Search Results (220)

Colorectal cancer (CRC) is a significant global health concern, ranking as the third most frequently diagnosed cancer and the second leading cause of cancer-related deaths. Advances in screening, such as the implementation of liquid biopsies (LB), have improved early detection, thus enhancing survival rates. This review summarizes the multifaceted nature of CRC, focusing on its genetic background, the complex tumor microenvironment, and the influence of gut microbiota, nutrition, and metabolic alterations. The development of CRC is influenced by various risk factors, including age, genetics, chronic diseases, and lifestyle choices. The genetic heterogeneity of CRC defines distinct molecular subtypes, characterized by different treatment responses and patient prognoses. Chronic inflammation and dysbiosis in the gut microbiota further contribute to CRC pathogenesis. In addition, nutritional factors play a crucial role in CRC, affecting carcinogenesis and treatment efficacy through direct interaction with the immune system and microbiome. Current therapeutic strategies include surgical interventions, chemo- and radiotherapy, targeted therapies, immunotherapy as well as dietary interventions, and microbiome modulation, highlighting the challenges posed by tumor heterogeneity and treatment resistance. In sum, a comprehensive understanding of CRC’s intrinsic and extrinsic drivers, including genetic, metabolic, and dietary influences, is essential for developing personalized treatment strategies and improving patient outcomes. Full article

Chronic kidney disease (CKD) is characterized by persistent exposure to uremic toxins (UTs), many of which originate from gut microbial metabolism and contribute to renal, cardiovascular, and metabolic complications. Current evidence indicates that CKD is associated with dysbiosis and the enrichment of microbial taxa carrying genes involved in UT precursor production. Diet is a major modulator of the gut microbiota and therefore represents a promising lever to reduce UT generation in synergy with current nephroprotective therapies. Beyond simple protein restriction, more specific dietary approaches, particularly plant-based low-protein diets, appear especially relevant. Additional factors, including amino acid composition, lipid quality, food processing, constipation, transit time, meal timing, and circadian rhythms, may also influence microbial metabolism and UT production. This review examines the role of nutrition in shaping the gut microbiota–UT–kidney axis and discusses how dietary modulation may support precision nutrition in the context of CKD. It also highlights future directions based on multidimensional phenotyping and robust biomarkers to capture interindividual variability, guide personalized interventions, and ultimately improve renal and cardiovascular outcomes in CKD. Full article

Sarcopenia, defined as the progressive loss of skeletal muscle mass and strength, is increasingly recognized as a significant concern in patients with chronic kidney disease (CKD) and particularly in kidney transplant recipients (KTx-ps). This review explores the complex interplay of pathophysiological mechanisms, prevalence, and management strategies of sarcopenia in the context of kidney transplantation. CKD contributes to sarcopenia through systemic inflammation, malnutrition, uremic toxin accumulation, and metabolic imbalances, all of which persist or are exacerbated after transplantation due to immunosuppressive therapies especially corticosteroids. Notably, the post-transplant period may introduce additional risks, such as altered body composition and reduced physical activity, further aggravating muscle wasting. Sarcopenia affects approximately 26% of KTx-ps, leading to adverse outcomes including decreased quality of life, increased risk of infection, frailty, delayed recovery, and graft loss. The diagnosis remains challenging due to variability in assessment tools and a lack of standardized criteria. Management strategies must be multifactorial, including personalized nutritional support, targeted physical activity, and, where appropriate, pharmacological interventions. Early identification through imaging and functional testing is critical, especially in older patients and those with prolonged dialysis vintage. Emerging therapies, such as myostatin inhibitors, offer promise but require further validation. Additionally, early steroid withdrawal may mitigate muscle loss without compromising graft survival in selected patients. This review underscores the need for heightened awareness and standardized protocols to identify and manage sarcopenia in kidney transplantation, ultimately improving long-term outcomes and patient-centered care. Full article

