Myocardial infarction augments sleep to limit cardiac inflammation and damage.

Sleep is integral to cardiovascular health1,2. Yet, the circuits that connect cardiovascular pathology and sleep are incompletely understood. It remains unclear whether cardiac injury influences sleep and whether sleep-mediated neural outputs contribute to heart healing and inflammation. Here we report that in humans and mice, monocytes are actively recruited to the brain after myocardial infarction (MI) to augment sleep, which suppresses sympathetic outflow to the heart, limiting inflammation and promoting healing. After MI, microglia rapidly recruit circulating monocytes to the brain's thalamic lateral posterior nucleus (LPN) via the choroid plexus, where they are reprogrammed to generate tumour necrosis factor (TNF). In the thalamic LPN, monocytic TNF engages Tnfrsf1a-expressing glutamatergic neurons to increase slow wave sleep pressure and abundance. Disrupting sleep after MI worsens cardiac function, decreases heart rate variability and causes spontaneous ventricular tachycardia. After MI, disrupting or curtailing sleep by manipulating glutamatergic TNF signalling in the thalamic LPN increases cardiac sympathetic input which signals through the ß2-adrenergic receptor of macrophages to promote a chemotactic signature that increases monocyte influx. Poor sleep in the weeks following acute coronary syndrome increases susceptibility to secondary cardiovascular events and reduces the heart's functional recovery. In parallel, insufficient sleep in humans reprogrammes ß2-adrenergic receptor-expressing monocytes towards a chemotactic phenotype, enhancing their migratory capacity. Collectively, our data uncover cardiogenic regulation of sleep after heart injury, which restricts cardiac sympathetic input, limiting inflammation and damage.

Variable Eating Patterns: A Potential Novel Risk Factor for Systemic Inflammation in Women.

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.

Sleep and Diet: Mounting Evidence of a Cyclical Relationship.

Two factors intrinsic to health are diet and sleep. These two behaviors may well influence one another. Indeed, that insufficient sleep adversely impacts dietary intakes is well documented. On the other hand, diet may influence sleep via melatonin and its biosynthesis from tryptophan. Experimental data exist indicating that provision of specific foods rich in tryptophan or melatonin can improve sleep quality. Whole diets rich in fruits, vegetables, legumes, and other sources of dietary tryptophan and melatonin have been shown to predict favorable sleep outcomes. Although clinical trials are needed to confirm a causal impact of dietary patterns on sleep and elucidate underlying mechanisms, available data illustrate a cyclical relation between these lifestyle factors. We recommend adopting a healthful diet to improve sleep, which may further promote sustained favorable dietary practices.

Evening Chronotype Is Associated with Poorer Habitual Diet in US Women, with Dietary Energy Density Mediating a Relation of Chronotype with Cardiovascular Health.

BACKGROUND: An innate preference for later timing of sleep and activity, termed evening chronotype, is linked to poorer cardiovascular health (CVH). However, associations of chronotype with specific health behaviors in US women are not well characterized. Of particular interest is habitual diet, because <1% of US adults meet recommendations for a healthful diet. OBJECTIVES: We aimed to evaluate cross-sectional and prospective associations of chronotype with diet quantity and quality in US women, and to assess whether dietary energy density (ED), a robust predictor of cardiometabolic outcomes, mediates an established chronotype-CVH relation. METHODS: Data were collected from participants in the AHA Go Red for Women Strategically Focused Research Network cohort (aged 20-76 y; 61% racial/ethnic minority) at baseline (n = 487) and 1-y follow-up (n = 432). Chronotype (evening compared with morning/intermediate) and habitual diet were ascertained from the Morningness-Eveningness Questionnaire and an FFQ, respectively. Multivariable-adjusted linear regression models evaluated cross-sectional and prospective associations of chronotype with diet. Causal mediation analyses assessed whether dietary ED mediated a relation between chronotype and CVH, quantified using AHA Life's Simple 7 score, derived from clinical measurements and validated assessments of CVH components. RESULTS: Evening compared with morning/intermediate chronotype was associated with poorer diet quality, including lower intakes of plant protein (cross-sectional: ß = -0.63 ± 0.24, P < 0.01; prospective: ß = -0.62 ± 0.26, P = 0.01), fiber (cross-sectional: ß = -2.19 ± 0.65, P < 0.001; prospective: ß = -2.39 ± 0.66, P < 0.001), and fruits and vegetables (cross-sectional: ß = -1.24 ± 0.33, P < 0.001; prospective: ß = -1.15 ± 0.36, P = 0.001). Evening chronotype was also associated with higher dietary ED at baseline (ß = 0.20 ± 0.05, P = 0.001) and 1 y (ß = 0.19 ± 0.06, P = 0.001). Dietary ED was a partial mediator of the association between evening chronotype and poorer CVH (24.6 ± 9.1%, P < 0.01). CONCLUSIONS: Evening chronotype could contribute to unhealthful dietary patterns in US women, with higher dietary ED partially mediating the relation between eveningness and poorer CVH. Behavioral interventions to reduce dietary ED might mitigate cardiovascular disease risk in women with evening chronotype.

