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.

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.

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.

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.

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.

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.

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 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.

Variability in Daily Eating Patterns and Eating Jetlag Are Associated With Worsened Cardiometabolic Risk Profiles in the American Heart Association Go Red for Women Strategically Focused Research Network.

Background Sleep variability and social jetlag are associated with adverse cardiometabolic outcomes via circadian disruption. Variable eating patterns also lead to circadian disruption, but associations with cardiometabolic health are unknown. Methods and Results Women (n=115, mean age: 33±12 years) completed a 1-week food record using the Automated Self-Administered 24-Hour Dietary Assessment Tool at baseline and 1 year. Timing of first and last eating occasions, nightly fasting duration, and %kcal consumed after 5 pm (%kcal 5 pm) and 8 pm (%kcal 8 pm) were estimated. Day-to-day eating variability was assessed from the SD of these variables. Eating jetlag was defined as weekday-weekend differences in these metrics. Multivariable-adjusted linear models examined cross-sectional and longitudinal associations of day-to-day variability and eating jetlag metrics with cardiometabolic risk. Greater jetlag in eating start time, nightly fasting duration, and %kcal 8 pm related to higher body mass index and waist circumference at baseline (P<0.05). In longitudinal analyses, a 10% increase in %kcal 8 pm SD predicted increased body mass index (ß, 0.52; 95% CI, 0.23-0.81) and waist circumference (ß, 1.73; 95% CI, 0.58-2.87); greater %kcal 8 pm weekday-weekend differences predicted higher body mass index (ß, 0.25; 95% CI, 0.07-0.43). Every 30-minute increase in nightly fasting duration SD predicted increased diastolic blood pressure (ß, 0.95; 95% CI, 0.40-1.50); an equivalent increase in nightly fasting duration weekday-weekend differences predicted higher systolic blood pressure (ß, 0.58; 95% CI, 0.11-1.05) and diastolic blood pressure (ß, 0.45; 95% CI, 0.10-0.80). Per 10% increase in %kcal 5 pm SD, there were 2.98 mm Hg (95% CI, 0.04-5.92) and 2.37mm Hg (95% CI, 0.19-4.55) increases in systolic blood pressure and diastolic blood pressure; greater %kcal 5 pm weekday-weekend differences predicted increased systolic blood pressure (ß, 1.83; 95% CI, 0.30-3.36). For hemoglobin A1c, every 30-minute increase in eating start and end time SD and 10% increase in %kcal 5 pm SD predicted 0.09% (95% CI, 0.03-0.15), 0.06% (95% CI, 0.001-0.12), and 0.23% (95% CI, 0.07-0.39) increases, respectively. Conclusions Variable eating patterns predicted increased blood pressure and adiposity and worse glycemic control. Findings warrant confirmation in population-based cohorts and intervention studies.

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.

Actigraphy-Derived Sleep Is Associated with Eating Behavior Characteristics.

Poor sleep is a determinant of obesity, with overconsumption of energy contributing to this relationship. Eating behavior characteristics are predictive of energy intake and weight change and may underlie observed associations of sleep with weight status and obesity risk factors. However, relationships between sleep and dimensions of eating behavior, as well as possible individual differences in these relations, are not well characterized. Therefore, the aim of this study was to evaluate whether sleep behaviors, including duration, timing, quality, and regularity relate to dietary restraint, disinhibition, and tendency towards hunger and to explore whether these associations differ by sex. This cross-sectional study included 179 adults aged 20-73 years (68.7% women, 64.8% with BMI ≥ 25 kg/m2). Sleep was evaluated by accelerometry over 2 weeks. Eating behavior dimensions were measured with the Three-Factor Eating Questionnaire. Prolonged wake after sleep onset (WASO) (0.029 ± 0.011, p = 0.007), greater sleep fragmentation index (0.074 ± 0.036, p = 0.041), and lower sleep efficiency (-0.133 ± 0.051, p = 0.010) were associated with higher dietary restraint. However, higher restraint attenuated associations of higher WASO and sleep fragmentation with higher BMI (p-interactions < 0.10). In terms of individual differences, sex influenced associations of sleep quality measures with tendency towards hunger (p-interactions < 0.10). Stratified analyses showed that, in men only, higher sleep fragmentation index, longer sleep onset latency, and lower sleep efficiency were associated with greater tendency towards hunger (ß = 0.115 ± 0.037, p = 0.003, ß = 0.169 ± 0.072, p = 0.023, ß = -0.150 ± 0.055, p = 0.009, respectively). Results of this analysis suggest that the association of poor sleep on food intake could be exacerbated in those with eating behavior traits that predispose to overeating, and this sleep-eating behavior relation may be sex-dependent. Strategies to counter overconsumption in the context of poor quality sleep should be evaluated in light of eating behavior traits.

