Search

Marie-Pierre St-Onge,1 Gary Zammit,2 David M Reboussin,3 Samuel T Kuna,4 Mark H Sanders,8 Richard Millman,6 Anne B Newman,5 Thomas A Wadden,4 Rena R Wing,6 F Xavier Pi-Sunyer,1 Gary D Foster7 Sleep AHEAD Research Group*1New York Obesity Research Center, St Luke's/Roosevelt Hospital, New York, NY, USA; 2Clinilabs, New York, NY, USA; 3Department of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA; 4Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA; 5Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA, USA; 6Department of Psychiatry and Human Behavior, Brown University, Providence, RI, USA; 7Center for Obesity Research and Education, Temple University, Philadelphia, PA, USA; 8Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, PA, USA*A full list of the members of the Sleep AHEAD Research Group is available in an online appendixPurpose: Some studies have found an association between sleep disturbances and metabolic risk, but none has examined this association in individuals with type 2 diabetes. The objective of this study was to determine the relationship between sleep disturbances and metabolic risk factors in obese patients with type 2 diabetes.Patients and methods: This study was a cross-sectional examination of the relationship between sleep parameters (apnea/hypopnea index [AHI], time spent in various sleep stages) and metabolic risk markers (fasting glucose, hemoglobin A1c, lipids) using baseline data of the Sleep AHEAD cohort. Subjects (n = 305) were participants in Sleep AHEAD (Action for Health in Diabetes), a four-center ancillary study of the Look AHEAD study, a 16-center clinical trial of overweight and obese participants with type 2 diabetes, designed to assess the long-term effects of an intensive lifestyle intervention on cardiovascular events. All participants underwent one night of in-home polysomnography and provided a fasting blood sample. Regression analyses estimated the relationship between sleep variables and metabolic risk factors. Models were adjusted for study center, age, sex, race/ethnicity, waist circumference, smoking, alcohol intake, diabetes duration, and relevant medications.Results: Of 60 associations tested, only one was significant: fasting glucose was associated with sleep efficiency (estimate −0.53 ± [standard error] 0.26, P = 0.041). No associations were found between any of the sleep variables and lipid profile or hemoglobin A1c.Conclusions: The present data show only weak associations between select sleep variables and metabolic risk factors and do not provide strong support for a role of sleep on metabolic abnormalities in obese patients with type 2 diabetes.Keywords: obesity, obstructive sleep apnea, metabolic risk, sleep, diabetes

St-Onge MP, Jones PJ. J Nutr 2002;132:329-332. Medium chain fatty acids (MCFA) are readily oxidized in the liver. Animal and human studies have shown that the fast rate of oxidation [...]

Background: The consumption of ultra-processed foods (UPF) is on the rise worldwide, and it has been linked to numerous health conditions, such as diabetes, obesity, and cancer. Few studies have focused on the effect of UPF consumption on sleep health and even fewer on chronic insomnia., Objective: This study investigated the association between UPF intake and chronic insomnia in a large population-based sample., Design: This was a cross-sectional analysis using the NutriNet-Santé study data, an ongoing Web cohort in France., Participants/setting: Thirty-eight thousand five hundred seventy adult males and females who had completed a sleep questionnaire (2014) and at least two 24-hour dietary records were included in the analysis., Main Outcomes Measures: Chronic insomnia was defined according to established criteria. Categorization of food and beverages as UPF was based on the NOVA-Group 4 classification., Statistical Analyses Performed: The cross-sectional association between UPF intake and chronic insomnia was assessed using multivariable logistic regression., Results: Among the 38,570 participants (mean age, 50.0 ±14.8 years, 77.0% female) included in the analysis, 19.4% had symptoms of chronic insomnia. On average, UPF represented 16% of the total amount (g/day) of the overall dietary intake. In the fully adjusted model, UPF consumption was associated with higher odds of chronic insomnia (odds ratio [OR] for an absolute 10% greater UPF intake in the diet = 1.06; 95% confidence interval [CI]: 1.02-1.09). Sex-specific OR for chronic insomnia for an absolute 10% greater UPF intake in the diet were 1.09 (1.01-1.18) among males and 1.05 (1.01-1.09) among females., Conclusions: This large epidemiological study revealed a statistically significant association between UPF intake and chronic insomnia, independent of sociodemographic, lifestyle, diet quality, and mental health status covariates. The findings provide insights for future longitudinal research as well as nutrition- and sleep-focused intervention and prevention programs., (Copyright © 2024 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.)

An emerging field of research has revealed a bidirectional relationship between sleep and diet, highlighting the potential role of a healthy diet in improving sleep. However, the impact of chrono-nutrition on sleep remains less explored. Here we conducted a systematic scoping review, considering the multiple dimensions of chrono-nutrition, to describe the extent, range, and nature of the existing literature in this area (PROSPERO: CRD42021274637). There has been a significant increase in the literature exploring this topic over the past six years (almost 67 % of the evolving literature). A breakdown of the included studies was performed according to three major chrono-nutritional dimensions: meal timing [n = 35], irregular eating patterns [n = 84], and frequency of eating occasions [n = 3]. Meal timing included three sub-dimensions: breakfast skipping [n = 13], late eating [n = 16], and earlier vs later meals schedules [n = 6]. Irregular meal patterns included three sub-dimensions: diurnal fasting [n = 65], intermittent fasting [n = 16], and daily meal patterns [n = 3]. Frequency was the least studied dimension (n = 3). We provided a synthetic and illustrative framework underlining important preliminary evidence linking the temporal characteristics of eating patterns to various facets of sleep health. Nonetheless, much work remains to be done to provide chrono-nutrition guidelines to improve sleep health in the general population., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Chrononutrition is a rapidly evolving field of nutritional epidemiology that addresses the complex relationship between temporal eating patterns, circadian rhythms, and metabolic health, but most prior research has focused on the cardiometabolic consequences of time-restricted feeding and intermittent fasting. The purpose of this topical review is to summarize epidemiological evidence from observational and intervention studies regarding the role of chrononutrition metrics related to eating timing and regularity in cardiometabolic health preservation and cardiovascular disease prevention. Observational studies are limited due to the lack of time-stamped diet data in most population-based studies. Findings from cohort studies generally indicate that breakfast skipping or the later timing of the first eating occasion, a later lunch and dinner, and a greater proportion of caloric intake consumed in the evening are associated with adverse cardiometabolic outcomes, including higher risk for coronary heart disease, hypertension, type 2 diabetes, obesity, dyslipidemia, and systemic inflammation. Randomized controlled trials are also limited, as most in the field of chrononutrition focus on the cardiometabolic consequences of time-restricted feeding. Overall, interventions that shift eating timing patterns to earlier in the day and that restrict evening caloric intake tend to have protective effects on cardiometabolic health, but small sample sizes and short follow-up are notable limitations. Innovation in dietary assessment approaches, to develop low-cost validated tools with acceptable participant burden that reliably capture chrononutrition metrics, is needed for advancing observational evidence. Culturally responsive pragmatic intervention studies with sufficiently large and representative samples are needed to understand the impact of fixed and earlier eating timing schedules on cardiometabolic health. Additional research is warranted to understand the modifiable determinants of temporal eating patterns, to investigate the role of chrononutrition in the context of other dimensions of diet (quantity, quality, and food and nutrition security) in achieving cardiometabolic health equity, and to elucidate underlying physiological mechanisms.

