Maria Erlin , Davrina Rianda , Fadilah Fadilah , Linda Erlina , Mega Diasty Rahayu , Erfi Prafiantini , Ali Sungkar , Anuraj H Shankar , Rina Agustina
{"title":"Association of Prepregnancy Body Mass Index with Gut Microbiota Diversity and Abundance in Pregnant Women","authors":"Maria Erlin , Davrina Rianda , Fadilah Fadilah , Linda Erlina , Mega Diasty Rahayu , Erfi Prafiantini , Ali Sungkar , Anuraj H Shankar , Rina Agustina","doi":"10.1016/j.tjnut.2025.02.006","DOIUrl":"10.1016/j.tjnut.2025.02.006","url":null,"abstract":"<div><h3>Background</h3><div>Understanding the link between prepregnancy nutritional status and gut microbiota during pregnancy may lead to novel maternal and child health interventions.</div></div><div><h3>Objective</h3><div>To explore the association of prepregnancy body mass index (BMI) status with gut microbiota diversity and abundance during pregnancy.</div></div><div><h3>Methods</h3><div>A cross-sectional study was conducted on 90 pregnant women from primary health centers in Jakarta, Indonesia. Trained staff interviewed women on sociodemographic characteristics and nutrient intake, gathered data on prepregnancy BMI from antenatal records, and obtained fecal samples. Samples were analyzed for microbiota diversity indices [Shannon, Faith phylogenetic diversity (Faith PD), and Chao1] and abundance using 16S ribosome ribonucleic acid sequencing. Multivariate logistic regression was performed adjusting for carbohydrate and protein intake, ethnicity, and education to determine the relationship between prepregnancy BMI and the alpha diversity indices and the presence of the phylum Firmicutes and genera <em>Prevotella</em> and <em>Blautia</em>.</div></div><div><h3>Results</h3><div>Pregnant women who were overweight or obese (BMI ≥23.0 kg/m<sup>2</sup>) before pregnancy had significantly lower odds of having gut microbiota diversity above the median of the Shannon index [adjusted odds ratio (aOR): 0.37, 95% confidence interval (CI): 0.14, 0.97, <em>P</em> = 0.042], Faith PD (aOR: 0.23, 95% CI: 0.07, 0.75, <em>P</em> = 0.015), and Chao1 (aOR: 0.25, 95% CI: 0.09, 0.67, <em>P</em> = 0.006) compared with those who were neither overweight nor obese. Prepregnant women who were overweight or obese also had significantly lower odds of having levels above the median of the phylum Firmicutes (aOR: 0.38, 95% CI: 0.15, 0.98, <em>P</em> = 0.045) and genus <em>Blautia</em> (aOR: 0.32, 95% CI: 0.12, 0.85, <em>P</em> = 0.022) compared with women who were neither overweight nor obese.</div></div><div><h3>Conclusions</h3><div>Prepregnancy overweight or obese status was associated with lower gut microbiota diversity and lower abundance of Firmicutes and <em>Blautia</em> among pregnant women in an urban community. These findings suggest that prepregnancy interventions to control BMI may improve gut flora and potentially benefit pregnant women.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1731-1740"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433182","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}
Jiaqi Yang , Lauren Bernard , Jingsha Chen , Valerie K Sullivan , Jennifer A Deal , Hyunju Kim , Bing Yu , Lyn M Steffen , Casey M Rebholz
{"title":"Plasma Proteins Associated with the Mediterranean-Dietary Approaches to Stop Hypertension Intervention for Neurodegenerative Delay (MIND) Diet and Incident Dementia","authors":"Jiaqi Yang , Lauren Bernard , Jingsha Chen , Valerie K Sullivan , Jennifer A Deal , Hyunju Kim , Bing Yu , Lyn M Steffen , Casey M Rebholz","doi":"10.1016/j.tjnut.2025.03.015","DOIUrl":"10.1016/j.tjnut.2025.03.015","url":null,"abstract":"<div><h3>Background</h3><div>The Mediterranean-Dietary Approaches to Stop Hypertension Intervention for Neurodegenerative Delay (MIND) diet slows cognitive decline and protects brain health, but the mechanisms are poorly understood.</div></div><div><h3>Objectives</h3><div>We aimed to determine the plasma proteins associated with the MIND diet score and their ability to predict incident dementia in the Atherosclerosis Risk in Communities study.