Journal of Nutrition最新文献

Background: B vitamin inadequacies are common in the US, particularly among African Americans. B vitamins play a key role in one-carbon metabolism, and poor status may influence cardiovascular health. We investigated associations of dietary intake of vitamins B6, B12, and folate, as well as plasma concentrations of vitamin B12 and folate, with incident coronary heart disease (CHD).

Methods: We analyzed data from the Jackson Heart Study (2000-2016), including 4,863 participants in the dietary analytic sample (309 CHD cases) and 4,906 in the plasma analytic sample (311 CHD cases). Dietary intake of B vitamins was energy-adjusted using the residual method. Cox proportional hazards regression with multiple imputation was applied to estimate hazard ratios (HRs) for incident CHD over a median of 13.8 years of follow-up (60,660 and 61,180 person-years in the dietary and plasma samples, respectively). Linearity of associations was evaluated using restricted cubic splines.

Results: In multivariable-adjusted models (per 1 SD), higher energy-adjusted dietary intake of vitamin B6 (HR = 1.07; 95% CI: 0.93-1.25), vitamin B12 (HR = 0.99; 95% CI: 0.87-1.12), or folate (HR = 0.97; 95% CI: 0.82-1.15) were not significantly associated with CHD risk. Similarly, plasma vitamin B12 (HR = 0.99; 95% CI: 0.84-1.18) and folate (HR = 0.97; 95% CI: 0.80-1.17) showed no statistically significant associations. Tests for non-linearity revealed no evidence of threshold or U-shaped relationships.

Conclusion: In this cohort of African American adults, neither dietary intake nor plasma concentrations of B vitamins were significantly associated with CHD risk. These findings do not support a strong association between B vitamin status and CHD risk in this cohort.

Background: Growing evidence shows that obesity influences iron status during pregnancy, however, it is unknown whether maternal obesity is associated with epigenetic changes in TfR2 and HJV.

Objective: To explore the association between adiposity and DNA methylation in TfR2 and HJV in early pregnancy and the mediating effect of inflammation on this association.

Methods: This cross-sectional study used data from a double-blind randomized controlled trial in singleton pregnant women with normal weight (BMI 18.5-24.9 kg/m²) and obesity (BMI ≥30.0 kg/m²). Maternal BMI, fat mass, visceral fat, iron/inflammatory markers and DNA methylation of TfR2 and HJV were measured at 12 gestational weeks (GW). Two primer sets were designed (TfR2 zone 1 and 2, (TfR2z1, TfR2z2); HJV zone 1 and 2 (HJVz1, HJVz2). An inflammation score was calculated using pro-inflammatory cytokines.

Results: 65 pregnant women were included, 34 with normal weight, and 31 with obesity. Compared to those of normal weight women, those with obesity showed: lower percentage of DNA methylation in TfR2z1 CpG sites 5, 6, 8-10 and the average in this zone (average CpG methylation 5.80 vs 6.92%, p=0.004); lower percentage of DNA methylation in TfR2z2 CpG sites 5 and 6 (12.5 vs 14.7%, p=0.035; 17.8 vs 20.1%, p=0.031); higher percentage methylation of DNA in HJVz1 CpG site 3 (HJVz1 CpG 3 45.3% vs 43.4%, p=0.010) and HJVz2 CpG site 2 and the average (HJVz2 CpG 2 43.2 vs 37.9%, p<0.001, average 65.9 vs 61.6%, p<0.001). Adjusting for covariates, TfR2z1 was negatively and HJVz2 positively associated with all adiposity measures (TfR2z1, BMI β=-0.288, p=0.030; HJVz2 β=0.459, p<0.001). Inflammation showed a mediating effect on the association between all adiposity measures and DNA methylation of HJVz1 (p=0.019).

Conclusions: Maternal adiposity is associated with epigenetic changes in the iron metabolism genes TfR2 and HJV in early pregnancy, part of which are inflammation-mediated changes in HJV.

Background: Consuming ≥20% of daily energy from pecans improves blood lipids and reduces dyslipidemia but exceeds dietary recommendations. The benefits of lower doses remain unclear.

Objective: Examine the effects of pecan consumption at doses of 6%, 13%, and 20% of total energy needs on fasting and postprandial blood lipids in adults with excess body weight and/or dyslipidemia, compared to the control. We hypothesized a dose-response relationship, with the 20% group showing the greatest lipid improvements, followed by 13% and 6%, and all would be better than the control.