The ketogenic diet (KD) is a critical, evidence-based intervention within medical nutrition therapy for managing neurological disorders. In this article, we reviewed the published research on the efficacy of the ketogenic diet and its variations in treating epilepsy, particularly for patients unresponsive to anti-epileptic drugs. The literature review was performed on PubMed between 2022 and 2025. The review of clinical studies across various age groups reveals that, while the KD is effective for both focal and generalized seizures, infants often achieve higher rates of seizure freedom compared to adults, potentially due to better dietary compliance. Despite its success, the restrictive nature of the diet presents significant challenges for individuals suffering from epilepsy. The key challenges that reduce compliance over time include side effects, such as gastrointestinal issues, potential for malnutrition, and a high risk of micronutrient deficiencies. The role of the registered dietitian is paramount in this interdisciplinary approach, ensuring personalized education by monitoring growth and adjusting nutritional plans to optimize health outcomes for children unresponsive to anti-epileptic drugs. Ultimately, integrating MNT with traditional pharmacological or surgical treatments offers the most promising path for significant seizure reduction and improved quality of life for epileptic patients. Full article

Global population aging has led to a substantial increase in the number of older adults receiving long-term pharmacological treatment, often involving polypharmacy. Long-term medication use is often linked to negative oral health outcomes, such as xerostomia, periodontal disease, dental caries, and changes in the oral microbiome, even if it is necessary for treating systemic conditions. The general health, nutritional state, and quality of life of elderly people are all significantly impacted by these diseases. This narrative review integrates recent data on biological causes, genetic vulnerability, and public health consequences to investigate oral self-care as a preventive strategy in older persons on medication. The effects of long-term medication therapy on oral tissues, salivary function, inflammatory responses, and microbial balance are given special attention, as is the role of genetic variants linked to immunological and inflammatory pathways on individual variability. The review also evaluates oral self-care interventions aimed at reducing medication-related oral complications, such as the use of fluoride, mechanical plaque control measures, and caregiver-assisted oral care practices. Oral self-care is viewed from a public health perspective as a scalable and affordable strategy for reducing oral health disparities in older populations. The results highlight the significance of preventative, individualized, and integrated oral health interventions within larger healthcare frameworks for older persons taking long-term medications. Full article

Background/Objectives: Pancreatic cancer-associated cachexia (CAC) is a complex, multifactorial and multi-organ metabolic syndrome affecting approximately 80% of patients with pancreatic ductal adenocarcinoma (PDAC). Recent epidemiological data show that cachexia is a primary cause of mortality in PDAC, directly accounting for approximately 30% of cancer-related deaths and significantly limiting the tolerability of cancer therapy and is associated with adverse effects of treatment. It is defined by systemic weight loss, skeletal muscle atrophy (sarcopenia), and adipose tissue depletion, often driven by systemic inflammation and metabolic dysregulation. Methods: The literature was searched in PubMed and Scopus using combinations of keywords. The search covers the literature between 2016 and 2026, but papers before this period were also included because of their historical importance. Studies with higher evidential value, such as prospective studies, randomized controlled trials, and meta-analyses, were prioritized and emphasized in our analysis. Results: CAC in PC arises from a systemic inflammatory response driven by tumor–host interactions and the release of pro-inflammatory mediators, such as growth differentiation factor 15 (GDF-15) and parathyroid hormone-related protein (PTHrP), which promotes anorexia and weight loss. The most commonly used diagnostic criteria include unintentional weight loss of more than 5% of body mass within 6 months, a body mass index (BMI) below 20 kg/m², or weight loss greater than 2% in the presence of sarcopenia. Emerging evidence supports the use of AI-based body composition analysis and novel biomarkers, including GDF-15 levels, to improve the detection and monitoring of cachexia. This review highlights that, despite the absence of pharmacological agents specifically approved for CAC in the United States and Europe, current guidelines recommend multimodal supportive care, including low-dose olanzapine, nutritional support, and exercise-based interventions. Furthermore, we identify recent phase 2 trials targeting the GDF-15 pathway, such as the GDF-15 inhibitor ponsegromab, which have demonstrated significant improvements in body weight and physical activity, suggesting a potential breakthrough in targeted therapies for CAC. Conclusions: CAC in PDAC represents a critical unmet medical need in oncology. It manifests as a lethal systemic pathology that demands early identification and targeted personalized pharmacological and nutritional interventions. Early diagnosis and targeted intervention represent promising strategies for improving survival and quality of life in this high-risk patient population. Full article