Sleep Regularity and Cardiometabolic Heath: Is Variability in Sleep Patterns a Risk Factor for Excess Adiposity and Glycemic Dysregulation?

PURPOSE OF REVIEW: Night-to-night variability in sleep patterns leads to circadian disruption and, consequently, could increase cardiometabolic risk. The purpose of this review is to summarize findings from studies published between 2015 and 2020 examining various measures of night-to-night variability in sleep in relation to metabolic syndrome (MetS), type 2 diabetes (T2D), and their risk factors. We illustrate a potential causal pathway between irregular sleep patterns and T2D, highlighting knowledge gaps along the way. RECENT FINDINGS: Across different measures of sleep variability, irregular sleep patterns were associated with poorer cardiometabolic outcomes. Higher standard deviations (SD) across nights of sleep duration and onset or midpoint of sleep were associated with increased odds of having MetS and clusters of metabolic abnormalities as well as greater adiposity and poorer glycemic control. Conversely, greater regularity of rest-activity patterns related to lower risk for T2D. Social jetlag was associated with glycemic dysregulation, adiposity, T2D, and MetS. These associations are often observed in both metabolically healthy and unhealthy individuals; both higher SD of sleep duration and social jetlag relate to poorer glucose regulation in individuals with diabetes. There is consistent evidence of associations of sleep variability with increased risk for adiposity, glucose dysregulation, T2D, and MetS. Although experimental evidence is needed to determine causation, there is support to recommend stabilizing sleep patterns for cardiometabolic risk prevention.

Variability in Sleep Patterns: an Emerging Risk Factor for Hypertension.

PURPOSE OF REVIEW: In this review, we summarize recent epidemiological data (2014-2019) that examine the association of sleep variability with blood pressure (BP), discuss potential underlying mechanisms, and highlight future research directions. RECENT FINDINGS: Higher standard deviations of sleep duration and sleep-onset timing were not related to BP. However, a higher Sleep Regularity Index score was associated with lower odds of hypertension. Studies on social jetlag, a prevalent form of sleep variability, reported null associations. In contrast, lower interdaily stability in circadian rest-activity rhythms, a measure of invariability in sleep-wake cycles between days and synchronization to light and dark cycles, was associated with higher BP and greater hypertension odds, particularly among non-shift workers. Sleep variability is consistently associated with risk factors for hypertension. Evidence on sleep variability and BP is limited and varies depending on the measure used to characterize day-to-day variability in sleep. Studies that identify and utilize a standard definition of sleep variability, incorporate a 24-h ambulatory BP monitoring, and ensure coinciding timing of sleep and BP measurements are necessary to disentangle these relationships.

Reciprocal Roles of Sleep and Diet in Cardiovascular Health: a Review of Recent Evidence and a Potential Mechanism.

PURPOSE OF REVIEW: This review investigates the potential bi-directional relation between sleep and diet in considering their contribution to cardiovascular health. We further explore the involvement of the gut microbiome in the relationships between poor sleep and dietary intakes and increased cardiovascular disease (CVD) risk. RECENT FINDINGS: There is strong evidence that sleep restriction leads to unhealthy food choices and increased energy intake. The diet may impact sleep, as well. Epidemiological studies show that higher adherence to a Mediterranean dietary pattern predicts healthier sleep. One factor that could underlie these relationships is the gut microbiome. Although data are mixed, there is some evidence that sleep restriction can influence the composition of the gut microbiome in humans. Similarly, Mediterranean diets and other plant-rich diets are related to increased diversity of the microbiota. At present, few studies have investigated the influence of the microbiome on sleep; however, limited evidence from epidemiological and intervention studies suggest that the composition of the microbiome may relate to sleep quality. More research is needed to better understand the role of the microbiome in the multi-directional relationship between sleep, diet, and CVD. There is growing evidence of a bi-directional relationship between sleep and the diet, which could act in concert to influence CVD risk. Diets such as the Mediterranean diet, comprised of high intakes of fruits, vegetables, and other plant-based foods, may promote healthy sleep and beneficial gut microflora. The gut microbiome may then underlie the relation between diet, sleep, and CVD risk.

