R01 HL148801, R01 EB030134, R01 HL157445, and U01 CA265719. All authors receive institutional support from NIH P30 DK120515, P30 DK063491, P30 CA014195, P50 AA011999, and UL1 TR001442.
REFERENCES
- 1.Schnabel L, Kesse-Guyot E, Alles B, et al. , Association Between Ultraprocessed Food Consumption and Risk of Mortality Among Middle-aged Adults in France, JAMA Intern Med, 179, 2019, 490–498. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Swinburn B, Egger G, Raza F. Dissecting obesogenic environments: the development and application of a framework for identifying and prioritizing environmental interventions for obesity. Prev Med 1999;29:563–70. [DOI] [PubMed] [Google Scholar]
- 3.Gill S, Panda S. A Smartphone App Reveals Erratic Diurnal Eating Patterns in Humans that Can Be Modulated for Health Benefits. Cell Metabol 2015;22(5): 789–98. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Allison DB, Heshka S. Emotion and eating in obesity? A critical analysis. Int J Eat Disord 1993;13:289–95. [DOI] [PubMed] [Google Scholar]
- 5.Hall KD, Farooqi IS, Friedman JM, et al. , The energy balance model of obesity: beyond calories in, calories out, Am J Clin Nutr, 115, 2022, 1243–1254. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Araujo J, Cai J, Stevens J. Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009–2016. Metab Syndr Relat Disord 2019;17:46–52. [DOI] [PubMed] [Google Scholar]
- 7.Epel E, Jimenez S, Brownell K, et al. Are stress eaters at risk for the metabolic syndrome? Ann N Y Acad Sci 2004;1032:208–10. [DOI] [PubMed] [Google Scholar]
- 8.Torres SJ, Nowson CA. Relationship between stress, eating behavior, and obesity. Nutrition 2007;23:887–94. [DOI] [PubMed] [Google Scholar]
- 9.Dallman MF, Pecoraro N, Akana SF, et al. Chronic stress and obesity: a new view of “comfort food. Proc Natl Acad Sci U S A 2003;100:11696–701. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Dallman MF. Stress-induced obesity and the emotional nervous system. Trends Endocrinol Metabol: TEM (Trends Endocrinol Metab) 2010;21:159–65. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Conway TL, Vickers RR Jr, Ward HW, et al. Occupational stress and variation in cigarette, coffee, and alcohol consumption. J Health Soc Behav 1981;22:155–65. [PubMed] [Google Scholar]
- 12.Mehlum L. Alcohol and stress in Norwegian United Nations peacekeepers. Mil Med 1999;164:720–4. [PubMed] [Google Scholar]
- 13.Laitinen J, Ek E, Sovio U. Stress-related eating and drinking behavior and body mass index and predictors of this behavior. Prev Med 2002;34:29–39. [DOI] [PubMed] [Google Scholar]
- 14.Smith JM, Serier KN, Belon KE, et al. Evaluation of the relationships between dietary restraint, emotional eating, and intuitive eating moderated by sex. Appetite 2020;155:104817. [DOI] [PubMed] [Google Scholar]
- 15.Ouwens MA, van Strien T, van der Staak CP. Tendency toward overeating and restraint as predictors of food consumption. Appetite 2003;40:291–8. [DOI] [PubMed] [Google Scholar]
- 16.Mouchacca J, Abbott GR, Ball K. Associations between psychological stress, eating, physical activity, sedentary behaviours and body weight among women: a longitudinal study. BMC Publ Health 2013;13:828. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Steptoe A, Lipsey Z, Wardle J. Stress, hassles and variations in alcohol consumption, food choice and physical exercise: A diary study. Br J Health Psychol 1998; 3:51–63. [Google Scholar]
- 18.Afari N, Herbert MS, Godfrey KM, et al. , Acceptance and commitment therapy as an adjunct to the MOVE! programme: a randomized controlled trial, Obes Sci Pract, 5, 2019, 397–407. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Corsica J, Hood MM, Katterman S, et al. Development of a novel mindfulness and cognitive behavioral intervention for stress-eating: a comparative pilot study. Eat Behav 2014;15:694–9. [DOI] [PubMed] [Google Scholar]
- 20.American psychiatric association. Washington, DC: American Psychiatric Association Publishing; 2022. p. 1, online resource. [Google Scholar]
- 21.Masheb RM, Grilo CM. Eating patterns and breakfast consumption in obese patients with binge eating disorder. Behav Res Ther 2006;44:1545–53. [DOI] [PubMed] [Google Scholar]
- 22.Harvey K, Rosselli F, Wilson GT, et al. Eating patterns in patients with spectrum binge-eating disorder. Int J Eat Disord 2011;44:447–51. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Hudson JI, Hiripi E, Pope HG Jr, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry 2007; 61:348–58. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Fairburn CG. Cognitive behavior therapy and eating disorders. New York: Guilford Press; 2008. p. 324, xii. [Google Scholar]
