Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-05-28DOI: 10.1016/j.tjnut.2026.101619
Dristi Sapkota, Dinesh Phuyal
{"title":"From Field to Faucet: Phosphorus-Driven Harmful Algal Blooms, Cyanotoxin Exposure, and Clinical Implications for Primary Care Physicians—A Narrative Review","authors":"Dristi Sapkota, Dinesh Phuyal","doi":"10.1016/j.tjnut.2026.101619","DOIUrl":"10.1016/j.tjnut.2026.101619","url":null,"abstract":"<div><h3>Background</h3><div>Agricultural phosphorus enrichment of freshwater ecosystems drives eutrophication and cyanobacterial harmful algal blooms (HABs) that contaminate drinking water, recreational sites, and food webs with cyanotoxins. Translating this environmental science into clinical practice for primary care physicians remains limited.</div></div><div><h3>Objectives</h3><div>This narrative review traced the causal chain from agricultural phosphorus transport and cyanobacterial bloom ecology through cyanotoxin-mediated health consequences. The goal is to give primary care physicians a practical, One Health–based resource for recognizing, managing, and counseling patients on cyanotoxin exposure.</div></div><div><h3>Methods</h3><div>A narrative, integrative review was conducted by searching PubMed, Web of Science, Scopus, and Google Scholar using terms related to phosphorus runoff, cyanobacterial HABs, cyanotoxin human health effects, and primary care environmental exposure. Peer-reviewed articles, key toxicology and epidemiology studies, and guidance documents from the World Health Organization, the United States Environmental Protection Agency, and the Centers for Disease Control and Prevention were prioritized and selected based on their relevance to the intersection of phosphorus contamination and human health outcomes in primary care settings. No statistical analysis was performed because this is a qualitative synthesis of existing literature.</div></div><div><h3>Results</h3><div>The review found that phosphorus from agricultural fertilizers, livestock production, urban runoff, and legacy soil stores drives freshwater eutrophication and harmful algal bloom formation. Climate change is intensifying these processes through increased extreme precipitation and prolonged thermal stratification. Cyanotoxins enter human exposure pathways via drinking water, recreational contact, aerosol inhalation, and bioaccumulation in fish and irrigated crops. Children, pregnant individuals, rural communities on small water systems, and occupational groups such as fishers face disproportionate exposure risk. Broad regulatory gaps persist globally: although some regional bodies, such as the European Food Safety Authority, have issued risk assessments and provisional guidance, no internationally harmonized maximum permissible limits for cyanotoxins in food crops have been established.</div></div><div><h3>Conclusions</h3><div>This narrative review demonstrates that phosphorus-driven HABs pose a growing multisystem health threat through contamination of water and food supplies with hepatotoxic, neurotoxic, and cytotoxic cyanotoxins. Primary care physicians, particularly those serving rural communities and communities disproportionately burdened by environmental hazards, must integrate environmental exposure history-taking into routine clinical practice to improve early recognition and reduce the health burden of cyanotoxin exposure.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101619"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148055098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-05-28DOI: 10.1016/j.tjnut.2026.101620
Eileen F Sullivan, Viviane Valdes, Talat Shama, Shahria Hafiz Kakon, Mary Zhuo Ke, Jasmine Siew, William A Petri, Rashidul Haque, Charles A Nelson
