Associations of dietary patterns with objective and subjective sleep duration and sleep quality in a population-based cohort study

Objective: To examine cross-sectional and longitudinal associations of various types of dietary patterns with self-reported sleep quality and with actigraphy-estimated sleep parameters in the prospective, population-based Rotterdam Study. Methods: For each participant, scores for five different dietary patterns were derived based on food frequency questionnaires; two pre-defined scores developed to estimate adherence to the Dutch dietary guidelines and to the Mediterranean diet; and three data-driven scores indicating a prudent, unhealthy and typical Dutch diet. In 2589 participants (median age 56.9 years; 58 % female), self-rated sleep quality was assessed with the Pittsburgh Sleep Quality Index. In 533 participants, actigraphs were worn for an average of 6.8 days (SD: 0.7) to estimate total sleep time, sleep onset latency, wake after sleep onset, and sleep efficiency. Sleep parameters were measured at baseline and 3–6 years later. Multiple linear regression was used to assess cross-sectional and longitudinal associations. Results: No statistically significant associations between dietary patterns and total sleep time, sleep onset latency, wake after sleep onset, sleep efficiency and subjective sleep quality were observed in cross-sectional or longitudinal analyses. To illustrate, the effect estimate for sleep duration was 2.7 min per night (95 % CI -2.1, 7.5) per 5 point increase in Mediterranean diet score in the cross-sectional analyses. Furthermore, in longitudinal analyses, the effect estimate for sleep duration was −1.0 min per night (95 % CI -5.2, 3.1) per SD increase in the prudent diet. Conclusions: Our results suggest that dietary patterns are not associated with sleep in this population-based cohort study. Trial registration: Netherlands National Trial Register and WHO International Clinical Trials Registry Platform (ICTRP; https://apps.who.int/trialsearch/) shared catalogue number NL6645/NTR6831. Registered November 13th, 2017.</p

Associations of dietary patterns with objective and subjective sleep duration and sleep quality in a population-based cohort study

Objective: To examine cross-sectional and longitudinal associations of various types of dietary patterns with self-reported sleep quality and with actigraphy-estimated sleep parameters in the prospective, population-based Rotterdam Study. Methods: For each participant, scores for five different dietary patterns were derived based on food frequency questionnaires; two pre-defined scores developed to estimate adherence to the Dutch dietary guidelines and to the Mediterranean diet; and three data-driven scores indicating a prudent, unhealthy and typical Dutch diet. In 2589 participants (median age 56.9 years; 58 % female), self-rated sleep quality was assessed with the Pittsburgh Sleep Quality Index. In 533 participants, actigraphs were worn for an average of 6.8 days (SD: 0.7) to estimate total sleep time, sleep onset latency, wake after sleep onset, and sleep efficiency. Sleep parameters were measured at baseline and 3–6 years later. Multiple linear regression was used to assess cross-sectional and longitudinal associations. Results: No statistically significant associations between dietary patterns and total sleep time, sleep onset latency, wake after sleep onset, sleep efficiency and subjective sleep quality were observed in cross-sectional or longitudinal analyses. To illustrate, the effect estimate for sleep duration was 2.7 min per night (95 % CI -2.1, 7.5) per 5 point increase in Mediterranean diet score in the cross-sectional analyses. Furthermore, in longitudinal analyses, the effect estimate for sleep duration was −1.0 min per night (95 % CI -5.2, 3.1) per SD increase in the prudent diet. Conclusions: Our results suggest that dietary patterns are not associated with sleep in this population-based cohort study. Trial registration: Netherlands National Trial Register and WHO International Clinical Trials Registry Platform (ICTRP; https://apps.who.int/trialsearch/) shared catalogue number NL6645/NTR6831. Registered November 13th, 2017.</p

Whole-diet interventions and cardiovascular risk factors in postmenopausal women: A systematic review of controlled clinical trials