- 25.Murphy R, Straebler S, Cooper Z, et al. Cognitive behavioral therapy for eating disorders. Psychiatr Clin North Am 2010;33:611–27. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Moberg LT, Solvang B, Saele RG, et al. Effects of cognitive-behavioral and psychodynamic-interpersonal treatments for eating disorders: a meta-analytic inquiry into the role of patient characteristics and change in eating disorder-specific and general psychopathology in remission. J Eat Disord 2021;9:74. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Atwood ME, Friedman A. A systematic review of enhanced cognitive behavioral therapy (CBT-E) for eating disorders. Int J Eat Disord 2020;53:311–30. [DOI] [PubMed] [Google Scholar]
- 28.Agras WS, Fitzsimmons-Craft EE, Wilfley DE. Evolution of cognitive-behavioral therapy for eating disorders. Behav Res Ther 2017;88:26–36. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Scheer FA, Hilton MF, Mantzoros CS, et al. Adverse metabolic and cardiovascular consequences of circadian misalignment. Proc Natl Acad Sci U S A 2009;106: 4453–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Petersen MC, Gallop MR, Flores Ramos S, et al. Complex physiology and clinical implications of time-restricted eating. Physiol Rev 2022;102:1991–2034. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Golombek DA, Rosenstein RE. Physiology of circadian entrainment. Physiol Rev 2010;90:1063–102. [DOI] [PubMed] [Google Scholar]
- 32.Zarrinpar A, Chaix A, Panda S. Daily Eating Patterns and Their Impact on Health and Disease. TEM (Trends Endocrinol Metab) 2016;27:69–83. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Mure LS, Le HD, Benegiamo G, et al. Diurnal transcriptome atlas of a primate across major neural and peripheral tissues. Science 2018;359:eaao0318. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Zhang R, Lahens NF, Ballance HI, et al. A circadian gene expression atlas in mammals: implications for biology and medicine. Proc Natl Acad Sci U S A 2014;111:16219–24. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Lopez-Otin C, Kroemer G. Hallmarks of Health. Cell 2021;184:33−−63. [DOI] [PubMed] [Google Scholar]
- 36.Valladares M, Obregon AM, Chaput JP. Association between genetic variants of the clock gene and obesity and sleep duration. J Physiol Biochem 2015;71: 855–60. [DOI] [PubMed] [Google Scholar]
- 37.Torrego-Ellacuria M, Barabash A, Matia-Martin P, et al. Influence of CLOCK Gene Variants on Weight Response after Bariatric Surgery. Nutrients 2022;14:3472. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.Wright KP Jr, McHill AW, Birks BR, et al. Entrainment of the human circadian clock to the natural light-dark cycle. Curr Biol 2013;23:1554–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Manella G, Sabath E, Aviram R, et al. The liver-clock coordinates rhythmicity of peripheral tissues in response to feeding. Nat Metab 2021;3:829–42. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Wang F, Zhang L, Zhang Y, et al. Meta-analysis on night shift work and risk of metabolic syndrome. Obes Rev 2014;15:709–20. [DOI] [PubMed] [Google Scholar]
- 41.Sun M, Feng W, Wang F, et al. Meta-analysis on shift work and risks of specific obesity types. Obes Rev 2018;19:28–40. [DOI] [PubMed] [Google Scholar]
- 42.Vyas MV, Garg AX, Iansavichus AV, et al. Shift work and vascular events: systematic review and meta-analysis. BMJ 2012;345:e4800. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Kim CW, Yun KE, Jung HS, et al. Sleep duration and quality in relation to non-alcoholic fatty liver disease in middle-aged workers and their spouses. J Hepatol 2013;59:351–7. [DOI] [PubMed] [Google Scholar]
- 44.Bernsmeier C, Weisskopf DM, Pflueger MO, et al. Sleep Disruption and Daytime Sleepiness Correlating with Disease Severity and Insulin Resistance in Non-Alcoholic Fatty Liver Disease: A Comparison with Healthy Controls. PLoS One 2015; 10:e0143293. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Imaizumi H, Takahashi A, Tanji N, et al. The Association between Sleep Duration and Non-Alcoholic Fatty Liver Disease among Japanese Men and Women. Obesity facts 2015;8:234–42. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46.Hsieh SD, Muto T, Murase T, et al. Association of short sleep duration with obesity, diabetes, fatty liver and behavioral factors in Japanese men. Intern Med 2011;50: 2499–502. [DOI] [PubMed] [Google Scholar]
- 47.Liu C, Zhong R, Lou J, et al. Nighttime sleep duration and risk of nonalcoholic fatty liver disease: the Dongfeng-Tongji prospective study. Ann Med 2016;48: 468–76. [DOI] [PubMed] [Google Scholar]