Background: Systemic inflammation is a key driver of heart failure (HF) progression across all ejection fraction (EF) phenotypes, with diet emerging as a modifiable factor influencing cardiac metabolism and inflammatory signaling. This narrative review integrates current evidence on the inflammatory mechanisms underlying HF, their links with common comorbidities and emerging anti-inflammatory therapeutic strategies, with a particular focus on the role of nutrition in supporting healthy cardiac metabolism. Methods: We searched MEDLINE/PubMed, EMBASE, Web of Science, the Cochrane Library, Scopus and reference lists of relevant publications using terms related to systemic inflammation, dietary patterns and HF prioritizing high-impact studies on nutrition–inflammation–HF interactions published from 2000 onward. Results: Major HF comorbidities sustain chronic, low-grade inflammation through elevated cytokine activity. Dietary patterns—especially those with high Dietary Inflammatory Index (DII)—substantially shape inflammatory milieu. The Mediterranean diet appears to have a favorable inflammatory profile with reduction in circulating pro-inflammatory biomarkers, especially C-reactive protein (CRP) and interleukin-6 (IL-6). Established therapies for HF with reduced ejection fraction and vagus nerve stimulation elicit anti-inflammatory efficacy through cytokine suppression. Sodium glucose cotransporter-2 (SGLT2) inhibitors demonstrate positive metabolic effects and anti-inflammatory actions through decrease in IL-6 and tumor necrosis factor-α (TNF-α). Interleukin-1 blockade has produced heterogeneous clinical outcomes, while definitive findings examining the role of IL-6 inhibitors in inflammation suppression and possible benefit on cardiac outcomes are anticipated. Preliminary data show the potential synergistic effects of dietary patterns/nutrients and pharmacological agents combination on improvement of endothelial function and attenuation of the fibrotic process, although there is a need for further research in large-scale trials. Conclusions: Systemic inflammation demonstrates a key role in HF initiation and progression, and the effect of diet on inflammatory pathways is central. Dietary patterns targeting inflammation-related mechanisms (inflammasome, gut dysbiosis) can lead to attenuation of systemic inflammatory response and restoration of cardiac metabolic flexibility. A deeper mechanistic discernment of cardiac inflammatory cascades, together with identification of HF subpopulations with excessive inflammatory activity, may facilitate the design of targeted randomized controlled trials (RCTs) aiming for novel personalized, inflammation-targeted HF therapies with potential clinical benefit. Full article

Background/Objectives: Responses to lifestyle interventions vary widely in obesity, and genetic factors may enhance outcomes. This study evaluated whether a 12-week genotype-informed personalized nutrition education (GEN) program improved weight and overall body composition among adults with obesity. Methods: Adults with a body mass index ≥ 25 kg/m² were randomized to a genotype-informed personalized nutrition education (GEN) group or a control group receiving standard nutrition education. The GEN group received weekly counseling tailored to nine obesity-related genetic traits. Changes were evaluated using paired t-tests and repeated-measures analysis of variance, with significance defined as p < 0.05. Results: Forty-three participants (GEN: n = 19; CON: n = 24) were analyzed. After 12 weeks, the GEN group showed significantly greater reductions than the CON group in body weight (−3.35 ± 0.7 vs. –0.91 ± 0.4 kg, p = 0.004), BMI (–1.17 ± 0.3 vs. –0.32 ± 0.1 kg/m², p = 0.005), and waist circumference (–5.56 ± 0.8 vs. –2.53 ± 0.7 cm, p < 0.001). Energy (–415 kcal, p = 0.003) and carbohydrate intake (–65 g, p = 0.003) also decreased significantly in the GEN group. Exploratory subgroup analyses suggested that participants classified as high genetic risk showed more pronounced improvements when receiving genotype-informed counseling. No serious adverse events were reported. Conclusions: The genotype-informed personalized nutrition program was associated with greater improvements in body composition than general nutrition education. Integrating genetic risk information into structured nutrition education may enhance perceived personal relevance and support effective weight management. Full article