This observational pilot study examined the association between diet, meal pattern and glucose over a 2-week period under free-living conditions in 26 adults with dysglycemia (D-GLYC) and 14 with normoglycemia (N-GLYC). We hypothesized that a prolonged eating window and late eating occasions (EOs), along with a higher dietary carbohydrate intake, would result in higher glucose levels and glucose variability (GV). General linear models were run with meal timing with time-stamped photographs in real time, and diet composition by dietary recalls, and their variability (SD), as predictors and glucose variables (mean glucose, mean amplitude of glucose excursions [MAGE], largest amplitude of glucose excursions [LAGE] and GV) as dependent variables. After adjusting for calories and nutrients, a later eating midpoint predicted a lower GV (β = -2.3, SE = 1.0, p = 0.03) in D-GLYC, while a later last EO predicted a higher GV (β = 1.5, SE = 0.6, p = 0.04) in N-GLYC. A higher carbohydrate intake predicted a higher MAGE (β = 0.9, SE = 0.4, p = 0.02) and GV (β = 0.4, SE = 0.2, p = 0.04) in N-GLYC, but not D-GLYC. In summary, our data suggest that meal patterns interact with dietary composition and should be evaluated as potential modifiable determinants of glucose in adults with and without dysglycemia. Future research should evaluate causality with controlled diets.

Study Objectives: Poor sleep in adolescents can increase the risk of obesity, possibly due to changes in dietary patterns. Prior neuroimaging evidence, mostly in adults, suggests that lacking sleep results in increased response to food cues in reward-processing brain regions. Needed is a clarification of the mechanisms by which food reward processing is altered by the kind of chronic sleep restriction (SR) typically experienced by adolescents. This study aimed to elucidate the impact of sleep duration on response to visual food stimuli in healthy adolescents using functional neuroimaging, hypothesizing increased reward processing response after SR compared to a well-rested condition., Methods: Thirty-nine healthy adolescents, 14-17 years old, completed a 3-week protocol: (1) sleep phase stabilization; (2) SR (~6.5 h nightly); and (3) healthy sleep (HS) duration (~9 h nightly). Participants underwent functional MRI while performing a visual food paradigm. Contrasts of food versus nonfood responses were compared within-subject between conditions of SR and HS., Results: Under SR, there was a greater response to food stimuli compared to HS in a voxel cluster including the left ventral tegmental area and substantia nigra. No change in food appeal rating due to the sleep manipulation was detected., Conclusions: Outcomes of this study suggest that SR, as commonly experienced by healthy adolescents, results in the elevated dopaminergic drive of the reward network that may augment motivation to seek food in the context of individual food appeal and inhibitory profiles. Countermeasures that reduce food salience could include promoting consistent HS habits., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: Although sleep affects a range of waking behaviors, the majority of studies have focused on sleep loss with relatively little attention on sustained periods of adequate sleep. The goal of this study was to use an experimental design to examine the effect of both of these sleep patterns on cognitive performance in healthy adults., Methods: This study used a randomized crossover design. Participants who regularly slept 7-9 hours/night completed two 6-week intervention conditions, adequate sleep (maintenance of habitual bed/wake times) and insufficient sleep (reduction in sleep of 1.5 hours relative to adequate sleep), separated by a 2-6weeks (median=43days) washout period. Cognitive functioning was evaluated at baseline and endpoint of each intervention using the NIH Toolbox Cognition Battery. General linear models contrasted scores following each condition to the baseline of the first condition; the baseline of the second condition was included to evaluate practice effects., Results: Sixty-five participants (age 35.9 ± 4.9years, 89% women, 52% non-White race/ethnicity) completed study procedures. There was improvement in performance on the List Sorting Working Memory task after the adequate sleep condition that exceeded practice effects. Cognitive performance after insufficient sleep did not reach the level expected with practice and did not differ from baseline. A similar pattern was found on the Flanker Inhibitory Control and Attention task., Conclusions: These findings contribute to our understanding of the complex interplay between sleep and cognition and demonstrate that consistent, stable sleep of at least 7 hours/night improves working memory and response inhibition in healthy adults., Clinical Trial Registration: The manuscript reports on data from two clinical trials: Impact of Sleep Restriction on Performance in Adults (URL: https://clinicaltrials.gov/ct2/show/NCT02960776, ID Number: NCT02960776) and Impact of Sleep Restriction in Women (URL: https://clinicaltrials.gov/ct2/show/NCT02835261, ID Number: NCT02835261)., Competing Interests: Declaration of conflict of interest The authors have no conflicts of interest., (Copyright © 2024 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.)

Objective/background: Experimental studies suggest that sleep loss affects psychological outcomes. However, most studies focus on acute severe in-laboratory sleep restriction, with limited ecological validity. This study examines the impact of sustained mild sleep restriction (SR) on stress and distress among healthy adults in a naturalistic home environment., Patients/methods: We analyzed data from two randomized crossover studies. Individuals who regularly slept 7-9 h/night completed two 6-wk intervention phases separated by a 6-wk washout: habitual sleep (HS: maintenance of habitual bed and wake times) and SR (delayed bedtime by 1.5 h/night and maintenance of habitual wake time). Adherence to sleep duration requirements was verified with wrist actigraphy and daily sleep diaries during each intervention phase. Measures of perceived stress, subjective anxiety, subjective depression, rumination, and cortisol were collected at baseline and endpoint of each intervention phase., Results: Sixty-two participants (age 36.4 ± 14.0 y, 85.5 % women, 63.3 % racial/ethnic minority) were included in our analyses. Mean total sleep time was 7.4 ± 0.4 h/night during HS and 6.2 ± 0.4 h/night during SR (p < 0.001). Higher perceived stress (3.6 ± 1.0, p = 0.0007) and subjective anxiety (1.1 ± 0.5, p = 0.039) were observed after SR compared to HS. No effect of sleep condition was observed on subjective depression, rumination, and cortisol., Conclusions: Our findings suggest that prolonged mildly insufficient sleep, similar to what commonly experienced in the real world, can lead to increased perceived stress and subjective anxiety in healthy adults. Addressing sleep loss, even if mild, should be a key component of interventions aimed at promoting mental health in the general population., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Marie-Pierre St-Onge reports financial support was provided by National Institutes of Health. Marie-Pierre St-Onge reports financial support was provided by. Brooke Aggarwal reports financial support was provided by American Heart Association. Giada Benasi reports financial support was provided by National Institutes of Health., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: The American Heart Association (AHA), in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and metabolic syndrome) that contribute to cardiovascular health. The AHA Heart Disease and Stroke Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs)., Methods: The AHA, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States and globally to provide the most current information available in the annual Statistical Update with review of published literature through the year before writing. The 2024 AHA Statistical Update is the product of a full year's worth of effort in 2023 by dedicated volunteer clinicians and scientists, committed government professionals, and AHA staff members. The AHA strives to further understand and help heal health problems inflicted by structural racism, a public health crisis that can significantly damage physical and mental health and perpetuate disparities in access to health care, education, income, housing, and several other factors vital to healthy lives. This year's edition includes additional global data, as well as data on the monitoring and benefits of cardiovascular health in the population, with an enhanced focus on health equity across several key domains., Results: Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics., Conclusions: The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.

