British Journal of Nutrition最新文献

Fine particulate matter (PM_2.5) is a known risk factor for heart failure (HF), while plant-based dietary patterns may help reduce HF risk. This study examined the combined impact of PM_2.5 exposure and a plant-based diet on HF incidence. A total of 190,092 participants from the UK Biobank were included in this study. HF cases were identified through linkage to the UK National Health Services register, with follow-up lasting until October 2022 in England, August 2022 in Scotland, and May 2022 in Wales. Annual mean PM_2.5 concentration was obtained using a land use regression model, while the healthful plant-based diet index (hPDI) was calculated using the Oxford WebQ tool based on two or more 24-hour dietary assessments of 17 major food groups. Cox proportional hazard models assessed the associations of PM_2.5 and hPDI with HF risk, and interactions were evaluated on additive and multiplicative scales. During a median of 13.4-year follow-up, 4,351 HF cases were recorded. Participants in the highest PM_2.5 tertile had a 23% increased HF risk (HR: 1.23, 95% CI: 1.14-1.32) compared to those in the lowest tertile. Moderate or high hPDI was associated with reduced HF risk relative to low hPDI. The lowest HF risk was observed in individuals with high hPDI and low PM_2.5 exposure, underscoring the protective role of a plant-based diet, particularly in areas with lower PM_2.5 levels. A healthy plant-based diet may mitigate HF risk, especially in populations exposed to lower PM_2.5 levels.

Dietary intervention is a key strategy for preventing and managing chronic kidney disease (CKD). However, evidence on specific foods' effects on CKD is limited. This study aims to clarify the impact of various foods on CKD risk. We used two-sample Mendelian randomization (TSMR) to analyze the causal relationships between the intake of 18 foods (e.g., cheese, processed meat, poultry, beef, non-oily fish) and CKD risk, as well as eGFRcr and eGFRcys levels. The inverse variance weighting (IVW) method, weighted median method, MR-Egger regression, simple mode and weighted mode were employed. Sensitivity analysis included Cochran's Q test and the Egger intercept test. Frequent alcohol intake was linked to higher CKD risk (P=0.007, 0.048). Protective factors included cheese (OR=0.71, [95%CI: 0.53, 0.94], P=0.017), tea (OR=0.66, [95%CI: 0.43, 1.00], P=0.048) and dried fruit (OR=0.78, [95%CI: 0.63, 0.98], P=0.033). Oily fish (β=0.051, [95%CI: 0.001, 0.102], p=0.046) and dried fruit (β=0.082, [95%CI: 0.016, 0.149], p=0.014) were associated with elevated eGFRcys. Salad/raw vegetables (β=0.024, [95%CI: 0.003, 0.045], p=0.028) and dried fruit (β=0.013, [95%CI: 0.001, 0.031], p=0.014) were linked to higher eGFRcr, while cereal intake (β=-0.021, [95%CI: -0.033, -0.010], p<0.001) was associated with lower eGFRcr. These findings provide insights for optimizing dietary strategies for CKD patients.

High-fat food intake is associated with atopic dermatitis (AD), but the role of habitual dietary habits related to the frequency of high-fat food intake remains unclear. To address this, we developed a frequency-based dietary index, Diet Quality based on Dietary Fat Score, to assess high-fat food intake and examined its association with AD in 13,561 young Chinese adults (mean age = 22.51 years, SD ± 5.90) from Singapore and Malaysia. Using an investigator-administered questionnaire aligned with the validated International Study of Asthma and Allergy in Childhood protocol, we conducted multivariable logistic regression adjusting for demographics, body mass index, genetic predisposition, and lifestyle factors, with false discovery rate correction for multiple comparisons. Frequent high-fat food intake was associated with higher odds of AD presentation (Adjusted Odds Ratios [AOR]: 1.525; 95% Confidence Intervals [CI]: 1.314-1.772; adjusted p < 0.001). The association remained significant regardless of total fat intake (AOR: 1.445; 95% CI: 1.054-1.801; adjusted p < 0.001) and among individuals with high fruit and vegetable intake (Adjusted Odds Ratios [AOR]: 1.489; 95% Confidence Intervals [CI]: 1.191-1.860; adjusted p < 0.001) or low energy intake (AOR: 1.399; 95% CI: 1.054-1.857; adjusted p < 0.05). No synergistic effects were observed between dietary factors. These findings highlight that frequent intake of high-fat foods is independently associated with AD, emphasizing the importance of dietary moderation in AD risk management.