{"title":"Trajectories of Physical Growth across Early Childhood Are Associated with Electroencephalography Power","authors":"Eileen F Sullivan, Viviane Valdes, Talat Shama, Shahria Hafiz Kakon, Mary Zhuo Ke, Jasmine Siew, William A Petri, Rashidul Haque, Charles A Nelson","doi":"10.1016/j.tjnut.2026.101620","DOIUrl":"10.1016/j.tjnut.2026.101620","url":null,"abstract":"<div><h3>Background</h3><div>Chronic malnutrition, commonly indexed using anthropometric indicators, is linked to deficits in multiple domains of children’s development. Alterations to brain development have been found to partially explain these links, yet the mechanisms and timing underlying these relations are not well understood. Electroencephalography (EEG) is well suited to examining early neural correlates of anthropometric indicators, but longitudinal evidence is limited.</div></div><div><h3>Objectives</h3><div>This study explored the presence and timing of relations between physical growth and EEG resting-state power across early childhood in a population with high rates of chronic malnutrition.</div></div><div><h3>Methods</h3><div>Data were drawn from a longitudinal, observational study of 130 children (74 females) living in Dhaka, Bangladesh. Anthropometric measures, including height-for-age <em>Z</em>-scores (HAZ) and stunting status, were collected 14 times from 3 to 54 mo old. Resting-state EEG power data were collected at ∼6 mo, 2 y, and 5.5 y old. Linear mixed-effects models were used to estimate growth trajectories and examine relations between anthropometric indicators and EEG power.</div></div><div><h3>Results</h3><div>Findings revealed nonlinear changes in both HAZ and EEG over the first 5 years. HAZ scores decreased from 9 to 24 mo (<em>b</em> = −0.03, SE = 0.004, <em>P</em> < 0.001) but increased from 30 to 54 mo (<em>b</em> = 0.02, SE = 0.00, <em>P</em> < 0.001). Substantial variation in recovery status from stunting was seen. Exposure to stunting or static measures of HAZ was not associated with EEG power, but steeper positive trajectories of HAZ were related to higher EEG power (<em>b</em> = 1.07, SE = 0.40, <em>P</em> = 0.008).</div></div><div><h3>Conclusions</h3><div>These results suggest that both physical growth and EEG power development are dynamic over the first 5 years of life. The findings also highlight how longitudinal measures, including growth trajectories, can provide nuanced insights to complement static measures of anthropometry in Bangladesh.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101620"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148055146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of Daily Lycium barbarum Consumption Regimens on Bone and Muscle in Aging Mice","authors":"Chuanxin Sun, Yuke He, Fangjun Liu, Jiao Meng, Xinhua Qiao, Chang Chen","doi":"10.1016/j.tjnut.2026.101645","DOIUrl":"10.1016/j.tjnut.2026.101645","url":null,"abstract":"<div><h3>Background</h3><div>Building on our previous findings that <em>Lycium barbarum</em> (“goji” berry, wolfberry) extracts mitigate age-related bone loss and improve muscle endurance, a key translational question emerges regarding its practical consumption. This study therefore investigates whether a common daily intake mode-simply soaking a small amount in hot water as tea or eating dried fruits directly confers comparable bone and muscle protective effects.</div></div><div><h3>Objectives</h3><div>This study aimed to determine whether 3 different daily consumption regimens of <em>L</em>. <em>barbarum</em> confer bone and muscle protective effects comparable to a concentrated extract in aging mice.</div></div><div><h3>Methods</h3><div>Two-month-old adult mice were used as controls. In a natural aging model, 14-mo-old male C57BL/6J mice were divided into 5 treatment groups (<em>n</em> = 8): aging control, <em>Lycium barbarum</em> extract (LBE, a concentrated aqueous decoction), hot water infusion without residue (LBHWI, daily water-soaked 15 goji berries), infusion with residue (LBHWI + Res), and whole fruit ingestion. After 16 wk of oral gavage, bone (microcomputed tomography, calcein labeling) and muscle (grip endurance, fiber typing) parameters were evaluated. Statistical analysis employed one-way analysis of variance followed by the Bonferroni post hoc test.