Background and Aims: Promising associations have been demonstrated between delayed last eating occasion and cardiorespiratory fitness in adults with heart failure (HF), however, it is unknown if time of eating is associated with clinical endpoints such as mortality. This study aimed to examine associations between time of eating variables and all-cause and cardiovascular mortality in the National Health and Nutrition Examination Survey (NHANES)., Methods and Results: Participants self-disclosed HF diagnosis. Two dietary recalls were obtained and categorical variables were created based on mean time of first eating occasion (8:31 AM), last eating occasion (7:33 PM) and eating window (11.02 h). Mortality was obtained through linkage to the National Death Index. Covariate-adjusted Cox proportional hazard regression models were created examining the association between time of eating and mortality. Participants (n = 991) were 68 (95 % CI 67-69) years of age, 52.6 (95 % CI 49.0-56.3)% men and had a body mass index of 32.5 (95 % CI 31.8-33.2) kg/m 2 with follow up time of 68.9 (95 % CI 64.8-72.9) person-months. When models were adjusted for time of eating variables and all other covariates, extending the eating window beyond 11.02 h was associated with decreased risk of cardiovascular (HR 0.36 [95 % CI 0.16-0.81]), but not all-cause mortality. Time of first and last eating occasions were not associated with mortality., Conclusions: In adults with HF, an extended eating window is associated with reduced risk for cardiovascular mortality. Randomized controlled trials should examine if extending the eating window can improve prognostic indicators such as cardiorespiratory fitness in this population., (Copyright © 2023 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Background: Sleep restriction (SR) has been shown to upregulate neuronal reward networks in response to food stimuli, but prior studies were short-term and employed severe SR paradigms., Objective: Our goal was to determine whether mild SR, achieved by delaying bedtimes by 1.5 h, influences neuronal networks responsive to food stimuli compared with maintained adequate sleep (AS) >7 h/night., Methods: A randomized controlled crossover study with 2 6-wk phases, AS (≥7 h sleep/night) and SR (-1.5 h/night relative to screening), was conducted. Adults with AS duration, measured using wrist actigraphy over a 2-wk screening period, and self-reported good sleep quality were enrolled. Resting-state and food-stimulated functional neuroimaging (fMRI) was performed at the endpoint of each phase. Resting-state fMRI data analyses included a priori region-of-interest seed-based functional connectivity, whole-brain voxel-wise analyses, and network analyses. Food task-fMRI analyses compared brain activity patterns in response to food cues between conditions. Paired-sample t tests tested differences between conditions., Results: Twenty-six participants (16 males; age 29.6 ± 5.3 y, body mass index 26.9 ± 4.0 kg/m 2 ) contributed complete data. Total sleep time was 7 h 30 ± 28 min/night during AS compared with 6 h 12 ± 26 min/night during SR. We employed different statistical approaches to replicate prior studies in the field and to apply more robust approaches that are currently advocated in the field. Using uncorrected P value of <0.01, cluster ≥10-voxel thresholds, we replicated prior findings of increased activation in response to foods in reward networks after SR compared with AS (right insula, right inferior frontal gyrus, and right supramarginal gyrus). These findings did not survive more rigorous analytical approaches (Gaussian Random Field theory correction at 2-tailed voxel P < 0.001, cluster P < 0.05)., Conclusions: The results suggest that mild SR leads to increased reward responsivity to foods but with low confidence given the failure to meet significance from rigorous statistical analyses. Further research is necessary to inform the mechanisms underlying the role of sleep on food intake regulation. This trial was registered at clinicaltrials.gov as NCT02960776., (Copyright © 2023 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

Objectives: This pilot randomized controlled study evaluates the feasibility and preliminary efficacy of a 7-week remote intervention combining well-being therapy and sleep hygiene to improve sleep and psychological outcomes among adults reporting poor sleep and distress., Methods: Thirty-one participants (81% women, 40.2 ± 13.0 y, 48% racial/ethnic minority) were recruited from the community during the COVID-19 pandemic through online and local advertisement, and randomized to well-being therapy+sleep hygiene or sleep hygiene-only. Study outcomes were evaluated by self-reported questionnaires administered at baseline and post-intervention and a daily sleep diary., Results: Compared to sleep hygiene-only, well-being therapy+sleep hygiene led to greater improvements in wake after sleep onset (time-by-group interaction: 3.6 ± 1.5 min, p  = .017), personal growth (β -3.0, 95%CI -5.2, -0.8, p  = .01), and purpose in life (β -3.5, 95%CI -6.1, -0.9, p  = .009). Anxiety, perceived stress, sleep quality, and insomnia symptoms improved similarly in both groups (between-group differences, p  > .05). Improvements in sleep quality, insomnia, and sleep duration were associated with reductions in multiple measures of psychological distress (all p  < .05)., Conclusions: These findings suggest that, in a non-clinical setting of individuals suffering from combined poor sleep and psychological distress, the addition of well-being therapy to sleep hygiene may provide additional benefits for sleep by promoting sleep continuity and well-being.

Objective: Insufficient sleep is associated with type 2 diabetes, yet the causal impact of chronic insufficient sleep on glucose metabolism in women is unknown. We investigated whether prolonged mild sleep restriction (SR), resembling real-world short sleep, impairs glucose metabolism in women., Research Design and Methods: Women (aged 20-75 years) without cardiometabolic diseases and with actigraphy-confirmed habitual total sleep time (TST) of 7-9 h/night were recruited to participate in this randomized, crossover study with two 6-week phases: maintenance of adequate sleep (AS) and 1.5 h/night SR. Outcomes included plasma glucose and insulin levels, HOMA of insulin resistance (HOMA-IR) values based on fasting blood samples, as well as total area under the curve for glucose and insulin, the Matsuda index, and the disposition index from an oral glucose tolerance test., Results: Our sample included 38 women (n = 11 postmenopausal women). Values are reported with ±SEM. Linear models adjusted for baseline outcome values demonstrated that TST was reduced by 1.34 ± 0.04 h/night with SR versus AS (P < 0.0001). Fasting insulin (β = 6.8 ± 2.8 pmol/L; P = 0.016) and HOMA-IR (β = 0.30 ± 0.12; P = 0.016) values were increased with SR versus AS, with effects on HOMA-IR more pronounced in postmenopausal women compared with premenopausal women (β = 0.45 ± 0.25 vs. β = 0.27 ± 0.13, respectively; P for interaction = 0.042). Change in adiposity did not mediate the effects of SR on glucose metabolism or change results in the full sample when included as a covariate., Conclusions: Curtailing sleep duration to 6.2 h/night, reflecting the median sleep duration of U.S. adults with short sleep, for 6 weeks impairs insulin sensitivity, independent of adiposity. Findings highlight insufficient sleep as a modifiable risk factor for insulin resistance in women to be targeted in diabetes prevention efforts., (© 2023 by the American Diabetes Association.)