Doggy bags and downsizing: Packaging uneaten food to go after a meal attenuates the portion size effect in women.

Serving larger portions leads to increased food and energy intake, but little is known about strategies to moderate this response. This study tested how the effect of portion size on meal intake was influenced by providing the option to take away uneaten food in a "doggy bag" (to-go container). Women were randomly assigned to one of two subject groups: a To-Go Group (n = 27) that was informed before each meal that their leftover food would be packaged to take away after the meal, and a Control Group (n = 26) that was not given this option. In a crossover design, subjects came to the lab once a week for four weeks to eat a dinner composed of five foods. Across meals, the portion size of all foods was varied (100%, 125%, 150%, and 175% of baseline). Results showed that the portion size effect, defined as the trajectory of intake across the weight of food served, differed significantly by subject group (P ≤ 0.025). In the Control Group, increasing the portion size of all foods led to substantial increases in intake (P < 0.0001); for every 100 g added to the baseline portion, women in this group consumed an additional mean (±SEM) of 64 ±â€¯12 g of food and 90 ±â€¯19 kcal, until intake leveled off. In contrast, intake of women in the To-Go Group increased by only 17 ±â€¯12 g and 19 ±â€¯18 kcal for every additional 100 g served; these increases did not differ significantly from zero (P > 0.15). Thus, the effect of portion size on intake was attenuated in the To-Go Group compared to the Control Group. These data indicate that packaging uneaten food after a meal could be an effective strategy to reduce overconsumption from large portions.

Comparing the portion size effect in women with and without extended training in portion control: A follow-up to the Portion-Control Strategies Trial.

Following a 1-year randomized controlled trial that tested how weight loss was influenced by different targeted strategies for managing food portions, we evaluated whether the effect of portion size on intake in a controlled setting was attenuated in trained participants compared to untrained controls. Subjects were 3 groups of women: 39 participants with overweight and obesity from the Portion-Control Strategies Trial, 34 controls with overweight and obesity, and 29 controls with normal weight. In a crossover design, on 4 different occasions subjects were served a meal consisting of 7 foods that differed in energy density (ED). Across the meals, all foods were varied in portion size (100%, 125%, 150%, or 175% of baseline). The results showed that serving larger portions increased the weight and energy of food consumed at the meal (P < .0001), and this effect did not differ across groups. Increasing portions by 75% increased food intake by a mean (±SEM) of 111 ±â€¯10 g (27%) and increased energy intake by 126 ±â€¯14 kcal (25%). Across all meals, however, trained participants had lower energy intake (506 ±â€¯15 vs. 601 ±â€¯12 kcal, P = .006) and lower meal ED (1.09 ±â€¯0.02 vs. 1.27 ±â€¯0.02 kcal/g; P = .003) than controls, whose intake did not differ by weight status. The lower energy intake of trained participants was attributable to consuming meals with a greater proportion of lower-ED foods than controls. These results further demonstrate the robust nature of the portion size effect and reinforce that reducing meal ED is an effective way to moderate energy intake in the presence of large portions.

Does the cost of a meal influence the portion size effect?

Serving larger portions leads to increased intake, but little is known about how the cost of a meal affects this response. Therefore, we tested whether the amount of money paid for a meal influenced the portion size effect at a lunch served in a controlled restaurant-style setting. In a crossover design, 79 adults (55 women; 24 men) came to the lab once a week for 4 weeks to eat a main dish of pasta with side dishes. Across weeks, the meal was varied in two factors: portion size of the main dish (400 g or 600 g) and cost of the meal (US$8 or $16). At discharge subjects completed questionnaires that assessed behaviors thought to influence the response to portion size and cost. Results showed that the portion size of the main dish had a significant effect on meal intake (P < 0.0001). The weight of food consumed at the meal increased by 18 ±â€¯2% (mean ±â€¯SEM 83 ±â€¯11 g) and energy intake increased by 20 ±â€¯2% (133 ±â€¯16 kcal) when the larger portion was served. These effects of portion size did not differ across the two levels of cost (both interactions P > 0.37) nor did meal cost have significant effects on meal intake (both P > 0.24). Subject scores for satiety responsiveness did, however, influence the effect of portion size on food intake (P = 0.0007). Serving larger portions led to increased intake in subjects with lower satiety responsiveness scores (P < 0.0001), but did not affect intake in those with higher scores. In summary, the effect of portion size on intake in a restaurant-style setting was not influenced by meal cost but was attenuated in individuals higher in satiety responsiveness.

