Vitamin C (ascorbic acid) degradation generates oxalic acid which has been implicated in oxalate-associated renal failure. The aim of this scoping review was to assess studies reporting an association of oral or intravenous (IV) vitamin C with acute renal failure presumed to be due to oxalate nephropathy to investigate the role of pre-existing renal dysfunction and other possible confounders of oxalate nephropathy. Of the 144 papers identified, 45 were included in the final review. These comprised 21 oral vitamin C case reports and 24 IV vitamin C case reports. Oral vitamin C cases were reported in people with pre-existing renal disease and/or gastrointestinal surgery or disorders leading to altered oxalate absorption, among other confounders such as dehydration and high dietary oxalates. IV vitamin C cases were reported in people with cancer, sepsis/burns, or other confounding conditions. In most cases, renal failure could be attributed to the primary disease and/or various medications and interventions used to treat the condition. Importantly, pre-existing renal dysfunction is a key risk factor for impaired clearance of large doses of vitamin C, thereby potentially contributing to hyperoxalosis and further renal damage. As such, it is vital for healthcare practitioners to monitor renal function both before and during high-dose vitamin C regimens.

Mediterranean and vegan diets have been extensively studied for health effects. This secondary analysis assessed animal vs plant-based processed foods. We hypothesized that greater intake of minimally processed plant foods and lower intake of animal foods, particularly processed and ultraprocessed, would be associated with lower body weight. In this randomized crossover trial, 62 overweight adults were randomized to a Mediterranean or low-fat vegan diet for 16 weeks, separated by a 4-week washout. Body weight was the primary outcome. Three-day diet records assessed intake of animal- and plant-based foods by NOVA processing category. Compared with the Mediterranean diet, the vegan diet produced greater reductions in minimally processed animal foods (P < .001) and greater increases in minimally processed plant foods (P = .003). Processed animal- and plant-based foods decreased on the vegan diet versus the Mediterranean diet (P <.001 and P = .005, respectively). In the first 16 weeks, changes in processed and ultraprocessed animal foods were nominally associated with weight gain (r = +0.30, P = .02; r = +0.36, P = .004), though neither survived Bonferroni correction. In the second 16 weeks, an increase in minimally processed animal foods was associated with weight gain (r = +0.42, P = .002), the only correlation surviving correction; a nominal inverse association emerged for minimally processed plant foods (r = -0.35, P = .01). In this exploratory analysis, increasing minimally processed plant foods while minimizing animal foods at all processing levels was associated with favorable weight outcomes. Trial registration: ClinicalTrials.gov, NCT03698955.

Insufficient sleep has been linked to diet, but its relation to longer term folate status is unclear. We hypothesized that red blood cell (RBC) folate measures would be inversely associated with insufficient sleep. We analyzed 4224 adults aged ≥20 years from the National Health and Nutrition Examination Survey 2021-2023, including 836 with insufficient sleep. Insufficient sleep was defined as a weekday/weekend weighted mean sleep duration <7 h/night. Survey-weighted logistic regression accounted for the complex sampling design. The weighted prevalence of insufficient sleep was 19.2%. In the primary model, each 1-standard deviation higher concentration was associated with lower odds of insufficient sleep for conventional RBC folate (odds ratio, 0.865; 95% confidence interval, 0.777-0.963), total washed RBC folate (0.847; 0.746-0.962), washed RBC 5-methyltetrahydrofolate (0.853; 0.764-0.953), and MeFox (0.842; 0.761-0.930); THF and 5,10-methenylTHF were not associated with the outcome. Estimates changed little after adjustment for day 1 energy intake, dietary folate equivalents, and supplement use. Restricted cubic spline models showed no evidence of nonlinearity. Model-standardized prevalence was 20.3% in the lowest and 15.2% in the highest quartile of total washed RBC folate. Results were similar in sensitivity analyses, including additional adjustment for serum cotinine. These cross-sectional findings are consistent with inverse associations for selected RBC folate measures but do not establish temporal direction or a benefit of folate supplementation.