Polyphenols are plant compounds with several biological activities. This review aims to summarize current knowledge on the potential role of polyphenols in modulating sleep. A total of 28 preclinical studies, 12 intervention studies and four observational studies exploring the role of polyphenol intake on sleep were identified. From animal studies, 26 out of the 28 studies found beneficial effects of polyphenols on sleep architecture. Three out of four human observational studies found a beneficial association between polyphenol intake and sleep parameters. And, among clinical intervention studies, eight from a total of 12 studies found some beneficial effect of polyphenol intake on various sleep parameters, although some discrepancies between studies were found. Overall, emerging evidence suggests a benefit of polyphenol intake on sleep. Several mechanisms of action have been suggested, ranging from effects on neurotransmitters to an action through the gut-brain axis. However, more research in this field is needed, emphasizing the use of nutritional doses in mechanistic studies and interventions targeting participants with sleep problems. This would allow to elucidate whether an additional biological effect of polyphenols is modulation of sleep, a behavior associated with adverse health outcomes., Competing Interests: Declaration of competing interest The authors have no conflict of interest to declare., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Purpose of Review: We summarized research on the bidirectional association between intake of ultra-processed food (UPF) and sleep., Recent Findings: Sleep contributes to cardiometabolic health in part via food intake patterns. Restricting sleep increases intakes of high-carbohydrate/high-fat foods, a profile representative of UPF. This systematic review covers the association of UPF intake, as an exposure or an outcome, and sleep. UPF was defined as NOVA Group 4. MEDLINE and EMBASE were searched through April 2023 for epidemiological studies with general-population adult samples. Fifteen studies met the inclusion criteria; all were cross-sectional, published between 2016 and 2023, with samples from Brazil (n = 8), Spain (n = 2), Italy (n = 1), the UK (n = 1), Paraguay (n = 1), Iran (n = 1) and China (n = 1). Thirteen studies examined UPF intake as the exposure whereas two tested UPF intake as the outcome. UPF intakes were determined using food frequency questionnaires (73%) or 24-h recalls (27%). Two studies assessed sleep via accelerometry; the remaining studies relied on self-reports of sleep quality, duration, anxiety-induced insomnia, and napping, with 60% using a single question. The average methodological quality across the studies was deemed "fair". Six of the 13 studies that examined UPF consumption as the exposure revealed inverse associations with sleep outcomes in adjusted (n = 5) or bivariate (n = 1) analyses. Both studies addressing UPF consumption as the outcome and sleep as the exposure showed significant inverse associations. Evidence for UPF-sleep associations is accumulating, although sleep assessment limitations are apparent. This review can provide impetus for research using comprehensive and validated sleep measures and nudge policymakers towards refining dietary guidelines worldwide., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Study Objectives: Insufficient sleep leads to overconsumption, but the factors contributing to this effect are poorly understood. Therefore, we assessed the influence of prolonged curtailment of sleep on free-living eating patterns linked with overconsumption and explored associations of these eating patterns with diet quality under different sleep conditions., Methods: Sixty-five adults (47 females) participated in outpatient randomized crossover studies with two 6-week conditions: adequate sleep (7-9 h/night) and sleep restriction (-1.5 h/night relative to screening). Food records were collected over 3 nonconsecutive days, from which we ascertained data on eating frequency, midpoint, and window and intakes of energy and nutrients. Linear mixed models were used to assess the impact of sleep condition on change in eating pattern (sleep × week interaction) and the relation between eating patterns and dietary intakes (sleep × eating pattern interaction)., Results: Sleep condition impacted the change in eating frequency across weeks, with eating frequency increasing in sleep restriction relative to adequate sleep (β = 0.3 ± 0.1; P = .046). Across conditions, eating more frequently tended to relate to higher energy intakes (β = 60.5 ± 34.6; P = .082). Sleep also influenced the relation of variability in eating midpoint with intakes of saturated fat (β = 6.0 ± 2.1; P = .005), polyunsaturated fat (β = -3.9 ± 2.0; P = .051), and added sugar (β = 17.3 ± 6.2; P = .006), with greater midpoint variability associated with more adverse changes in these diet quality components in sleep restriction vs adequate sleep., Conclusions: Chronic short sleep increases eating frequency and adversely influences associations of variability in meal timing with components of diet quality. These findings help to explain how short sleep leads to overconsumption and obesity., Clinical Trial Registration: Registry: ClinicalTrials.gov; Name: Impact of Sleep Restriction in Women; URL: https://clinicaltrials.gov/ct2/show/NCT02835261; Identifier: NCT02835261 and Name: Impact of Sleep Restriction on Performance in Adults; URL: https://clinicaltrials.gov/ct2/show/NCT02960776; Identifier: NCT02960776., Citation: Barragán R, Zuraikat FM, Tam V, RoyChoudhury A, St-Onge M-P. Changes in eating patterns in response to chronic insufficient sleep and their associations with diet quality: a randomized trial. J Clin Sleep Med . 2023;19(11):1867-1875., (© 2023 American Academy of Sleep Medicine.)

Background Insufficient sleep is associated with increased cardiovascular disease risk, but causality is unclear. We investigated the impact of prolonged mild sleep restriction (SR) on lipid and inflammatory profiles. Methods and Results Seventy-eight participants (56 women [12 postmenopausal]; age, 34.3±12.5 years; body mass index, 25.8±3.5 kg/m 2 ) with habitual sleep duration 7 to 9 h/night (adequate sleep [AS]) underwent two 6-week conditions in a randomized crossover design: AS versus SR (AS-1.5 h/night). Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol, triglycerides, and inflammatory markers (CRP [C-reactive protein], interleukin 6, and tumor necrosis factor-α) were assessed. Linear models tested effects of SR on outcomes in the full sample and by sex+menopausal status (premenopausal versus postmenopausal women+men). In the full sample, SR increased high-density lipoprotein cholesterol compared with AS (β=1.2±0.5 mg/dL; P =0.03). Sex+menopausal status influenced the effects of SR on change in total cholesterol ( P -interaction=0.04), LDL-C ( P -interaction=0.03), and interleukin 6 ( P -interaction=0.07). Total cholesterol and LDL-C decreased in SR versus AS in premenopausal women (total cholesterol: β=-4.2±1.9 mg/dL; P =0.03; LDL-C: β=-6.3±2.0 mg/dL; P =0.002). Given paradoxical effects of SR on cholesterol concentrations, we explored associations between changes in inflammation and end point lipids under each condition. Increases in interleukin 6 and tumor necrosis factor-α during SR tended to relate to lower LDL-C in premenopausal women (interleukin 6: β=-5.3±2.6 mg/dL; P =0.051; tumor necrosis factor-α: β=-32.8±14.2 mg/dL; P =0.027). Conclusions Among healthy adults, prolonged insufficient sleep does not increase atherogenic lipids. However, increased inflammation in SR tends to predict lower LDL-C in premenopausal women, resembling the "lipid paradox" in which low cholesterol associates with increased cardiovascular disease risk in proinflammatory conditions. Registration URL: https://www.clinicaltrials.gov; Unique identifiers: NCT02835261, NCT02960776.

Sleep restriction is associated with increased cardiovascular risk, which is more pronounced in female than male persons. We reported recently first causal evidence that mild, prolonged sleep restriction mimicking "real-life" conditions impairs endothelial function, a key step in the development and progression of cardiovascular disease, in healthy female persons. However, the underlying mechanisms are unclear. In model organisms, sleep restriction increases oxidative stress and upregulates antioxidant response via induction of the antioxidant regulator nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Here, we assessed directly endothelial cell oxidative stress and antioxidant responses in healthy female persons (n = 35) after 6 weeks of mild sleep restriction (1.5 h less than habitual sleep) using randomized crossover design. Sleep restriction markedly increased endothelial oxidative stress without upregulating antioxidant response. Using RNA-seq and a predicted protein-protein interaction database, we identified reduced expression of endothelial Defective in Cullin Neddylation-1 Domain Containing 3 (DCUN1D3), a protein that licenses Nrf2 antioxidant responses, as a mediator of impaired endothelial antioxidant response in sleep restriction. Thus, sleep restriction impairs clearance of endothelial oxidative stress that over time increases cardiovascular risk.Trial Registration: NCT02835261 ., (© 2023. Springer Nature Limited.)

