Clinical nutrition ESPEN最新文献

Background & aims: The impact of serum Omega-6 fatty acids on cardiovascular health is debated, with evidence supporting both protective and harmful effects. To investigate the association between serum Omega-6 fatty acid and mortality from all causes and cardiovascular disease (CVD), utilizing advanced statistical methodologies including competing risk models and multivariate Mendelian randomization.

Methods: Data of 5,070 participants from National Health and Nutrition Examination Survey (NHANES) in 2011 to 2014 wave were analyzed, with follow-up data on mortality sourced from the National Death Index. Serum Omega-6 fatty acids level was measured at baseline. Cox proportional hazards regression and competing risks models was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and CVD mortality by baseline Omega-6 fatty acids level. Restricted cubic splines were used to explore the nonlinearity. Mendelian randomization to assess the causal relationships between Omega-6 levels and mortality.

Results: 438 all-cause deaths and 137 CVD deaths were observed during an 83 months median follow-up. Restricted cubic spline analysis demonstrated a U-shaped correlation between baseline serum Omega-6 fatty acid levels with all-cause and CVD mortality risks. Subgroup analysis indicated that for the low-level Omega-6 fatty acid participants, the hazard ratios were 0.68 (95% CI, 0.55-0.85) for all-cause mortality and 0.62 (95% CI, 0.40-0.95) for CVD mortality. Conversely, for the high-level participants, the hazard ratios were 1.14 (95% CI, 1.01-1.28) for all-cause mortality and 1.23 (95% CI, 1.05-1.44) for CVD mortality. Both univariate and multivariate Mendelian randomization analyses confirmed a positive causal relationship between higher serum Omega-6 fatty acid levels and increased CVD mortality risk.

Conclusions: The findings suggest a U-shaped relationship between serum Omega-6 fatty acid levels and mortality risks, with elevated levels linked causally to increased CVD mortality. These results underscore the need for balanced dietary Omega-6 fatty acid intake to optimize cardiovascular health.

Background & aims: Semaglutide has demonstrated efficacy in both glycemic control and weight loss. This systematic review and meta-analysis aimed to assess the efficacy and safety of the combined use of semaglutide and basal insulin in individuals diagnosed with type 2 diabetes mellitus (T2DM).

Methods: PubMed, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), and China Science and Technology Journal Database (VIP) were searched to identify relevant publications. The primary outcome measure was the change in HbA1c levels. Secondary outcome measures encompassed change in body weight, fluctuations in FPG levels, occurrence of adverse events, serious adverse events, hypoglycemic episodes, and gastrointestinal reactions including nausea, vomiting, and diarrhea. Mean differences (MDs) and relative risk (RR) with confidence intervals (CI) of 95% were used to analyze the deference.

Results: 7 RCTs with 2354 patients were incorporated into the study. Compared to placebo or other active treatment, the addition of semaglutide to basal insulin demonstrated significant reductions in hemoglobin A1c (HbA1c) [mean differences (MD): -1.17%, P<0.00001], body weight [MD -5.99 kg, P<0.00001], and fasting blood glucose (FPG) [MD -1.08%, P<0.00001]. No evidence indicated a higher risk of adverse events [RR 1.46, P=0.13]. However, it did result in increased rates of gastrointestinal adverse events, including nausea, vomiting and diarrhea.

Conclusions: The combination treatment of semaglutide and basal insulin demonstrates significant improvements in glycemic control and reduction in body weight, without an increased risk of hypoglycemia. Our findings provided support for the utilization of a combination therapy involving semaglutide and basal insulin in T2DM.

Background: The circadian clock, which governs periodic physiological changes, is influenced by various environmental factors, and its disruptions can lead to non-communicable chronic diseases (NCDs). Among the genes that control the circadian clock are ARNTL, CLOCK, CRY1, PER1, PER2, NR1D2, and MTNR1B, with several polymorphisms associated with diseases such as diabetes and hypertension. Therefore, this study aimed to determine the association between SNPs in the aforementioned genes and markers of non-communicable chronic diseases (NCDs) in a young population, stratified by gender.

Methods: A sample of 346 individuals of both sexes aged 18 to 27 underwent clinical and nutritional evaluations to determine clinical markers associated with NCDs. Using isothermal PCR, 119 polymorphisms in the ARNTL, CLOCK, CRY1, PER1, PER2, NR1D2, and MTNR1B genes were determined. Subsequently, binary logistic regression analyses and mean comparisons using Student's t-test and one-way ANOVA with Bonferroni adjustment were performed.

Results: Polymorphisms were associated with risk factors such as elevated waist circumference, BMI, insulin, and lipid imbalances, while some acted protectively. Notable SNPs included rs6486122, rs77486964, rs11022756, rs72869158 from ARNTL; rs7309618, rs10778528 from CRY1; rs2304911 from PER1; rs72620839, rs58574366 from PER2; rs6832769, rs1056547 from CLOCK; and rs4858095, rs11922577 from NR1D2, providing insights into the associations of genetic markers with clinically relevant markers for NCDs.

Conclusion: Clock gene polymorphisms exhibit associations with clinical markers of NCDs, emphasizing the intricate interaction between the biological clock and risk factors. This underscores the importance of genetic testing and personalized clinical approaches for prevention and treatment. Further research is needed to understand the underlying mechanisms and long-term health impacts of these genetic variations.