The co-occurring experience of food insecurity and stress may result in the over- and underconsumption of nutrients that may impact cognitive function (CF). The objective of this study was to determine if food security status (FSS) and/or stress influences domains of CF and dietary intake in a diverse population of college students. It was hypothesized that decreasing FSS and increasing levels of stress would be associated with poorer indicators of CF and dietary quality. This cross-sectional study (n = 230) included a series of computerized tasks using Cambridge Neuropsychological Test Automated Battery to assess CF domains. Diet quality and nutrient intake were estimated using Diet ID. Perceived stress, FSS, and sociodemographic information were collected. Multivariable linear regression models were constructed to explore the associations between FSS and/or stress on dietary and CF outcomes.Participants experienced food insecurity (31%), moderate to high stress (84%), and clinically relevant adverse childhood experiences (19%). There was an inverse relationship between carotenoid, fiber, and protein intake with higher stress (P < .05). FSS was associated with increased sodium and protein intake (P < .05). Differences were observed in three out of five CF domains, with increasing stress associated with lower scores on the Cambridge Gambling Task and Rapid Visual Processing (P < .01) and low FSS was associated with greater time to decision-making on the Delayed Match to Sample (P < .01) and lower scores on Rapid Visual Processing (P < .05). Differences in FSS and/or higher levels of stress was associated with various domains of CF, including decision-making, impulsivity, and planning, which may provide insight into dietary behaviors in this population.

Neurodegenerative diseases are defined as progressive and irreversible disorders involving the degeneration of neurons in the brain, giving rise to both cognitive deterioration and motor dysfunction. Diseases such as Alzheimer's, Parkinson's, and Huntington's pose major public health challenges, particularly in aging populations, and are driven by complex mechanisms including oxidative stress, neuroinflammation, and abnormal protein aggregation. Recent evidence suggests that alterations in gut microbiota composition are closely linked to the onset and progression of these disorders. Saponins have been reported to modulate gut microbiota composition and preclinical studies indicate that certain saponins may exert neuroprotective actions in specific models of neurodegeneration. This review summarizes and interprets the emerging, preliminary role of saponins in modulating pathways implicated in neurodegeneration, with a particular focus on their capacity to influence the gut microbiota-brain axis. Specifically, we summarize scientific evidence on how the structural features of saponins shape gut microbial composition and activity, thereby influencing their potential to modulate the development and progression of neurodegenerative disorders. Microbial metabolites, neuroinflammatory cascades, and redox balance represent key pathways potentially influenced by saponins in preclinical contexts, 2 central drivers of neurodegenerative progression. This review also highlights the preliminary nature of current evidence on these potential mechanisms and discusses major knowledge gaps, including saponin toxicity and the need for clinical studies before meaningful translation.

The epidemiological findings on specific vitamin D metabolites and health outcomes remain inconsistent and limited. We hypothesized that vitamin D metabolites may have distinct associations with all-cause and cardiovascular disease (CVD) mortality. This study included 24,592 participants from the National Health and Nutrition Examination Survey 2007 to 2018. Baseline serum vitamin D metabolites, including 25(OH)D3, its epimer 3‑epi-25(OH)D3, and 25(OH)D2, were quantified using standardized liquid chromatography-tandem mass spectrometry. Data on death and causes were obtained through the National Death Index records. Cox proportional-hazard models were used to estimate the hazard ratios and 95% confidence intervals (CIs). During a median follow-up of 6.4 years, 1397 all-cause deaths and 371 CVD deaths were documented. Serum 25(OH)D3 and total 25(OH)D exhibited L-shaped inverse associations with all-cause and CVD mortality, whereas 25(OH)D2 showed no association. When comparing extreme quartiles, the multivariable-adjusted hazard ratios for 25(OH)D3 were 0.68 (95% CI: 0.56-0.83) for all-cause mortality and 0.71 (95% CI: 0.50-0.99) for CVD mortality. For 3‑epi-25(OH)D3, we observed a nonlinear inverse association with all-cause mortality that attenuated to null at around 10.7 nmol/L. Moreover, mediation analysis suggested that alkaline phosphatase and albumin collectively explained 20.0% and 20.4% of the associations of 25(OH)D3 and total 25(OH)D with CVD mortality, respectively. In a nationally representative population, serum 25(OH)D3 was inversely associated with all-cause and CVD mortality, while 3‑epi-25(OH)D3 and 25(OH)D2 showed distinct patterns of association with mortality. Our findings highlight the importance of distinguishing among vitamin D metabolites in mortality risk assessment.