Background: Daytime sleepiness is common in older adults and may result from poor nighttime sleep due to sleep disordered breathing, fragmented sleep, or other sleep disorders. Daytime sleepiness may be associated with cognition in older adults., Objectives: We investigated the association between self-reported daytime sleepiness and cognitive function in the Look AHEAD clinical trial., Design: Observational follow-up of a randomized clinical trial of an intensive lifestyle intervention., Setting: Clinic., Participants: Participants (n=1,778) aged 45-76 years at baseline with type 2 diabetes and overweight or obesity., Interventions: Participants were randomized to an intensive lifestyle intervention for weight loss or a control condition of diabetes support and education., Measurements: Participants provided self-reported levels of daytime sleepiness at baseline and years 12-13. Cognitive function was assessed with a neurocognitive battery at years 12-13 and 18-20., Results: Participants who reported having frequent daytime sleepiness (often or always) performed significantly worse than others on the cognitive composite (-0.35; p-value=0.014) after controlling for covariates. When stratified by intervention arm, participants assigned to the intensive lifestyle intervention who reported often/always having daytime sleepiness performed worse on Digit Symbol Coding (-0.63; p-value=0.05) and Trail Making Part-B (-0.56; p-value=0.02) after controlling for covariates. Statistical interactions revealed associations between daytime sleepiness and the following covariates: race and ethnicity, APOE ε4 carrier status, baseline history of cardiovascular disease, and depression., Conclusions: Daytime sleepiness over ~13 years predicted poorer cognitive performance in older individuals who, by virtue of having diabetes and overweight/obesity, are at high risk for sleep disorders and cognitive impairment., Competing Interests: Adam Spira received honoraria for serving as a consultant to Merck and from Springer Nature Switzerland AG for guest editing special issues of Current Sleep Medicine Reports. The other authors report no conflicts of interest., (© The Authors 2023.)

Obesity and type 2 diabetes (T2D) are increasingly common worldwide. While these disorders have increased in prevalence over the past several decades, there has been a concomitant reduction in sleep duration. Short sleep duration has been associated with higher rates of obesity and T2D, and the causality of these associations and their directionality, continue to necessitate evaluation. In this review we consider the evidence that sleep is an intrinsic factor in the development of obesity and chronic metabolic disorders, such as insulin resistance and T2D, while evaluating a potential bi-directional association. We consider the evidence that diet and meal composition, which are known to impact glycemic control, may have both chronic and acute impact upon sleep. Moreover, we consider that postprandial nocturnal metabolism and peripheral glycemia may affect sleep quality. We propose putative mechanisms whereby acute effects of nighttime glucose excursions may lead to increased sleep fragmentation. We conclude that dietary manipulations, particularly with respect to carbohydrate quality, may confer sleep benefits. Future research may seek to evaluate the effectiveness of synergistic nutrient strategies to promote sleep quality, with particular attention to carbohydrate quality, quantity, and availability as well as carbohydrate to protein ratio., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Ultra-processed foods (UPF) are ubiquitous in the modern-day food supply and widely consumed. High consumption of these foods has been suggested to contribute to the development of obesity in adults. The purpose of this review is to present and evaluate current literature on the relationship between UPF consumption and adult obesity. Cross-sectional studies (n = 9) among different populations worldwide show a positive association between UPF consumption and obesity. Longitudinal studies (n = 7) further demonstrate a positive association between UPF consumption and development of obesity, suggesting a potential causal influence of UPF consumption on obesity risk. However, only one randomized controlled trial has tested the causality of this association. The study included in this review found greater energy intake and weight gain with consumption of a high UPF diet compared to a high unprocessed food diet. The potential mechanisms by which UPF increase the risk of obesity include increased energy intake due to increased sugar consumption, decreased fiber consumption, and decreased protein density; however, more research is needed. Overall, the evidence identified in the current review consistently support a positive relation between high UPF consumption and obesity. While there is a need for more experimental research to establish causality and elucidate the mechanisms, the sum of the evidence supports a need for research on treatment modalities that include reductions in UPF consumption for the management of adult obesity., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)

Objective: The aim of this study was to investigate the effect of sleep restriction (SR) on insulin sensitivity and energy metabolism in postmenopausal women., Methods: In a randomized crossover trial, 14 women underwent four nights of habitual sleep (HS, 100% normal sleep) and SR (60% of HS) while following a eucaloric diet. Outcomes included the following: (1) insulin sensitivity by hyperinsulinemic-euglycemic clamp, defined as the glucose infusion rate (GIR); (2) resting metabolism and substrate oxidation by indirect calorimetry; and (3) glucose, insulin, and C-peptide concentrations following a standard meal test., Results: Nine postmenopausal women (mean [SD], age 59 [4] years, BMI 28.0  [2.6] kg/m 2 ) were analyzed. Accelerometer-determined total time in bed was 8.4 ± 0.6 hours during HS versus 5.0 ± 0.4 hours during SR (38% reduction, p < 0.0001). SR reduced low-dose insulin GIR by 20% (HS: 2.55 ± 0.22 vs. SR: 2.03 ± 0.20 mg/kg/min; p = 0.01) and high-dose insulin GIR by 12% (HS: 10.48 ± 0.72 vs. SR: 9.19 ± 0.72 mg/kg/min; p < 0.001). SR reduced fat oxidation during high-dose insulin infusion (p < 0.01), and it did not alter resting energy metabolism., Conclusions: Four nights of SR reduced insulin sensitivity and fat oxidation in postmenopausal women. These findings underscore the role of insufficient sleep in metabolic dysfunction following menopause. Larger trials investigating how sleep disturbances cause metabolic dysfunction during menopause are needed across all stages of menopause., (© 2023 The Obesity Society.)

Objective: The aim of this study was to assess the prevalence and severity of sleep-disordered breathing (SDB) across racial/ethnic groups in 3702 pregnant people at 6 to 15 and 22 to 31 weeks gestational age, examine whether BMI modifies the association between race/ethnicity and SDB, and investigate whether interventions to reduce weight might reduce racial/ethnic disparities in SDB., Methods: Differences by race/ethnicity in SDB prevalence and severity were quantified via linear, logistic, or quasi-Poisson regression. Controlled direct effect was used to estimate whether intervening on BMI would remove/diminish differences by race/ethnicity in SDB severity., Results: This study comprised 61.2% non-Hispanic White (nHW), 11.9% non-Hispanic Black (nHB), 18.5% Hispanic, and 3.7% Asian people. SDB prevalence was higher for nHB compared with nHW pregnant people at 6 to 15 weeks (odds ratio [OR] 1.81, 95% CI [1.07, 2.97]), whereas at 21 to 32 weeks, Asian pregnant people had a higher SDB prevalence than nHW (OR 2.2, 95% CI [1.1, 4.0]). The severity of SDB differed across racial/ethnic groups in early pregnancy, with nHB pregnant people having a higher apnea-hypopnea index (AHI) (OR 1.35, 95% CI [1.07, 1.69]) compared with nHW. Having overweight/obesity was associated with a higher AHI (β = 2.36, 95% CI [1.97, 2.84]). Controlled direct effect analyses indicated that in early pregnancy, nHB and Hispanic pregnant people would have a lower AHI compared with nHW people had they had normal weight., Conclusions: This study extends knowledge on racial/ethnic disparities in SDB to a pregnant population., (© 2023 The Obesity Society.)