Purpose: Cachexia, characterized by involuntary weight loss, muscle wasting, and metabolic dysfunction, is prevalent in advanced cancer and chronic illnesses. Despite its impact, outpatient treatment models in the U.S. remain limited and unstandardized. Here, we aim to describe the structure, implementation, patient characteristics, and real-world clinical trajectories of a multidisciplinary clinic for cancer cache as well as other forms of unintentional weight loss clinic within an academic endocrinology practice. Methods: We conducted a retrospective observational cohort study of 103 patients referred to a single-center unintentional weight loss clinic over five years. Patients received comprehensive assessments (weight trajectory, nutrition status, 5× sit-to-stand test, handgrip strength) and personalized interventions including nutrition counseling, resistance training, and pharmacologic therapies. Results: Among 103 patients (median age 69.7 years; 53% male), 64% had cancer, while 36% were referred for non-malignant causes of weight loss or cachexia. Reduced appetite or food intake was reported in 43%, and functional impairment was common, with low handgrip strength in 47% and impaired 5× sit-to-stand performance in 79% of assessed patients. Systemic abnormalities were frequent, including elevated hs-CRP (57%), elevated neutrophil-to-lymphocyte ratio (43%), and hypoalbuminemia (26%). Among patients with available paired follow-up data, the median rate of weight change shifted from −0.5 kg/month prior to enrollment to 0.0 kg/month three months after the initial visit (p < 0.0001). Five-times sit-to-stand performance improved modestly at three months (p = 0.042), while handgrip strength was unchanged. Half of patients that engaged with the clinic returned for at least follow-up, but there was no identifiable difference between the population of patients that returned versus those that did not. Conclusions: A structured, multidisciplinary unintentional weight loss clinic in an endocrinology setting was associated with stabilization of weight and modest changes in physical function in this single-center cohort among patients who engaged in follow-up. These findings highlight the successful implementation of integrated outpatient care models and provide practice-based context for future interventions and therapeutic evaluations. Full article

Background: Incretin-based therapies, including glucagon-like peptide-1 (GLP-1) receptor agonists and dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP) receptor co-agonists, advance obesity treatment by promoting weight loss and lowering the risk of type 2 diabetes and cardiovascular disease. Methods: This narrative review synthesizes clinical evidence to highlight the role of dietitians in obesity management when incretin-based therapies are used. Results: GLP-1 receptor agonists and dual GLP-1/GIP receptor co-agonists achieve 15–21% weight loss and reduce cardiometabolic risk. Their effectiveness and safety are optimized when integrated with medical nutrition therapy (MNT) and personalized nutrition strategies. In Italy’s aging population, the rising burden of sarcopenic obesity requires dietitian-led care to preserve fat-free mass while reducing fat mass. Dual GLP-1/GIP co-agonists show superior reductions in visceral adiposity, but effects on fat-free mass remain inconclusive, underscoring the need for dietitian oversight to prevent adverse body-composition changes. Sarcopenic obesity is associated with increased mortality and functional decline. Dietitians are uniquely qualified to ensure adequate protein intake and protect muscle during pharmacologic interventions. In Italy, role clarity in clinical nutrition remains limited; however, under national law (DM 744/94; Law 42/1999), dietitians are recognized as the professionals authorized to provide medical nutrition therapy (MNT). Conclusions: The dietitian’s expertise maximizes therapeutic efficacy, minimizes adverse effects, and safeguards long-term outcomes. Integrating dietitians into pharmacological treatment pathways is essential to optimize outcomes, ensure patient safety, and safeguard long-term metabolic health. Full article