Maternal body mass index (BMI) reflects nutritional status, metabolic adaptation, and energy balance during pregnancy and the postpartum period. Longitudinal BMI trajectories may therefore represent distinct nutritional-metabolic phenotypes with implications for subsequent cardiometabolic risk. However, such trajectory patterns extending from pregnancy into the postpartum period remain insufficiently characterized, particularly in Asian populations. This study aimed to identify distinct BMI trajectories from early pregnancy to 6 months postpartum and evaluate their associations with hypertension risk. In this prospective birth cohort, 502 women were recruited at a medical center in Taiwan between August 2022 and August 2023, with scheduled follow-up from early pregnancy to 6 months postpartum. After exclusions, 444 singleton pregnancies were included in the pregnancy trajectory analysis. Among them, 348 women with available postpartum BMI measurements were included in the postpartum trajectory analysis. Latent class trajectory modeling characterized longitudinal BMI patterns, and multinomial logistic regression examined associations between trajectory groups and demographic, clinical, and biochemical factors, including hypertension status. Three prenatal BMI trajectories and 2 postpartum weight-loss patterns were identified and integrated into 3 composite nutritional-metabolic profiles: Majority-Rapid Decline (MR), High-Rapid Decline (HR), and High-Slow Decline (HS). Compared with MR, the HS group exhibited a markedly elevated risk of hypertension (adjusted odds ratio 7.63; 95% CI: 2.05-28.38). Women in the HS group had higher early-pregnancy BMI and demonstrated attenuated postpartum weight loss, suggesting a more adverse metabolic response to pregnancy. Maternal BMI trajectories represent meaningful nutritional phenotypes that extend across pregnancy and postpartum. A pattern combining high early BMI with limited postpartum weight loss was associated with increased hypertension risk, underscoring the importance of tailored nutritional and weight-management strategies to improve maternal cardiometabolic health.

Menopause is a physiological transition characterized by the cessation of ovarian function and a decline in estrogen production, contributing to metabolic dysfunction, adipose tissue remodeling, oxidative stress, and chronic low-grade inflammation. Due to contraindications of hormone therapy for some women, natural compounds have been investigated. We hypothesized that açaí seed extract (ASE) would improve metabolic parameters and reduce white and brown adipose tissue (BAT) remodeling through antioxidant and anti-inflammatory mechanisms. Sprague-Dawley rats (90 days old) underwent bilateral ovariectomy (OVX), with Sham rats as controls. ASE supplementation (200 mg/kg/day) started 4 weeks after surgery and lasted 8 weeks. Food intake and body weight were assessed. Body composition was evaluated by nuclear magnetic resonance. After treatment, animals were euthanized by decapitation. Plasma lipid profile, 17 β-estradiol, leptin, and thyroid hormones were assessed. Retroperitoneal white adipose tissue (rWAT) and BAT were isolated for morphometric analysis and assessment of oxidative damage, antioxidant activity, and proinflammatory cytokines. UCP-1 immunostaining was evaluated in BAT. 17 β-estradiol concentrations and uterine weight were reduced by OVX and were not modified by ASE. ASE attenuated OVX-induced alterations in body fat mass, dyslipidemia, leptin, and total T3; prevented adipocyte hypertrophy in rWAT; reduced interleukin 6 and oxidative damage; and improved antioxidant activity in rWAT and BAT. The extract reduced body weight gain, body fluid, and tumor necrosis factor alpha concentrations and increased UCP-1 immunostaining, independent of ovarian status. The results suggest that ASE has potential to mitigate metabolic alterations associated with OVX, with some effects occurring independently of ovarian status.