Objectives: Menopause is accompanied by many metabolic changes, increasing the risk of cardiometabolic diseases. The impact of diet, as a modifiable lifestyle factor, on cardiovascular health in general populations has been well established. The purpose of this systematic review is to summarize the evidence on the effects of whole diet on lipid profile, glycemic indices, and blood pressure in postmenopausal women. Methods: Embase, Medline, Cochrane Central Register of Controlled Trials, and Google Scholar were searched from inception to February 2021. We included controlled clinical trials in postmenopausal women that assessed the effect of a whole-diet intervention on lipid profile, glycemic indices, and/or blood pressure. The risk of bias in individual studies was assessed using RoB 2 and ROBINS-I tools. Summary of evidence: Among 2,134 references, 21 trials met all eligibility criteria. Overall, results were heterogenuous and inconsistent. Compared to control diets, some studies showed that participants experienced improvements in total cholesterol (TC), low-density lipoprotein cholesterol (LDL), systolic blood pressure (SBP), fasting blood sugar (FBS), and apolipoprotein A (Apo-A) after following fat-modified diets, but some adverse effects on triglycerides (TG), very low-density lipoprotein cholesterol (VLDL), lipoprotein(a) (Lp(a)), and high-density lipoprotein cholesterol (HDL) concentrations were also observed. A limited number of trials found some effects of the Paleolithic, weight-loss, plant-based, or energy-restricted diets, or of following American Heart Association recommendations on TG, TC, HDL, insulin, FBS, or insulin resistance. Conclusion: Current evidence suggests that diet may affect levels of some lipid profile markers, glycemic indices, and blood pressure among postmenopausal women. However, due to the large heterogeneity in intervention diets, comparison groups, intervention durations, and population characteristics, findings are inconclusive. Further well-designed clinical trials are needed on dietary interventions to reduce cardiovascular risk in postmenopausal women

Circulating lipoprotein (a) and all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis

Aims: To investigate the association between circulating lipoprotein(a) (Lp(a)) and risk of all-cause and cause-specific mortality in the general population and in patients with chronic diseases, and to elucidate the dose-response relations. Methods and results: We searched literature to find prospective studies reporting adjusted risk estimates on the association of Lp(a) and mortality outcomes. Forty-three publications, reporting on 75 studies (957,253 participants), were included. The hazard ratios (HRs) and 95% confidence intervals (95%CI) for the top versus bottom tertile of Lp(a) levels and risk of all-cause mortality were 1.09 (95%CI: 1.01–1.18, I2: 75.34%, n = 19) in the general population and 1.18 (95%CI: 1.04–1.34, I2: 52.5%, n = 12) in patients with cardiovascular diseases (CVD). The HRs for CVD mortality were 1.33 (95%CI: 1.11–1.58, I2: 82.8%, n = 31) in the general population, 1.25 (95%CI: 1.10–1.43, I2: 54.3%, n = 17) in patients with CVD and 2.53 (95%CI: 1.13–5.64, I2: 66%, n = 4) in patients with diabetes mellitus. Linear dose-response analyses revealed that each 50 mg/dL increase in Lp(a) levels was associated with 31% and 15% greater risk of CVD death in the general population and in patients with CVD. No non-linear dose-response association was observed between Lp(a) levels and risk of all-cause or CVD mortality in the general population or in patients with CVD (Pnonlinearity > 0.05). Conclusion: This study provides further evidence that higher Lp(a) levels are associated with higher risk of all-cause mortality and CVD-death in the general population and in patients with CVD. These findings support the ESC/EAS Guidelines that recommend Lp(a) should be measured at least once in each adult person’s lifetime, since our study suggests those with higher Lp(a) might also have higher risk of mortality

Circulating lipoprotein (a) and all-cause and cause-specific mortality : A systematic review and dose-response meta-analysis

To investigate the association between circulating lipoprotein(a) (Lp(a)) and risk of all-cause and cause-specific mortality in the general population and in patients with chronic diseases, and to elucidate the dose-response relations. Methods and results: We searched literature to find prospective studies reporting adjusted risk estimates on the association of Lp(a) and mortality outcomes. Forty-three publications, reporting on 75 studies (957,253 participants), were included. The hazard ratios (HRs) and 95% confidence intervals (95%CI) for the top versus bottom tertile of Lp(a) levels and risk of all-cause mortality were 1.09 (95%CI: 1.01–1.18, I2: 75.34%, n = 19) in the general population and 1.18 (95%CI: 1.04–1.34, I2: 52.5%, n = 12) in patients with cardiovascular diseases (CVD). The HRs for CVD mortality were 1.33 (95%CI: 1.11–1.58, I2: 82.8%, n = 31) in the general population, 1.25 (95%CI: 1.10–1.43, I2: 54.3%, n = 17) in patients with CVD and 2.53 (95%CI: 1.13–5.64, I2: 66%, n = 4) in patients with diabetes mellitus. Linear dose-response analyses revealed that each 50 mg/dL increase in Lp(a) levels was associated with 31% and 15% greater risk of CVD death in the general population and in patients with CVD. No non-linear dose-response association was observed between Lp(a) levels and risk of all-cause or CVD mortality in the general population or in patients with CVD (Pnonlinearity > 0.05). Conclusion: This study provides further evidence that higher Lp(a) levels are associated with higher risk of all-cause mortality and CVD-death in the general population and in patients with CVD. These findings support the ESC/EAS Guidelines that recommend Lp(a) should be measured at least once in each adult person’s lifetime, since our study suggests those with higher Lp(a) might also have higher risk of mortality