Association of meal timing of energy, macronutrients and foods with hypercholesterolaemia in the US adults.

Few studies examined the association of energy, macronutrients and food consumption at dinner v. breakfast with hypercholesterolaemia. A total of 27 911 participants from the National Health and Nutrition Examination Survey (2003-2016) were included in the cross-sectional study. Energy, macronutrients and food consumption at breakfast, dinner and the difference at dinner v. breakfast (Δratio) were calculated. Multiple logistic regression models and substitution effects of foods at dinner with breakfast were also performed. After adjustment for potential covariates, compared with the lowest quintile, participants in the highest quintile of Δratio in terms of energy had a higher risk of prevalent hypercholesterolaemia (ORΔratio of energy 1·16, 95 % CI (1·01, 1·33)) mainly due to Δratio of low-quality carbohydrates and plant protein (ORΔratio of low-quality carbohydrates 1·19; 95 % CI (1·05, 1·35)); ORΔratio of plant protein 1·13; 95 % CI (1·01, 1·28)). ΔAdded sugars and Δnuts were associated with hypercholesterolaemia (ORΔadded sugars 1·01; 95 % CI (1·00, 1·02)); ORΔnuts 1·08; 95 % CI (1·01, 1·16)). Furthermore, the substitution of added sugars, nuts and processed meat at dinner with breakfast could reduce the OR of hypercholesterolaemia. This study indicated that among US adults, overconsumption of energy, macronutrients including low-quality carbohydrates and plant protein at dinner than breakfast was significantly associated with a higher risk of prevalent hypercholesterolaemia. The replacing of added sugar, nuts and processed meat at dinner with breakfast reduced the risk of prevalent hypercholesterolaemia. This study emphasised the importance of meal timing in the prevention of hypercholesterolaemia.

Exposure to N,N-diethyl-m-toluamide and cardiovascular diseases in adults.

Although growing evidence suggests that N,N-diethyl-m-toluamide (DEET) has adverse effects on public health, the relationship of DEET with cardiovascular disease (CVD) is still largely unknown. The purpose of this study was, therefore, to evaluate the association between DEET exposure and total and specific CVD among the US adults. In this cross-sectional study, a total of 5,972 participants were selected from the National Health and Nutrition Examination Survey (NHANES) 2007-2014. CVD was defined as a combination of congestive heart failure (CHF), coronary heart disease (CHD), angina, heart attack, or stroke. Logistic regression models were used to evaluate the association between DEET metabolites and the risks of total and specific CVD. Compared to the lowest quartile, 3-(diethylcarbamoyl) benzoic acid (DCBA) in the highest quartile was associated with the increased risks of CVD (odds ratio [OR]: 1.32, 95% CI: 1.03-1.68, P for trend = 0.025) and CHD (OR: 1.57, 95% CI: 1.10-2.25, P for trend = 0.017), after adjustment for potential covariates. Nevertheless, exposure to DCBA was not significantly associated with heart attack, CHF, angina, and stroke. Further studies are required to confirm these findings and identify the underlying mechanisms.

Relationship Between Carbohydrate Intake (Quantity, Quality, and Time Eaten) and Mortality (Total, Cardiovascular, and Diabetes): Assessment of 2003-2014 National Health and Nutrition Examination Survey Participants.

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.

The Association Between Exposure to Acrylamide and Mortalities of Cardiovascular Disease and All-Cause Among People With Hyperglycemia.

Background: Acrylamide is a common environmental volatile organic compound that humans are frequently exposed to in their daily lives. However, whether exposure to acrylamide is associated with long-term survival in patients with hyperglycemia remains largely unknown. Methods and Results: A total of 3,601 hyperglycemic people were recruited in this study, including 1,247 people with diabetes and 2,354 people with pre-diabetes, who enrolled in the National Health and Nutrition Examination survey (2003-2004, 2005-2006, and 2013-2014). The acrylamide exposure was measured by the serum hemoglobin adduct of acrylamide (HbAA) and glycidamide (HbGA), and the ratio of HbAA and HbGA (HbAA/HbGA) was calculated, which were all categorized into quintiles. The National Death Index was used to identify the participants' death information until 2015. Cox proportional hazards (CPHs) regression models were performed to examine the survival relationship between these biomarkers and mortality. During the 28,652 person-year follow-up, 268 deaths due to the cardiovascular disease (CVD) were documented. After adjustment for multiple confounders, compared with participants in the lowest quintile of HbAA/HbGA, the participants in the highest quintile were more likely to die due to CVD (hazard ratio [HR] = 1.61, 95% CI: 1.09-2.39) and all-cause (HR = 1.59, 95% CI: 1.25-2.01). Moreover, subgroup analysis showed that the highest quintile of HbAA/HbGA in the people with diabetes or pre-diabetes was related to mortalities risk of CVD (HR diabetes = 1.92, 95% CI: 1.11-3.31; HR pre-diabetes = 1.78, 95% CI: 1.01-3.14) and all-cause mortality (HR diabetes = 1.81, 95% CI: 1.27-2.58; HR pre-diabetes = 1.59, 95% CI: 1.14-2.20). Additionally, no significant association between the levels of HbAA or HbGA and CVD mortality was observed among people with diabetes or pre-diabetes. Conclusion: Higher levels of HbAA/HbGA are associated with greater mortalities of CVD and all-cause among hyperglycemic people.

