Search Results (748)

Background: Nutritional status assessment is the cornerstone of the Nutrition Care Process, guiding diagnosis, intervention, and monitoring. The classical ABCD model (Anthropometry, Biochemical, Clinical, Dietary) has been widely applied; however, it presents limitations in addressing current nutritional and epidemiological challenges. Objective: This narrative review aims to synthesize and update the scientific evidence on the expanded nutritional assessment model, known as ABCDEFG, which incorporates the Ecological–microbiota (E), Functional (F), and Genomic–nutrigenomic (G) approaches. Methods: A narrative review of the literature was conducted through PubMed, Scopus, and Web of Science, covering publications from 2013 to 2025. Articles were selected based on relevance to at least one of the seven assessment domains. Findings were synthesized descriptively and critically, highlighting applications, strengths, and limitations. Results: The ABCDEFG framework offers a multidimensional perspective of nutritional assessment. While anthropometric, biochemical, clinical, and dietary methods remain essential, the inclusion of ecological dimensions (gut microbiota, environmental influences), functional measures (e.g., muscle strength, physical performance), and genomics enables a more sensitive and personalized evaluation. This integrative approach supports better clinical decision-making and research innovation in nutrition and health sciences. Conclusions: The seven-method model broadens the scope of nutritional assessment, bridging traditional and emerging tools. Its application enhances the capacity to identify nutritional risks, design targeted interventions, and advance precision nutrition. Full article

Background: Depression and Metabolic Dysfunction-Associated Steatotic Fatty Liver Disease (MASLD) are common chronic diseases, respectively. However, the causal and molecular links between them remain unclear. In order to explore whether depression contributes to an increased risk of MASLD and whether inflammation mediates this effect, we integrated multi-level evidence from the epidemiology of the National Health and Nutrition Examination Survey (NHANES), the genetics of GWAS, the transcriptomes of GEO, and single-cell RNA sequencing datasets. Methods: A multi-level integrative analysis strategy was used to validate this pathway. First, a cross-sectional epidemiological analysis based on NHANES data was used to reveal the association between depression and MASLD, and to explore the mediating role of inflammation and liver injury markers. Secondly, a two-sample Mendelian randomization analysis was used to infer the causal direction of depression and MASLD, and to verify the mediating effect of systemic inflammation and liver injury indicators at the genetic level. Then, the transcriptome co-expression network analysis and machine learning were used to screen the common hub genes connecting the two diseases. Finally, single-cell transcriptome data were used to characterize the dynamic expression of potential key genes during disease progression at cellular resolution. Results: Depression significantly increased the risk of MASLD, especially in women (OR = 1.39, 95%CI [1.17–1.65]). Parallel mediation analysis showed that high-sensitivity C-reactive protein (hs-CRP) (p < 0.001), γ-glutamyltransferase (GGT) (p < 0.001), and alkaline phosphatase (ALP) (p < 0.001) mediated this relationship. Mendelian randomization analysis confirmed the unidirectional causal effect of depression on MASLD, and there was no reverse association (β = 0.483, SE = 0.146, p = 0.001). Weighted gene co-expression network analysis and machine learning identified CD40LG as a potential molecular bridge between depression-associated immune modules and MASLD. In addition, single-cell data analysis revealed a stage-specific trend of CD40LG expression in CD4⁺ T cells during MASLD progression, while its receptor CD40 was also activated in B cells. In the female sample, CD40LG maintained an upward trend. However, the stability of this result is limited by the limited sample size. Conclusions: This study provides converging multi-omics evidence that depression plays a causal role in MASLD through inflammation-mediated immune signaling. The CD40LG-CD40 axis has emerged as an immune mechanism that transposes depression into the pathogenesis of MASLD, providing a potential target for the intervention of gender-specific metabolic liver disease. Full article

Pests contribute significantly to the loss of Apis mellifera colonies in a multifactorial context that includes viruses, pesticides, nutritional deficiencies, and climate change. This review critically summarises diagnostic techniques (morphological, molecular, automated) and epidemiological methods for the main parasites (Varroa destructor, Vairimorpha spp., Acarapis woodi, Tropilaelaps spp., Aethina tumida, Lotmaria passim, Crithidia mellificae), evaluating trade-offs between sensitivity, specificity, cost, and practicality. There is no universal gold standard; the methodological choice must be contextualised. A decision-making framework structured on four pillars (Primary objective, Resource constraints, Epidemiological context, Ethics/Regulatory) is proposed to guide optimal selections, with application examples and testable hypotheses for future validation. Limitations of emerging technologies (reduced accuracy in the field for AI and LAMP), gaps in multi-pathogen synergies (including viruses and bacteria), interactions with pesticides, and climate impacts with explicit uncertainties are discussed. A global perspective and a One Health approach are adopted, identifying research priorities for integrated diagnostic tools, validated predictive models, and sustainable strategies. Full article