</div></div><div><h3>Results</h3><div>LBE significantly increased bone mineral density by 43.5% (<em>P</em> < 0.05) and type IIa muscle fibers by 29.1% (<em>P</em> < 0.05) compared with aging controls. <em>In vitro</em>, LBE raised alkaline phosphatase activity from 0.034 to 0.047 nmoL/mg protein/min (<em>P</em> < 0.01) and upregulated <em>Bglap</em> expression 1.43-fold (<em>P</em> < 0.01). In contrast, none of the 3 daily consumption regimens (LBHWI, LBHWI + Res, whole fruit) improved any major <em>in vivo</em> endpoint (all <em>P</em> > 0.05).</div></div><div><h3>Conclusions</h3><div>The efficacy of <em>L</em>. <em>barbarum</em> is highly dependent on its form of administration. These findings suggest that conventional dietary intake may be insufficient, whereas standardized extracts offer a potent, evidence-based strategy for supporting skeletal and muscle health during aging; how to eat <em>L</em>. <em>barbarum</em> indeed matters.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101645"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148176053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-06-02DOI: 10.1016/j.tjnut.2026.101625
Marianne Bråtveit , Johnny Laupsa−Borge , Tonje Bjørnstad , Cathrine Sommersten , Adrian McCann , Gülen Arslan Lied , Ottar Nygård , Gunnar Mellgren , Jutta Dierkes , Simon Nitter Dankel
{"title":"Marked Changes in One-Carbon Metabolism on a Low-Carbohydrate High-Fat Diet: A Randomized Controlled Trial (CARBFUNC)","authors":"Marianne Bråtveit , Johnny Laupsa−Borge , Tonje Bjørnstad , Cathrine Sommersten , Adrian McCann , Gülen Arslan Lied , Ottar Nygård , Gunnar Mellgren , Jutta Dierkes , Simon Nitter Dankel","doi":"10.1016/j.tjnut.2026.101625","DOIUrl":"10.1016/j.tjnut.2026.101625","url":null,"abstract":"<div><h3>Background</h3><div>Studying the impact of dietary carbohydrates and fat on markers of one-carbon metabolism could provide important insight into distinct metabolic adaptations and how diets affect disease risk.</div></div><div><h3>Objectives</h3><div>This study aimed to determine changes in plasma one-carbon metabolites and B-vitamers on isocaloric diets differing in carbohydrate processing or amount.</div></div><div><h3>Methods</h3><div>A total of 193 individuals with obesity were randomly assigned to equal-energy and protein diets either with more processed, acellular carbohydrates [acellular, high-carbohydrate low-fat (A-HCLF), comparator arm], minimally processed cellular carbohydrates [cellular high-carbohydrate low-fat diet (C-HCLF)] [both designed with 45 energy percent (E%) carbohydrates and 38 E% fat], or a low-carbohydrate, high-fat (LCHF) diet designed with 8 E% carbohydrate and ∼75 E% fat, including 30 E% saturated fat. To address secondary outcomes of the trial, we analyzed changes in plasma one-carbon metabolites and B-vitamers, and dietary B-vitamin intakes after 3, 6, 9, and 12 mo, using constrained linear mixed-effect modeling.</div></div><div><h3>Results</h3><div>After 3 mo, the relative change score after the LCHF diet was significantly different from the A-HCLF comparator for plasma α-hydroxybutyrate (LCHF/A-HCLF: +41.3%∗/–1.56%, <em>P</em> < 0.001; ∗: significant within-group change), methylmalonic acid (MMA) (–5.69%∗/+8.64%∗, <em>P</em> < 0.001), methionine (−7.81%∗/+1.44%, <em>P</em> = 0.001), nicotinamide (−19.7%∗/+14.0%, <em>P</em> = 0.007), 1-methylnicotinamide (mNAM) (−14.1%∗/+14.1%, <em>P</em> = 0.003), pyridoxal (−2.42%/+18.9%∗), 4-pyridoxic acid (−12.4%∗/+21.4%∗, <em>P</em> < 0.001), and cysteine (−3.00%∗/+1.10%). Between-group differences for most of these metabolites remained significant after 6 and 9 mo. Comparing C-HCLF with A-HCLF, significant differences in relative change scores were found for mNAM after 3 mo (C-HCLF/A-HCLF: −11.5%/+14.1%, <em>P</em> = 0.012) and 9 mo (−14.9%∗/+18.6%, <em>P</em> = 0.001). Plasma changes in one-carbon metabolites and B-vitamers showed weak correlations with dietary B-vitamins.