Background: There are bi-directional relationships between sleep disturbances and obesity, both of which are prevalent in patients with heart failure with preserved ejection fraction (HFpEF). However, little is known about the sleep-obesity association in HFpEF., Objectives: To determine associations of multidimensional sleep health, night movement, sleep fragmentation, and sleep-disordered breathing (SDB) risk with overall and regional adiposity in HFpEF patients., Methods: Men and women with HFpEF (n = 49) were assessed via 14-day actigraphy, Pittsburgh Sleep Quality Index, and Epworth Sleepiness Scale to derive multidimensional sleep health. SDB risk was assessed via Berlin Questionnaire. Body composition was measured using anthropometry; MRI quantification of epicardial, abdominal, liver, and thigh adipose tissue was performed in a subsample (n = 22). Spearman correlation (rs) and linear regression analyses (β coefficient) were used to estimate bivariate and age-adjusted associations., Results: Multidimensional sleep health was inversely associated with BMI (rs = -0.50, p < .001; unadjusted: β = -4.00, 95%CI: -5.87, -2.13; age-adjusted: β = -2.48, 95%CI: -4.65, -0.30), thigh subcutaneous adipose tissue (rs = -0.50, p = .018; unadjusted: β = -36.95, 95%CI: -67.31, -6.59), and thigh intermuscular fat (age-adjusted: β = -0.24, 95%CI: -0.48, -0.01). Night movement and sleep fragmentation were associated with greater intermuscular thigh and lower liver fat. High SDB risk was associated with a higher visceral-to-subcutaneous ratio of abdominal adiposity and lower thigh adiposity., Conclusions: Adverse multidimensional sleep health is associated with higher adiposity measures in HFpEF patients. Further studies are needed to determine whether intervening on sleep could ameliorate excess adiposity or whether weight loss could improve sleep quality in HFpEF., Competing Interests: Declaration of Competing Interest Dr. Shah has received research grants from Actelion, AstraZeneca, Corvia, Novartis, and Pfizer; and consulting fees from Abbott, Actelion, AstraZeneca, Amgen, Aria CV, Axon Therapies, Bayer, Boehringer-Ingelheim, Boston Scientific, Bristol-Myers Squibb, Cardiora, Coridea, CVRx, Cyclerion, Cytokinetics, Edwards Lifesciences, Eidos, Eisai, Imara, Impulse Dynamics, Intellia, Ionis, Ironwood, Lilly, Merck, MyoKardia, Novartis, Novo Nordisk, Pfizer, Prothena, Regeneron, Rivus, Sanofi, Shifamed, Tenax, Tenaya, and United Therapeutics. All other authors do not have any conflicts of interest to disclose related to the present submission., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Healthy individuals exhibit blood pressure variation over a 24-hour period with higher blood pressure during wakefulness and lower blood pressure during sleep. Loss or disruption of the blood pressure circadian rhythm has been linked to adverse health outcomes, for example, cardiovascular disease, dementia, and chronic kidney disease. However, the current diagnostic and therapeutic approaches lack sufficient attention to the circadian rhythmicity of blood pressure. Sleep patterns, hormone release, eating habits, digestion, body temperature, renal and cardiovascular function, and other important host functions as well as gut microbiota exhibit circadian rhythms, and influence circadian rhythms of blood pressure. Potential benefits of nonpharmacologic interventions such as meal timing, and pharmacologic chronotherapeutic interventions, such as the bedtime administration of antihypertensive medications, have recently been suggested in some studies. However, the mechanisms underlying circadian rhythm-mediated blood pressure regulation and the efficacy of chronotherapy in hypertension remain unclear. This review summarizes the results of the National Heart, Lung, and Blood Institute workshop convened on October 27 to 29, 2021 to assess knowledge gaps and research opportunities in the study of circadian rhythm of blood pressure and chronotherapy for hypertension.

Poor sleep quality and insufficient sleep affect a large portion of the population. This is concerning given increasing evidence that poor sleep health is a behavioral risk factor for the development of cardiometabolic diseases. A healthy diet is associated with a plethora of favorable health outcomes, and emerging research now highlights diet as a potential determinant of sleep health that could be leveraged to improve sleep quality. Dairy products are notably rich in tryptophan (Trp), a key substrate for serotonin and melatonin production, which are instrumental for initiating and maintaining sleep. Furthermore, dairy products provide a range of micronutrients that serve as cofactors in the synthesis of melatonin from Trp, which could contribute to sleep-promoting effects. In this review, we evaluate population studies and clinical trials to examine a possible link between dairy consumption and sleep. Available epidemiologic studies illustrate positive associations between dairy intake and sleep outcomes. Moreover, some intervention studies support a causal effect of dairy intake on sleep. Given these data, we discuss potential mechanisms, invite additional clinical research on this topic, and provide insights on how limitations of current studies can be addressed in future trials., (Copyright © 2023 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure, and glucose control) that contribute to cardiovascular health. The Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, congenital heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs)., Methods: The American Heart Association, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current information available in the annual Statistical Update with review of published literature through the year before writing. The 2023 Statistical Update is the product of a full year's worth of effort in 2022 by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. The American Heart Association strives to further understand and help heal health problems inflicted by structural racism, a public health crisis that can significantly damage physical and mental health and perpetuate disparities in access to health care, education, income, housing, and several other factors vital to healthy lives. This year's edition includes additional COVID-19 (coronavirus disease 2019) publications, as well as data on the monitoring and benefits of cardiovascular health in the population, with an enhanced focus on health equity across several key domains., Results: Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics., Conclusions: The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.

Circadian rhythms regulate the sleep-wake and feeding-fasting cycles. Sleep and feeding constitute a complex cycle that is determined by several factors. Despite the importance of sleep duration and mealtimes for many obesity phenotypes, most studies on dietary patterns have not investigated the contribution of these variables to the phenotypes analyzed. Likewise, they have not investigated the factors related to sleep or mealtimes. Thus, our aims were to investigate the link between taste perception and eating/sleep patterns and to analyze the effect of the interactions between sleep/meal patterns and genetic factors on obesity phenotypes. We conducted a cross-sectional analysis on 412 adults from the Mediterranean population. We measured taste perception (bitter, sweet, salty, sour, and umami) and assessed sleep duration and waketime. The midpoint of sleep and social jetlag was computed. From the self-reported timing of meals, we estimated the eating window, eating midpoint, and eating jetlag. Adherence to the Mediterranean diet was measured with a validated score. Selected polymorphisms in the TAS2R38, CLOCK, and FTO genes were determined, and their associations and interactions with relevant phenotypes were analyzed. We found various associations between temporal eating, sleep patterns, and taste perception. A higher bitter taste perception was associated with an earlier eating midpoint ( p = 0.001), breakfast time ( p = 0.043), dinner time ( p = 0.009), waketime ( p < 0.001), and midpoint of sleep ( p = 0.009). Similar results were observed for the bitter taste polymorphism TAS2R38-rs713598, a genetic instrumental variable for bitter perception, increasing the causality of the associations. Moreover, significant gene-sleep interactions were detected between the midpoint of sleep and the TAS2R38-rs713598 ( p = 0.032), FTO-rs9939609 ( p = 0.037), and CLOCK-rs4580704 ( p = 0.004) polymorphisms which played a role in determining obesity phenotypes. In conclusion, our study provided more information on the sleep and mealtime patterns of the general Spanish Mediterranean population than on their main relationships. Moreover, we were able to show significant associations between taste perception, specifically bitter taste; sleep time; and mealtimes as well as an interaction between sleep time and several genetic variants linked to obesity phenotypes. However, additional research is needed to better characterize the causality and mechanisms behind these associations.