Background/Objectives: Chronic low-grade inflammation and nutritional deficiencies, particularly vitamin D deficiency, have emerged as important contributors to Metabolic syndrome (MetS) pathogenesis but remain underexplored. This study aimed to comprehensively evaluate the associations between dietary intake, vitamin D status, and inflammatory biomarkers (high-sensitivity C-reactive protein -CRP- and ferritin) in patients with MetS. Methods: A cross-sectional observational study was conducted on 141 adult MetS patients at a Mexican hospital. Clinical, anthropometric, dietary (using a validated food frequency questionnaire), and biochemical data including serum 25-hydroxyvitamin D, CRP, ferritin, and neutrophil-to-lymphocyte ratio (NLR) were collected. Vitamin D deficiency was defined as serum 25(OH)D < 20 ng/mL, and high inflammation as CRP ≥ 3 mg/L. Logistic regression models adjusted for confounders were used to analyze associations. Mediation analysis assessed whether vitamin D deficiency mediated the link between dietary intake and high CRP or ferritin. Results: Patients with elevated CRP had significantly lower serum vitamin D levels (14.0 ± 5.1 vs. 22.1 ± 7.0 ng/mL; p < 0.001). Multivariable analysis showed vitamin D deficiency (adjusted OR 7.1; 95% CI 2.5–19.4; p < 0.001) and hyperferritinemia (ferritin ≥ 200 μg/L; aOR 8.0, 95% CI 3.5–18.2, p < 0.001) as predictors of high CRP. Conversely, hyperferritinemia was predicted by vitamin D deficiency (aOR 24.69; 95% CI 3.76–162.16; p = 0.001), elevated CRP (aOR 5.06; p = 0.014), Hb (aOR 63.23; p < 0.001), and inversely by grade 2 obesity (aOR 0.11; 95% CI 0.02–0.60; p = 0.03), confirming bidirectional CRP-ferritin associations and hyperferritinemia as an inflammation marker rather than iron overload indicator. Although Hb > 14.3 g/dL associated with hyperferritinemia, it did not independently predict CRP in multivariate analyses. Frequent consumption of vitamin D-rich foods (milk, fish, Manchego and Oaxaca cheese) was associated with lower inflammation. Mediation analysis confirmed that vitamin D deficiency mediated dietary intake-CRP and dietary intake-ferritin links (Sobel test p < 0.05). Conclusions: Vitamin D deficiency is a key mediator linking inadequate dietary vitamin D intake to systemic inflammation in MetS. Nutritional strategies emphasizing vitamin D repletion and consumption of vitamin D fortified foods may effectively reduce chronic inflammation and improve metabolic outcomes. Full article

Background: The belief that “sugar feeds cancer” is widespread and has strongly influenced public perceptions, patient behavior, and dietary recommendations, despite uncertainty regarding its scientific validity. This belief largely stems from misinterpretation of the Warburg effect, which describes altered glucose metabolism in cancer cells rather than dietary sugar dependence. The objective of this review was to critically evaluate whether dietary sugar intake directly contributes to cancer development or progression by examining the totality of epidemiological, experimental, and mechanistic evidence. Methods: We conducted a narrative review of human epidemiological studies, experimental animal and cell-based models, and mechanistic investigations published between 1980 and July 2025. Evidence was synthesized across cancer types, sugar sources, and biological pathways, with careful consideration of study design, exposure relevance, and key confounders, including obesity, insulin resistance, and overall dietary patterns. Results: Across cancer types, epidemiological evidence showed predominantly null or inconsistent associations between sugar intake and cancer risk or outcomes, with positive findings largely confined to metabolically susceptible subgroups and often attenuated after adjustment for adiposity and energy intake. Experimental studies suggested potential tumor-promoting effects under non-physiological conditions, while mechanistic data indicated that sugar influences cancer risk indirectly through insulin signaling, inflammation, and metabolic dysfunction rather than direct tumor fueling. Conclusions: Current evidence does not support the hypothesis that dietary sugar directly “feeds” cancer in humans. Overemphasis on sugar avoidance risks nutritional and psychological harm, particularly among cancer patients. Evidence-based guidance should prioritize overall dietary quality, metabolic health, and patient well-being rather than isolated sugar restriction. Full article

