OBJECTIVE In this study we investigated the association of the quantity, quality, and timing of carbohydrate intake with all-cause, cardiovascular disease (CVD), and diabetes mortality. RESEARCH DESIGN AND METHODS This secondary data analysis included use of National Health and Nutrition Examination Survey (2003–2014) and National Death Index data from adults (n = 27,623) for examination of the association of total daily and differences in carbohydrate intake with mortality. Participants were categorized into four carbohydrate intake patterns based on the median values of daily high- and low-quality carbohydrate intake. The differences (Δ) in carbohydrate intake between dinner and breakfast were calculated (Δ = dinner − breakfast). Cox regression models were used. RESULTS The participants who consumed more high-quality carbohydrates throughout the day had lower all-cause mortality risk (hazard ratio [HR] 0.88; 95% CI 0.79–0.99), whereas more daily intake of low-quality carbohydrates was related to greater all-cause mortality risk (HR 1.13; 95% CI: 1.01–1.26). Among participants whose daily high- and low-quality carbohydrate intake were both below the median, the participants who consumed more high-quality carbohydrates at dinner had lower CVD (HR 0.70; 95% CI 0.52–0.93) and all-cause mortality (HR 0.82; 95% CI 0.70–0.97) risk; an isocaloric substitution of 1 serving low-quality carbohydrates intake at dinner with high-quality reduced the CVD and all-cause mortality risks by 25% and 19%. There was greater diabetes mortality among the participants who consumed more low-quality carbohydrates at dinner (HR 1.78; 95% CI 1.02–3.11), although their daily high-quality carbohydrate intake was above the median. CONCLUSIONS Consuming more low-quality carbohydrates at dinner was associated with greater diabetes mortality, whereas consuming more high-quality carbohydrates at dinner was associated with lower all-cause and CVD mortality irrespective of the total daily quantity and quality of carbohydrates.
Background Although accumulating evidence has demonstrated that consumption time of energy and macronutrients plays an important role in maintaining health, the association between consumption time of different foods and cardiovascular disease, cancer, and all‐cause mortalities is still largely unknown. Methods and Results A noninstitutionalized household population of the US 21 503 participants from National Health and Nutrition Examination Survey was included. Meal patterns and snack patterns throughout a whole day were measured using 24‐hour dietary recall. Principal component analysis was performed to establish dietary patterns. Cox proportional hazards models were used to evaluate the association between dietary patterns across meals and cardiovascular disease (CVD), cancer, and all‐cause mortalities. During the 149 875 person‐years of follow‐up, 2192 deaths including 676 deaths because of CVD and 476 because of cancer were documented. After adjusting for potential confounders, participants consuming fruit‐lunch had lower mortality risks of all‐cause (hazard ratio [HR], 0.82; 95% CI, 0.72–0.92) and CVD (HR, 0.66; 95% CI, 0.49–0.87); whereas participants who consumed Western‐lunch were more likely to die because of CVD (HR, 1.44; 95% CI, 1.10–1.89). Participants who consumed vegetable‐dinner had lower mortality risks of all‐cause, CVD, and cancer (HR all‐cause , 0.69; 95% CI, 0.60–0.78; HR CVD , 0.77; 95% CI, 0.61–0.95; HR cancer , 0.63; 95% CI, 0.48–0.83). For the snack patterns, participants who consumed fruit‐snack after breakfast had lower mortality risks of all‐cause and cancer (HR all‐cause , 0.78; 95% CI, 0.66–0.93; HR cancer , 0.55; 95% CI, 0.39–0.78), and participants who consumed dairy‐snack after dinner had lower risks of all‐cause and CVD mortalities (HR all‐cause , 0.82; 95% CI, 0.72–0.94; HR CVD , 0.67; 95% CI, 0.52–0.87). Participants who consumed a starchy‐snack after main meals had greater mortality risks of all‐cause (HR after‐breakfast , 1.50; 95% CI, 1.24–1.82; HR after‐lunch , 1.52; 95% CI, 1.27–1.81; HR after‐dinner , 1.50; 95% CI, 1.25–1.80) and CVD (HR after‐breakfast , 1.55; 95% CI, 1.08–2.24; HR after‐lunch , 1.44; 95% CI, 1.03–2.02; HR after‐dinner , 1.57; 95% CI, 1.10–2.23). Conclusions Fruit‐snack after breakfast, fruit‐lunch, vegetable‐dinner, and dairy‐snack after dinner was associated with lower mortality risks of CVD, cancer, and all‐cause; whereas Western‐lunch and starchy‐snack after main meals had greater CVD and all‐cause mortalities.