</div></div><div><h3>Methods</h3><div>We analyzed 10,230 Black and White participants at visit 3 (1993–1995) with food frequency questionnaire and proteomics data and randomly divided them into discovery (<em>n =</em> 6850) and replication (<em>n =</em> 3380) samples. We examined associations between the MIND diet score and 4955 proteins using multivariable linear regression and elastic net regression. C-statistics were calculated to assess if proteins improved the prediction of high MIND diet adherence beyond participant characteristics. Cox proportional hazards models were used to assess associations between significant diet-related proteins and incident dementia over 2 decades. C-statistics assessed the ability of significant proteins to improve dementia prediction beyond known risk factors.</div></div><div><h3>Results</h3><div>Of 316 proteins associated with the MIND diet score in the discovery sample at a false discovery rate <0.05, 62 were internally replicated. Of these, 21 proteins selected by the elastic net individually improved MIND diet score prediction. After a median follow-up of 21 y, there were 2311 dementia cases. Five diet-related proteins, thrombospondin-2 [hazard ratio (HR): 1.19; 95% confidence interval (CI): 1.11, 1.29], protein ABHD14A (HR: 1.23; 95% CI: 1.11, 1.37), structural maintenance of chromosomes protein 3 (HR: 1.19; 95% CI: 1.08, 1.31), epidermal growth factor receptor (HR: 0.68; 95% CI: 0.53, 0.86), and interleukin-12 subunit beta (HR: 1.14; 95% CI: 1.05, 1.25) were significantly associated with incident dementia. All 5 proteins individually and together improved the prediction of dementia risk.</div></div><div><h3>Conclusions</h3><div>Using high-throughput proteomics, we identified candidate biomarkers of the MIND diet score and incident dementia, which are implicated in neural signaling, angiogenesis, and anti-inflammatory pathways.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1710-1721"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673969","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}
Jigna M Dharod , Jeffrey D Labban , Helen Tadese , Valerie L Flax , Maureen M Black
{"title":"Added Sugar Intake from Infant Formula and Complementary Foods: A Longitudinal Investigation and Implications for Infant Weight Gain","authors":"Jigna M Dharod , Jeffrey D Labban , Helen Tadese , Valerie L Flax , Maureen M Black","doi":"10.1016/j.tjnut.2025.03.025","DOIUrl":"10.1016/j.tjnut.2025.03.025","url":null,"abstract":"<div><h3>Background</h3><div>Infant formula contains added sugar, although national recommendations are that added sugar should be avoided for infants.</div></div><div><h3>Objectives</h3><div>This study aims to estimate average daily added sugar intake from formula and complementary foods and examine associations between added sugar intake from formula and complementary foods and weight status among infants in low-income households.</div></div><div><h3>Methods</h3><div>Between August 2019 and November 2021, mother–infant dyads were recruited from a pediatric clinic primarily serving Medicaid recipients, regardless of feeding type. 24-h feeding recalls were conducted on infants aged 6, 9, and 12 mo. For directly breast-fed infants, we used the average expected milk volume intake by age. Weight-for-age and weight-for-length <em>z</em>-scores were calculated from health record measurements. Descriptives, bivariate tests, and multilevel linear growth modeling were used.</div></div><div><h3>Results</h3><div>Most participants (<em>n =</em> 234) were African American (39%) or Latino (38%). Infants’ daily added sugar intake was on average 7 g from complementary foods and 33 g from formula, with formula being the major source at 6 and 9 mo. Daily intake of calories due to added sugar was significantly higher among formula-fed infants compared with breast milk or sugar-free formula-fed infants (<em>P</em> = 0.034). For every 10 g of added sugar from formula daily, infants’ weight-for-length <em>z</em>-scores increased by an average of 0.060 (SE = 0.018, <em>P</em> = 0.001).</div></div><div><h3>Conclusions</h3><div>Formula significantly contributes to added sugar intake among infants compared with complementary foods. A significant positive association between added sugar from formula and infant weight gain suggests the need for regulations limiting added sugar in formula and including added sugar information on formula food labels.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1870-1877"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743105","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}
Longgang Zhao , Yun Chen , Alyssa Clay-Gilmour , Jiajia Zhang , Xuehong Zhang , Susan E Steck