- 48.Marin-Alejandre BA, Abete I, Cantero I, et al. Association between Sleep Disturbances and Liver Status in Obese Subjects with Nonalcoholic Fatty Liver Disease: A Comparison with Healthy Controls. Nutrients 2019;11:322. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 49.Saran AR, Dave S, Zarrinpar A. Circadian Rhythms in the Pathogenesis and Treatment of Fatty Liver Disease. Gastroenterology 2020;158:1948–1966 e1941. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 50.Sutton EF, Beyl R, Early KS, et al. , Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes, Cell Metabol, 27, 2018, 1212–1221 e1213. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 51.Che T, Yan C, Tian D, et al. Time-restricted feeding improves blood glucose and insulin sensitivity in overweight patients with type 2 diabetes: a randomised controlled trial. Nutr Metab 2021;18:88. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 52.Domaszewski P, Konieczny M, Pakosz P, et al. Effect of a Six-Week Intermittent Fasting Intervention Program on the Composition of the Human Body in Women over 60 Years of Age. Int J Environ Res Public Health 2020;17:4138. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 53.Peeke PM, Greenway FL, Billes SK, et al. Effect of time restricted eating on body weight and fasting glucose in participants with obesity: results of a randomized, controlled, virtual clinical trial. Nutr Diabetes 2021;11:6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 54.Jamshed H, Steger FL, Bryan DR, et al. , Effectiveness of Early Time-Restricted Eating for Weight Loss, Fat Loss, and Cardiometabolic Health in Adults With Obesity: A Randomized Clinical Trial, JAMA Intern Med, 182, 2022, 953–962. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 55.Kotarsky CJ, Johnson NR, Mahoney SJ, et al. Time-restricted eating and concurrent exercise training reduces fat mass and increases lean mass in overweight and obese adults. Physiol Rep 2021;9:e14868. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 56.Cai H, Qin YL, Shi ZY, et al. Effects of alternate-day fasting on body weight and dyslipidaemia in patients with non-alcoholic fatty liver disease: a randomised controlled trial. BMC Gastroenterol 2019;19:219. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 57.Chow LS, Manoogian ENC, Alvear A, et al. , Time-Restricted Eating Effects on Body Composition and Metabolic Measures in Humans who are Overweight: A Feasibility Study, Obesity, 28, 2020, 860–869. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 58.Lin YJ, Wang YT, Chan LC, et al. Effect of time-restricted feeding on body composition and cardio-metabolic risk in middle-aged women in Taiwan. Nutrition 2022; 93:111504. [DOI] [PubMed] [Google Scholar]
- 59.Liu D, Huang Y, Huang C, et al. Calorie Restriction with or without Time-Restricted Eating in Weight Loss. N Engl J Med 2022;386:1495–504. [DOI] [PubMed] [Google Scholar]
- 60.Lowe DA, Wu N, Rohdin-Bibby L, et al. Effects of Time-Restricted Eating on Weight Loss and Other Metabolic Parameters in Women and Men With Overweight and Obesity: The TREAT Randomized Clinical Trial. JAMA Intern Med 2020;180:1491–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 61.Thomas EA, Zaman A, Sloggett KJ, et al. Early time-restricted eating compared with daily caloric restriction: A randomized trial in adults with obesity. Obesity 2022;30:1027–38. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 62.Isenmann E, Dissemond J, Geisler S. The Effects of a Macronutrient-Based Diet and Time-Restricted Feeding (16:8) on Body Composition in Physically Active Individuals-A 14-Week Randomised Controlled Trial. Nutrients 2021;13:3122. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 63.Phillips NE, Mareschal J, Schwab N, et al. The Effects of Time-Restricted Eating versus Standard Dietary Advice on Weight, Metabolic Health and the Consumption of Processed Food: A Pragmatic Randomised Controlled Trial in Community-Based Adults. Nutrients 2021;13:1042. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 64.Manoogian ENC, Zadourian A, Lo HC, et al. Feasibility of time-restricted eating and impacts on cardiometabolic health in 24-h shift workers: The Healthy Heroes randomized control trial. Cell Metabol 2022;34:1442–56.e7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 65.Zarrinpar A, Chaix A, Yooseph S, et al. Diet and feeding pattern affect the diurnal dynamics of the gut microbiome. Cell Metabol 2014;20:1006–17. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 66.Dantas Machado AC, Brown SD, Lingaraju A, et al. Diet and feeding pattern modulate diurnal dynamics of the ileal microbiome and transcriptome. Cell Rep 2022;40:111008. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 67.Russell BJ, Brown SD, Siguenza N, et al. , Intestinal transgene delivery with native E. coli chassis allows persistent physiological changes, Cell, 185, 2022, 3263–3277 e3215. [DOI] [PMC free article] [PubMed] [Google Scholar]