Increasing the size of portion options affects intake but not portion selection at a meal.

In an environment with large portion sizes, allowing consumers more control over their portion selection could moderate the effects on energy intake. We tested whether having subjects choose a portion from several options influenced the amount selected or consumed when all portion sizes were systematically increased. In a crossover design, 24 women and 26 men ate lunch in the lab once a week for 3 weeks. At each meal, subjects chose a portion of macaroni and cheese from a set of 3 portion options and consumed it ad libitum. Across 3 conditions, portion sizes in the set were increased; the order of the conditions was counterbalanced across subjects. For women the portion sets by weight (g) were 300/375/450, 375/450/525, and 450/525/600; for men the portions were 33% larger. The results showed that increasing the size of available portions did not significantly affect the relative size selected; across all portion sets, subjects chose the smallest available portion at 59% of meals, the medium at 27%, and the largest at 15%. The size of portions offered did, however, influence meal intake (P < 0.0001). Mean intake (±SEM) was 16% greater when the largest set was offered (661 ± 34 kcal) than when the medium and smallest sets were offered (both 568 ± 18 kcal). These results suggest that portions are selected in relation to the other available options, and confirm the robust effect of portion size on intake. Although presenting a choice of portions can allow selection of smaller amounts, the sizes offered are a critical determinant of energy intake. Thus, the availability of choices could help to moderate intake if the portions offered are within an appropriate range for energy needs.

Emolabeling increases healthy food choices among grade school children in a structured grocery aisle setting.

Health literacy, the ability to acquire health-related knowledge and make appropriate health-related decisions, is regarded as a key barrier to meaningfully convey health information to children and can impact food choice. Emolabeling is an image-based labeling strategy aimed at addressing this problem by conveying health information using emotional correlates of health using emoticons (happy = healthy; sad = not healthy). To test the utility of such a method to promote healthy food choices among children, 64 children (59% girls, <5% non-White, mean BMI = 52nd percentile) in kindergarten through 5th grade were first given a brief 5-min lesson on how to use the emoticons, then asked to choose any 4 foods in each of 2 aisles structured to mimic a grocery aisle - there were 12 identical foods placed in the same location in each aisle with half being low calorie and half high calorie snacks. Foods were emolabeled in one aisle; no emolabels were used in the other aisle; the order that children were brought in each aisle was counterbalanced. Results showed that adding emolabels increased the number (M ± SD) of healthy foods chosen (3.6 ± 0.7 with vs. 2.3 ± 1.1 without emolabels present [95% CI 1.0, 1.5], R(2) = .67) and reduced the total calories (M ± SD) of foods chosen (193.5 ± 88.5 Cal with vs. 374.3 ± 152.6 Cal without emolabels present [95% CI -212.6, -149.0], R(2) = .70). Hence, adding emolabels was associated with healthier food choices among children, thereby demonstrating one possible strategy to effectively overcome health literacy barriers at these ages.

Proximity of foods in a competitive food environment influences consumption of a low calorie and a high calorie food.

The objective of this study was to test if proximity of a food or preference for a food influences food intake in a competitive food environment in which one low calorie/low fat (apple slices) and one higher calorie/higher fat (buttered popcorn) food was available in the same environment. The proximity of popcorn and apple slices was manipulated and 56 participants were randomly assigned to groups. In Group Apples Near, apple slices were placed near (within arms reach) a participant and popcorn was placed far (2m away). In Group Popcorn Near, buttered popcorn was placed near and apple slices were placed far. As a control for the absence of a proximity manipulation, Group Both Near had both test foods placed near. Although participants rated the popcorn as more liked than apples, the food that was placed closer to the participant was consumed most in the two experimental groups, regardless of preference (R(2)=0.38). Total energy intake was reduced most when popcorn was placed far from a participant compared to when it was placed near (R(2)=0.24). The effects reported here were not moderated by BMI and did not vary by sex. In all, the results support the hypothesis that making a low calorie food more proximate will reduce total energy intake and increase intake of a low calorie food, even when a higher calorie and more preferred food is also available, but less proximate.

