International Journal for Vitamin and Nutrition Research最新文献

Background: Nonalcoholic fatty liver disease (NAFLD) was clinically documented to be accompanied by iron homeostasis imbalances, however, the causal relationship between them remains unclear. Therefore, this study aimed to examine the relationship between iron homeostasis indicators (serum iron, ferritin, transferrin, total iron binding capacity (TIBC), and transferrin saturation (TSAT)) and NAFLD risk.

Methods: We applied two-sample Mendelian randomization (MR) to assess the effects of genetic liability to iron homeostasis indicators (N = 43,220-246,139) on NAFLD risk (N = 377,988) in individuals of European ancestry. Reverse direction MR, multivariable MR, and two-step MR were performed to estimate reverse association, causal effects independent of smoking or drinking, and the mediating effect of lipid metabolism, respectively. Smoking and drinking as confounders were considered confounders.

Results: Genetically predicted serum iron, ferritin, and TSAT were significantly associated with a higher risk of NAFLD (odds ratio (OR): 1.286, 95% confidence interval (CI): 1.075-1.539; p = 0.0059; OR: 1.260, 95% CI: 1.050-1.500, p = 0.0195; and OR: 1.223, 95% CI: 1.067-1.402; p = 0.0039, respectively). Reverse direction MR analysis suggested that genetic liability to NAFLD had no significant causal effect on iron homeostasis. Sex-specific MR exhibited a stronger effect size for the association of elevated ferritin with NAFLD risk in males (OR: 1.723, 95% CI: 1.338-2.219; p = 2.48 × 10^-5). Two-step MR revealed that elevated triglycerides (TGs) mediated approximately 3%-5% of the observed effect of serum iron and TSAT on NAFLD risk, while decreased low-density lipoprotein cholesterol (LDL-C) mediated 9%-10%.

Conclusion: Genetic liability to iron status imbalance may causally affect NAFLD. This evidence may support the clinical treatment of NAFLD in the target population.

Folate and folic acid (FA) are two forms of vitamin B9, a B-complex nutrient essential for the human body. Folate is the natural form of vitamin B9 and is found in foods such as citrus fruits, leafy green vegetables, and beans. In contrast, FA is the synthetic form and is commonly found in supplements and added to fortified foods. The metabolism of folate and FA plays a crucial role in DNA synthesis and methylation; therefore, understanding the mechanism through which a decrease in folate and FA consumption affects the development of breast cancer (BC) is important. DNA hypermethylation can inhibit the transcription of tumor suppressor genes, while DNA hypomethylation may have the same effect and activate oncogene transcription. However, some genetic variants exist, such as rs1801133 and rs1801131 in the MTHFR gene and rs1051266 in the RFC gene. The MTHFR gene encodes an enzyme that facilitates the utilization of folate to support essential bodily functions, while the RFC gene is responsible for transporting folate into cells and acts as an anion exchanger. Both genes intervene in the transport and absorption of FA and are related to an increased risk of cancer. Studies investigating the relationship between FA and BC often rely on in vitro and in vivo models; however, the findings may not fully translate to humans due to significant physiological and metabolic differences across species. This article explores how changes in FA metabolism due to malabsorption defects, a deficient diet or genetic variants may impact methylation processes and their relationship with BC.

Background: This study aimed to investigate how education centering around nutrition can influence diet quality and health-related behavior in the Spanish population.

Methods: A descriptive cross-sectional study was performed, and the validated NutSo-HH (Nutritional and Social Healthy Habits) questionnaire was administered. The overall sample was 1087 Spanish adults, 48.11% of whom had studied or were studying a degree in health sciences, compared to 51.89% who had no studies or were studying another subject. Differences between groups were assessed using statistical analyses.

Results: The results indicated that people with higher nutrition education exhibited an increased consumption of vegetables (3.64 vs. 3.50), cereals (3.09 vs. 2.70), legumes (2.19 vs. 2.10) and water (3.47 vs. 3.34) (all p < 0.001) and a lower consumption of red meat (1.60 vs. 1.73) (p < 0.001). No statistically significant differences were observed in the consumption of the remaining analyzed food products. People with health literacy reported better self-perceived health (3.94 vs. 3.76) (p < 0.001) and had a lower body mass index (BMI) (23.68 kg/m² vs. 24.75 kg/m²) (p < 0.001) than those without health literacy. No significant differences were observed in the time spent in sports practice and sedentary lifestyle or in variables related to eating disorders.