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.

Does sex influence the effects of experimental sleep curtailment and circadian misalignment on regulation of appetite?

Sleep curtailment and circadian misalignment disrupt energy sensing and eating behaviors, which can contribute to weight gain and obesity-related comorbidities. Herein, we review the effects of experimental manipulations of sleep duration and circadian alignment on circulating concentrations of appetite hormones, specifically leptin and ghrelin. Further, we focus on sex differences in hormonal and behavioral responses related to food intake. The studies reviewed suggest potential sex-specific effects of sleep curtailment on key hormones involved in the gut-brain axis, presumably leading to downstream effects on neural processes involved in food seeking and consumption behaviors. However, there is insufficient evidence to declare any sex-specific effects of circadian misalignment on appetite regulation. More research is needed to elucidate the complex sex-specific relationships between sleep, circadian rhythms, energy homeostasis, and appetite regulating mechanisms. Greater knowledge of these mechanisms would aid in the development of targeted methods to mitigate risk for obesity and related metabolic diseases.

Habitual Nightly Fasting Duration, Eating Timing, and Eating Frequency are Associated with Cardiometabolic Risk in Women.

Nightly fasting duration (NFD) and eating timing and frequency may influence cardiometabolic health via their impact on circadian rhythms, which are entrained by food intake, but observational studies are limited. This 1-year prospective study of 116 US women (33 ± 12y, 45% Hispanic) investigated associations of habitual NFD and eating timing and frequency with cardiovascular health (CVH; American Heart Association Life's Simple 7 score) and cardiometabolic risk factors. NFD, eating timing and frequency, and nighttime eating levels were evaluated from 1-week electronic food records completed at baseline and 1 y. In multivariable-adjusted linear regression models, longer NFD was associated with poorer CVH (ß = -0.22, p = 0.016 and ß = -0.22, p = 0.050) and higher diastolic blood pressure (DBP) (ß = 1.08, p < 0.01 and ß = 1.74, p < 0.01) in cross-sectional and prospective analyses, respectively. Later timing of the first eating occasion at baseline was associated with poorer CVH (ß = -0.20, p = 0.013) and higher DBP (ß = 1.18, p < 0.01) and fasting glucose (ß = 1.43, p = 0.045) at 1 y. After adjustment for baseline outcomes, longer NFD and later eating times were also associated with higher waist circumference (ß = 0.35, p = 0.021 and ß = 0.27, p < 0.01, respectively). Eating frequency was inversely related to DBP in cross-sectional (ß = -1.94, p = 0.033) and prospective analyses (ß = -3.37, p < 0.01). In cross-sectional analyses of baseline data and prospective analyses, a higher percentage of daily calories consumed at the largest evening meal was associated with higher DBP (ß = 1.69, p = 0.046 and ß = 2.32, p = 0.029, respectively). Findings suggest that frequent and earlier eating may lower cardiometabolic risk, while longer NFD may have adverse effects. Results warrant confirmation in larger multi-ethnic cohort studies with longer follow-up periods.

A Mediterranean Dietary Pattern Predicts Better Sleep Quality in US Women from the American Heart Association Go Red for Women Strategically Focused Research Network.

Consumption of a Mediterranean diet has been linked to better sleep health in older, European populations. However, whether this dietary pattern is predictive of sleep quality in US women, a group prone to poor sleep, is unknown. This prospective cohort study of 432 US women (20-76 y; 60% racial/ethnic minority) evaluated whether compliance with a Mediterranean diet at baseline predicted sleep quality at 1-y follow-up. Alternate Mediterranean (aMed) diet scores and habitual sleep quality were computed from the validated Block Brief Food Frequency Questionnaire and Pittsburgh Sleep Quality Index (PSQI), respectively. Linear regression models evaluated prospective associations of the aMed diet pattern and its components with measures of sleep quality, after adjustment for age, BMI, race/ethnicity, education, and health insurance status. Higher baseline aMed scores were associated with lower PSQI scores (ß = -0.30 ± 0.10, p < 0.01), indicative of better sleep quality, higher sleep efficiency (ß = 1.20 ± 0.35, p < 0.001), and fewer sleep disturbances (ß = -0.30 ± 0.12, p = 0.01) at 1-y. Fruit and vegetable consumption also predicted lower PSQI scores, higher sleep efficiency and fewer sleep disturbances (all p < 0.05). Higher legume intake predicted better sleep efficiency (ß = 1.36 ± 0.55, p = 0.01). These findings suggest that adherence to a Mediterranean diet pattern should be evaluated as a strategy to promote sleep quality in US women.