Chronic Insufficient Sleep in Women Impairs Insulin Sensitivity Independent of Adiposity Changes: Results of a Randomized Trial.

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 (ß = 6.8 ± 2.8 pmol/L; P = 0.016) and HOMA-IR (ß = 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 (ß = 0.45 ± 0.25 vs. ß = 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.

Psychobiological regulation of plasma and saliva GDF15 dynamics in health and mitochondrial diseases.

GDF15 (growth differentiation factor 15) is a marker of cellular energetic stress linked to physical-mental illness, aging, and mortality. However, questions remain about its dynamic properties and measurability in human biofluids other than blood. Here, we examine the natural dynamics and psychobiological regulation of plasma and saliva GDF15 in four human studies representing 4,749 samples from 188 individuals. We show that GDF15 protein is detectable in saliva (8% of plasma concentration), likely produced by salivary glands secretory duct cells. Using a brief laboratory socio-evaluative stressor paradigm, we find that psychosocial stress increases plasma (+3.5-5.9%) and saliva GDF15 (+43%) with distinct kinetics, within minutes. Moreover, saliva GDF15 exhibits a robust awakening response, declining by ~40-89% within 30-45 minutes from its peak level at the time of waking up. Clinically, individuals with genetic mitochondrial OxPhos diseases show elevated baseline plasma and saliva GDF15, and post-stress GDF15 levels in both biofluids correlate with multi-system disease severity, exercise intolerance, and the subjective experience of fatigue. Taken together, our data establish that saliva GDF15 is dynamic, sensitive to psychological states, a clinically relevant endocrine marker of mitochondrial diseases. These findings also point to a shared psychobiological pathway integrating metabolic and mental stress.

Exploring the Role of Dairy Products In Sleep Quality: From Population Studies to Mechanistic Evaluations.

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.

Changes in eating patterns in response to chronic insufficient sleep and their associations with diet quality: a randomized trial.

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 (ß = 0.3 ± 0.1; P = .046). Across conditions, eating more frequently tended to relate to higher energy intakes (ß = 60.5 ± 34.6; P = .082). Sleep also influenced the relation of variability in eating midpoint with intakes of saturated fat (ß = 6.0 ± 2.1; P = .005), polyunsaturated fat (ß = -3.9 ± 2.0; P = .051), and added sugar (ß = 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.

Paradoxical Effects of Prolonged Insufficient Sleep on Lipid Profile: A Pooled Analysis of 2 Randomized Trials.

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/m2) 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 (ß=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: ß=-4.2±1.9 mg/dL; P=0.03; LDL-C: ß=-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: ß=-5.3±2.6 mg/dL; P=0.051; tumor necrosis factor-α: ß=-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.

Dimensions of sleep quality are related to objectively measured eating behaviors among children at high familial risk for obesity.

OBJECTIVE: The aim of this study was to evaluate whether dimensions of sleep quality were associated with homeostatic and hedonic eating behaviors among children with healthy weight (BMI-for-age < 90%) but varying maternal weight status. METHODS: A total of 77 children (mean [SD], age: 7.4 [0.6] years; BMI z score: -0.10 [0.7]) with healthy weight and high (n = 32) or low (n = 45) familial obesity risk based on maternal weight status were served an ad libitum meal (homeostatic eating) followed by palatable snacks to assess eating in the absence of hunger (EAH; hedonic eating). Habitual sleep quality was quantified from seven nights of wrist actigraphy. Partial correlations, adjusted for child energy needs, pre-meal hunger, food liking, and socioeconomic status, evaluated associations of sleep with meal intake and EAH. Additionally, sleep-by-obesity risk interactions were assessed. RESULTS: Greater sleep fragmentation was associated with higher homeostatic meal energy intake, but only among children at high familial obesity risk (p value for interaction = 0.001; ß high risk = 48.6, p = 0.001). Sleep fragmentation was not associated with total EAH but was related to higher and lower intake of carbohydrates (r = 0.33, p = 0.003) and fat (r = -0.33, p = 0.003), respectively. CONCLUSIONS: Adverse associations of poor sleep with energy intake may be amplified among children already predisposed to obesity. Furthermore, that fragmented sleep relates to preferential intake of carbohydrates over fat during EAH may suggest alterations in taste preferences with poor sleep.

Sleep exerts lasting effects on hematopoietic stem cell function and diversity.

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.