A Newly Developed Indicator of Overeating Saturated Fat Based on Serum Fatty Acids and Amino Acids and Its Association With Incidence of Type 2 Diabetes: Evidence From Two Randomized Controlled Feeding Trials and a Prospective Study.

Objective: Hyper-caloric intake of saturated fatty acids (SFAs) is common in modern societies, probably contributing to the epidemic of type 2 diabetes mellitus (T2DM). This study conducted two randomized controlled trials (RCTs) for developing a new indicator that can assess the nutritional status and examined its association with incidence of T2DM. Methods: In RCT 1, healthy participants were randomly assigned into three groups, namely, control group (n = 40), overfeeding group 1 (100 g butter per day, n = 37), and overfeeding group 2 (120 g butter per day, n = 37). In RCT 2, healthy subjects were randomly assigned into two groups, namely, control group (n = 52) and high-fat group (300-extra kcal/day from diet that was designed by high-fat diet, n = 58). In the prospective cohort, 4,057 participants aged 20-74 years were enrolled and followed up over 5.3 years. Serum profiles of fatty acids and amino acids were measured. Results: In RCT 1, serum fatty acids, including C14:0 and C18:0, increased, whereas C18:2, C20:4, C22:5, and C22:6 decreased; serum amino acids, including tyrosine, alanine, and aminobutyric acid, increased, whereas histidine and glycine decreased (p < 0.05). Among these serum fatty acids and amino acids, changes in C14:0, C20:4, tyrosine, histidine, and glycine were also observed in RCT 2. An indicator was developed based on the five fatty acids and amino acids, namely, C14:0 × tyrosine × 1,000/[C20:4 × (glycine + histidine)], and it significantly identified participants in the intervention group with area under the curve (AUC) (95% CI) being 0.85 (0.77-0.92). The indicator was significantly associated with incidence of T2DM in the prospective cohort with HRs (95% CIs) from bottom quartile to top quartile being 1,1.21 (0.82-1.77), 1.60 (1.12-2.30), 2.04 (1.42-2.94). Conclusion: The newly developed indicator in RCTs can be used in assessing the nutritional status of hypercaloric intake of SFA and predicting the development of T2DM.

The Association of Dietary Vitamin Intake Time Across a Day With Cardiovascular Disease and All-Cause Mortality.

Background: Chrono-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). Methods: A 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. Results: Compared 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. Conclusion: This 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.

Fetal malnutrition is associated with impairment of endogenous melatonin synthesis in pineal via hypermethylation of promoters of protein kinase C alpha and cAMP response element-binding.

This study investigated whether and how fetal malnutrition would influence endogenous melatonin synthesis, and whether such effect of fetal malnutrition would transmit to the next generation. We enrolled 2466 participants and 1313 of their offspring. The urine 6-hydroxymelatonin sulfate and serum melatonin rhythm were measured. Methylation microarray detection and bioinformatics analysis were performed to identify hub methylated sites. Additionally, rat experiment was performed to elucidate mechanisms. The participants with fetal malnutrition had lower 6-hydroxymelatonin sulfate (16.59 ± 10.12 µg/24 hours vs 24.29 ± 11.99 µg/24 hours, P < .001) and arear under curve of melatonin rhythm (67.11 ± 8.16 pg/mL vs 77.11 ± 8.04 pg/mL, P < .001). We identified 961 differentially methylated sites, in which the hub methylated sites were locating on protein kinase C alpha (PRKCA) and cAMP response element-binding protein (CREB1) promoters, mediating the association of fetal malnutrition with impaired melatonin secretion. However, such effects were not observed in the offspring (all P > .05). Impaired histomorphology of pineal, decreased melatonin in serum, pineal, and pinealocyte were also found in the in vivo and in vitro experiments (P < .05 for the differences of the indicators). Hypermethylation of 10 CpG sites on the PRKCA promoter and 8 CpG sites on the CREB1 promoter were identified (all P < .05), which down-regulated PRKCA and CREB1 expressions, leading to decreased expression of AANAT, and then resulting in the impaired melatonin synthesis. Collectively, fetal malnutrition can impair melatonin synthesis through hypermethylation of PRKCA and CREB1 promoters, and such effects cannot be transmitted to the next generation.