Conclusions: This study concluded that although health science education showed some benefits in eating habits and perceptions of well-being, did not significantly influence all aspects of nutritional habits and lifestyles. Further studies with a more holistic approach could provide a more complete picture of the influence of health education on overall well-being.

Background: Remnant cholesterol (RC) is a risk factor for the development of atherosclerosis. Vitamin E has antioxidant properties, making it a potentially effective management tool for preventing cardiovascular disease (CVD). However, the relationship between vitamin E intake and RC remains unclear.

Methods: We conducted a cross-sectional study using data from the National Health and Nutrition Examination Survey (NHANES) Survey 2007-2020. 11,585 participants (aged ≥20, 48% male) were included. Information on vitamin E intake (dietary vitamin E intake and total vitamin E intake) was collected. RC was defined as serum total cholesterol minus high-density lipoprotein and low-density lipoprotein cholesterol. Survey-weighted linear regression models and a restricted cubic spline (RCS) were used to test the relationship between vitamin E intake and RC. Subgroup analyses and interaction tests were also performed to verify the robustness of the results.

Results: After adjusting for all potential confounders (demographics, socioeconomic status, lifestyle, diet, and comorbidities), dietary vitamin E intake was negatively associated with RC (β = -0.21, 95% CI: (-0.29, -0.12), p < 0.0001), and this negative association was also present between total vitamin E intake and RC (β = -0.12, 95% CI: (-0.18, -0.06), p < 0.0001). The RCS analysis revealed a nonlinear negative association between vitamin E intake and RC. The negative correlation existed in different subgroups, with no interaction except for the "use of vitamin E supplements" subgroup.

Conclusion: Vitamin E intake showed a protective association with RC. The results suggest that increasing dietary vitamin E intake may help reduce RC levels and CVD risk.

Background: Vitamin D (VD) and gut microbiota (GM) are important variables in pediatric hematopoietic stem cell transplantation (HSCT) recipients with bloodstream infections (BSI). Both VD and GM play significant roles in immune regulation and in maintaining intestinal barrier function.

Methods: This prospective case-control study included 48 consecutive pediatric patients who underwent HSCT, as well as 20 healthy children from the community. Plasma samples were collected pre- and post-HSCT, together with post-HSCT fecal samples. Serum 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D3 (1,25(OH)₂D₃) were measured using chemiluminescence and enzyme linked immunosorbent assay, respectively. GM was analyzed by 16S rDNA next generation sequencing.

Results: The incidence of BSI in pediatric HSCT recipients was 33.3% (16/48). No significant differences in serum 25(OH)D or 1,25(OH)₂D₃ levels were observed between the BSI and non-BSI groups either before or after transplantation, or with the healthy control group. The α-diversity of GM in BSI and non-BSI patients was significantly lower than in healthy subjects. Proteobacteria were significantly more abundant in BSI patients than in non-BSI patients (p = 0.0434) or healthy controls (p = 0.0193). Pediatric HSCT patients showed significantly higher levels of Staphylococcus (p < 0.001), Pseudomonas (p < 0.001), Enterococcus (p < 0.001), Clostridium innocuum (p = 0.0175) and Enterobacter (p = 0.0394) compared to the controls, whereas the levels of Firmicutes (p = 0.009), Actinobacteria (p < 0.001), Bifidobacterium (p < 0.001) and Faecalibacterium (p < 0.001) were significantly lower. β-diversity analysis revealed significant population differences between the three groups.

Conclusions: These results indicate there is no practical value in monitoring VD in HSCT patients. During HSCT and BSI, the GM experiences a loss of probiotics and an increase in potential pathogens.

Background: Dry Eye Disease (DED) significantly impacts global populations, causing discomfort and vision problems. This review explores the effects of lutein supplementation on DED symptoms and signs.

