Search Results (2,290)

Climate change poses a threat to global rice production by increasing the frequency and intensity of extreme weather events. The widespread cultivation of genetically uniform modern varieties has narrowed the genetic base of rice, increasing its vulnerability to these increased pressures. Rice landraces are traditional rice varieties that have been cultivated by farming communities for centuries and are considered crucial resources of genetic diversity. These landraces are adapted to a wide range of agro-ecological environments and exhibit valuable traits that provide tolerance to various biotic stresses, including drought, salinity, nutrient-deficient soils, and the increasing severity of climate-related temperature extremes. In addition, many landraces possess diverse alleles associated with resistance to biotic stresses, including pests and diseases. In addition, rice landraces exhibit great grain quality characters including high levels of essential amino acids, antioxidants, flavonoids, vitamins, and micronutrients. Hence, their preservation is vital for maintaining agricultural biodiversity and enhancing nutritional security, especially in vulnerable and resource-limited regions. However, rice landraces are increasingly threatened by genetic erosion due to widespread adoption of modern high-yielding varieties, habitat loss, and changing farming practices. This review discusses the roles of rice landraces in developing resilient and climate-smart rice cultivars. Moreover, the Pantiange Heigu landrace, cultivated at one of the highest altitudes globally in Yunnan Province, China, has been used as a case study for integrated conservation by demonstrating the successful combination of in situ and ex situ strategies, community engagement, policy support, and value-added development to sustainably preserve genetic diversity under challenging environmental and socio-economic challenges. Finally, this study explores the importance of employing advanced genomic technologies with supportive policies and economic encouragements to enhance conservation and sustainable development of rice landraces as a strategic imperative for global food security. By preserving and enhancing the utilization of rice landraces, the agricultural community can strengthen the genetic base of rice, improve crop resilience, and contribute substantially to global food security and sustainable agricultural development in the face of environmental and socio-economic challenges. Full article

As age progresses and the population increases, the prevalence of dementia also increases. Pharmacological interventions are used to treat cognitive decline. Alternative approaches to traditional pharmacology, such as dietary interventions, may help combat cognitive decline in aging populations. This review summarizes existing investigations using complementary and alternative approaches as mitigating interventions. We also briefly note other important modifiable factors to decrease the risk of cognitive decline, and Alzheimer’s disease and related dementias. Such approaches include nutrition and dietary interventions that show promising results for mitigating cognitive decline, as well as additional lifestyle modifying factors that are important to note (e.g., sleep, cardiovascular diseases, environmental factors, physical, social and leisure activities, cognitive stimulation, psychosocial factors, and sensory functioning) for their impact on cognition in aging. Despite the limited findings and support for complementary and alternative approaches in combating existing cognitive decline, findings suggest that such approaches may be most beneficial prior to the onset of cognitive impairment. Specific nutrition components, including flavonoids and omega fatty acids, may mitigate cognitive decline, and emerging evidence suggests that these nutrients may promote a healthy gut microbiota. Of the complementary and alternative approaches, adhering to specific diets, generally, has the most consistent support to combat cognitive decline. It is important to note that other non-nutritional or non-dietary modifiable lifestyle factors also show promising benefits in mitigating further cognitive decline. Future investigations and clinical trials with replication studies are needed to elucidate these complementary and alternative approaches as effective treatment options for clinicians. Full article

