Journal of Nutrition最新文献

Background: Linoleic acid biomarkers are associated with positive health outcomes including lower risk of diabetes and cardiovascular disease. The effect of consuming linoleate-fortified foods (compared with palm oil-fortified foods) in a randomized controlled, double-masked crossover study to change linoleic acid biomarkers without changing bodyweight is unknown.

Objectives: The aim of this study was to determine the effect of delivering soybean and palm oils through study foods on the linoleic acid content of blood fractions and body weight in adults.

Methods: In this crossover pilot study, 4 male and 6 female adults, ages 25-76 y and body mass index from 26 to 41 kg/m², were randomly assigned to consume: 30 g of soybean and palm oil delivered in 3 study foods/d for 4 wk separated by a 2-wk washout period. Bodyweight, fatty acid profile of plasma, erythrocytes, peripheral blood mononuclear cells (PBMC), and dried blood spots, and PBMC cardiolipin were measured before and after each intervention period. Dietary intake was assessed using 24-h recalls. The outcomes were analyzed using the Wilcoxon Signed Rank Test.

Results: After 4 wk of consuming 3 foods/d, plasma linoleic acid decreased during the palm oil intervention (-1.60, P = 0.04), whereas it tended to increase in plasma (2.35, P = 0.07) and erythrocytes (1.09, P = 0.05) during the soybean oil intervention. The percentage of PBMC tetralinoleoyl cardiolipin marginally increased during the soybean oil intervention (2.31, P = 0.05) but did not change during the palm oil intervention. There was no difference in energy intake between the 2 interventions (P = 0.65) and no change in bodyweight during either intervention (P > 0.40).

Conclusions: Foods can be used to deliver 30 g/d of dietary oil for 4 wk to impact linoleic acid biomarkers without incurring body weight changes. These foods are useful for future randomized controlled double-masked clinical trials assessing the impact of dietary oils on energy metabolism. The study was registered at clinicaltrials.gov as NCT04975763 (https://clinicaltrials.gov/study/NCT04975763).

Background: Maternal selenium deficiency is hypothesized to contribute to risk of adverse outcomes including low birth weight and prematurity, possibly through its role as an antioxidant and/or in thyroid hormone function.

Objectives: We assessed relationships between maternal selenium concentrations during pregnancy with offspring outcomes including birth measurements, low birth weight (<2500 g), prematurity (<37 wk), and small for gestational age (birth weight <10th percentile for gestational age).

Methods: This was a secondary analysis of the Women First Trial (NCT01883193), a randomized controlled study investigating the effect of small-quantity lipid-based nutrition supplement (sqLNS) with 130 μg selenium on fetal growth. sqLNS was started ≥3 mo prior to conception, around 12 wk of gestation, or not at all in women in Guatemala, India, and Pakistan. At 12 and 34 wk of gestation and 3 mo postpartum, maternal serum selenium was measured by inductively coupled plasma mass spectrometry (n = 145-325 per timepoint per site). We used generalized linear models adjusted for study arm, study site, and markers of inflammation to test for associations between maternal selenium status and offspring outcomes including birth anthropometry.

Results: Mean selenium concentrations decreased over the course of pregnancy and were lowest 3 mo postpartum. Selenium was lowest in Pakistan and did not increase with maternal supplementation. Across all sites, we found no significant associations between maternal selenium at 12 and 34 wk with birth weight- length-, or head circumference-for-age z-scores. There were also no associations with low birth weight, small for gestational age, or prematurity.

Conclusions: Maternal selenium supplementation did not impact serum concentrations, suggesting that supplementation may not overcome the impact of low intake and the high demands of pregnancy and early lactation. Larger studies in high-risk regions are needed to further clarify the relationship between maternal selenium deficiency and infant outcomes. This trial was registered at clinicaltrials.gov as NCT01883193 (registered 18 June 2013).

Background: Adequate concentrations of long-chain omega-3(LC n-3) PUFAs, specifically EPA and DHA, are critical for maternal health and fetal development during pregnancy. Despite their importance, global data on maternal blood concentrations of EPA+DHA remain sparse and inconsistent, partially due to differences in measurement methodologies.