Methods: A systematic review was conducted following PRISMA guidelines, examining clinical trials from databases including PubMed, Web of Science, EMBASE, and the Cochrane Library. Six randomized controlled trials (RCTs) involving 584 subjects were included. Meta-analysis was not conducted due to heterogeneity in study designs, dosages, and outcome measures.

Results: Lutein dosages ranged from 3 mg/day to 20 mg/day, with treatment durations from 4 to 12 weeks. Improvements were observed in subjective symptoms, with significant reductions in Ocular Surface Disease Index (OSDI) scores in some studies. Objective measures also showed positive results: tear break-up time (TBUT) increased significantly in some trials. However, other studies reported no significant differences between treatment and control groups, reflecting heterogeneity in outcomes. Schirmer's test and corneal-conjunctival staining results varied, with some showing significant improvements and others not.

Conclusions: Lutein supplementation may benefit DED patients by improving symptoms and tear film stability. However, due to study heterogeneity, larger, well-designed RCTs are needed to establish standardized dosing and confirm these findings.

Background: This study aimed to elucidate correlations between obesity-related indicators and vitamin D (VD) status in a nationally representative sample of U.S. adults.

Methods: We analysed data from 9168 adults aged 20-59 years obtained from the 2011-2018 National Health and Nutrition Examination Survey. Serum 25 hydroxyvitamin D [25(OH)D] levels were measured and categorised into quartiles. Anthropometric measurements, including weight, waist circumference, and fat mass in various body regions quantified through dual-energy X-ray absorptiometry, were collected. Multiple imputation was employed to replace missing data. The importance of obesity-related indicators and serum 25(OH)D concentration was explored using multiple linear regression adjusted for demographics, lifestyle factors, dietary intake, and clinical biomarkers, and stepwise regression.

Results: Weight, waist circumference, and fat mass across all body regions were inversely associated with serum 25(OH)D levels (all p < 0.001). Notable differences were observed between men and women. Stepwise regression revealed a strong inverse correlation between visceral adipose tissue and serum 25(OH)D concentration in men [β 95% CI: -13.04 (-18.10, -7.99), p < 0.001], whereas in women, only weight was significantly correlated with serum 25(OH)D concentration [β 95% CI: -0.20 (-0.28, -0.12), p < 0.001]. Demographic attributes, seasonal sunlight exposure, dietary VD, calcium, phosphorus, and magnesium intake, and biomarkers including alkaline phosphatase and creatinine also emerged as significant predictors.

Conclusions: Besides conventional obesity measures, abdominal fat metrics exhibit robust associations with VD deficiency, especially in men. Public health initiatives and clinical management strategies for hypovitaminosis D in obese populations should consider nuanced aspects of adiposity distribution alongside other demographic, lifestyle, and dietary factors influencing VD.

Background: A growing body of evidence indicates the regulating effects of alpha-lipoic acid on iron metabolism. However, findings from clinical trials are equivocal. This systematic review and meta-analysis aimed to evaluate the quantitative effect of alpha lipoic acid (ALA) supplementation on iron metabolism parameters including serum iron, total iron binding capacity, hemoglobin, and ferritin.

Methodology: Online databases, including PubMed, Scopus, and Web of Science were searched, up to 29 May 2022, to obtain all relevant studies.

Results: A total of 1901 publications were identified in the systematic search; of which, 10 studies with a total of 529 participants were included in this meta-analysis. Pooled analysis of the studies showed no statistically significant effects of ALA on ferritin (weighted mean difference (WMD) = -11.01 ng/mL; 95% CI: -40.07, 18.05 ng/mL; I² = 0.0%, p = 0.670), serum iron (WMD = -0.47 μ/dL; 95% CI: -24.48, 23.54 μ/dL; I² = 94.7%, p < 0.001), hemoglobin (WMD = 0.49 g/dL; 95% CI: -0.54, 1.52 g/dL; I² = 95.7%, p < 0.001), and total iron binding capacity (TIBC) (WMD = 3.95 μ/dL; 95% CI: -21.3, 29.2 μ/dL; I² = 53.1%, p = 0.094). In subgroup analysis, ALA significantly increased hemoglobin in patients with hematological disorders (WMD = 1.23 g/dL; 95% CI: 1.00, 1.45 g/dL; I² = 96.6%, p < 0.001) and in studies with durations longer than 8 weeks (WMD = 1.03 g/dL; 95% CI: 0.82, 1.25 g/dL; I² = 96.5%, p = 0.02).