Background: Ultra-processed foods (UPFs) have emerged as a critical component of diet quality, yet data on the associations between UPF and nutrient intakes remain limited. This study aimed to evaluate nutrient consumption in relation to UPF intake and adherence to international dietary guidelines for non-communicable disease (NCD) prevention. Methods: Data from 469 individuals aged 2–18 years enrolled in the Hellenic National Nutrition and Health Survey (HNNHS) were analyzed. Intakes were assessed using two 24 h recalls, and foods were classified according to the NOVA system. Participants were categorized by UPF energy intake tertiles. Nutrient adequacy was assessed using Nordic Nutrition Recommendations, European Society of Cardiology guidelines for macronutrients, and the Institute of Medicine’s Estimated Average Requirements and Adequate Intake values for micronutrients. Results: Children in the highest UPF tertile had significantly higher intakes of energy, carbohydrates, added sugars, saturated fats, polyunsaturated fats, and cholesterol, but lower intakes of protein compared to those in the lowest tertile. Fiber intake remained inadequate across all tertiles, with no significant differences. Regarding adherence to NCD prevention guidelines, children in the 3rd UPF tertile had a 2.3 times higher prevalence ratio for exceeding added sugar recommendations, while their protein intake prevalence ratio was 0.8 times lower. For micronutrients, the highest UPF tertile showed significantly elevated intakes of vitamins E, B₁, folate, calcium, iron, copper, and sodium, but lower potassium intake compared to the lowest tertile. Conclusions: Our results underscore the need for effective public health strategies to improve diet quality in children and adolescents and prevent diet-related NCDs. Full article

Background: Chronic kidney disease (CKD) represents a state of persistent, sterile low-grade inflammation in which sustained innate immune activation accelerates renal decline and cardiovascular complications. Diet-induced gut dysbiosis and intestinal barrier dysfunction lower mucosal immune tolerance, promote metabolic endotoxemia, and position the gut as an upstream modulator of systemic inflammatory signaling along the gut–kidney axis. Scope: Most studies address microbiota-derived metabolites, food-derived bioactive peptides, or omega-3 fatty acids separately. This review integrates evidence across these domains and examines their convergent actions on epithelial barrier integrity, immune polarization, oxidative-inflammatory stress, and inflammasome-dependent pathways relevant to CKD progression. Key mechanisms: CKD-associated dysbiosis is characterized by reduced short-chain fatty acid (SCFA) production and increased generation and accumulation of uremic toxins and co-metabolites, including indoxyl sulfate, p-cresyl sulfate, trimethylamine N-oxide, and altered bile acids. Reduced SCFA availability weakens tight junction-dependent barrier function and regulatory immune programs, favoring Th17-skewed inflammation and endotoxin translocation. Bioactive peptides modulate inflammatory mediator networks and barrier-related pathways through effects on NF-κB/MAPK signaling and redox balance, while omega-3 fatty acids and specialized pro-resolving mediators support resolution-phase immune responses. Across these modalities, shared control points include barrier integrity, metabolic endotoxemia, oxidative stress, and NLRP3 inflammasome activation. Conclusions: Although evidence remains heterogeneous and largely preclinical, combined nutritional modulation targeting these convergent pathways may offer greater immunomodulatory benefit than isolated interventions. Future multi-omics-guided, factorial trials are required to define responder phenotypes and translate precision immunonutrition strategies into clinical CKD care. Full article

Osteoporosis and chronic conditions such as type 2 diabetes mellitus, cardiovascular disease, heart failure, and chronic kidney disease share several common biological mechanisms, including chronic inflammation, oxidative stress, hormonal dysregulation, and metabolic alterations. In this context, multimorbidity presents an increasing clinical challenge, particularly in older populations, where osteoporosis remains frequently underdiagnosed and undertreated. This review aims to explore the complex interplay between skeletal fragility and cardiometabolic diseases, emphasizing the role of nutritional deficiencies (such as iron and vitamin C), shared molecular pathways (advanced glycation end-products, Renin–Angiotensin–Aldosterone System, RANK Ligand, RANK), and the systemic impact of chronic inflammation and tissue hypoperfusion. The review also addresses the effects of various drug classes—antidiabetics, antihypertensives, anticoagulants, and anti-osteoporotic agents—on bone metabolism and cardiovascular risk. Special focus is given to the implementation of integrated and personalized care models, particularly multidisciplinary team-based approaches, which have demonstrated significant reductions in mortality and refracture rates, despite their still limited adoption in clinical practice. In conclusion, this review highlights the shared mechanisms between osteoporosis and cardiometabolic conditions in the context of multimorbidity, underscoring persistent clinical challenges related to diagnosis, drug interactions, and care fragmentation that warrant further research into integrated care models. Full article