Westernized dietary patterns (WDPs), characterized by processed foods, red meats, refined grains, and added sugars, may contribute to gastric cancer (GC) development. We hypothesized that alignment with WDPs, as measured by the Westernized diet index (WDI), is associated with an increased risk of GC. In this incidence case-control study, 82 newly diagnosed GC patients and 95 age- and sex-matched controls were recruited. Dietary intake was assessed using a validated 168‑item food frequency questionnaire. Logistic regression models estimated odds ratios and 95% confidence intervals for GC across WDI categories, adjusting for major demographic, lifestyle, and clinical covariates, including Helicobacter pylori infection. To assess construct validity, fully adjusted linear regression evaluated associations between WDI scores and circulating inflammatory markers (high-sensitivity C-reactive protein, interleukin [IL]‑6, IL‑1β, IL‑10, tumor necrosis factor-alpha), oxidative stress (total antioxidant capacity, malondialdehyde), and metabolic biomarkers (body mass index, fasting glucose, lipid profile). Higher alignment with WDPs (lower WDI scores) was associated with significantly increased GC risk. Individuals in the highest WDI global Z‑score categories-WDI-G (food groups-nutrient based) and WDI-FG (food group based)-had 85% and 78% lower odds of GC, respectively (odds ratio = 0.15 and 0.19; both P < .001). Greater WDP alignment (lower WDI scores) was also associated with higher concentrations of high-sensitivity C-reactive protein, IL‑6, tumor necrosis factor-alpha, and IL‑1β, and lower IL‑10, along with an adverse metabolic profile (higher LDL‑c, lower HDL‑c). Overall, greater alignment with WDPs was associated with elevated GC risk and unfavorable biomarker patterns. These findings support the WDI as a biologically plausible indicator of Western dietary exposure and underscore the potential role of WDPs in gastric carcinogenesis.

Excessive gestational weight gain (GWG) is linked to poor pregnancy outcomes and increased maternal obesity. Current interventions moderately reduce GWG, but have limited impact on maternal health. Dietary fiber supports weight management and diet quality outside of pregnancy, yet its effects during pregnancy remain unclear. We hypothesized that a high fiber (HFib) intervention would reduce GWG, decrease fat accrual, and improve diet quality compared with standard prenatal care. In this randomized controlled pilot trial, the HFib group completed an 18-week intervention beginning at 12 to 20 weeks gestation, which included behavioral education and daily HFib snacks. Of n = 51 participants randomized, n = 31 were included in the final analysis (HFib: n = 16, usual care: n = 15). GWG, body composition, dietary intake, and diet quality were assessed at baseline and intervention end. Total GWG was lower in the HFib group (mean difference -5.5 kg, P = .029) compared to controls, and by the end of the intervention, the HFib group also showed smaller increases in body fat percentage (1.6% vs 4.5%, P = .033) and fat mass (mean difference -2.7 kg, P = .029). Fiber intake increased from 21.8 ± 7.5 to 35.1 ± 7.4 g/d in the HFib group, while the usual care group remained near 19 g/d. Diet quality improved in the HFib group (+7.6 points) and declined in usual care (P = .003). In conclusion, the HFib intervention, combining HFib snacks and behavioral education, significantly increased fiber intake and improved adherence to a food-based HFib dietary pattern. These findings suggest the approach is feasible and may help reduce GWG and fat accrual. This trial was registered at clinicaltrials.gov (NCT04868110).

