Background: Dietary inorganic nitrate from vegetable sources has been shown to lower blood pressure (BP) and improve endothelial function. However, the impact of nitrate from different dietary sources on BP remains unclear.
Objectives: The objective of this study was to determine the relationships between dietary nitrate and nitrite from vegetables (with drinking water) and processed meats with BP and other cardiovascular disease (CVD) risk markers in a representative United Kingdom population.
Methods: Data from the cross-sectional National Diet and Nutrition Survey years 1‒8, adults (19‒64 y) were used. For the analysis, a database of nitrate and nitrite concentrations in vegetables, drinking water, processed meats, and composite dishes was developed. The population was stratified into quartiles of increasing total and daily nitrate or nitrite intakes from vegetables (including drinking water) and processed meats to determine the relationships with biomarkers of CVD risk (BP, lipid profile, C-reactive protein, anthropometric measures, and glycemic control) using an analysis of covariance.
Results: This dataset included 3338 adults (59% female) with a mean age of 43 y (standard deviation 12). Across increasing quartiles of vegetable nitrate intake, systolic BP (SBP), diastolic BP, waist circumference, waist-to-hip ratio, and glycated hemoglobin were lower in Q3 (95‒130 mg/d nitrate) than in Q1 (3‒65 mg/d) (P ≤ 0.038). Participants in Q4 (>131 mg/d) had lower pulse pressure, glucose, C-reactive protein, and total cholesterol concentrations than Q1 (P ≤ 0.05). Similar beneficial associations on SBP and lipid profiles were also evident for dietary nitrite intake from vegetables (P ≤ 0.05). In contrast, there was no difference in CVD risk biomarkers across quartiles of nitrate intake from processed meats, with higher SBP in Q4 (1.8‒3 mg/d nitrate) than Q1 (0.1‒0.8 mg/d) (P = 0.010).
Conclusions: These data suggest that the dietary source of dietary nitrate and nitrite may play an important role in determining the relationship with BP and other CVD risk biomarkers in a representative United Kingdom population. This trial was registered at clinicaltrials.gov as NCT05178875.
Background: Cottonseed oil (CSO) has displayed beneficial effects regarding blood lipids, albeit in relatively high doses.
Objectives: The aim was to examine the effects of 3 doses of CSO compared with a control (CON) diet on blood lipids in adults at risk of cardiovascular disease (CVD).
Methods: Ninety-one adults with obesity and/or hypercholesterolemia completed this randomized, parallel clinical trial with a 4-wk partial outpatient feeding intervention. Participants were randomly assigned into 1 of 4 groups: intervention group received 10% estimated energy needs (EEN) from cottonseed oil (LOW) (n = 23), intervention group received 20% EEN from cottonseed oil (MID) (n = 23), or intervention group received 30% EEN from cottonseed oil (HIGH) (n = 22) providing 10%, 20%, or 30% of EEN from CSO, respectively, or control (CON) (n = 23), receiving 10% of EEN from a combination of oils. Fasting blood lipids were obtained at preintervention and postintervention visits, followed by a high-fat meal challenge (35% EEN) with 5-h postprandial blood draws to evaluate lipid metabolism.
Results: Compared with the control diet, total cholesterol decreased in LOW, MID, and HIGH, respectively (-10.2 mg/dL; -12.5 mg/dL; -13.9 mg/dL, respectively; P < 0.05 for all). Similarly, non-high-density lipoprotein cholesterol decreased in LOW, MID, and HIGH (-10.2 mg/dL; -15.8 mg/dL; -16.5, respectively; P < 0.05 for all) compared with CON. Low-density lipoprotein cholesterol reduced in MID and HIGH (-11.7 mg/dL and -12.9 mg/dL, respectively; P < 0.05 for both) with a trend for reduction in LOW (-6.8 mg/dL; P = 0.08) compared with no change in CON. Postprandial triglycerides were reduced in HIGH (-14.7 mg/dL, P = 0.02) compared with LOW, MID, and CON.
Conclusions: Enriching diets with 10%, 20%, and 30% CSO improved fasting blood lipids in CVD at-risk adults, with the best results in the 20% and 30% doses. This trial was registered at clinicaltrials.gov as NCT05686954.
Background: Intake of added sugars, such as sucrose, is high globally. In rats, a maternal high-sucrose diet (HSD) from 10 wk before pregnancy to embryonic day (E)19.5 has widespread impacts on maternal, placental, and fetal blood and brain steroid levels, including glucocorticoids, androgens, and aldosterone.
Objectives: This study examined whether maternal HSD during pregnancy alone is sufficient to alter maternal, placental, and fetal steroids.
Methods: Pregnant rats received either a control diet (1% kcal sucrose) or an isocaloric, nutrient-matched HSD (26% kcal sucrose) between E0.5 and 19.5. On E19.5, we collected maternal serum, placenta, fetal blood and brain, and amniotic fluid. We microdissected the placenta and fetal brain and measured 14 steroids using liquid chromatography tandem mass spectrometry (n = 12-15/diet/sex).