Background/Objectives: Patients in need of specialized palliative care are clinically highly complex, with pain being the most prevalent problem. Furthermore, in these patients, a self-report for characterization of pain could be difficult to obtain. This cross-sectional, exploratory study investigates the use of clinical parameters and peripheral blood biomarkers for potentially identifying and characterizing pain (assessed using Pain Assessment in Advanced Dementia (PAINAD) and Numeric Scale (NS)) in patients under palliative care, including a population with dementia where pain is often underdiagnosed. Methods: Fifty-three patients with non-oncological diseases were analyzed in a cross-sectional study using medical and nursing records. Among previous biomarkers related to monocytes and platelets assessed by flow cytometry, we selected the most significative ones for pain characterization in a logistic regression analysis (multivariate analysis), alongside patient-specific characteristics such as renal function, nutritional status, and age. Results: Our exploratory findings suggest strong relationships between chronic pain and advanced age, reduced glomerular filtration rate (GFR), and malnutrition within this cohort. Furthermore, the percentage of lymphocytes, total and classical monocytes, the relative expression in monocytes of CD206, CD163, the CD163/CD206 ratio, and the relative expression in platelets of CD59 emerged as potential predictors of pain. Statistical analyses highlighted the challenges of multicollinearity among variables such as age, GFR, and nutritional status. A classification model further suggested that all patients over 65 years in our specific sample reported pain. Conclusions: This pilot study provides preliminary support for prior evidence linking chronic pain to aging, nutritional deficits, and renal impairment, and highlights potential novel peripheral blood biomarkers for pain assessment. This work emphasizes the promise of clinical and molecular biomarkers to improve pain detection and management, contributing to personalized and effective palliative care strategies. Full article

Background/Objectives: Metabolism is fundamental to all living organisms. It comprises a highly complex network of fine-tuned chemical reactions that sustain life but also generate by-products that damage cellular biomolecules, including DNA, thereby contributing to aging and disease. As metabolism can be largely modified by dietary alterations, it has the potential to positively or negatively affect health and disease. Interestingly, many aging-associated illnesses known to be influenced by diet also show a causal relation with DNA damage. As DNA keeps all instructions for life, and DNA lesions, if unrepaired, interfere with vital processes such as DNA replication and transcription, DNA damage may be an important mediator of the impact of nutrition on health and aging. Methods: Here, we discuss the genome-protective effects of various oral interventions in mice, aiming to elucidate which nutritional alterations lower DNA damage and promote overall health. Results: Our analysis covers a wide range of interventions with reported positive impacts on genomic stability, including modified diets (e.g., dietary restriction, probiotics, micronutrients, fatty acids, and hormones), NAD+ precursors (e.g., nicotinamide riboside), plant derivatives, and synthetic drugs. Among these, caloric and dietary restriction emerge as the most potent, generic modulators of DNA damage and repair processes, enhancing aspects of repair efficiency through metabolic recalibration and improved cellular resilience. Other interventions, like NAD+ precursors, activate partly similar pathways without necessitating reduced food intake. Conclusions: While many interventions show promise, their effects are often less pronounced or are process-specific compared to caloric or dietary restriction. Additionally, many substances lack comprehensive exploration of their genome-protective effects in mice, with often only a small number of studies examining their impact on genome stability. Moreover, the heterogeneity between studies limits direct comparison. However, the observed overlap in mechanistic effects between treatments lends credibility to their potential efficacy. Ultimately, a deeper understanding of these mechanisms could pave the way for translating these findings into, e.g., combination treatments to promote healthy aging in humans. Full article