Objectives: This study assessed global maternal blood concentrations of EPA+DHA during pregnancy by synthesizing data from observational studies and RCTs from the last 20 y (2004-2025).

Methods: Non-red blood cells (RBC) based EPA+DHA blood concentrations from published studies were standardized using conversion equations to estimate relative EPA+DHA percentages in RBCs [estimated omega-3 index (eO3I)]. Country mean eO3I levels were classified into 4 categories based on literature-defined thresholds.

Results: An analysis of 66 studies involving 33,390 pregnant women from 28 countries revealed significant geographical disparities in eO3I levels. Only the Seychelles, Norway, and Ghana achieved desirable levels (>8%). Some Asian countries (Japan, Taiwan, and Singapore), Malawi, Tanzania, and northern european nations (Belgium, Netherlands, Iceland, Denmark, and Sweden) exhibited sufficient/moderate levels (>6%-8%). Most countries, including the United States, Canada, Mexico, Brazil Chile, Australia, the United Kingdom, Germany, Switzerland, Italy, Croatia, and Spain, demonstrated insufficient/low levels (>4%-6%). Meanwhile, China, India, and Iran showed very low/undesirable levels (≤4%).

Conclusions: These findings highlight widespread insufficiency in maternal EPA+DHA status globally, with particularly severe deficiencies observed in Asia and parts of Europe. This study underscores the need for more research to ultimately define the optimal EPA+DHA concentrations during pregnancy using standardized blood biomarkers, along with pregnancy-specific reference ranges, to facilitate targeted nutritional strategies aimed at optimizing health outcomes for both mother and child. Future studies should focus on addressing data gaps, refining intake recommendations, and promoting accessible supplementation strategies.

Background: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may improve inflammatory conditions. We previously demonstrated that supplementation with EPA+DHA in adults elevates anti-inflammatory oxylipins in human plasma and adipose tissue. However, the localization of EPA/DHA in plasma lipid pools [phosphatidylcholines (PC), triglycerides (TAG), cholesteryl esters (CE), and nonesterified fatty acids (NEFA)] and how this relates to the downstream oxylipin levels remains unknown.

Objectives: This study aimed to identify the incorporation of supplemental EPA+DHA into plasma PC, TAG, CE, NEFA, and the impact on downstream oxylipins.

Methods: We conducted an exploratory analysis with available samples (n = 21, 20 female, 1 male, age 35-49 y) from a previous double-blind, placebo-controlled trial of participants randomly assigned to consume either 3 g of EPA+DHA concentrate (1.1 g EPA + 0.8 g DHA) or corn oil (CO) [1.65 g linoleic acid (LA) + 0.81 g oleic acid] daily for 12 wk. Plasma was analyzed using gas chromatography and mass spectrometry to quantify fatty acids and oxylipins, respectively.

Results: EPA+DHA supplementation increased EPA levels across PC, CE, NEFA, and TAG pools, and increased DHA levels in PC, CE, and TAG pools. Conversely, supplementation decreased LA levels in PC, CE, and NEFA pools, and decreased arachidonic acid (AA) levels in PC and NEFA pools. EPA+DHA supplementation also led to significant shifts in oxylipin concentrations compared with baseline, with predominant increases in anti-inflammatory and decreases in proinflammatory oxylipins. CO supplementation decreased TAG AA levels and modified concentrations of several AA-derived oxylipins. Levels of EPA+DHA and derived oxylipins were significantly higher across lipid pools following supplementation with EPA+DHA compared with CO.

Conclusions: These findings offer insights into supplemental EPA+DHA localization to different circulating lipid pools, which have implications for understanding how to mitigate systemic inflammation. Furthermore, studies are needed to evaluate relationships between the changes in polyunsaturated fatty acids, oxylipins, and markers of inflammation. The study was registered at www.isrctn.com as ISRCTN96712688.

Background: In a recent double-blind randomized controlled trial (RCT) in Nepal, we found a negative effect of maternal vitamin B-12 supplementation during pregnancy on motor performance in their young infants.

