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Background: The association of the meal timing of dietary total antioxidant capacity (DAC) with mortality is unclear. We aimed to investigate the association between the meal timing of DAC and all-cause, cardiovascular disease (CVD), and cancer mortality in general adult populations. Methods: A total of 56,066 adults who participated in the US National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018 were recruited for this study. Dietary intake (quantity and timing) was evaluated by nonconsecutive 24-h dietary recalls. The main exposure variables were the DAC across three meals (total, breakfast, lunch, and dinner; without coffee) and the difference between dinner and breakfast DAC (Δ = dinner-breakfast; without coffee). The outcomes were all-cause, CVD, and cancer mortality. The adjusted hazard ratios [aHRs] and 95% confidence intervals [CI] were imputed by Cox proportional hazards regression. Results: Among the 56,066 participants, there were 8566 deaths from any cause, including 2196 from CVD and 1984 from cancer causes. Compared to participants in the lowest quintiles of the total DAC, those in the highest quintiles had 34% and 27% decreased risks of all-cause and CVD mortality, respectively (all-cause mortality: aHRs 0.66 [95% CI 0.57–0.76]; CVD mortality: aHRs 0.73 [95% CI 0.57–0.94]). More importantly, participants in the highest quintiles of the dinner DAC, but not those in that of breakfast or lunch, had a 24% decrease in all-cause mortality (aHRs 0.76 [95% CI 0.67–0.87]) compared with those in the lowest quintiles. Inverse associations were further confirmed for Δ DAC (aHRs 0.84 [95% CI 0.74–0.96]). Above associations did not change when including DAC from snacks or tea. Mediation analysis showed that the total associations of total, dinner or Δ DACs with reduced all-cause mortality were 24%, 13% and 6%, respectively, mediated by serum CRP. Additionally, all-cause mortality was decreased by 7% in models replacing 10% breakfast DAC (aHRs 0.93 [95% CI 0.9–0.97]) with an equivalent proportion of dinner DAC. For cancer mortality, no statistical significance was detected in the adjusted models. Conclusions: The findings emphasize the putative beneficial relationship of a diet rich in antioxidants and meal timing on serum CRP and all-cause mortality. [ABSTRACT FROM AUTHOR]

The long-term impact of eating duration on the risk of all-cause mortality remains unclear, with limited exploration of how different levels of energy intake and physical activity might influence this impact. To investigate, 24 484 American adults from the National Health and Nutrition Examination Survey spanning 1999-2018 were included. Eating duration was assessed via 24-h dietary recall, and all-cause mortality data were sourced from the National Death Index. The relationship between eating duration and all-cause mortality was analysed using Cox proportional hazards regression models, restricted cubic splines and stratification analysis with complex weighted designs. The median (IQR) of eating duration for participants was 12·5 (11·0, 14·0) h. In this study, 2896 death events were observed, and the median follow-up time (IQR) was 125 (77, 177) months. After multivariable adjustment, compared with Q1, Q2, Q3 and Q4 had reduced risks of all-cause mortality by 17, 15 and 13 %, respectively. Furthermore, each additional hour of eating duration was correlated with a 2 % decrease in the risk of all-cause mortality. Additionally, a non-linear dose-response relationship was observed between eating duration and the risk of all-cause mortality, showing a U -shaped relationship from 8·9 h to 15·3 h ( P for non-linearity < 0·05). Interestingly, the non-linear dose-response relationship was observed exclusively among individuals with high energy intake or a lightly active physical activity level. These findings suggest potential health benefits from adjusting eating duration, though further prospective studies are needed for validation.