Methods: This single-blind, randomized, controlled superiority trial enrolled 102 adults with excess body weight (BMI ≥28kg/m²) or dyslipidemia. Participants were randomized to 6% (n=26), 13% (n=26), or 20% (n=25) pecan-intake groups, or to a control group (n=25) that maintained a habitual, nut-free diet. Participants completed pre- and post-intervention visits, which included fasting lipid assessments and a high-fat meal challenge (17% of total energy), followed by 4-h postprandial blood draws.

Results: Change in total cholesterol, LDL cholesterol, Apolipoprotein B, non-HDL cholesterol, and TC/HDL cholesterol ratio all decreased from pre- to post-intervention in MID (-13.3±3.4, -12.7±3.3, -9.2±2.3, -13.9±3.2, and -0.3±0.1 mg/dL, respectively; p<0.05 for all) and HIGH (-12.7±3.6, -11.9±3.4, -7.8±1.9, -13.8±3.6, and -0.3±0.1 mg/dL, respectively; p<0.05 for all) vs. no change in LOW or CON. Change from baseline postprandial non-esterified fatty acids (NEFAs) decreased from pre-to-post intervention in MID (p=0.01) vs. no changes in CON, HIGH, or LOW (p>0.05 for all). Fasting triglycerides (TGs), fasting NEFAs, and postprandial TGs did not differ between groups (p>0.05 for all).

Conclusions: Pecan intake providing 20% and 13%, but not 6%, of daily energy improved fasting blood lipid profiles versus the control, with postprandial NEFA reductions observed only at 13%. These findings offer the first evidence that moderate doses of daily pecan consumption confer cardioprotective benefits.

Clinical trial registry: This trial was registered at clinicaltrials.gov as NCT05949879 and available from: https://clinicaltrials.gov/study/NCT05949879. The date of initial trial registration was July 18, 2023.

Background: Gut dysbiosis is associated with malnutrition and inflammation in chronic kidney disease (CKD); however, the causality remains unclear.

Objectives: This study aimed to determine whether fecal microbiota from patients with stage 5 CKD can directly induce nutritional impairment and inflammatory responses in recipient rats.

Methods: Fecal microbiota from patients with stage 5 CKD and healthy controls were transplanted into rats treated with antibiotics. After 2 weeks, we assessed nutritional parameters, inflammatory markers, and microbial composition.

Results: Compared with the healthy-FMT group, rats receiving CKD-derived microbiota exhibited a significant reduction in body weight (466.70 ± 12.60 g vs. 433.90 ± 20.10 g) and serum albumin concentrations (22.87 ± 5.43 g/L vs. 20.36 ± 7.51 g/L). In contrast, serum inflammatory markers were significantly elevated in the CKD-FMT group, including C-reactive protein (12.10 ± 3.10 vs. 15.40 ± 5.00 mg/L) and interleukin-6 (14.30 ± 1.80 vs. 18.80 ± 2.10 pg/L) (all p < 0.01). Microbial analysis revealed enrichment of Enterobacteriaceae and depletion of beneficial genera such as Lactobacillus and Ruminococcaceae.

Conclusions: Our results provide direct evidence that gut microbiota from patients with uremia can impair nutritional status and aggravate systemic inflammation in recipient rats, underscoring a pathogenic role of dysbiosis in CKD complications.

Computational approaches are transforming nutrition science by integrating data from wearables, digital health platforms, and multi-omics technologies to unravel complex diet-health interactions. Traditional statistical models cannot adequately capture the temporal, nonlinear, and individual variability inherent in such data. Computational nutrition, integrating data science, machine learning, and systems modeling, has therefore emerged as a distinct and rapidly developing field. Landmark studies have demonstrated its potential to improve dietary assessment, predict metabolic responses, and design personalized interventions. From an early-career perspective, however, the rise of computational nutrition also exposes structural and educational gaps. Early-career researchers (ECRs) often encounter fragmented training, limited mentorship, and restricted access to interoperable data and computational infrastructure. Empowering ECRs through integrated curricula, equitable data access, and recognition of interdisciplinary contributions will be essential for ensuring that computational nutrition evolves into a transparent, reproducible, and inclusive discipline capable of advancing both personalized and population-level nutrition.