Objectives: The objective of this study is to examine whether the negative effect of the vitamin B-12 supplementation on motor performance in these infants aged 8 to 12 wk differed by baseline maternal characteristics.

Methods: These are secondary analyses of an RCT where 800 pregnant women were randomly assigned to receive vitamin B-12 or placebo from early pregnancy to 6 mo postpartum. The outcome was motor development measured by the test of infant motor performance (TIMP) in 712 infants at age 8 to 12 wk. We examined whether plasma markers of baseline maternal vitamin B-12 status [cobalamin, total homocysteine (tHcy), methylmalonic acid (MMA), and cB12], folate and hemoglobin concentration, and socioeconomic status (SES) modified the effect of vitamin B-12 on the TIMP scores. The subgrouping variables were categorized according to predefined cutoffs and included as interaction terms in generalized linear models, with treatment group as the exposure and TIMP scores (continuous and categorical) as the outcomes.

Results: Overall, the negative effect of the vitamin B-12 supplementation was observed in most subgroups. Except for plasma folate concentration (P-interaction = 0.015), the maternal baseline characteristics did not significantly modify the effect of vitamin B-12 supplementation on the TIMP scores. There was a tendency for a stronger negative effect of vitamin B-12 among infants of women with adequate baseline vitamin B-12 status (i.e. concentrations of cobalamin >220, tHcy <10, MMA <0.26, and cB12 values >-0.5) and with folate concentration in the lower tertile.

Conclusions: The negative effect of vitamin B-12 supplementation on infant motor performance cannot be explained by any subgroup specific effects. However, the effect appears to be more pronounced in mothers with adequate B-12 status. This trial was registered at clinicaltrials.gov as NCT03071666 (https://www.

Clinicaltrials: gov/study/NCT03071666).

Background: Binge eating, a transdiagnostic behavior present in both binge eating disorder (BED) and bulimia nervosa (BN), has increasingly been conceptualized as a manifestation of reward system dysregulation. Although BN is marked by compensatory behaviors and heightened emotional reactivity, BED is frequently associated with obesity, hormonal imbalance, and diminished inhibitory control. Despite their clinical relevance, the neurobiological substrates underpinning binge eating remain insufficiently integrated, particularly regarding the interplay between reward sensitivity, affective instability, and cognitive dysfunction.

Objectives: The objective of this review was to propose an integrative theoretical model centered on reward sensitivity as a core mechanism underlying binge-eating behavior in BED and BN, synthesizing multidimensional evidence to support precision-based interventions across cognitive, emotional, neurobiological, and nutritional domains.

Methods: A comprehensive scoping review was conducted across PubMed, Web of Science, CrossRef, and Google Scholar, yielding 81 studies selected for methodological rigor, diagnostic specificity, and relevance to reward processing frameworks. Inclusion was guided by the Population, Intervention, Comparison, Outcome strategy and evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system.

Results: Evidence converges on a constellation of traits-impulsivity, negative urgency, and executive dysfunction-interacting with aberrant dopaminergic and serotonergic signaling. Reinforcement learning mechanisms, particularly model-free pathways, appear to mediate the transition from episodic to compulsive binge eating. Neuroimaging implicates frontostriatal and limbic circuits in reward anticipation and valuation.

Conclusions: The proposed integrative model identifies reward hypersensitivity as a central mechanism in binge-eating pathology, shaped by neurobiological, behavioral, nutritional, and environmental factors. Distinct profiles between BED and BN-especially in compensatory behaviors, hormonal signaling, and neuroplasticity-highlight the need for precision-based treatments, including neuromodulation, cognitive flexibility training, nutritional rehabilitation, and pharmacogenetic strategies.

Protein quality is an important concept in nutrition, but specific food information remains fragmented across multiple databases and not readily available to anyone except protein experts. This article presents the development of a novel Protein Quality Hub providing a consolidated, global protein quality database and illustrates its use for applied dietary and research applications. The Protein Quality Hub offers the first structured, searchable, and transparent platform for protein quality scoring and evaluations with corresponding metadata across various food types and analytical methodologies. The database currently includes 7775 protein correction factors comprising 1186 human patterns; 6589 animal profiles; and all 33 published Indicator Amino Acid Oxidation values. The article demonstrates 4 applications of the Hub ranging from simple queries for Protein Digestibility-Corrected Amino Acid Score and Digestible Indispensable Amino Acid Score values to complex research applications to assess the essential amino acid content of meals with multiple protein sources and a unique comparison of digestibility compared with metabolic availability data. The Protein Quality Hub is an important advancement in making protein quality information accessible for research and health applications.