Results: Maternal HSD during pregnancy alone did not alter maternal food intake, maternal body mass, and litter size (all P values ≥ 0.29, Student's t-test) but increased the percentage of males in a litter (P = 0.03, Student's t-test). Maternal HSD did not alter steroids in the maternal serum (all P values ≥ 0.21, Student's t-test), placenta [all P values ≥ 0.07, 2-way analysis of variance (ANOVA)], and fetal blood (all P values ≥ 0.13, 2-way ANOVA). Nonetheless, maternal HSD increased testosterone in the fetal nucleus accumbens (P = 0.04, 2-way ANOVA), decreased allopregnanolone in the fetal amygdala (P = 0.01, 2-way ANOVA), and decreased 11-dehydrocorticosterone in the amniotic fluid (P = 0.05, 2-way ANOVA).
Conclusions: Maternal HSD during pregnancy alone does not affect steroid levels in the maternal serum, placenta, or fetal blood of rats, but disrupts testosterone and allopregnanolone levels in critical regions of the fetal brain that regulate reward-seeking and emotion. Thus, although a long-term maternal HSD is necessary for widespread endocrine effects, the fetal brain is sensitive to short-term increases in maternal sucrose consumption during pregnancy.
Background: Prenatal supplementation with the essential nutrient choline improves insulin sensitivity in Wistar rat offspring. Whether these benefits extend to choline's oxidized derivative, betaine, and how they relate to gut microbiota composition and function remains unclear.
Objectives: We investigated the effects of prenatal choline or betaine supplementation on metabolic phenotypes and whether gut microbiota features predict functional outcomes in offspring.
Methods: Pregnant Wistar rats (n = 11/group) were fed an AIN-93G diet and randomly assigned to receive either 0.25% choline, 0.25% betaine, or no supplementation (control) in their drinking water during pregnancy. One female and one male offspring from each dam (n = 11/group) were weaned to a high-fat diet for 12 wk. Metabolic measures were analyzed using analysis of variance models, gut microbiota profiles were evaluated with Analysis of Composition of Microbiomes with Bias Correction, and predictive capacity was tested using nested cross-validation.
Results: Offspring of choline- and betaine-supplemented dams showed lower body weight (8% in females, P < 0.0001; 7% in males, P < 0.01) and food intake (7% in females, 10% in males; both P < 0.05) compared with control, with variations in fasting blood glucose, plasma glucagon, and insulin. Colon total glucagon-like peptide-1 (GLP-1) concentrations were higher in both supplemented groups (50% in females, 40% in males; P < 0.0001), with betaine exerting 80% higher circulating total GLP-1 in males (P < 0.001). Prenatal choline and betaine produced distinct, sex-specific gut microbiota signatures, with 40% higher fecal butyrate concentrations (P < 0.0001). Machine learning identified Akkermansia and Adlercreutzia, overlapping with betaine exposure, as predictors of fecal butyrate (r = 0.48, P < 0.001) and colon GLP-1 concentrations (r = 0.34, P < 0.05).
Conclusions: Prenatal supplementation of choline or betaine enhances features of the glucoregulatory system in offspring in concert with shifts in gut microbiota composition that were predictive of metabolic function.
Background: Previous evidence on the associations of dairy intake with risk of cardiometabolic diseases has been inconsistent with studies showing inverse, null, or positive associations.
Objectives: We aimed to assess these associations in China, where dairy consumption level is low and cardiometabolic disease patterns differ from those in the West.
Methods: The China Kadoorie Biobank is a prospective cohort study with ∼512,000 adult participants recruited from 10 diverse localities in China during 2004-2008. At baseline and periodic resurveys, information on the consumption frequency of major food groups was collected using a validated interviewer-administered laptop-based questionnaire. During ∼ 5.4 million person-years of follow-up, 18,306 diabetes, 33,946 ischemic heart diseases [IHD, including 3888 acute myocardial infarction (MI)], 33,670 ischemic stroke, 7191 intracerebral hemorrhage (ICH) cases, and 13,241 cardiovascular deaths were recorded. Cox regression was used to calculate adjusted hazard ratios (HRs) relating dairy intake to cardiometabolic disease risk.
Results: At baseline, 10.7% of participants regularly consumed (i.e., ≥4 d/wk) dairy products, whereas 70.0% reported never or rare consumption. After adjusting for potential confounders including body mass index, dairy consumption was significantly and positively associated with IHD but inversely associated with risks of acute MI, ICH and cardiovascular death, with HRs for regular consumers compared with nonconsumers being 1.09 (95% CI: 1.06, 1.12), 0.88 (0.80, 0.98), 0.69 (0.62, 0.76), and 0.82 (0.77, 0.87), respectively, but not with diabetes and IS. These associations were largely independent of systolic blood pressure.
Conclusions: In Chinese adults, higher dairy consumption was associated with lower risks of acute MI, ICH, and cardiovascular death. Future studies are warranted to further elucidate these relationships and their causality.