{"title":"Metabolomic and Proteomic Signatures of Ultra-processed Foods Are Positively Associated with Adverse Liver Outcomes","authors":"Longgang Zhao , Yun Chen , Alyssa Clay-Gilmour , Jiajia Zhang , Xuehong Zhang , Susan E Steck","doi":"10.1016/j.tjnut.2025.04.034","DOIUrl":"10.1016/j.tjnut.2025.04.034","url":null,"abstract":"<div><h3>Background</h3><div>Higher consumption of ultra-processed foods is associated with increased risk of obesity and type 2 diabetes; however, evidence on liver diseases and the underlying mechanisms remain limited.</div></div><div><h3>Objectives</h3><div>This study aimed to evaluate associations between metabolomic and proteomic signatures of ultra-processed food intake and adverse liver outcomes.</div></div><div><h3>Methods</h3><div>Data of participants aged 40 to 69 y from the UK Biobank (<em>N</em> = 173,840) were analyzed. Ultra-processed food intake was assessed using multiple 24-h dietary recalls. Plasma metabolites were measured using nuclear magnetic resonance spectroscopy, and plasma proteome was profiled using the Olink platform. Adverse liver outcomes (metabolic dysfunction-associated steatotic liver disease [MASLD], cirrhosis, liver cancer, and severe liver disease) were ascertained using data from the in-hospital records or cancer or death registries. We used elastic net regression to calculate omics signatures of ultra-processed foods and Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for ultra-processed foods and their omics signatures and adverse liver outcomes, adjusting for multiple potential confounding factors.</div></div><div><h3>Results</h3><div>With a median follow-up of 8.9 years, an increase of 1 standard deviation (SD) in metabolic signature score of ultra-processed foods was associated with increased risk of MASLD (HR: 1.61; 95% CI: 1.38, 1.87). An increase of 1 SD in proteomic signature score of ultra-processed foods was associated with increased risk of MASLD (HR: 1.84; 95% CI: 1.45, 2.35), cirrhosis (HR: 1.49; 95% CI: 1.16, 1.91), and severe liver disease (HR: 1.48; 95% CI: 1.07, 2.03). Thirty-four metabolites and 65 proteins were significantly associated with ultra-processed food intake and were enriched in biological pathways such as lipid metabolism, immune, and inflammatory response. About half of these metabolites and proteins are significantly associated with risk of MASLD and cirrhosis.</div></div><div><h3>Conclusions</h3><div>Ultra-processed food intake and its metabolic and proteomic signatures are positively associated with risk of MASLD.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1851-1858"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987200","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}
Min Liu , Ning Ma , Sheng Li , Zeyue Kang , Minghui Wang , Dan Wang , Jingpeng Zhao , Hongchao Jiao , Yunlei Zhou , Xiaojuan Wang , Haifang Li , Hai Lin
{"title":"Prevotella-Produced Succinate Alleviates Hepatic Steatosis by Enhancing Mitochondrial Function in Layer-Type Chickens","authors":"Min Liu , Ning Ma , Sheng Li , Zeyue Kang , Minghui Wang , Dan Wang , Jingpeng Zhao , Hongchao Jiao , Yunlei Zhou , Xiaojuan Wang , Haifang Li , Hai Lin","doi":"10.1016/j.tjnut.2025.04.018","DOIUrl":"10.1016/j.tjnut.2025.04.018","url":null,"abstract":"<div><h3>Background</h3><div>A higher abundance of <em>Prevotella</em> species in the gut microbiota is associated with the consumption of high-fiber diets and can be reproduced by dietary supplementation with L-arabinose. The effect of <em>Prevotella</em> and its metabolite succinate on hepatic lipid metabolism remains unclear.</div></div><div><h3>Objectives</h3><div>This study aimed to elucidate the effects of <em>Prevotella</em> and its metabolite succinate on hepatic steatosis in layer-type pullets.</div></div><div><h3>Methods</h3><div>In experiment 1, 4-wk-old female layer-type chickens (Isa Brown) were randomly divided into 4 dietary groups and fed a basal diet supplemented with 0%, 2%, 4%, or 6% L-arabinose for 11 wk. In experiments 2 and 3, 10-wk-old chickens were orally administered <em>Prevotella</em> (10<sup>6</sup> CFU) or fed a diet supplemented with 0.2% sodium succinate for 4 wk. The growth performance, plasma lipid metabolites, hepatic lipid accumulation and gene expression, and cecal microbiota were determined. In in vitro experiment, chicken embryo hepatocytes were treated with <em>Prevotella’</em>s metabolites or 0.1 mM succinate in the absence or presence of 4c, a succinate receptor 1 (SUCNR1) inhibitor, or shRNA-PGC1β. Lipid deposition and mitochondrial function were measured. Data were analyzed with a 1-way analysis of variance followed by Tukey’s test.