Conclusion: ALA supplementation had no statistically significant effect on iron-related parameters. Subgroup analysis revealed a significant increasing effect of ALA on hemoglobin in patients with hematological disorders and in studies with durations >8 weeks.

Background: Parkinson's disease (PD) is a chronic progressive neurodegenerative disease, and the exact etiology of PD has not been fully elucidated. Changes in dietary patterns play an important role in the onset and progression of PD. However, the association between specific dietary factors and PD remains unclear.

Methods: A total of 14,309 subjects from the National Health and Nutrition Examination Survey (NHANES) (2007-2016) were included. Logistic regression was used to analyze the association between 34 nutrients and PD. The regression model was adjusted for potential confounders and effect modifiers including age, gender, race, education, hypertension, and stroke.

Results: The data showed negative associations of the intake of protein (0.99 (0.98, 1.00), p = 0.018), fiber (0.96 (0.93, 0.99), p = 0.003), vitamin E (0.91 (0.86, 0.97), p = 0.005), copper (0.55 (0.36, 0.86), p = 0.009) with PD. Alpha carotene (p = 0.042), beta-carotene (p = 0.006), phosphorus (p = 0.018), magnesium (p = 0.002), sodium (p = 0.035), potassium (p = 0.001) had a potential negative correlation with PD. The intake of carbohydrate, sugars, fat, cholesterol, vitamin A, beta-cryptoxanthin, lycopene, lutein zeaxanthin, vitamin B1, vitamin B2, niacin, vitamin B6, folate, vitamin B12, vitamin C, vitamin D, vitamin K, calcium, iron, zinc, selenium, caffeine, theobromine, alcohol was not associated with PD (p > 0.05).

Conclusions: Some specific dietary elements are associated with PD, and supplementation of dietary elements may have potentially beneficial effects. However, the observed associations between dietary factors and PD may be influenced by changes in diet resulting from the disease itself, rather than diet influencing PD risk. Further longitudinal studies are needed to establish causal relationships and directionality.

Background: Non-alcoholic fatty liver disease (NAFLD) has become the primary cause of chronic liver disease. Although malnutrition is a common late-stage clinical consequence during the course of organ dysfunction and death in critical patients, it has not received sufficient attention in the context of NAFLD. The aim of this study was to explore the prevalence and prognostic significance of malnutrition in patients with NAFLD using three simple tools for nutrition assessment.

Methods: Participants (n = 3908) in the National Health and Nutrition Examination Survey (NHANES) database were divided into NAFLD (n = 1737) and non-NAFLD (n = 2171) groups. The controlling nutritional status (CONUT) score, prognostic nutrition index (PNI), and nutrition risk index (NRI) were applied to investigate the association between malnutrition and mortality among NAFLD patients.

Results: The median age of participants was 54.0 years, with females accounting for 52.2% of the study cohort. A majority of elderly male participants had NAFLD, and up to 18% of NAFLD patients suffered from malnutrition. During the average period of follow-up (24.4 ± 7.2 months), 36 all-cause deaths occurred in the NAFLD group. Multivariate analysis revealed that malnutrition was associated with significantly higher mortality compared with normal nutrition. The adjusted hazard ratio (HR) for PNI was 4.44 (95% CI: 2.07-9.53, p < 0.001), and for NRI it was 6.98 (95% CI: 1.47-33.11, p = 0.014). The CONUT score also showed a trend for association with higher mortality.

Conclusion: Malnutrition is a common comorbidity in NAFLD patients and is closely associated with poor prognosis and higher mortality. The three nutrition assessment tools employed in this study could be used to improve the predictive ability of nutritional status for mortality among NAFLD patients.