Patients with primary mitochondrial oxidative phosphorylation (OxPhos) defects present with fatigue and multi-system disorders, are often lean, and die prematurely, but the mechanistic basis for this clinical picture remains unclear. By integrating data from 17 cohorts of patients with mitochondrial diseases (n = 690) we find evidence that these disorders increase resting energy expenditure, a state termed hypermetabolism. We examine this phenomenon longitudinally in patient-derived fibroblasts from multiple donors. Genetically or pharmacologically disrupting OxPhos approximately doubles cellular energy expenditure. This cell-autonomous state of hypermetabolism occurs despite near-normal OxPhos coupling efficiency, excluding uncoupling as a general mechanism. Instead, hypermetabolism is associated with mitochondrial DNA instability, activation of the integrated stress response (ISR), and increased extracellular secretion of age-related cytokines and metabokines including GDF15. In parallel, OxPhos defects accelerate telomere erosion and epigenetic aging per cell division, consistent with evidence that excess energy expenditure accelerates biological aging. To explore potential mechanisms for these effects, we generate a longitudinal RNASeq and DNA methylation resource dataset, which reveals conserved, energetically demanding, genome-wide recalibrations. Taken together, these findings highlight the need to understand how OxPhos defects influence the energetic cost of living, and the link between hypermetabolism and aging in cells and patients with mitochondrial diseases., (© 2023. The Author(s).)

Background: The timing and regularity of eating patterns could play a role in systemic inflammation, as circadian clocks responsible for daily rhythms of inflammatory signaling are entrained by food intake., Purpose: To evaluate associations of intra-weekly and weekday-weekend differences in eating timing patterns with high-sensitivity C-reactive protein (hsCRP)., Methods: A community-based sample of 103 U.S. women from the American Heart Association Go Red for Women Strategically Focused Research Network completed a meal-timing questionnaire and provided a blood sample for measurement of hsCRP. Differences in weekday versus weekend eating start time, eating end time, and nightly fasting duration were calculated as eating jetlag metrics. Intra-weekly variability in eating timing patterns was defined by the standard deviation (SD) of these variables. Multivariable linear regression models were used to evaluate cross-sectional associations of eating timing variability metrics with hsCRP., Results: Each additional 30-min difference in weekday-weekend eating end time was related to 13% higher hsCRP (p = .023). Similarly, every 30-min increase in eating end time SD, reflecting greater variability in timing of last eating occasion, was associated with 29% higher hsCRP. Per 1-hr weekday-weekend difference in nightly fasting duration, there was a 45% elevation in hsCRP (p = .003). Every 30-min increase in nightly fasting duration SD, representing greater variability in span of the daily fasting/eating periods, was associated with 46% higher hsCRP., Conclusions: Variable eating timing patterns were associated with higher hsCRP. Intervention studies are needed to determine whether stabilizing the timing of eating occasions may represent a novel strategy to reduce chronic inflammation., (© Society of Behavioral Medicine 2022. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Objective: This study investigated the effects of circadian misalignment (CM), induced by delaying mealtimes, independent of sleep timing and duration and eating window duration, on energy expenditure (EE), respiratory quotient (RQ), and substrate oxidation., Methods: Healthy adults, aged 20 to 49 years, participated in this randomized crossover study under controlled feeding conditions. Eating window duration was identical in both conditions (circadian alignment [CA]: 9:00 am-7:00 pm; CM: 1:00 pm-11:00 pm), and bedtimes were constant (11:30 pm-8:00 am). EE, RQ, and substrate oxidation were obtained over 23 hours in a metabolic chamber on days 3 and 4 and days 14 and 15 in each condition. Twenty-four-hour and post-meal outcomes were analyzed using a linear mixed-effects model including condition, day, and day-by-condition interaction as main predictors and sex as a covariate., Results: Three men and four women (age 37.4 ± 8.8 years, BMI 30.4 ± 3.3 kg/m 2 ) completed the study. Twenty-four-hour EE did not differ between conditions. Post-meal RQ for dinner and snack was higher in CM versus CA (both p < 0.001) with correspondingly higher glucose oxidation (both p < 0.01) and lower fat oxidation (dinner only p = 0.0001)., Conclusions: CM, induced by delaying mealtimes by 4 hours relative to CA, independently shifts nutrient metabolism toward greater carbohydrate and lower fat oxidation., (© 2022 The Obesity Society.)

Background: Daily rhythms are observed in humans and almost all other organisms. Most of these observed rhythms reflect both underlying endogenous circadian rhythms and evoked responses from behaviours such as sleep/wake, eating/fasting, rest/activity, posture changes and exercise. For many research and clinical purposes, it is important to understand the contribution of the endogenous circadian component to these observed rhythms., Content: The goal of this manuscript is to provide guidance on best practices in measuring metrics of endogenous circadian rhythms in humans and promote the inclusion of circadian rhythms assessments in studies of health and disease. Circadian rhythms affect all aspects of physiology. By specifying minimal experimental conditions for studies, we aim to improve the quality, reliability and interpretability of research into circadian and daily (i.e., time-of-day) rhythms and facilitate the interpretation of clinical and translational findings within the context of human circadian rhythms. We describe protocols, variables and analyses commonly used for studying human daily rhythms, including how to assess the relative contributions of the endogenous circadian system and other daily patterns in behaviours or the environment. We conclude with recommendations for protocols, variables, analyses, definitions and examples of circadian terminology., Conclusion: Although circadian rhythms and daily effects on health outcomes can be challenging to distinguish in practice, this distinction may be important in many clinical settings. Identifying and targeting the appropriate underlying (patho)physiology is a medical goal. This review provides methods for identifying circadian effects to aid in the interpretation of published work and the inclusion of circadian factors in clinical research and practice., (© 2022 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.)

A sleepless night may feel awful in its aftermath, but sleep's revitalizing powers are substantial, perpetuating the idea that convalescent sleep is a consequence-free physiological reset. Although recent studies have shown that catch-up sleep insufficiently neutralizes the negative effects of sleep debt, the mechanisms that control prolonged effects of sleep disruption are not understood. Here, we show that sleep interruption restructures the epigenome of hematopoietic stem and progenitor cells (HSPCs) and increases their proliferation, thus reducing hematopoietic clonal diversity through accelerated genetic drift. Sleep fragmentation exerts a lasting influence on the HSPC epigenome, skewing commitment toward a myeloid fate and priming cells for exaggerated inflammatory bursts. Combining hematopoietic clonal tracking with mathematical modeling, we infer that sleep preserves clonal diversity by limiting neutral drift. In humans, sleep restriction alters the HSPC epigenome and activates hematopoiesis. These findings show that sleep slows decay of the hematopoietic system by calibrating the hematopoietic epigenome, constraining inflammatory output, and maintaining clonal diversity., (© 2022 McAlpine et al.)