</div></div><div><h3>Results</h3><div>L-arabinose decreased (–68%) hepatic and plasma TG (–52%) and enhanced the abundance of cecal <em>Prevotella</em> (+45-fold) (<em>P</em> < 0.001). Oral administration of <em>Prevotella melaninogenica</em> reduced plasma TG (–22%, <em>P</em> < 0.05) and increased succinate (+66%, <em>P</em> < 0.01). Succinate feeding reduced hepatic (–51%, <em>P</em> < 0.001) and plasma TG (–40%, <em>P</em> < 0.05). Both <em>Prevotella</em> and succinate administration reduced fatty acid synthase (FAS) activity with the induction of mitochondrial function-associated proteins. In vitro experiments showed that <em>Prevotella</em> and succinate alter mitochondrial function and lipid metabolism via SUCNR1, wherein PGC1β plays a critical role.</div></div><div><h3>Conclusions</h3><div>Succinate produced by <em>Prevotella</em> is a likely metabolite that reduces hepatic lipid deposition by suppressing FAS activity and activating mitochondrial function.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1751-1767"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031145","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":"Plant-Based Diet and Erectile Dysfunction: A Narrative Review","authors":"Mariana del Carmen Fernández-Fígares Jiménez","doi":"10.1016/j.tjnut.2025.04.019","DOIUrl":"10.1016/j.tjnut.2025.04.019","url":null,"abstract":"<div><div>Evidence shows that the consumption of plant foods, particularly those in their whole form (fruits, vegetables, whole grains, nuts, seeds, and legumes from which no edible part has been removed), improves cardiometabolic risk factors and is associated with reduced risk of cardiovascular diseases (CVDs), diabetes, cancer, chronic kidney disease and mortality compared with animal (meat, fish, eggs and dairy) and nonwhole plant foods (sugar-sweetened beverages, refined grains, etc.). Erectile dysfunction (ED) is considered a strong predictor of CVD. The underlying defect in arteriogenic ED is endothelial dysfunction. A plant-based diet focused on whole plant foods could enhance penile erection as it improves endothelial function through various mechanisms. First, it provides nitrates, L-arginine, and L-citrulline, substrates for nitric oxide production. In addition, this diet lowers low-density lipoprotein cholesterol, trimethylamine N-oxide, postprandial triglycerides, advanced glycation end product, inflammation, and vasoconstrictors levels, contributing to higher nitric oxide concentrations, increased endothelial progenitor cells preservation and decreased arterial stiffness. This review explores the epidemiological evidence of a plant-based diet emphasizing whole plant foods on ED and the potential biological pathways involved.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1644-1652"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016172","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":"High-Cellulose Diet Ameliorates Cognitive Impairment by Modulating Gut Microbiota and Metabolic Pathways in Mice","authors":"Moeka Tanabe , Kazuo Kunisawa , Imari Saito , Haruto Ojika , Kuniaki Saito , Toshitaka Nabeshima , Akihiro Mouri","doi":"10.1016/j.tjnut.2025.04.004","DOIUrl":"10.1016/j.tjnut.2025.04.004","url":null,"abstract":"<div><h3>Background</h3><div>Nutrition is a key factor in cognitive function, and safe dietary interventions are promising to prevent cognitive impairment in pediatric psychiatric disorders. We previously demonstrated that childhood social isolation (SI) stress affects colonic function, leading to cognitive impairment. Cellulose, an insoluble dietary fiber, shows benefits to intestinal health, but its potential impact on cognitive impairment has not been explored.</div></div><div><h3>Objectives</h3><div>This study investigated whether a high-cellulose diet ameliorates cognitive impairment induced by SI through modulation of gut microbiota and metabolic pathways.