Background Intake time of diet has recently been demonstrated to be associated with the internal clock and circadian pattern. However, whether and how the intake time of minerals would influence the natural course of cancer was largely unknown. Methods This study aimed to assess the association of mineral intake at different periods with cancer and all-cause mortality. A total of 27,455 participants aged 18–85 years old in the National Health and Nutrition Examination Survey were recruited. The main exposures were the mineral intakes in the morning, afternoon and evening, which were categorized into quintiles, respectively. The main outcomes were mortality of cancer and all causes. Results During the 178,182 person-years of follow-up, 2680 deaths, including 601 deaths due to cancer, were documented. After adjusting for potential confounders, compared to the participants who were in the lowest quintile(quintile-1) of mineral intakes at dinner, the participants in the highest quintile intake(quintile-5) of dietary potassium, calcium and magnesium had lower mortality risks of cancer (HRpotassium = 0.72, 95% CI:0.55–0.94, P for trend = 0.023; HRcalcium = 0.74, 95% CI:0.57–0.98, P for trend = 0.05; HRmagnesium = 0.75, 95% CI:0.56–0.99, P for trend = 0.037) and all-cause (HRpotassium = 0.83, 95% CI:0.73–0.94, P for trend = 0.012; HRcalcium = 0.87, 95% CI:0.76–0.99, P for trend = 0.025; HRmagnesium = 0.85, 95% CI:0.74–0.97, P for trend = 0.011; HRcopper = 0.80, 95%CI: 0.68–0.94, P for trend = 0.012). Further, equivalently replacing 10% of dietary potassium, calcium and magnesium consumed in the morning with those in the evening were associated with lower mortality risk of cancer (HRpotassium = 0.94, 95%CI:0.91–0.97; HRcalcium = 0.95, 95%CI:0.92–0.98; HRmagnesium = 0.95, 95%CI: 0.92–0.98). Conclusions This study demonstrated that the optimal intake time of potassium, calcium and magnesium for reducing the risk of cancer and all-cause mortality was in the evening.
BackgroundChrono-nutrition emphasized the importance of the intake time; however, less is known about the impact of dietary vitamin intake time on health. This study aimed to examine our hypothesis about which vitamin intake time could influence the natural course of cardiovascular disease (CVD).MethodsA total of 27,455 adults enrolled in the National Health and Nutrition Examination Survey (NHANES) during 2003–2014 were recruited. The 12 dietary vitamin intakes in the morning, afternoon, and evening were categorized into tertiles or quartiles. Cox-proportional hazard regression models were developed to evaluate the association of vitamin intake time with CVD and all-cause mortalities.ResultsCompared with participants in the lowest quartile, participants in the highest quartile of dietary VB2 intake in the morning had significantly lowest mortality risk of CVD [hazard ratio (HR)VB2 = 0.75, 95% CI: 0.60–0.94, p = 0.017]; whereas, participants in the highest quartile of dietary-vitamin B6 (VB6), vitamin C (VC), vitamin E (VE), and folate-equivalent consumed in the evening showed the lowest risks of CVD (HRVB6 = 0.77, 95% CI: 0.60–0.99, p = 0.103; HRVC = 0.80, 95% CI: 0.65–0.98, p = 0.050; HRVE = 0.75, 95% CI: 0.56–0.99, p = 0.032; HRfolate–equivalent = 0.78, 95% CI: 0.63–0.97, p = 0.116) and all-cause mortalities (HRVB6 = 0.81, 95% CI: 0.71–0.93, p = 0.006; HRVC = 0.85, 95% CI: 0.76–0.95, p = 0.004; HRVE = 0.84, 95% CI: 0.72–0.97, p = 0.011; HRfolate–equivalent = 0.80, 95% CI: 0.71–0.90, p = 0.001). Moreover, equivalently replacing 10% intake of dietary VB6, VC, VE, and folate-equivalent in the morning with evening were associated with 4% (HRVB6 = 0.96, 95% CI: 0.92–0.99), 5% (HRVC = 0.95, 95% CI: 0.92–0.99), 4% (HRVE = 0.96, 95% CI: 0.91–0.99), and 5% (HRfolate–equivalent = 0.95, 95% CI: 0.92–0.99) lower risk of CVD mortality.ConclusionThis study found that the optimal intake time of dietary VB2 was in the morning, and the optimal intake times of dietary VB6, VC, VE, and folate-equivalent were in the evening.
Although there has been increasing recognition that famine exposure in the fetal stage damages liver function in adulthood, this deteriorated effect could be extended to the next generation remains vague. This study aimed to explore whether famine exposure was associated with liver function in the two consecutive generations, and its association with the mediation role of inflammatory markers. We analyzed the data of 2,681 participants from Suihua rural area, Heilongjiang Province, China. According to the date of birth, the participants were classified as fetal exposed and nonexposed. The F2 subjects were classified as having no parents exposed to famine, maternal famine exposure, paternal famine exposure, or parental famine exposure. In the mixed-effect models, prenatal exposure to famine was associated with the elevation of Δ aspartate aminotransferase (ΔAST) (β: 0.22, 95% CI: 0.01, 0.43) and Δ alanine aminotransferase (ΔALT) (β: 0.42, 95% CI: 0.19, 0.66) levels in F1 adults. The mediation analysis showed that the inflammatory markers including serum C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) might mediate the famine-liver function association. This longitudinal data were consistent with the hypothesis that the inflammatory markers explained part of the influence of prenatal famine exposure on liver function injury, and the natal mechanism was needed to be elucidated in the future study.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.