Background Although sufficient and healthy sleep is inversely associated with cardiovascular disease (CVD) and its risk factors, the American Heart Association's Life's Simple 7 (LS7), as a measure of cardiovascular health (CVH), did not include sleep. We evaluated an expanded measure of CVH that includes sleep as an eighth metric in relation to CVD risk. Methods and Results The analytic sample consisted of MESA (Multi-Ethnic Study of Atherosclerosis) Sleep Study participants who had complete data on sleep characteristics from overnight polysomnography, 7-day wrist actigraphy, validated questionnaires, and the outcome. We computed the LS7 score and 4 iterations of a new CVH score: score 1 included sleep duration, score 2 included sleep characteristics linked to CVD in the literature (sleep duration, insomnia, daytime sleepiness, and obstructive sleep apnea), scores 3 and 4 included sleep characteristics associated with CVD in MESA (score 3: sleep duration and efficiency, daytime sleepiness, and obstructive sleep apnea; score 4: score 3+sleep regularity). Multivariable-adjusted logistic and Cox proportional hazards models evaluated associations of the LS7 and CVH scores 1 to 4 with CVD prevalence and incidence. Among 1920 participants (mean age: 69±9 years; 54% female), there were 95 prevalent CVD events and 93 incident cases (mean follow-up, 4.4 years). Those in the highest versus lowest tertile of the LS7 score and CVH scores 1 to 4 had up to 80% lower odds of prevalent CVD. The LS7 score was not significantly associated with CVD incidence (hazard ratio, 0.62 [95% CI, 0.37-1.04]). Those in the highest versus lowest tertile of CVH score 1, which included sleep duration, and CVH score 4, which included multidimensional sleep health, had 43% and 47% lower incident CVD risk (hazard ratio, 0.57 [95% CI, 0.33-0.97]; and hazard ratio, 0.53 [95% CI, 0.32-0.89]), respectively. Conclusions CVH scores that include sleep health predicted CVD risk in older US adults. The incorporation of sleep as a CVH metric, akin to other health behaviors, may enhance CVD primordial and primary prevention efforts. Findings warrant confirmation in larger cohorts over longer follow-up.

Insufficient sleep is highly prevalent in society and has tremendous negative health consequences. Despite the available treatments, there is continued demand for novel and natural strategies to promote better sleep. Dietary modifications could be a viable new target to improve sleep. A literature review using PubMed was conducted on studies that examined the relationship between diet composition (ie, macronutrients or special diets) and objectively assessed sleep quality. Twenty human studies (6 observational and 14 interventional) published between 1975 and March 2021 met the eligibility criteria and were included. The amount of dietary carbohydrates and fats was associated with both better and worse sleep quality indices. However, the type of carbohydrate and fat was an important factor in these associations, with diets higher in complex carbohydrates (eg, fiber) and healthier fats (eg, unsaturated) being associated with better sleep quality. Diets higher in protein were associated with better sleep quality. In general, diets rich in fiber, fruits, vegetables, and anti-inflammatory nutrients and lower in saturated fat (eg, Mediterranean diet) were associated with better sleep quality. The connection between diet and sleep quality warrants further investigation. Rigorous interventional studies of longer duration assessing the effects of whole foods, rather than isolated nutrients, and under free-living conditions, rather than in a research laboratory setting, as well as mechanistic studies are needed to better understand how dietary patterns relate to sleep quality. Future research could provide insights into whether dietary modifications could be an effective, personalized strategy for improving sleep quality in millions of Americans., (Copyright © 2022 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.)

Aging is a risk factor for several pathologies, restricting one's health span, and promoting chronic diseases (e.g., cardiovascular and neurodegenerative diseases), as well as cancer. Telomeres are regions of repetitive DNA located at chromosomal ends. Telomere length has been inversely associated with chronological age and has been considered, for a long time, a good biomarker of aging. Several lifestyle factors have been linked with telomere shortening or maintenance. However, the consistency of results is hampered by some methodological issues, including study design, sample size, measurement approaches, and population characteristics, among others. Therefore, we aimed to systematically review the current literature on the effects of three relevant lifestyle factors on telomere length in human adults: physical activity, smoking, and sleep. We conducted a qualitative systematic review of observational and intervention studies using the Preferred Reporting Item for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. The systematic literature search covered articles published in MEDLINE and EMBASE databases (from 2010 to 2020). A total of 1400 studies were identified; 83 were included after quality control. Although fewer sedentary activities, optimal sleep habits, and non- or ex-smoker status have been associated with less telomere shortening, several methodological issues were detected, including the need for more targeted interventions and standardized protocols to better understand how physical activity and sleep can impact telomere length and aging. We discuss the main findings and current limitations to gain more insights into the influence of these lifestyle factors on the healthy aging process.

Objectives: This brief narrative review aims to give an up-to-date overview of intuitive and mindful eating (I/ME) interventions with specific focus on cardiometabolic risk factors, including glucose, lipid profile, blood pressure and inflammatory markers., Content: I/ME intervention studies in adults which measured at least one physiological parameter other than weight were identified from PubMed. The clinical trial/randomized controlled trial filters and publication dates 2001 through April 2021 with variations of the following keywords were applied: intuitive eating, mindful eating, weight neutral. Ten articles were identified., Summary and Outlook: Of the 10 studies, seven showed I/ME interventions were more effective than control in at least one cardiometabolic outcome, two showed significant I/ME within-group improvements but no between-group differences, and one showed neither within-group nor between-group differences. Specifically, I/ME improved glucose levels among pregnant women with or without gestational diabetes, lipid profile among adults with overweight or obesity, blood pressure among participants with overweight and inflammatory markers among post-menopausal women with obesity. However, the positive impact of I/ME on each of these cardiometabolic parameters was not consistent across studies: of the six studies that examined glucose regulation, two demonstrated positive outcomes for I/ME group, whereas four found no effect compared to control. Three out of five studies had positive lipid effects, one out of five demonstrated systolic blood pressure (SBP) improvements and one of two showed improvements in inflammatory markers. Given these mixed results, more research is needed to understand the possible effectiveness of I/ME to improve cardiometabolic health., (© 2021 Walter de Gruyter GmbH, Berlin/Boston.)

The human circadian system consists of the master clock in the suprachiasmatic nuclei of the hypothalamus as well as in peripheral molecular clocks located in organs throughout the body. This system plays a major role in the temporal organization of biological and physiological processes, such as body temperature, blood pressure, hormone secretion, gene expression, and immune functions, which all manifest consistent diurnal patterns. Many facets of modern life, such as work schedules, travel, and social activities, can lead to sleep/wake and eating schedules that are misaligned relative to the biological clock. This misalignment can disrupt and impair physiological and psychological parameters that may ultimately put people at higher risk for chronic diseases like cancer, cardiovascular disease, and other metabolic disorders. Understanding the mechanisms that regulate sleep circadian rhythms may ultimately lead to insights on behavioral interventions that can lower the risk of these diseases. On February 25, 2021, experts in sleep, circadian rhythms, and chronobiology met virtually for the Keystone eSymposium "Sleep & Circadian Rhythms: Pillars of Health" to discuss the latest research for understanding the bidirectional relationships between sleep, circadian rhythms, and health and disease., (© 2021 New York Academy of Sciences.)