</div></div><div><h3>Methods</h3><div>C57BL/6J male mice (3 wk old; <em>n</em> = 10–15/group) were randomly divided into 2 groups: individually housed (SI) group and housed 5 mice per cage (group-housed) group. Each group received either a normal diet (5% cellulose) or a high-cellulose diet (30% cellulose) for 5 wk daily until the end of the behavioral testing. We evaluated behavior abnormalities, gut microbiota composition, and metabolites, and performed 2-way analysis of variance.</div></div><div><h3>Results</h3><div>Intake of a high-cellulose diet ameliorated cognitive impairment, including decreased time spent in a novel location of SI mice in novel object location test (NOLT; +30%; <em>P</em> < 0.01) with reduction of Iba-1 positive cells, microglia, in the hippocampus (–33%; <em>P</em> < 0.05). The high-cellulose diet indicated a significant difference in gut microbiota clustering plots (<em>P</em> < 0.01) and enhanced the variation in malate-aspartate shuttle pathways in SI mice (<em>P</em> < 0.01). Notably, fecal microbiota transplantation (FMT) from SI mice fed a high-cellulose diet after antibiotic treatment, replicated amelioration of cognitive impairment in NOLT (+46%; <em>P</em> < 0.01). Additionally, the FMT replicated a decrease of Iba-1 positive cells indicating suppressed hippocampal microglial activation (–52%; <em>P</em> < 0.01), and enhanced the variation in malate-aspartate shuttle pathways (<em>P</em> < 0.01).</div></div><div><h3>Conclusions</h3><div>These findings suggest that a high-cellulose diet may ameliorate pediatric-specific cognitive impairment through modulation of the gut microbiota and metabolic pathways.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1689-1699"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021790","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":"Dietary Gluten Intake and Cardiovascular Disease Mortality in Japanese Adults in the Takayama Study","authors":"Michiko Tsuji , Keiko Wada , Michiyo Yamakawa , Masaaki Sugino , Tomoka Mori , Chisato Nagata","doi":"10.1016/j.tjnut.2025.03.005","DOIUrl":"10.1016/j.tjnut.2025.03.005","url":null,"abstract":"<div><h3>Background</h3><div>There is growing attention toward the gluten-free diet in Japan, in spite of a low prevalence of celiac disease and high consumption of rice.</div></div><div><h3>Objectives</h3><div>The present study examined whether gluten intake is associated with an increased risk of cardiovascular disease (CVD) mortality in Japanese adults.</div></div><div><h3>Methods</h3><div>In 1992, 13,355 men and 15,724 women, ≥35 y of age, in the Takayama study, completed a self-administered questionnaire. Gluten intake was estimated using a food frequency questionnaire as a baseline. Mortality was ascertained during 16 y of follow-up. Hazard ratios (HRs) and 95% confidence intervals (CIs) for CVD mortality were calculated according to gluten intake quartiles.</div></div><div><h3>Results</h3><div>During 16.1 y of follow-up, 775 CVD deaths in men and 903 CVD deaths in women occurred. Compared with the lowest quartile of intake, the highest quartile of gluten intake was significantly associated with a decreased risk of CVD mortality after controlling for age, sex, and other covariates (HR = 0.73; 95% CI: 0.62, 0.86, <em>P</em>-trend = 0.0003).</div></div><div><h3>Conclusions</h3><div>Our data showed a significant inverse association between gluten intake and CVD mortality. The present study does not support the notion that gluten avoidance should have a beneficial effect on CVD mortality.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1933-1937"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585952","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}
Min Zhuang , Bing Wang , Yanchuan Shi , Zhongkai Zhou
{"title":"Multiorgan Regulation Mechanisms and Nutritional Intervention Strategies in Gestational Diabetes Mellitus","authors":"Min Zhuang , Bing Wang , Yanchuan Shi , Zhongkai Zhou","doi":"10.1016/j.tjnut.2025.04.008","DOIUrl":"10.1016/j.tjnut.2025.04.008","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) affects millions of pregnant women worldwide and leads to both short- and long-term complications for mothers and their fetuses. Managing GDM through diet, physical activity, and medical interventions can significantly reduce these risks. Studies have identified the individual and combined roles of organs regulated by placental hormones, cytokines, and gut microbiota as key pathways contributing to impaired glucose homeostasis. In this context, placental hormones mediate the crosstalk among the placenta, pancreas, and