</div></div><div><h3>Conclusions</h3><div>Compared with A-HCLF, the LCHF diet was followed by significantly different changes in plasma α-hydroxybutyrate, MMA, methionine, nicotinamide, mNAM, pyridoxal, 4-pyridoxic acid, and cysteine. These shifts were largely independent of vitamin consumption and may rather reflect ketoadaptive mechanisms, including enhanced fatty acid oxidation and upregulated antioxidant defense. Carbohydrate quality had less impact on the one-carbon metabolites.</div><div>This trial was registered at <span><span>clinicaltrials.gov</span><svg><path></path></svg></span> as NCT03401970 (<span><span>https://clinicaltrials.gov/study/NCT03401970</span><svg><path></path></svg></span>).</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101625"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-02-18DOI: 10.1016/j.tjnut.2026.101427
Eulália Rebeca Silva-Araújo, Ana Elisa Toscano, Henrique José Cavalcanti Bezerra Gouveia, Paula Brielle Pontes, Joaci Pereira dos Santos-Júnior, Osmar Henrique dos Santos-Júnior, Maria Daniele Teixeira Beltrão de Lemos, Nathalia Caroline de Oliveira Melo, Janaina Viana de Melo, Eduardo Padrón-Hernández, Raul Manhães-de-Castro
{"title":"Unraveling Riboflavin-Mediated Mitochondrial Modulation as a Therapeutic Pathway in Neurological Disorders: An Integrative Systematic Review","authors":"Eulália Rebeca Silva-Araújo, Ana Elisa Toscano, Henrique José Cavalcanti Bezerra Gouveia, Paula Brielle Pontes, Joaci Pereira dos Santos-Júnior, Osmar Henrique dos Santos-Júnior, Maria Daniele Teixeira Beltrão de Lemos, Nathalia Caroline de Oliveira Melo, Janaina Viana de Melo, Eduardo Padrón-Hernández, Raul Manhães-de-Castro","doi":"10.1016/j.tjnut.2026.101427","DOIUrl":"10.1016/j.tjnut.2026.101427","url":null,"abstract":"<div><div>Mitochondrial dysfunction is recognized as a key pathophysiological mechanism in neurodegenerative diseases. Alterations in mitochondrial dynamics—including imbalances in fission and fusion, impaired biogenesis, and disrupted mitophagy—contribute to the onset and progression of neurological disorders. In this context, mitochondrial modulation has emerged as a promising therapeutic strategy. This systematic review examined the role of riboflavin, a water-soluble vitamin and essential mitochondrial cofactor, in neurological interventions through mitochondrial modulation, with emphasis on elucidating the underlying molecular mechanisms. A search of the PubMed, Embase, Scopus, and Web of Science databases identified 23 eligible studies, comprising 6 in vitro experiments, 10 rodent models, and 7 clinical trials. These studies evaluated the effects of riboflavin in monogenic, neurodegenerative, and demyelinating mitochondrial diseases, cerebrovascular/hypoxic injury, and pain/migraine. Clinical evidence indicated that riboflavin may regulate oxidative stress in stroke and perinatal asphyxia, with associated functional improvements. Preclinical findings revealed mechanisms of action involving energy homeostasis, cell cycle regulation, and mitochondrial dynamics across monogenic mitochondrial disorders, neurodegenerative diseases, hypoxic injury, and models of pain and migraine. Possibly through mitochondrial modulation, riboflavin appeared to reduce α-synuclein aggregation in Parkinson’s disease, increase the number of tyrosine-hydroxylase-positive neurons in Alzheimer’s disease models, enhance neuronal survival in Brown-Vialetto–Van Laere and Huntington’s disease models, and normalize neuronal excitability in ataxia and migraine. In contrast, no therapeutic effects were observed in demyelinating diseases. Overall, the findings suggest that riboflavin may promote neuroprotection through redox modulation and gene regulation, stabilization of membrane potential, and enhanced mitochondrial complex activity via flavin cofactors, ultimately supporting neuronal metabolism and functional outcomes. Despite advances in mechanistic understanding, clinical applications in humans remain insufficiently defined for most conditions, with clearer dosage regimens currently established only for stroke and migraine.