Urinary metals as influencing factors of coronary heart disease among a population in Guangzhou, China.

The cardiovascular system is highly sensitive to toxic metal exposure and trace element dysregulation. However, previous findings relating to metal exposure and coronary heart disease (CHD) have partially been conflicting and difficult to exhibit the combined effect of metal mixtures. This case-control study investigated urinary concentrations of ten metal/metalloids among clinically-diagnosed CHD patients and healthy adults during May to December 2021 in Guangzhou, China. We found that cadmium (Cd) status in urine from CHD patients was remarkably higher than its reference, while chromium (Cr), nickel (Ni), copper (Cu) and selenium (Se) concentrations were lower (p < 0.05). Spearman correlation analysis showed that urinary arsenic (As) and Se were highly correlated (rs=0.830, p < 0.001), indicating their similar sources. Principal component analysis (PCA) exhibited denser distribution of Cd-Sn in cases than in controls. Logistic regression analysis exhibited significant associations between urinary Cd (adjusted OR: 1.965, 95% CI: 1.222-3.162), Se (0.787, 95% CI: 0.695-0.893), Ni (0.493, 95% CI: 0.265-0.916) and CHD risk. Quantile g-computation showed negative joint effect of metal mixtures on CHD (adjusted OR: 0.383, 95% CI: 0.159-0.932) (p < 0.05), suggesting the need for supplementing essential trace elements. The negative partial effect was primarily attributed to Se and Ni, while positive partial effect was mainly due to tin (Sn) and Cd. Nevertheless, we also found a quantile increase of Cd-Sn level was negatively correlated with 8.26% (95% CI: 3.44-13.08%) decrease of high-density lipoprotein cholesterol (p < 0.001), and 71.2% of the joint effect attributed to Cd. Based on random forest, Se, Cd and Ni were found to be the dominant influencing factors of CHD. The role of Ni in CHD is yet to be uncovered, while excessive Cd exposure and low Se status among CHD patients need to be mitigated.

Egg consumption improves vascular and gut microbiota function without increasing inflammatory, metabolic, and oxidative stress markers.

Egg consumption is one of the many inconsistencies in evidence linking dietary cholesterol to cardiovascular disease (CVD). In addition, the gut microbiota and its metabolite, trimethylamine-N-oxide (TMAO), have been shown to play a crucial role in the development of CVD. The fact that egg is rich in choline suggests that excessive egg consumption may increase TMAO production by altering the gut microbiota. However, the effects of egg consumption on vascular function and gut microbiota remain unclear. Here, the diet of nine young male subjects was supplemented with two boiled eggs daily for 2 weeks. Changes in vascular function, inflammation, metabolism, oxidative stress, and gut microbiota were examined. We found that egg consumption increased flow-mediated dilation and decreased brachial-ankle pulse wave velocity. Furthermore, egg consumption positively modulated the gut microbiota function but had no effects on the levels of C-reactive protein, glucose, lipid profile, malondialdehyde, superoxide dismutase, or TMAO. The current study provides evidence that egg consumption improves vascular function, which may be related to the alterations seen in the gut microbiota. Therefore, moderate egg consumption may help to improve vascular and intestinal function in individuals at low risk of developing CVD and other metabolic disorders.

First-Trimester Maternal Folic Acid Supplementation Modifies the Effects of Risk Factors Exposures on Congenital Heart Disease in Offspring.

This study aimed to examine effect modification of maternal risk factor exposures and congenital heart disease (CHD) by maternal folic acid supplementation (FAS)/non-FAS. We included 8379 CHD cases and 6918 CHD-free controls from 40 clinical centers in Guangdong Province, Southern China, 2004-2016. Controls were randomly chosen from malformation-free fetuses and infants and frequency matched to the echocardiogram-confirmed cases by enrollment hospital and year of birth. We used multiple regression models to evaluate interactions between FAS/non-FAS and risk factors on CHDs and major CHD categories, adjusted for confounding variables. We detected statistically significant additive and multiplicative interactions between maternal FAS/non-FAS and first-trimester fever, viral infection, and threatened abortion on CHDs. An additive interaction on CHDs was also identified between non-FAS and living in a newly renovated home. We observed a statistically significant dose-response relationship between non-FAS and a greater number of maternal risk factors on CHDs. Non-FAS and maternal risk factors interacted additively on multiple critical CHDs, conotruncal defects, and right ventricular outflow tract obstruction. Maternal risk factor exposures may have differential associations with CHD risk in offspring, according to FAS. These findings may inform the design of targeted interventions to prevent CHDs in highly susceptible population groups.

Maternal folic acid supplementation mediates the associations between maternal socioeconomic status and congenital heart diseases in offspring.

Low maternal socioeconomic status (SES) is considered as a risk factor of congenital heart diseases (CHDs) in offspring. However, the pathways underpinning the SES-CHDs associations are unclear. We assessed if first trimester maternal folic acid supplementation (FAS) is a mediator of the SES-CHDs associations. This case-control study included 8379 CHD cases and 6918 CHD-free controls from 40 participating centers in Guangdong, Southern China, 2004-2016. All fetuses were screened for CHDs using ultrasound and cases were confirmed by echocardiogram. We collected SES and FAS information during face-to-face interview by obstetricians using a structured questionnaire. Low SES was defined as education attainment <12 years, household individual income <3000 Chinese Yuan/person/month or unemployment. FAS referred to at least 0.4 mg of daily folic acid intake over 5 days/week continuously. We used causal mediation analysis to estimate the direct, indirect and proportion mediated by FAS on the SES-CHDs associations adjusted for confounders. Both low maternal income and education were significantly associated with increased risks of CHDs and lower prevalence of FAS. Low maternal FAS prevalence mediated 10% [95%CI:5%,13%] and 3% [95%CI:1%,5%] of the maternal low income-CHDs and the maternal low education-CHDs associations, respectively. In addition, FAS mediated the highest proportion of the associations between income and multiple critical CHDs [46.9%, 95%CI:24.7%,77%] and conotruncal defects [31.5%, 95%CI:17.1%,52.0%], respectively. Maternal FAS partially mediated the SES-CHDs associations, especially among the most critical and common CHDs. Promoting FAS in low SES women of childbearing age may be a feasible intervention to help prevent CHDs.