Background/Objectives: Recessive dystrophic epidermolysis bullosa (RDEB) is a severe congenital genodermatosis characterized by skin and mucosa fragility, chronic inflammation, recurrent infections and high nutritional demands due to increased metabolism and epithelial barrier-related losses, placing patients at risk of zinc deficiency. We aimed to investigate the clinical relevance and biochemical determinants of zinc deficiency as a potentially modifiable contributor to disease burden in RDEB. Methods: In this cross-sectional study (n = 84), serum zinc levels were analyzed in association with sex, age, disease severity, percentage of body surface area (BSA) affected, inflammatory markers, infection burden, and common clinical complications including anemia and growth impairment. Results: Zinc deficiency, defined as levels below 670 µg/L, was identified in 35% of patients and became more frequent after age 5 and during adulthood, particularly among those with more severe disease. Deficiency was strongly associated with anemia, inflammation, infection burden, growth impairment, and extensive skin involvement. A revised cutoff of 780 µg/L is proposed, showing improved diagnostic performance for identifying patients at risk of systemic complications, and offering a more suitable threshold for starting preventive supplementation. Multivariate logistic modeling confirmed that low serum zinc independently predicted anemia risk, alongside transferrin saturation and C- reactive protein levels. Serum albumin was identified as the strongest determinant of zinc levels, partially mediating the effects of inflammation and skin involvement. Conclusions: These findings identify serum zinc as a clinically relevant marker of nutritional status and complication burden in RDEB. While no causal or therapeutic effects can be inferred from this cross-sectional study, the strong and biologically plausible associations observed suggest a rationale for systematic monitoring and correction of zinc deficiency as part of comprehensive supportive care, and warrant prospective studies to assess clinical benefit. Full article

Background: Intestinal failure-associated liver disease (IFALD) is a serious complication in patients receiving parenteral nutrition, often exacerbated by inflammation, lipid overload, and oxidative stress. Nobiletin (NOB), a polymethoxylated flavone, is known for its anti-inflammatory and lipid-regulating properties. Methods: We employed an in vitro model using THLE-2 human hepatocytes and primary human cholangiocytes exposed to Intralipid (INT) and lipopolysaccharide (LPS) to simulate IFALD conditions. NOB was tested at non-toxic concentrations (10 and 25 µM) to assess its protective effects. MTT viability assays, multiplex bead-based immunoassays (MAGPIX), RT-qPCR, and Western blotting were used to evaluate changes in inflammation markers, gene expression, and protein signaling. Moreover, ALT and AST activities were used to assess hepatocellular injury. Results: NOB maintained high cell viability in THLE-2 hepatocytes and cholangiocytes, confirming its low cytotoxicity. NOB normalized ALT and AST activities in both tested cell lines, but the effect reached statistical significance only for ALT in cholangiocytes. Under IFALD-like conditions (LPS+INT), NOB significantly preserved metabolic activity in both cell types. In THLE-2 and cholangiocytes, NOB markedly reduced the phosphorylation of pro-inflammatory proteins JNK, NF-κB, and STAT3, indicating a broad inhibition of inflammatory signaling. Moreover, in THLE-2 cells, NOB upregulated lipid metabolism-related genes (PRKAA2, CYP7A1, and ABCA1) and decreased oxidative stress, thereby enhancing the nuclear translocation of Nrf2 and increasing SOD1 level, which supports the activation of antioxidant defenses. Conclusions: NOB exhibits hepatoprotective properties under IFALD-like conditions in vitro, likely through modulation of inflammation-related signaling and lipid metabolism pathways. Full article