Background: Nutritional deficiency anemias—including iron, vitamin B12, and folate deficiencies—are common worldwide and are increasingly recognized as potential contributors to venous thromboembolism (VTE). Mechanistic and epidemiologic data suggest that anemia may promote thrombosis through hypoxia, endothelial activation, reactive thrombocytosis, and hyperhomocysteinemia. However, a focused synthesis of clinical and genetic evidence specifically linking nutritional deficiency anemia to VTE has been lacking. Methods: We conducted a systematic search of PubMed and the Cochrane Library from inception to 30 September 2025 to identify studies assessing nutritional deficiency anemia in relation to VTE outcomes. Eligible studies included observational designs, case reports, case series, and Mendelian randomization (MR) analyses. Quality assessment followed the Newcastle–Ottawa Scale (NOS), Joanna Briggs Institute (JBI) checklists, and ROB-MR. The review was registered in PROSPERO (CRD420251235479). Results: Seven studies met the inclusion criteria. Observational analytical studies consistently showed that anemia was associated with adverse VTE-related outcomes. Lower hemoglobin predicted higher short-term mortality in acute pulmonary embolism (HR 1.16 per 1 g/dL decrease), increased symptomatic VTE among hospitalized patients (RR 1.94), and greater long-term bleeding and mortality risk in VTE cohorts (HRs 1.41–2.89). Iron-deficiency anemia increased the odds of VTE in population-based data (OR 1.43), and case reports described unprovoked DVT in young adults with moderate to severe anemia. The MR study indicated a potential causal association between anemia traits and thrombosis at unusual anatomical sites (OR 1.446). No study demonstrated a significant association with recurrent VTE. Most analytical studies were rated as good–high quality. Conclusion: Across multiple study designs, anemia—particularly iron-deficiency anemia and low baseline hemoglobin—appears to be an underrecognized factor associated with elevated VTE risk and adverse VTE-related outcomes. However, direct evidence for vitamin B12- and folate-deficiency anemia remains limited, and further well-designed prospective studies are required to confirm causality and clarify the contribution of specific nutritional deficiency subtypes, as well as to support integration of anemia assessment into VTE risk models. Full article

Background: Gestational diabetes mellitus (GDM) is a frequent pregnancy pathology with poor maternal and fetal outcomes and risk of type 2 diabetes in later life. Despite known risk factors, such as obesity, age, and familial history, new data suggest that environmental exposure to agents, such as pesticides, can play a role in the etiogenesis of GDM. Objective: The epidemiologic, experimental, and mechanistic evidence between pesticide exposure and GDM risk is summarized here, and we concentrate on recent research (2000–2025). Methods: We conducted a literature search in PubMed, Embase, and the Cochrane Library for studies published from January 2000 to December 2025 using combinations of the terms “fertilizers”, “herbicides”, and “pesticides” with “diabetes mellitus” and “gestational diabetes”. After deduplication, 12 unique studies met inclusion criteria for qualitative synthesis (GDM endpoint or pregnancy glycemia with pesticide exposure). Results: Occupational and agricultural exposure to pesticides during first pregnancy was determined to be associated with a significantly increased risk of GDM through various epidemiologic studies. New studies have implicated new classes of pesticides, including pyrethroids and neonicotinoids, with higher GDM risk with first-trimester exposure. Experimental studies suggest that pesticides provide potential endocrine-disrupting chemicals that can induce insulin resistance through disruption of hormonal signaling, oxidative stress, inflammation, β-cell toxicity, and epigenetic modifications. However, significant limitations exist. Most of the evidence is observational, measurement of exposure is often indirect, and confounding factors are difficult to exclude. Notably, low dietary and residential exposure is not well studied, and dose–response relationships are undefined. Conclusions: New data indicate that pesticide exposure during early pregnancy and occupational exposure may increase the risk of GDM. Prospective cohort studies using biomonitoring, chemical mixture exposure, and geographic variation in pesticide exposure should be the focus of future research. Due to potential public health implications, preventive strategies to ensure the quality of nutrition and to reduce maternal exposure to pesticides during pregnancy are rational. Full article

