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

BackgroundThe 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.PurposeTo evaluate associations of intra-weekly and weekday-weekend differences in eating timing patterns with high-sensitivity C-reactive protein (hsCRP).MethodsA 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.ResultsEach 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.ConclusionsVariable 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

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 (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

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 (β = -0.22, p = 0.016 and β = -0.22, p = 0.050) and higher diastolic blood pressure (DBP) (β = 1.08, p < 0.01 and β = 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 (β = -0.20, p = 0.013) and higher DBP (β = 1.18, p < 0.01) and fasting glucose (β = 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 (β = 0.35, p = 0.021 and β = 0.27, p < 0.01, respectively). Eating frequency was inversely related to DBP in cross-sectional (β = -1.94, p = 0.033) and prospective analyses (β = -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 (β = 1.69, p = 0.046 and β = 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

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 (β, 0.52; 95% CI, 0.23-0.81) and waist circumference (β, 1.73; 95% CI, 0.58-2.87); greater %kcal 8 pm weekday-weekend differences predicted higher body mass index (β, 0.25; 95% CI, 0.07-0.43). Every 30-minute increase in nightly fasting duration SD predicted increased diastolic blood pressure (β, 0.95; 95% CI, 0.40-1.50); an equivalent increase in nightly fasting duration weekday-weekend differences predicted higher systolic blood pressure (β, 0.58; 95% CI, 0.11-1.05) and diastolic blood pressure (β, 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 (β, 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