Background: Sarcoidosis is a heterogeneous, multisystem inflammatory disease with an unpredictable clinical course and limited prognostic markers. Increasing attention has focused on nutritional and metabolic factors—particularly obesity, body composition, and calcium–vitamin D metabolism—as potentially modifiable elements associated with disease development and clinical phenotype. However, the available literature remains fragmented and methodologically heterogeneous. Objective: To systematically map current evidence on the relationship between nutritional status and the development, clinical course, and prognosis of sarcoidosis, and to identify key gaps requiring further research. Methods: A scoping review was conducted in accordance with the Joanna Briggs Institute methodology and the PRISMA-ScR guidelines. PubMed, Scopus, Web of Science, Cochrane Library, EBSCO, and Google Scholar were searched for studies published between 2015 and 2025. Eligible studies included adult patients with sarcoidosis and addressed nutritional status broadly defined, encompassing anthropometric measures, body composition, immunonutritional indices, nutrition-related biomarkers, dietary factors, and supplementation practices. Due to substantial heterogeneity in exposure definitions and outcome measures, no quantitative synthesis or formal methodological quality appraisal was performed. Results: Eighteen studies, predominantly observational, were included. The most consistent findings concerned anthropometric parameters, with overweight and obesity showing the strongest association with an increased risk of sarcoidosis and, in selected studies, with reduced exercise capacity and greater disease burden. Evidence linking nutritional status to prognosis was indirect, while direct data on sarcoidosis-specific survival were lacking. Disturbances in calcium–vitamin D metabolism were frequent and clinically relevant, particularly in the context of supplementation-related hypercalcemia. Conclusions: Current evidence suggests that nutritional status—particularly excess body weight—and selected metabolic and immunonutritional factors are associated with sarcoidosis. However, given the largely observational nature of the available data and the lack of formal assessment of methodological quality, these results should be interpreted as association mapping and hypothesis generation rather than as evidence of causality. Well-designed prospective and interventional studies using standardized nutritional assessment tools and clinically relevant endpoints are needed to clarify the role of nutritional factors in sarcoidosis. Full article

Inflammatory Bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic gastrointestinal conditions that are prone to malnutrition due to poor oral intake, intestinal compromise of nutrient absorption, and increase in metabolic demand. Screening and diagnosing malnutrition in this population is necessary to treat and prevent worsening malnutrition. The use of Oral Nutritional Therapy (ONS) can provide the macronutrients that patients need to maintain their nutrition, however their role in within stages of diseases, active disease, remission, perioperative, and maintenance in relation to other nutritional therapies, such as enteral nutrition or parenteral nutrition, is unclear. This review will highlight the principles of diagnosing malnutrition, the evidence of ONS in disease and remission states, and the role of oral vitamins in the management of IBD. Full article

DNA methylation is a central epigenetic mechanism that mediates the interaction between nutritional exposures and gene regulation. Emerging evidence demonstrates that diet, bioactive compounds, genetic background, and lifestyle factors collectively shape the human methylome, influencing metabolic function, disease susceptibility, and biological aging. This review synthesizes current knowledge on the molecular and biochemical mechanisms of DNA methylation, the role of nutrients and dietary patterns in modulating methylation dynamics, and findings from human clinical trials evaluating nutritional interventions. Genotype-specific responses, including polymorphisms in one-carbon metabolism and metabolic pathways, are discussed as key determinants of interindividual variation in methylation outcomes. The review further highlights the advances in epigenetic clocks, systems biology, and multi-omics integration that support the development of precision nutrition frameworks. Ethical considerations and future challenges related to data interpretation, accessibility, and the regulation of epigenetic testing are also examined. Collectively, this review provides an integrative perspective on how DNA methylation serves as a dynamic interface between diet and health and outlines opportunities for implementing personalized nutrition strategies to improve metabolic resilience and promote healthy aging. Full article