The associations between plasma long-chain fatty acids and hypertension remain incompletely understood, particularly in middle-aged and older adults, and the underlying mechanisms are still unclear. This study aimed to investigate the associations between plasma long-chain fatty acids and hypertension and to explore the underlying molecular mechanisms using an integrated network pharmacology and molecular docking approach. We included 2092 middle-aged and older adults with available measurements of plasma long-chain fatty acid concentrations. Stepwise adjusted logistic regression and Bayesian kernel machine regression were used to assess the associations of individual fatty acids and mixed fatty acid exposure with hypertension. Potential targets of fatty acids and hypertension were identified from public databases, followed by protein-protein interaction network construction, hub target identification, enrichment analyses, and molecular docking. After adjustment for sex, age, sociodemographic characteristics, lifestyle factors, and body mass index, myristoleic acid, arachidonic acid, erucic acid, and docosahexaenoic acid were inversely associated with hypertension, whereas eicosapentaenoic acid and docosatetraenoic acid were positively associated. Mixed-exposure analysis suggested a modest overall effect, with the main contributions arising from these key fatty acids. MAPK3, PTGS2, and ESR1 were identified as hub targets and were mainly involved in inflammation, immune responses, lipid metabolism, and vascular function. In conclusion, plasma long-chain fatty acid profiles were associated with hypertension in middle-aged and older adults and may provide new epidemiological evidence and mechanistic insights into hypertension risk.

Body mass index (BMI) is widely used to assess obesity-related cardiometabolic risk, but the adiposity measures corresponding to a given BMI may differ across populations. We hypothesized that in Korean adults, a BMI of 25 kg/m[2] would correspond to substantial metabolic syndrome (MetS) risk at lower adiposity levels than previously reported in Western populations and that BMI and adiposity measures would demonstrate differential discriminatory performance for MetS. We analyzed adults aged 18-80 years from the Korea National Health and Nutrition Examination Survey were analyzed, including 3023 participants with dual-energy X-ray absorptiometry (DXA)-derived whole-body fat percentage (WBF%) and trunk fat percentage (2008-2011) and 9185 participants with bioelectrical impedance analysis (BIA)-derived WBF% (2022-2023). Age- and sex-adjusted complex-sample logistic regression was used to estimate the probability of MetS at BMI 25 kg/m[2] and the corresponding adiposity measures. The estimated prevalence of MetS at BMI 25 kg/m[2] was 29.6% in DXA-based dataset and 29.7% in BIA-based dataset. Corresponding WBF% values were 22.3% in men and 33.2% in women in DXA-based dataset, and 24.7% and 33.2%, respectively, in BIA-based dataset. Corresponding trunk fat percentages were 24.4% in men and 33.2% in women. BMI demonstrated greater discriminatory performance for MetS than WBF% in both datasets, and trunk fat percentage outperformed WBF% in DXA dataset. These findings support the hypothesis that Korean adults experience substantial metabolic risk at lower adiposity levels than reported in U.S. populations and highlight the importance of considering both total and regional adiposity in nutritional and metabolic risk assessment.

This secondary analysis aimed to examine the associations between biochemical biomarkers, lipid profiles and clinical outcomes in individuals with migraine. A cross-sectional study including 72 adults with a confirmed migraine diagnosis according to the ICHD-III criteria was conducted. Clinical outcomes comprised pressure pain thresholds (PPTs) at trigeminal and extratrigeminal sites, migraine-related disability (MIDAS), perceived stress (PSS-14), and handgrip strength. Biochemical parameters included serum vitamin D concentrations, the (Neutrophil-to-Lymphocyte Ratio (NLR), lipid profile and fasting glucose. Independent associations were assessed using adjusted multiple linear regression models. Higher NLR was associated with greater migraine-related disability (MIDAS; r = 0.38, p < .05) and higher perceived stress (PSS-14; r = 0.43, p < .05). Vitamin D concentrations were significantly and positively correlated with higher PPTs, particularly at the anterior temporalis (r = 0.36, p < .05), middle temporalis (r = 0.24, p < .05), and sternocleidomastoid muscles (r = 0.28, p < .05). Regression models further showed that elevated NLR was linked to increased disability (B = -0.35, 95% CI -0.47 to -0.17, p = .001) and lower PPTs at masseter (B = -0.40, 95% CI -0.75 to -0.14, p = .01) and middle temporalis (B = -0.34, 95% CI -0.46 to -0.13, p = .009). Also, lower vitamin D concentrations were associated with decreased PPTs at the middle temporalis (B = -0.38, 95% CI -0.52 to -0.22, p = .001). Higher NLR, as a marker of systemic inflammation, was associated with greater migraine-related disability and increased pain sensitivity, whereas lower vitamin D concentrations were associated with increased pain sensitivity.

