Background: Evidence is limited regarding the association between lifestyles and cardiovascular disease (CVD), and the extent to which healthy lifestyles could offset the genetic risk of CVD in females with breast cancer (BC). Methods: Females diagnosed as BC, who were free of CVD at baseline, from UK Biobank were included. Five modifiable lifestyle factors were considered to calculate the healthy lifestyle score, namely body mass index (BMI), smoking, alcohol drinking, dietary habits, and physical activity. The polygenetic risk score (PRS) was derived for coronary heart disease (CHD), ischemic stroke (IS), and heart failure (HF). Results: In 13,348 female BC survivors, there were 986 CVD events (736 CHD, 165 IS, and 353 HF) over a median of 8.01 years of follow-up. Participants with 4–5 healthy lifestyle components were associated with a decreased risk of incident CVD (HR: 0.50; 95%CI: 0.37, 0.66), CHD (HR: 0.49; 95%CI: 0.35, 0.69), IS (HR: 0.35; 95%CI: 0.19, 0.65), and HF (HR: 0.59; 95%CI: 0.36, 0.97), compared with those with 0–1 lifestyle components. Evidence for the genetic–lifestyle interaction was observed for CHD (p = 0.034) and HF (p = 0.044). Among participants at high genetic risk, a healthy lifestyle was associated with a lower risk of CHD (HR: 0.37; 95%CI: 0.24, 0.56), IS (HR: 0.37; 95%CI: 0.15, 0.93) and HF (HR: 0.39; 95%CI: 0.21, 0.73). Conclusions: Our findings suggest that BC survivors with a high genetic risk could benefit more from adherence to a healthy lifestyle in reducing CVD risk.

Aim: Alcohol intake alters DNA methylation profiles and methylation might mediate the association between alcohol and disease, but limited number of positive CpG sites repeatedly replicated. Materi...

Background: Strategies to stabilize and support overall infant health by increasing the number of Bifidobacterium longum in the infant gut are of interest, but few studies have systematically addressed this issue. We aimed to evaluate the efficacy and safety of Bifidobacterium longum use in infants using meta-analysis. Methods: We searched PubMed, EMBASE, Cochrane Library of Systematic Reviews, and SinoMed for publications until 27 July 2022. The main outcomes of interest were weight gain, risk of necrotizing enterocolitis (NEC), and adverse events. Two authors independently performed study screening, risk of bias assessment, and data extraction. Outcome data were extracted from each included study and combined using mean difference (MD) or risk ratio (RR) and finally combined using a fixed-effect model or random-effect model. Results: A total of 4481 relevant studies were identified, of which 15 were found to be eligible for randomized controlled trials and were included in the meta-analysis. The combined extracted data showed that the intervention group containing Bifidobacterium longum had a significantly lower risk of NEC (RR = 0.539, 95% CI: 0.333, 0.874) compared to the control group. There was no statistical difference between the intervention and control groups regarding weight gain (MD = 0.029, 95% CI: −0.032, 0.090), the occurrence of adverse events (RR = 0.986, 95% CI: 0.843, 1.153), and serious adverse events (RR = 0.881, 95% CI: 0.493, 1.573). Conclusions: Bifidobacterium longum may significantly reduce the risk of NEC in infants as well as being safe; thus, further research evidence is needed on whether there is a benefit on weight gain.

Background: While parental type 2 diabetes (T2D) is a known risk factor for offspring T2D, the differential impact of maternal versus paternal transmission remains debated. Methods: This prospective family-based cohort study enrolled 4508 diabetes-free adults from Northern China with a median 7.32-year follow-up. Using Cox proportional hazards models, we examined parent-of-origin effects on T2D incidence, adjusting for lifestyle, adiposity, and metabolic covariates. Results: Parental T2D conferred elevated offspring risk (adjusted HR = 1.82, 95% CI:1.44–2.30), and was predominantly driven by maternal transmission. Maternal T2D was robustly associated with offspring risk (HR = 1.89, 95% CI: 1.47–2.43), whereas paternal T2D showed no significant effect (HR = 1.27, 95% CI: 0.88–1.84). Offspring with only maternal T2D history exhibited the highest risk (HR = 2.55, 95% CI: 1.87–3.50; p = 4.70 × 10⁻⁹), persisting after full adjustment, while no significant association was observed for paternal diabetes. Lifestyle modified this association: healthy diet (diet score > 2 vs. ≤2: HR = 1.34 vs. 2.76; p_interaction = 9.10 × 10⁻⁴) and regular exercise (regular vs. unregular: HR = 1.13 vs. 2.10; p_interaction = 4.20 × 10⁻²) attenuated maternal transmission. Conclusions: Maternal T2D confers greater intergenerational risk than paternal T2D, with modifiable lifestyle factors mitigating this association. These findings highlight the importance of integrating maternal diabetes history into clinical risk stratification tools and prioritizing lifestyle interventions in the offspring of affected mothers to mitigate inherited risk.

(1) Background: Previous studies suggest that exposure to nitrogen dioxide (NO₂) has a negative impact on health. But few studies have explored the association between NO₂ and blood lipids or fasting plasma glucose (FPG), as well as gene–air pollution interactions. This study aims to fill this knowledge gap based on a pedigree cohort in southern China. (2) Methods: Employing a pedigree-based design, 1563 individuals from 452 families participated in this study. Serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDLC), and FPG were measured. We investigated the associations between short-term NO₂ exposure and lipid profiles or FPG using linear mixed regression models. The genotype–environment interaction (GenoXE) for each trait was estimated using variance component models. (3) Results: NO₂ was inversely associated with HDLC but directly associated with TG and FPG. The results showed that each 1 μg/m³ increase in NO₂ on day lag0 corresponded to a 1.926% (95%CI: 1.428–2.421%) decrease in HDLC and a 1.400% (95%CI: 0.341–2.470%) increase in FPG. Moreover, we observed a significant genotype–NO₂ interaction with HDLC and FPG. (4) Conclusion: This study highlighted the association between NO₂ exposure and blood lipid profiles or FPG. Additionally, our investigation suggested the presence of genotype–NO₂ interactions in HDLC and FPG, indicating potential loci-specific interaction effects. These findings have the potential to inform and enhance the interpretation of studies that are focused on specific gene–environment interactions.