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101427"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-05-08DOI: 10.1016/j.tjnut.2026.101586
Lisa Heggie, Zeynep Nas, Rana Conway, Alison Fildes, Andrea Smith, Edith Feskens, Jason CG Halford, Joanne A Harrold, Anne Raben, Clare H Llewellyn
{"title":"Genetic and Environmental Influences on Free Sugar and Nonnutritive Sweetener Intake in Toddlerhood and Middle Childhood Using Data from the Gemini Twin Cohort: Findings from the SWEET Project","authors":"Lisa Heggie, Zeynep Nas, Rana Conway, Alison Fildes, Andrea Smith, Edith Feskens, Jason CG Halford, Joanne A Harrold, Anne Raben, Clare H Llewellyn","doi":"10.1016/j.tjnut.2026.101586","DOIUrl":"10.1016/j.tjnut.2026.101586","url":null,"abstract":"<div><h3>Background</h3><div>Exceeding recommended free sugar (FS) intake is linked to poorer metabolic health. Nonnutritive sweeteners (NNS) offer an alternative to FS, and emerging evidence suggests that many children regularly consume them. Understanding the etiology of variation in FS and NNS intake in childhood can inform population-level strategies to reduce sugar consumption.</div></div><div><h3>Objectives</h3><div>This study aimed to examine genetic and environmental influences on variation in FS and NNS intakes in toddlerhood and middle childhood, and investigate stability and change over time.</div></div><div><h3>Methods</h3><div>FS (as % energy intake) and NNS (categorized as non-, low-, and high consumers) were estimated using 3-d dietary data at 21 mo (<em>n</em> = 2592) with repeated measures in a subsample at 7 y (<em>n</em> = 592) from British twins in the Gemini cohort. Longitudinal Cholesky twin models estimated genetic and environmental influences on FS and NNS intakes at both ages.</div></div><div><h3>Results</h3><div>Shared environmental factors strongly influenced both FS and NNS intakes at 21 mo [FS: 0.88; 95% confidence interval (CI): 0.86, 0.90; NNS: 0.99; 95% CI: 0.99, 1] and 7 y (FS: 0.58; 95% CI: 0.45, 0.69; NNS: 0.92; 95% CI: 0.86, 1), but the effect decreased significantly over time for FS. There was no significant genetic influence on NNS at either age; genetic influence on FS intake increased significantly from toddlerhood (FS: 0.09; 95% CI: 0.08, 0.11) to middle childhood (FS: 0.33; 95% CI: 0.22, 0.47). Small longitudinal correlations indicated greater change than stability in intakes over time for FS (<em>r</em> = 0.28, <em>P</em> < 0.001) and NNS <em>(r =</em> 0.35, <em>P</em> < 0.001), explained predominantly by novel shared environmental influences in middle childhood and the emergence of novel genetic influence on FS.</div></div><div><h3>Conclusions</h3><div>Shared environmental factors predominantly shape individual differences in FS and NNS intake during early life. Although increasing genetic influence from toddlerhood to middle childhood reflects growing autonomy in dietary choices for FS intake, variation in NNS intake remains overwhelmingly environmentally driven across both developmental periods. Findings emphasize the need for both age-specific public health interventions and food industry legislation to shape FS and NNS intakes in childhood.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101586"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-05-22DOI: 10.1016/j.tjnut.2026.101611
Malak Ali, Fiona O’Dwyer, Brona Murphy, Heleena Moni Bottu, Martina Rooney, Torres Sweeney, Sharleen L O’ Reilly, Aifric M O’Sullivan