adipose tissue, stimulating endocrine pancreas adaptation and adipose tissue expansion. However, insufficient maternal physiological adaptations, such as dysregulated adipocytokines, adipokines, and oxidative stress in the pancreas, can create an environment conducive to the onset of GDM. Furthermore, gut dysbiosis implies potential mechanisms of gut–host interaction associated with the occurrence of GDM, with short-chain fatty acids possibly serving as crucial targets. Nutritional therapy is recognized as the first-line approach for managing GDM, encompassing dietary guidance and supplementation with micro- and macronutrients as well as bioactive components. Importantly, combined interventions involving multiple nutrients, such as probiotics and prebiotics with vitamins or minerals, may exert stronger beneficial effects on the prevention and treatment of GDM and its complications. This review paper discusses the regulatory role of multiorgans in GDM and the implementation of nutritional therapy for its prevention and management, along with associated complications.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1614-1626"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026750","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}
Allison C Sylvetsky , Ying Wang , Ananya G Reddy , Caroline Y Um , Rebecca A Hodge , Cari Lichtman , Diane Mitchell , Anuj Nanavati , Michael Pollak , Ye Wang , Alpa V Patel , Marjorie L McCullough
{"title":"Nonnutritive Sweetener Consumption, Metabolic Risk Factors, and Inflammatory Biomarkers Among Adults in the Cancer Prevention Study-3 Diet Assessment Sub-Study","authors":"Allison C Sylvetsky , Ying Wang , Ananya G Reddy , Caroline Y Um , Rebecca A Hodge , Cari Lichtman , Diane Mitchell , Anuj Nanavati , Michael Pollak , Ye Wang , Alpa V Patel , Marjorie L McCullough","doi":"10.1016/j.tjnut.2025.03.020","DOIUrl":"10.1016/j.tjnut.2025.03.020","url":null,"abstract":"<div><h3>Background</h3><div>Nonnutritive sweeteners (NNSs) are widely used to replace added sugars, yet their role in metabolic health and chronic disease prevention is debated.</div></div><div><h3>Objective</h3><div>The objective of this study was to examine associations between NNS consumption, metabolic risk factors, and inflammatory biomarkers.</div></div><div><h3>Methods</h3><div>This cross-sectional analysis included 624 adults in the American Cancer Society’s Cancer Prevention Study-3 Diet Assessment Substudy (DAS). Consumption of NNS, including aspartame, saccharin, sucralose, and acesulfame-potassium, was estimated using the mean quantities reported in 6 24-h dietary recalls over 1 y. Fasting insulin, C-peptide, hemoglobin A1c (HbA1c), leptin, adiponectin, C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) were measured in fasting blood samples collected twice, 6 mo apart. Multivariable linear regression was used to examine associations between NNS consumption and the mean levels of each metabolic or inflammatory biomarker. Base models were adjusted for age, sex, race, education, smoking, and physical activity; full models were further adjusted for body mass index (BMI), diet quality (Healthy Eating Index 2020), and energy intake.</div></div><div><h3>Results</h3><div>More than half (55%) of participants reported consuming NNS (mean daily NNS consumption 7, 38, and 221 mg across tertiles). NNS consumption was positively associated with leptin (<em>P</em>-trend = 0.0006) and CRP (<em>P</em>-trend = 0.02), but associations were attenuated after adjustment for BMI, diet quality, and energy intake. NNS consumption was not associated with insulin, C-peptide, HbA1c, adiponectin, TNF-α, or IL-10. In analyses stratified by BMI, NNS consumption was positively associated with IL-6 among participants with BMI ≥25kg/m<sup>2</sup> but not BMI <25kg/m<sup>2</sup>.</div></div><div><h3>Conclusions</h3><div>Findings in the full sample were null after adjustment for energy intake and BMI, but NNS consumption was positively associated with IL-6 among participants with overweight or obesity. Investigation of mechanisms through which NNS consumption may impact inflammatory pathways is warranted.</div></div>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":"155 6","pages":"Pages 1952-1961"},"PeriodicalIF":3.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700663","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}