Background: Diet plays a critical role in colorectal cancer (CRC) prevention. Pesco-vegetarians, who consume both high fiber and fish containing n-3 (ω-3) polyunsaturated fatty acid (PUFA), have the lowest CRC risk. Ferroptosis is a form of regulated cell death characterized by the accumulation of lipid hydroperoxides that has emerged as a target for anticancer therapies.

Objectives: This study aimed to assess the broad utility of diet modulation as a promising avenue to modulate ferroptosis in the colon.

Methods: 1) Immortalized young adult mouse colonic epithelial cells (YAMC) were treated with control linoleic acid or docosahexaenoic acid (DHA) ± butyrate (But), followed by cell viability and lipid peroxidation measurements, 2) mice were fed diets containing fish oil and highly fermentable pectin (FP) compared with control corn oil and poorly fermentable cellulose (CC). Colons were isolated and used for bulk and single-cell ribonucleic acid-sequencing (RNA)-seq analysis, 3) a crossover pilot study was conducted by supplementing 30 healthy adults with soluble corn fiber (33 g/d) + fish oil (7.7 g/d n-3 PUFA) (SCF+FO) or maltodextrin + corn oil (MD+CO) for 30 d followed by a 60 d wash period and then 30 d of MD+CO or SCF+FO. Exfoliated colonocyte mRNA was isolated from stool and RNA-seq was performed for transcriptomic analysis.

Results: In vitro treatment of DHA and But reduced YAMC cell viability (P < 0.05), increased lipid peroxidation, a key biomarker of ferroptosis, compared with the counterpart group. In vivo FP-fed mice promoted lipid peroxidation in colonocytes relative to the control CC-fed mice (P < 0.05), and the induction of ferroptosis transcriptional networks exclusively in colonic epithelial cells. Furthermore, human subjects supplemented with SCF+FO exhibited an upregulation in intestinal ferroptosis-related gene expression, as compared with similar doses of MD+CO.

Conclusions: Our findings demonstrate that dietary fish oil and fermentable fiber combination induces ferroptosis exclusively in colonocytes. The human pilot study was registered at clinicaltrials.gov as NCT04211766.

Pancreatic beta cells play a pivotal role in the advancement of type 1 and type 2 diabetes mellitus. Ferroptosis, a distinct type of regulated cell death, is characterized by the accumulation of iron-dependent lipid peroxides in cell membranes, causing disruptions in cellular iron homeostasis and an impaired antioxidant system. Glutathione peroxidase 4 (GPx4) is a key antioxidant enzyme that protects cells against ferroptosis by mitigating oxidative damage and reducing lipid peroxides, thereby maintaining cellular redox balance. In this study, we aim to identify a natural compound as a potent ferroptosis inhibitor using in silico and in vitro approaches. We screened a bioactive compound library using in silico tools and identified polydatin (PD) as a potential GPx4 activator with a strong binding affinity of -7.8 kcal/mol. Its activity was validated using an in-house developed luciferase-based reporter assay system. We further investigated the effects of PD in an in vitro model using mouse pancreatic beta cells exposed to high-glucose conditions. Polydatin exhibited more than 90% cell viability and a dose-dependent protection against ferroptosis and enhanced cellular antioxidant capacity, as evidenced by the upregulation of key ferroptosis-associated markers, including GPx4, solute carrier family 7, ferritin, and transferrin, which were statistically significant. Notably, PD also activated the master antioxidant transcription factor nuclear factor erythroid 2-related factor 2 and its downstream genes, supporting its role in mitigating oxidative stress-related induced beta cell dysfunction. Collectively, our findings highlight PD as a promising ferroptosis inhibitor and support its potential as a therapeutic agent for preserving pancreatic beta cell function in diabetes.