{"title":"Vitamins A, D, E, and K Intakes, Status, and Breastmilk Concentrations in Breastfeeding Women in Ireland","authors":"Malak Ali, Fiona O’Dwyer, Brona Murphy, Heleena Moni Bottu, Martina Rooney, Torres Sweeney, Sharleen L O’ Reilly, Aifric M O’Sullivan","doi":"10.1016/j.tjnut.2026.101611","DOIUrl":"10.1016/j.tjnut.2026.101611","url":null,"abstract":"<div><h3>Background</h3><div>Fat-soluble vitamins A, D, E, and K are critical during the postpartum period for maternal recovery and infant development.</div></div><div><h3>Objectives</h3><div>To determine the concentrations of vitamins A, D, E, and K in maternal serum and breastmilk during the early postpartum period in breastfeeding women.</div></div><div><h3>Methods</h3><div>This was a secondary analysis of the WellFed 4-wk randomized controlled trial. Dietary recalls, serum, and breastmilk samples were collected from breastfeeding women at 4 and 8 wk postpartum (<em>n</em> = 48). Vitamin status and metabolic biomarkers were quantified using liquid chromatography–tandem mass spectrometry and a clinical analyzer, respectively. Associations were analyzed using correlation, regression, and mediation analysis (PROCESS macro for SPSS; IBM Corp).</div></div><div><h3>Results</h3><div>Mean daily intakes for vitamins A, D, and E were 1230 ± 633 μg, 6.5 ± 4.6 μg and 13.3 ± 8.1 mg, respectively. All women were sufficient in serum retinol (2.1 ± 0.4, 2.1 ± 0.3 μmol/L), α-tocopherol (45.5 ± 9.5, 39.3 ± 8.7 μmol/L), and phylloquinone (1.0 ± 0.5, 1.1 ± 0.7 nmol/L) at weeks 4 and 8, respectively. Sixty-five percent of the cohort were vitamin D sufficient (61.7 ± 22.2 nmol/L, 56.7 ± 19.2 nmol/L). Vitamin A intake was positively associated with serum retinol concentrations (<em>r</em> = 0.386, <em>P</em> = 0.012, adjusted <em>P</em> = 0.048). Breastmilk retinol (3.7 ± 1.2, 3.2 ± 1.1 μmol/L) and α-tocopherol (15.3 ± 7.4, 12.4 ± 5.1 μmol/L) concentrations were adequate at both timepoints, 25(OH)D<sub>2</sub> and 25(OH)D<sub>3</sub> were below the analytical detection limit. Serum and breastmilk α-tocopherol were correlated (<em>r</em> = 0.363, <em>P</em> = 0.013, adjusted <em>P</em> = 0.026). Total cholesterol, triglycerides, and CRP predicted up to 56% of serum α-tocopherol variance.</div></div><div><h3>Conclusions</h3><div>Maternal serum concentrations of vitamins A, E, and K are adequate, whereas approximately two-thirds of women are vitamin D sufficient. Breastmilk vitamins A and E are adequate and higher than previously reported, whereas vitamin D metabolites are undetectable. Dietary intake is positively associated with serum vitamins A and D, whereas serum vitamin E is associated with lipid-related biomarkers and correlated with breastmilk α-tocopherol, highlighting a potential link between maternal metabolic health and vitamin E in breastmilk.</div><div>This trial is registered at <span><span>clinicaltrials.gov</span><svg><path></path></svg></span> as NCT05924633 (<span><span>https://clinicaltrials.gov/study/NCT05924633</span><svg><path></path></svg></span>).</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101611"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gut Feeling: Microbiota as a Hidden Regulator of Hypertension","authors":"Lovepreet Singh, Gurman Bhullar, Sonia Shaik, Varsha Ganesh, Hemanth Kesani, Manju Rai","doi":"10.1016/j.tjnut.2026.101623","DOIUrl":"10.1016/j.tjnut.2026.101623","url":null,"abstract":"<div><div>Emerging evidence identifies the gut microbiota as a key regulator of blood pressure (BP) through its role in metabolizing dietary substrates into bioactive compounds that influence vascular, immune, and neurohumoral pathways. This review synthesizes recent mechanistic, preclinical, and clinical evidence linking gut microbial dysbiosis to hypertension, with particular emphasis on nutrition-dependent microbial metabolism and its translational