Background: The growing body of evidence linking dietary factors to oral and periodontal health is characterized by substantial heterogeneity in study design, dietary assessment methods, and reported outcomes, warranting a comprehensive narrative synthesis. Diet is a key determinant of oral and periodontal health, influencing inflammation, oxidative stress, salivary composition, and the oral microbiome. Objectives: This narrative review aims to synthesize current clinical, epidemiological, and mechanistic evidence on how dietary patterns and specific nutrients affect oral and periodontal health, focusing on inflammatory pathways, microbiome modulation, nutrient-dependent tissue mechanisms, and clinical outcomes. Methods: A structured narrative search was conducted in PubMed, Scopus, Web of Science, and Google Scholar (2000–2025). Studies examining diet, nutrients, the oral microbiome, caries, gingival inflammation, or periodontal disease were screened through a multistep process, resulting in 98 included articles. Results: High-sugar and ultra-processed diets trigger inflammation and oral dysbiosis, increasing caries and periodontal susceptibility. In contrast, nutrient-rich and anti-inflammatory diets improve immune regulation, support microbial balance, and are associated with better periodontal parameters. Conclusions: Dietary habits significantly shape oral and periodontal outcomes through interconnected metabolic, microbial, and immunological pathways. Integrating targeted nutritional counseling into dental care may strengthen prevention strategies and improve long-term oral health. Full article

Purpose: Candida bloodstream infections remain a major global health challenge, with mortality rates approaching 40%. Beyond classical immunocompromised status, recent evidence highlights additional risk factors, including iatrogenic immunosuppression, advanced age, prolonged hospitalization, exposure to broad-spectrum antibiotics, and total parenteral nutrition. While Candida albicans (C. albicans) remains the most common species in Europe and the USA, non-albicans species, particularly Nakaseomyces glabratus (N. glabratus), Candida tropicalis (C. tropicalis), and Candida parapsilosis (C. parapsilosis), are emerging worldwide. Methods: This retrospective observational cohort study was conducted at the University Hospital “San Giovanni di Dio e Ruggi d’Aragona” in Salerno, Italy, from January 2015 to December 2024. It included all patients with at least one positive blood culture for Candida species. Demographic data, hospital ward of admission, and antifungal susceptibility profiles were collected and analyzed using SPSS software (IBM SPSS Statistics for Mac, version 30 (IBM Corp., Armonk, NY, USA)). Results: The incidence rate is 48.7 new isolates per one thousand patient-days, with a trend of increasing episodes over time among a total of 364 patients. Most cases occurred in medical wards (59.5%), where patients were older (median age 76 (17). C. albicans accounted for 57.9% of isolates, and a significant association was found between species distribution and hospital unit (p < 0.05). Resistance to fluconazole, voriconazole, and amphotericin B increased among C. albicans, with similar trends in N. glabratus and C. parapsilosis. Conclusions: This large single-center cohort highlights both the persistent dominance of C. albicans and the worrisome rise in resistance among C. parapsilosis. Given the aging patient population and increasing antifungal resistance, local epidemiological data are crucial to guide empirical therapy. Our findings underscore the need for multidisciplinary antifungal stewardship programs to optimize personalized treatment strategies and contain the emergence of resistant strains. Full article

Background/Objectives: The growing prevalence of mental health problems among medical students is a global concern, with dietary patterns emerging as potential modifiable factors. This study aimed to explore and evaluate whether higher consumption of ultra-processed foods may be associated with greater symptoms of anxiety and depression. Methods: This was an exploratory cross-sectional study integrated into a previous cohort of medical students, conducted based on the guidelines for Strengthening the Reporting of Observational Studies in Epidemiology. Sixty-seven medical students completed a Food Frequency Questionnaire-based index. Dietary patterns and the associations between these patterns and symptoms of anxiety and/or depression were assessed statistically. Results: There were differences in the consumption of unprocessed or minimally processed foods, including fruits, vegetables, legumes and unsweetened juices between groups with/without anxiety or depression (p < 0.05). A higher intake of ultra-processed foods such as pizza, hot dogs, cereals high in fat and sugar, processed beverages and sweets was linked to greater symptoms (p < 0.05; Cohen’s d = 0.3–0.7). Three to four dietary patterns were identified, explaining between 60% and 86% of the variance. High consumption of cereals with added fat and sugars increased the risk by 7.4 times (OR = 7.4, 95% CI 1.2–12.2, p < 0.05). Conclusions: Dietary intake was associated, but not causally linked, to emotional symptoms among medical students. Lower consumption of unprocessed foods and higher intake of ultra-processed foods formed consistent behavioral profiles associated with anxiety and depression. Consuming more than three daily servings of cereals with added fat and sugar increased the risk of severe depressive symptoms by more than sevenfold, highlighting a strong dietary determinant. Future research should assess nutritional interventions aimed to improve mental health and academic performance in medical students. Full article