The association of minerals intake in three meals with cancer and all-cause mortality: the U.S. National Health and Nutrition Examination Survey, 2003-2014.

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.

Association of Meal and Snack Patterns With Mortality of All-Cause, Cardiovascular Disease, and Cancer: The US National Health and Nutrition Examination Survey, 2003 to 2014.

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 (HRall-cause, 0.69; 95% CI, 0.60-0.78; HRCVD, 0.77; 95% CI, 0.61-0.95; HRcancer, 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 (HRall-cause, 0.78; 95% CI, 0.66-0.93; HRcancer, 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 (HRall-cause, 0.82; 95% CI, 0.72-0.94; HRCVD, 0.67; 95% CI, 0.52-0.87). Participants who consumed a starchy-snack after main meals had greater mortality risks of all-cause (HRafter-breakfast, 1.50; 95% CI, 1.24-1.82; HRafter-lunch, 1.52; 95% CI, 1.27-1.81; HRafter-dinner, 1.50; 95% CI, 1.25-1.80) and CVD (HRafter-breakfast, 1.55; 95% CI, 1.08-2.24; HRafter-lunch, 1.44; 95% CI, 1.03-2.02; HRafter-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.

Association of Prenatal Famine Exposure With Inflammatory Markers and Its Impact on Adulthood Liver Function Across Consecutive Generations.

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) (ß: 0.22, 95% CI: 0.01, 0.43) and Δ alanine aminotransferase (ΔALT) (ß: 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.

Effects of epidermal growth factor on the growth of human gastric cancer cell and the implanted tumor of nude mice.

AIM: Epidermal growth factor (EGF) plays an important role in the regulation of gastrointestinal tissue growth and development, and it can stimulate epithelial proliferation, cell differentiation and growth. It has been established that the EGF can promote gastric cytoprotection and ulcer healing. But the potential ability of EGF to regulate the gastric cancer growth is unknown. This study is to investigate the influence of EGF on human gastric cancer cell and the implanted tumor growth of nude mice. METHODS: The cell growth rates of human gastric adenocarcinoma cell lines MKN-28, MKN-45, SGC-7901 and normal human gastric epithelial cells 3T3 were assessed when incubated with recombinant human EGF (rhEGF, 0.05, 0.1, 0.5, 1.0, 10, 50, 100 mg.L(-1)) using MTT method. The cells of MKN-28, MKN-45, SGC-7901 (gastric cancer tissue 1.5mm(3)) were implanted in the BALB/cA nude mice for 10 days. The EGF was given intraperitoneally (15, 30, 60 microg.kg(-1)) for 3 weeks. The body weights of the tumor-bearing animals and their tumor mass were measured afterwards to assess the mitogenic effect of rhEGF in the nude mice. RESULTS: Within the concentration range of 0.05-100mg.L(-1), rhEGF could increase the cell growth of normal 3T3 cells (cell growth rate 100% vs 102.8%, P<0.05), but partially restrain the gastric cancer cell growth. The latter effect was related to cell differentiation. In 15-60 microg/kg rhEGF groups, the mean implanted tumor mass of MKN-28 cell were 1.75 g, 1.91 g, 2.08 g/NS group 1.97 g (P>0.05), the mean tumor mass of SGC-7901 cell were 1.53 g, 1.07 g, 1.20 g/NS group 1.07 g (P>0.05), and for MKN-45 cell, the tumor mass were respectively 1.92 g, 1.29 g, 1.77 /NS group 1.82 g (P>0.05). So rhEGF had no obvious effect on implanted MKN-28, SGC-7901 and MKN-45 tumor growth. CONCLUSION: EGF has no stimulating effect on the human gastric cancer cell growth neither in vitro nor in vivo.