Research on the association between the Chinese visceral adiposity index (CVAI) and hyperuricemia (HUA) is scarce, and whether the association differs by sex is unclear. This research aimed to explore sex-specific associations between CVAI and HUA and to compare CVAI's predictive performance with other adiposity indices using data from 22,171 adults (30-79 years) in the China Multi-Ethnic Cohort (CMEC) study (Chongqing region). The prevalence of HUA was 20.9% in men and 9.7% in women. Multivariable logistic regression analyses were utilized to assess the adjusted odds ratios (ORs) and 95% confidence intervals (CIs). After multivariable adjustment, CVAI was associated with HUA in men (OR Q4 vs. Q1 = 3.31, 95% CI 2.73, 4.03) and women (OR Q4 vs. Q1 = 7.20, 95% CI 5.12, 10.12). Moreover, Significant interactions were observed between BMI and CVAI on HUA in both sexes (all P_interaction <0.001), with the strongest associations in those with BMI <24.0 kg/m². The ORs (95% CI) across different BMI groups (<24.0, 24.0-27.9, ≥28.0 kg/m²) were 1.87 (1.63, 2.13), 1.65 (1.48, 1.85), and 1.30 (1.14, 1.49) for men, and 2.76 (2.18, 3.51), 2.46 (1.98, 3.07), and 1.87 (1.47, 2.39) for women, respectively. Additionally, CVAI showed satisfactory predictive performance for HUA in women, with the largest area under the receiver operating characteristic curve (AUROC) of 0.735, but not in men (0.660). These findings suggest a close association between CVAI and HUA, particularly pronounced in those with BMI <24.0 kg/m², and a stronger association in women than in men.

Despite previous observational studies suggesting that malnutrition could be involved in venous thromboembolism (VTE), definitive causality still lacks in high-quality research evidence. This study aims to explore the genetic causal association between malnutrition and VTE. The study was performed using summary statistics from genome-wide association studies (GWAS) for VTE (cases =23,367; controls =430,366). Single nucleotide polymorphism (SNP) associated with exposure was selected based on quality control steps. The primary analysis employed the Inverse-variance weighted (IVW) method, with additional support from MR-Egger, weighted median, and weighted mode approaches. MR-Egger, leave-one-SNP-out analysis and MR-PRESSO was used for sensitivity analysis. Cochran's Q test was used to assess heterogeneity between instrumental variables (IVs). IVW suggested that overweight have a positive genetic casual effect on VTE (OR=1.1344, 95% CI= 1.056-1.2186, p<0.001). No genetic casual effect of malnutrition (IVW: OR=0.9983, 95% CI= 0.9593-1.0388, p=0.9333) was found on VTE. Cochran's Q test suggests no possible heterogeneity in both related exposures. The results of the MR-Egger regression suggest that the analysis is not affected by horizontal pleiotropy. The results of the MR-PRESSO suggest that there are no outliers. The results revealed a statistical genetical association where overweight correlate with an increased risk of VTE. Meanwhile, no genetical causal link was observed between malnutrition and VTE. Further research is warranted to deepen our understanding of these associations.

This study elucidated the impacts of coenzyme Q10 (COQ10) supplementation in a high-fat diet on growth, lipid metabolism, and mitochondrial function in spotted seabass (Lateolabrax maculatus). Totally five diets were formulated: a diet with normal fat content (11% lipid, NFD), a high-fat diet (17% lipid, HFD), and three additional diets by supplementing 5, 20 or 80 mg/kg of COQ10 to the HFD. After an 8-week culture period, samples were collected and analyzed. The results demonstrated that COQ10 inclusion prevented the HFD-induced deterioration of growth performance and feed utilization. COQ10 alleviated the deposition of saturated fatty acids following HFD intake and promoted the assimilation of n-3 and n-6 polyunsaturated fatty acids. Moreover, COQ10 administration inhibited the surge in serum transaminase activity and reduced hepatic lipid content following HFD ingestion, which was consistent with the results of oil red O staining. In addition, HFD feeding led to reduced hepatic citrate synthase and succinate dehydrogenase activities, and decreased ATP content. Notably, COQ10 administration improved these indices, and up-regulated the expression of mitochondrial biogenesis-related genes (pgc-1α, pgc-1β, nrf-1, tfam) and autophagy-related genes (pink1, mul1, atg5). In summary, supplementing 20-80 mg/kg of COQ10 in the HFD promoted growth performance, alleviated hepatic fat accumulation, and enhanced liver mitochondrial function in spotted seabass.

Inflammation and oxidative stress contribute to the progression of chronic diseases, and the volume of research in this area is rapidly expanding. Various dietary indices have been developed to determine the overall inflammatory or oxidative stress potential of a diet; however, few have been validated in cardiometabolic disease populations. This review aimed to explore the association between dietary indices and biomarkers of inflammation and oxidative stress in adults with cardiometabolic conditions. Four databases were systematically searched for literature in any language (Embase, CINAHL, CENTRAL, and MEDLINE) with 12,177 deduplicated records identified. Seventeen studies of adults with metabolic syndrome, cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease or chronic kidney disease were included. Fourteen studies were observational studies, one study was a clinical trial, and one was a randomised controlled trial. Four dietary indices were reported on with most studies (n=11) reporting on the dietary inflammatory index. The most reported biomarker was C-reactive protein. The findings were narratively synthesised. Results were inconclusive due to the heterogeneity of dietary indices and their use, disease states, and biomarkers reported. Only one study reporting on the dietary inflammatory index assessed all 45 parameters. Observational studies, particularly retrospective designs (n=7) are subject to recall and selection biases, potentially presenting overestimated results. Further research is required to determine the relationship between dietary indices and biomarkers of inflammation and oxidative stress in cardiometabolic disease populations. Future research should be rigorous, prospective, assess the full range of index parameters, and examine biomarkers the tool was developed for.