Methyl-donor nutrients, including folate, vitamin B12, vitamin B6, choline, betaine, and methionine, play indispensable roles in one-carbon metabolism and govern key processes such as DNA methylation, nucleotide synthesis, and genomic maintenance. Yet despite decades of research, their relationship with cancer remains paradoxical and frequently misunderstood. Much of the confusion arises from an overreliance on epidemiological studies that use cancer incidence as a late-stage endpoint, thereby obscuring how the biological actions of methyl donors differ fundamentally across the continuum from precancerous lesions to established tumors. By synthesizing evidence from mechanistic studies, precancerous lesion research, and early-stage carcinogenic models, this review suggests that adequate methyl-donor availability may be protective during the earliest phases of cancer development. However, these same nutrients may later become substrates hijacked by neoplastic cells to fuel rapid proliferation, maintain oncogenic methylation programs, and enhance tumor progression in established malignancies and high-risk populations. Therefore, this review proposes a reframing that methyl donors may not be evaluated merely as protective or harmful, but rather as context-dependent modifiers whose influence is shaped by timing, metabolic status, and the underlying biology of the target tissue. Such a shift is promising for advancing precision nutrition and the prevention or targeted suppression of cancer. Full article

Vitamin D, traditionally regarded as a nutrient, is increasingly recognized as a pharmacologically active secosteroid with pleiotropic effects extending beyond calcium homeostasis and bone integrity. Together with vitamin K2, it participates in the fine-tuning of mineral metabolism and vascular health, potentially modulating cardiometabolic risk through intertwined endocrine and paracrine pathways. Despite widespread fortification and supplementation, vitamin D deficiency remains a major global health concern, driven by limited sun exposure, obesity, and metabolic dysfunction. Observational and mechanistic studies consistently link low serum 25(OH)D concentrations with hypertension, insulin resistance, heart failure, and increased cardiovascular mortality. At the molecular level, vitamin D exerts pharmacological actions—modulating the renin–angiotensin–aldosterone system, exerting anti-inflammatory and antifibrotic effects, and influencing endothelial and cardiomyocyte signaling. While experimental and epidemiological evidence suggests potential cardiovascular benefits, large randomized controlled trials (RCTs) provide conflicting results, particularly regarding hypertension and heart failure. However, these often-neutral results do not preclude a targeted action. On the contrary, clinical efficacy is strongly dependent on baseline deficiency status and the presence of metabolic cofactors. In this context, high-dose supplementation of Vitamin D, in combination with Vitamin K2 to prevent vascular calcification, elevates the supplement to a genuine pharmacological agent, with a distinct therapeutic potential for modulating cardiometabolic risk in selected patient subgroups. Emerging evidence supports the concept that vitamin D, when appropriately dosed and combined with K2, may act more as a low-potency pharmacological modulator than a simple nutritional supplement. This review synthesizes current mechanistic, observational, and interventional evidence, aiming to clarify whether vitamin D should be reclassified—from a micronutrient to a pharmacologically relevant agent—in cardiometabolic prevention and therapy, proposing a paradigm shift toward personalized and targeted dosing strategies, characteristic of precision pharmacology. Full article