Neuroprotective peptides, a class of bioactive peptides naturally derived from food sources, exhibit strong potential in neuroprotection and the promotion of neural development. These peptides are characterized by high bioavailability, favorable safety profiles, and multifunctional physiological benefits. Notably, specific peptides such as PW5 (Pro-Trp-Trp-Trp-Trp-Trp) and WHP (Trp-His-Pro) have demonstrated significant efficacy in reducing oxidative stress, inhibiting neuroinflammation, and attenuating neuronal apoptosis in both in vitro and in vivo models of cognitive impairment. These actions are comparable to neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF), contributing to improved synaptic plasticity and enhanced cognitive function. Clinically, these peptides offer promising adjunct or alternative strategies for managing neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD), especially in early-stage interventions or dietary-based therapies. This review summarizes recent advances in food-derived neuroprotective peptides, with particular emphasis on their neuroprotective mechanisms, bioavailability challenges, BBB transport, and delivery approaches. It further highlights current research gaps and provides perspectives for future investigations aimed at facilitating the rational development and potential application of these peptides. Current research faces key limitations, including the incomplete understanding of structure-activity relationships, insufficient evidence regarding blood-brain barrier (BBB) permeability, limited knowledge of peptide stability in complex biological environments, and the lack of comprehensive long-term safety evaluations. Future studies should prioritize systematic peptide screening, mechanism-oriented structure optimization, and advanced delivery strategies to improve the bioavailability and functional efficacy of food-derived neuroprotective peptides.

Paternal obesity results in altered metabolic health and cognitive dysfunction in the offspring. Docosahexaenoic acid (DHA) supplementation has been reported to improve metabolic inflammation, insulin sensitivity, and sperm quality. This study investigated whether paternal DHA supplementation in healthy male rats could prevent metabolic dysfunction induced by a high-calorie diet in their offspring, with a special focus on liver lipid metabolism and sex-specific outcomes. Male Wistar rats received daily saline or DHA-rich fish oil by oral gavage from weaning to adulthood before mating with untreated females. Offspring were then fed either a standard diet or exposed to a free-choice high-fat, high-sugar (FcHFHS) diet. Supplementation with DHA did not alter body weight, circulating lipid profiles, or glucose concentration in the founder males. In offspring, FcHFHS diet feeding induced increased body weight and adiposity in both sexes regardless of paternal DHA supplementation. However, female offspring exhibited greater susceptibility than males to FcHFHS diet-induced dyslipidemia and liver triglyceride accumulation, together with altered hepatic expression of genes involved in lipogenesis and lipid export. Three-way ANOVA analyses revealed that sex and postnatal diet were the primary determinants of these gene expression changes, as well as strong interaction effects between sex and paternal DHA supplementation for key lipogenic genes, including GPAM, SCD1, and FAS. These results show that paternal DHA supplementation did not protect offspring from obesity or metabolic dysfunction. Instead, it induced sex- and diet-dependent programming effects of lipid metabolism driven by strong interactive influences of paternal diet, offspring sex, and postnatal nutritional environment.