Evidence of an association between metabolic syndrome (MetS) and irritable bowel syndrome (IBS) is emerging but is still inconclusive. The current cross-sectional study was conducted to explore the relationship between the two syndromes in a sample of Lebanese adults (n=221; mean age: 43.36 years; 62.9% females), recruited from a large urban university and its neighboring community. MetS was diagnosed based on the International Diabetes Federation criteria, and IBS was assessed using the Birmingham IBS scale. Logistic regression analyses were performed taking MetS and its components as dependent variables, and IBS and its subscales as independent variables. Covariates included sociodemographic, dietary, and lifestyle variables. MetS was positively associated with Visual Analogue Scale (VAS)-IBS (total scale (Beta=4.59, p=0.029) and VAS-Diarrhea subscale (Beta=4.96, p=0.008). Elevated blood pressure (Beta=5.02, p=0.007), elevated fasting blood sugar (Beta=4.19, p=0.033), and elevated waist circumference (Beta=5.38, p=0.010) were positively associated with VAS- Diarrhea subscale. MetS and IBS were found to be positively associated in a sample of the Lebanese adult population. We suggest that it might be of value to screen for either condition if one of the syndromes exists. Future longitudinal studies are essential to establish a causal relationship between the two syndromes to further understand the commonality related to pathogenesis and explore potential underlying mechanisms.

Dietary guidelines often combine plant and animal protein intake recommendations, yet some evidence suggests they may have distinct associations with diet quality and obesity. This study aimed to examine relationships between animal and plant protein intake, based on different protein classification approaches, and diet quality and obesity. Plant and animal protein contents of foods reported by 7637 adult participants aged ≥19 years during the 2011-12 Australian National Nutrition and Physical Activity Survey were estimated using Australian food composition databases. Usual animal, plant, and total protein intakes were estimated using Multiple Source Method. Diet quality was assessed using the 2013-Dietary Guidelines Index (DGI), and obesity measures included BMI and waist circumference (WC). Sex-stratified multiple linear and logistic regressions were performed and adjusted for potential confounders. Plant and animal protein intakes were positively associated with DGI scores [Plant protein: men, β=0.74(95%CI: 0.64, 0.85); women, β=0.78(0.67, 0.89); Animal protein: men, β=0.15(0.12, 0.18); women, β=0.26(0.22, 0.29)]. These associations were consistent when examining high-quality plant protein (i.e., high-protein-containing plant-based foods with comparable nutritional values to animal proteins) and non-dairy animal protein intakes. Plant protein intake was inversely associated with BMI and WC in men but not women. Animal protein intake was positively associated with BMI in men and women and WC in men only [β=0.04(0.02, 0.07)]. Plant protein intake was inversely associated with obesity [OR=0.97(0.96, 0.99)] and central obesity [OR=0.97(0.95, 0.98)] among men only. Further studies are needed to examine the influence of different animal protein sources by accounting for energy intake and sex-specific associations.

The sulfur microbial diet (SMD), a dietary pattern associated with 43 sulfur-metabolizing bacteria, may influence gut microbiota composition and contribute to aging process through gut-produced hydrogen sulfide (H₂S). We aimed to explore the association between SMD and biological age acceleration, using the cross-sectional study included 71,579 individuals from the UK Biobank. The SMD score was calculated by multiplying β-coefficients by corresponding serving sizes and summing them, based on dietary data collected using the Oxford WebQ, a 24-hour dietary assessment tool. Biological age (BA) was assessed using Klemerae-Doubal (KDM) and PhenoAge methods. The difference between BA and chronological age refers to the age acceleration (AgeAccel), termed "KDMAccel" and "PhenoAgeAccel". Generalized linear regression was performed. Mediation analyses were used to investigate underlying mediators including body mass index (BMI) and serum aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio. Following adjustment for multiple variables, a positive association was observed between consuming a dietary pattern with a higher SMD score and both KDMAccel (β_Q4vsQ1 = 0.35, 95%CI = 0.27 to 0.44, P<0.001) and PhenoAgeAccel (β_Q4vsQ1 = 0.32, 95%CI = 0.23 to 0.41, P<0.001). Each 1-standard deviation increase in SMD score was positively associated with the acceleration of biological age by 7.90% for KDMAccel (P<0.001) and 7.80% for PhenoAgeAccel (P<0.001). BMI and AST/ALT mediated the association. The stratified analysis revealed stronger accelerated aging impacts in males and smokers. Our study indicated a higher SMD score is associated with elevated markers of biological aging, supporting the potential utility of gut microbiota-targeted dietary interventions in attenuating the aging process.