Background: Growth impairment and poor nutritional status are recognized complications of pediatric inflammatory bowel disease (IBD), yet data specific to ulcerative colitis (UC) are limited. This systematic review aims to provide an overview of current knowledge on growth, nutritional status, and body composition in children and adolescents with UC. Methods: A systematic literature search was performed up to August 2025. Studies including patients aged 5–22 years with confirmed UC were reviewed. Results related to growth, nutritional status, and body composition were narratively synthesized to summarize findings. Results: Fifteen studies with 1575 patients with UC met inclusion criteria, comprising 5 prospective, 5 cross-sectional, and 5 retrospective designs. Although the included studies were conducted in broader IBD cohorts, only UC-specific outcomes were reported. The data were limited by sample size, heterogeneity in patient characteristics, outcome definitions, and assessment methods. The majority of patients had prolonged disease with remission or mild activity. Growth failure prevalence ranged from 7% to 36%, with weight deficits being more common than height deficits. Undernutrition affected up to 25% of patients, with variability across studies. Overweight and obesity were also observed, though most studies showed no significant differences between UC patients and controls. Only five very small studies assessed body composition, reporting inconsistent findings regarding reductions in lean body mass. Conclusions: Growth impairment and poor nutritional status can occur in children and adolescents with UC. Larger, standardized, high-quality studies focused specifically on UC are needed to better characterize its impact on growth and nutritional status, including the essential integration of body composition assessment. Full article

Aging is a multifactorial process marked by a progressive decline in physiological function and increased vulnerability to diseases such as neurodegeneration, cancer, cardiovascular disorders, and infections. A central feature of aging is inflammaging, a state of chronic low-grade inflammation driven by cellular senescence, mitochondrial dysfunction, and oxidative stress. Recently, two regulated forms of non-apoptotic cell death—ferroptosis and cuproptosis—have emerged as critical mechanisms linking redox imbalance, mitochondrial stress, and disrupted metal homeostasis to age-related pathology. Ferroptosis, an iron-dependent process characterized by lipid peroxidation and impaired glutathione peroxidase 4 (GPX4) activity, and cuproptosis, a copper-dependent mechanism associated with protein lipoylation stress, both intersect with aging-related changes in mitochondrial and metabolic function. Importantly, these two forms of cell death should not be viewed as entirely separate pathways but rather as interconnected axes within a broader metal–redox–metabolic network. Disturbances in copper or iron homeostasis, glutathione (GSH)/GPX4 dysfunction, mitochondrial and iron-sulfur (Fe–S) cluster compromise, and enhanced lipid peroxidation may converge to lower cellular survival thresholds, thereby exacerbating oxidative damage, immune dysfunction, and tissue degeneration and ultimately fueling aging and inflammaging. This review offers a unique integrated perspective that situates ferroptosis and cuproptosis within a unified framework of aging biology, emphasizing their roles in age-related diseases and the therapeutic potential of targeting these pathways through nutritional, pharmacological, and lifestyle interventions. Full article

Tooth resorption (TR) is a common and painful dental disease in cats. The contributions of skull type, diet, and chronic gingivostomatitis (CGS) to its development remain unclear. We retrospectively reviewed 166 cats with TR confirmed radiographically to evaluate these associations. Brachycephalic cats (N = 33) were significantly younger than non-brachycephalic cats (7.1 ± 2.6 vs. 8.7 ± 3.8 years, p = 0.026) and had a higher prevalence of advanced Stage 4 TR lesions (p = 0.018). There was no significant difference between two groups of cats in sex distribution, diet type or wet food consumption. CGS occurred more often in non-brachycephalic cats (57.9% vs. 21.2%, p < 0.001) but was not associated with TR severity. In both skull groups, mandibular premolars and molars were most commonly affected (p < 0.01). Cats with owner-reported premium diets had more Stage 4 lesions (p = 0.013), particularly in non-brachycephalic cats but not in brachycephalic cats. These findings suggest that TR severity is associated with younger age and advanced lesions in brachycephalic breeds, as well as diet-related differences in non-brachycephalic cats. Further studies are warranted to evaluate early dental screening and targeted nutritional strategies to mitigate the progression of tooth resorption in cats. Full article