Background/Objectives: Obesity is a major global public health and economic challenge. Governments worldwide have implemented nutrition-focused policies such as sugar-sweetened beverage taxes, front-of-pack labeling, food assistance reforms, and school nutrition standards to improve diet quality and reduce obesity. Because large-scale randomized controlled trials are often infeasible and conventional epidemiologic methods overlook population heterogeneity and behavioral feedback, microsimulation modeling has become a key tool for evaluating long-term and distributional policy impacts. This scoping review examined the application of microsimulation to obesity-related nutrition policies, focusing on model structure, behavioral parameterization, and integration of economic and equity analyses. Methods: Following PRISMA guidelines (PROSPERO CRD42024599769), five databases were searched for peer-reviewed studies. Data were extracted on policy mechanisms, model design, parameterization, and equity analysis. Study quality was assessed using a customized 21-item checklist adapted from CHEERS and NIH tools. Results: Twenty-nine studies met the inclusion criteria, with most policy settings based in the United States. Most employed dynamic, stochastic, individual-level microsimulation models with diverse behavioral assumptions, obesity equations, and calibration approaches. While most studies stratified outcomes by socioeconomic or demographic group, only one used a formal quantitative equity metric. Conclusions: Microsimulation modeling provides valuable evidence on the long-term health, economic, and distributional impacts of nutrition policies. Future work should strengthen methodological transparency, standardize equity assessment, and expand application beyond high-income settings to improve the comparability, credibility, and policy relevance of simulation-based nutrition policy research. Full article

Background: Tanzania is undergoing a rapid nutrition and epidemiological transition that has shifted dietary patterns and lifestyles toward more Westernised models, contributing to an increase in diet-related non-communicable diseases (NCDs), including obesity. Youth aged 15–35 years are particularly vulnerable to these shifts. Objectives: The objective of this scoping review was to map the available evidence on youth obesity in Tanzania, focusing on (1) data gaps in epidemiological reporting; (2) the ongoing nutrition transition; and (3) existing food system and health-related policies targeting youth. Methods: A targeted search was conducted in PubMed, Scopus, and the grey literature. The PCC (Population/Concept/Context) framework guided the study selection, focusing on youth and general young adults aged 15–35 years in Tanzania. Eligible studies published between 2000 and June 2025 were included. Results: The search yielded 247 peer-reviewed articles, of which 35 met the inclusion criteria. The findings reveal substantial gaps in epidemiological reporting, particularly limited regional data and inconsistent age disaggregation, which often obscures youth-specific patterns. Evidence on nutrition and lifestyle transitions is limited and fragmented, while available policies addressing obesity and related risk factors are broad in scope and rarely tailored to the youth population. Conclusions: This review demonstrates that evidence on obesity among Tanzanian youth is scarce, unevenly reported, and insufficiently specific to this age group. Clear gaps exist in epidemiological surveillance, research on nutrition transition, and youth-focused policy design. Strengthening age-specific monitoring systems, generating context-specific evidence, and developing targeted, measurable, and actionable strategies for youth could enhance Tanzania’s efforts to curb the rising burden of obesity and related NCDs. Full article

Background: Parkinson’s disease (PD) and frailty frequently co-occur and may interact bidirectionally through shared mechanisms of aging biology, mitochondrial dysfunction, inflammation, and reduced physiological reserve. Objective: We aimed to synthesize current evidence on prevalence, directionality, clinical overlap, adverse outcomes, and management implications of the PD–frailty nexus. Methods: A narrative review of epidemiologic, cohort, and interventional studies was performed, examining frailty in PD and PD risk in prefrail/frail populations, plus trials of multimodal interventions. Results: Frailty is common in PD, affecting approximately one-third of patients overall and becoming more prevalent as the disease advances. It independently predicts falls, cognitive decline, hospitalization, institutionalization, and mortality. Large cohorts suggest prefrailty/frailty is associated with incident PD risk, supporting a potential bidirectional association rather than direct causation. Diagnostic complexity arises because PD motor and non-motor features overlap with frailty constructs, risking misclassification. Management based on Comprehensive Geriatric Assessment (CGA) enhances personalized, multidisciplinary care. Exercise, particularly combined aerobic and resistance training reduces frailty and improves mobility, postural control, and quality of life. Complementary nutritional strategies, including muscle-targeted supplementation, can further strengthen rehabilitation outcomes, while careful attention to social determinants and polypharmacy remains essential to optimizing overall health and functional independence. Conclusions: Frailty is best understood as a clinical marker of vulnerability within PD and a correlate of more adverse trajectories rather than a proven causal determinant. Systematic frailty assessment integrated into PD care may help refine prognosis, individualize treatment, and support efforts to preserve independence. Priorities include PD-adapted frailty tools, CGA implementation, and rigorous trials of combined exercise–nutrition programs. Full article