implications. Experimental studies demonstrate that depletion of short-chain fatty-acid (SCFA)–producing bacteria and enrichment of proinflammatory and trimethylamine-producing taxa contribute to endothelial dysfunction, immune activation, and renin–angiotensin–aldosterone system dysregulation. Fecal microbiota transplantation and germ-free animal models provide causal evidence that hypertensive microbiota can directly elevate BP. Human multiomics and metabolomic studies further show that microbial functional capacity and metabolite production, rather than taxonomic composition alone, are strongly associated with hypertensive phenotypes and therapeutic responsiveness. Importantly, dietary interventions, including high-fiber diets, resistant starch, and the Dietary Approaches to Stop Hypertension diet, modulate microbial composition and enhance SCFA production, providing a mechanistic basis for their antihypertensive effects. Microbiota–drug interactions have also emerged as a novel determinant of antihypertensive treatment efficacy. Collectively, these findings support a metabolite-centered framework in which diet–microbiota interactions influence BP regulation. Targeting the gut microbiota through nutritional and microbiome-based strategies represents a promising adjunctive approach for hypertension prevention and personalized management. However, large-scale longitudinal and interventional human studies are needed to establish causality and optimize microbiota-targeted therapies.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101623"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-06-06DOI: 10.1016/j.tjnut.2026.101644
Kun Xu, Yiming Zhang, Gaixia Hou, Yongheng Zhao, Xuefeng Xi
{"title":"Orange Peel Powder Improves Constipation-Related Phenotypes and Is Associated with Coordinated Colonic and Brain-Related Changes in a Doxorubicin- and Loperamide-Treated Rat Model","authors":"Kun Xu, Yiming Zhang, Gaixia Hou, Yongheng Zhao, Xuefeng Xi","doi":"10.1016/j.tjnut.2026.101644","DOIUrl":"10.1016/j.tjnut.2026.101644","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to determine whether orange peel powder (OP) improves constipation-related phenotypes in a doxorubicin- and loperamide-treated rat model and whether such improvement is accompanied by coordinated histological and molecular changes in colon and brain tissues.</div></div><div><h3>Methods</h3><div>Forty-eight 12-wk-old male Sprague–Dawley rats were randomly assigned to 6 groups (<em>n</em> = 8/group): blank control (BC), aging control (AG), aging constipation control (ACG), and low-, medium-, and high-dose OP groups (0.1575, 0.315, and 0.63 g/kg, respectively). An aging-like phenotype was induced by intraperitoneal doxorubicin (2 mg/kg) for 4 wk, followed by loperamide gavage (2 mg/kg) for 14 d. OP was then administered by gavage for 4 wk. Body weight, defecation frequency, fecal moisture content, and small-intestinal propulsion rate were assessed. Gastrointestinal hormones, inflammatory markers, and oxidative stress indices were measured in serum, colon tissue, and/or brain tissue, as appropriate. Colon and brain histology were examined by hematoxylin–eosin staining. Tight junction proteins (ZO-1, occludin, and claudin-1) and endocannabinoid system–related proteins (CB1, CB2, and FAAH) in colon and brain tissues were assessed by western blotting.</div></div><div><h3>Results</h3><div>Compared with the BC group, the AG and ACG groups showed lower body weight gain and worse constipation-related phenotypes. The ACG group also exhibited a higher inflammatory and oxidative stress–related burden, altered gastrointestinal hormone profiles, histological abnormalities in the colon and brain, and lower expression of tight junction proteins in the colon and brain. OP intervention, particularly at the medium dose, improved defecation frequency, fecal moisture content, and small-intestinal propulsion rate; reduced interleukin-6, tumor necrosis factor-α, vasoactive intestinal peptide, and malondialdehyde; increased gastrin, motilin, and total superoxide dismutase activity; and upregulated ZO-1, occludin, and claudin-1 expression in the colon and brain.</div></div><div><h3>Conclusions</h3><div>OP improved constipation-related phenotypes in this composite model and was associated with coordinated systemic, colonic, and brain-related changes. These findings are descriptive and do not establish restoration of barrier function or a direct gut–brain mechanistic pathway.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101644"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148194813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal of NutritionPub Date : 2026-07-01Epub Date: 2026-06-02DOI: 10.1016/j.tjnut.2026.101629
Yuzuki Ando, Taro Murakami
{"title":"Isometric Contraction Attenuates Leucine-Stimulated 4E-Binding Protein 1 Phosphorylation in Contralateral Noncontracted Skeletal Muscle in Mice","authors":"Yuzuki Ando, Taro Murakami","doi":"10.1016/j.tjnut.2026.101629","DOIUrl":"10.1016/j.tjnut.2026.101629","url":null,"abstract":"<div><h3>Background</h3><div>Skeletal muscle contraction can influence anabolic signaling in distant noncontracted muscle. However, whether unilateral contraction alters nutrient-stimulated mechanistic target of rapamycin complex 1 (mTORC1) signaling in contralateral muscle remains unclear.</div></div><div><h3>Objectives</h3><div>This study aimed to determine whether unilateral isometric contraction attenuates leucine-stimulated mTORC1 signaling and protein synthesis in contralateral noncontracted muscle in mice.</div></div><div><h3>Methods</h3><div>Ten-wk-old male C57BL/6J mice fed a standard chow diet (CE-2) were assigned to resting or unilateral isometric contraction conditions and received water or leucine (1.35 g/kg body weight) 2 h after contraction (<em>n</em> = 8/group). Gastrocnemius muscles were collected 3 h postcontraction. Regulated in development and DNA damage responses 1 (REDD1) protein abundance, mTORC1 signaling, protein synthesis, and serum branched-chain amino acid (BCAA) concentrations were measured. Data were analyzed using 2-way analysis of variance (ANOVA) followed by Holm-adjusted post hoc tests.</div></div><div><h3>Results</h3><div>Unilateral contraction increased REDD1 protein abundance in contralateral noncontracted muscle, with a significant interaction between leucine and contraction (<em>P</em> = 0.0499). REDD1 protein abundance was higher in the isometric contraction groups than in the resting groups under water and leucine conditions. Two-way ANOVA revealed a significant interaction between leucine and contraction for 4E-binding protein 1 (4E-BP1) phosphorylation (<em>P</em> = 0.046). Under resting conditions, leucine increased 4E-BP1 phosphorylation compared with water, whereas this response was attenuated under contraction conditions. Ribosomal protein S6 kinase 1 phosphorylation was unchanged. Protein synthesis was increased by leucine (main effect, <em>P</em> < 0.001) and reduced by contraction (main effect, <em>P</em> < 0.001), with no significant interaction. Serum BCAA concentrations were increased by leucine (main effect, <em>P</em> < 0.001), with no effect of contraction or interaction.</div></div><div><h3>Conclusions</h3><div>In male C57BL/6J mice, unilateral isometric contraction attenuated leucine-stimulated 4E-BP1 phosphorylation in contralateral noncontracted skeletal muscle. Protein synthesis was reduced by contraction independently of leucine treatment. These effects occurred without differences in circulating BCAA availability, suggesting altered anabolic signaling responsiveness to nutritional stimulation.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"156 7","pages":"Article 101629"},"PeriodicalIF":4.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}