Long-term oncological outcomes are significantly influenced by dietary patterns and nutritional status. Emerging evidence suggests that specific nutrients and dietary behaviors modulate the biological pathways involved in cancer initiation, progression, and therapeutic response. Understanding these nutritional mechanisms is essential for optimizing cancer prevention strategies, improving treatment efficacy, and enhancing long-term prognosis. Dieting is a modifiable factor influencing cancer prevention, progression, and survivorship. This review is a molecular, clinical, and epidemiological data amalgamation that aims to figure out the first of the three aspects, i.e., how dietary patterns and nutrients affect carcinogenesis, therapeutic tolerance, and long-term outcomes in long-term oncology. The current review moves from diet-dependent core cancer mechanisms that lead cancer pathways through metabolic reprogramming, inflammation, oxidative stress regulation, and epigenetic alterations. Protective dietary patterns, e.g., plant-based, Mediterranean-style, fiber-rich, and omega-3-fed diets, typically provide lower oxidative and inflammatory loads while also facilitating immune surveillance and metabolic stability. Therapy-personalized nutrition that is high in energy–protein and functional foods is instrumental to treatment tolerance, reduction in complication incidence, and cachexia relief. The newest research highlights the significant influence of epigenetic remodeling and the gut–brain–immune axis as the main processes that connect nutrition to tumor behavior and psychosocial outcomes. Translation into clinical practice changes is still dependent on thoughtfully designed trials, the existence of standard guidelines, and the provision of equal access to digital nutrition tools, despite this advancement. Diet is positioned as a low-toxicity co-therapeutic strategy that supports prevention, treatment efficacy, and long-term survivorship. Full article

Background/Objectives: The coexistence of chronic obstructive pulmonary disease (COPD) and type 2 diabetes mellitus (T2D) poses significant clinical challenges due to overlapping mechanisms of systemic inflammation, oxidative stress, hypoxia, and metabolic dysregulation. Patients with both conditions face higher risks of exacerbations, prolonged hospitalizations, cardiovascular events, and reduced quality of life. This review aims to summarize current evidence on the pathophysiological interplay between COPD and T2D and to evaluate the impact of lifestyle and pharmacologic interventions. Methods: A narrative review of the literature was conducted to evaluate the pathophysiological links between COPD and T2D, assess the effects of pharmacologic and lifestyle interventions, and highlight key gaps and priorities for future research, with an emphasis on integrated, evidence-based management for this high-risk population. Results: Lifestyle interventions, including smoking cessation and structured physical activity, remain foundational to management. Emerging evidence indicates that antidiabetic therapies, such as glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium–glucose cotransporter-2 inhibitors (SGLT-2is), may confer additional pulmonary, metabolic, and cardiovascular benefits. These agents modulate systemic inflammation, oxidative stress, endothelial function, and insulin sensitivity, potentially reducing COPD exacerbations, improving lung function, and enhancing survival. Safety concerns, including glucocorticoid-induced hyperglycaemia and hypoxia-related metabolic complications, underscore the need for careful monitoring and individualized therapy COPD patients. Conclusions: Optimal care requires a multidisciplinary, patient-centred approach integrating pulmonology, endocrinology, primary care, nutrition, and rehabilitation, alongside shared decision-making and patient education. Despite promising findings, critical knowledge gaps remain. Large, well-designed randomized controlled trials and standardized definitions are needed to guide personalized therapeutic strategies. Full article

Background: Elevated low-density lipoprotein cholesterol (LDL-C) is a major risk factor for atherosclerosis and cardiovascular disease (CVD). Statins are the cornerstone of LDL-C reduction and are highly effective in secondary prevention. However, their benefit in primary prevention among individuals at low-to-moderate cardiovascular risk remains controversial, and long-term adherence is often limited by adverse effects. Methods: This narrative review summarizes current evidence on the clinical effectiveness of statin therapy, with particular attention paid to the role of nutritional status in modulating statin efficacy, safety, and interpretation of clinical outcomes. Results: In primary prevention the effectiveness of statins in reducing cardiovascular events remains mixed. Furthermore, 20–30% of patients in secondary or high-risk prevention do not achieve clinically meaningful benefits despite adequate LDL-C lowering. More than half of statin-treated patients discontinue therapy within two years, most commonly because of adverse effects, without a corresponding increase in cardiovascular mortality. Emerging evidence suggests that malnutrition and sarcopenia may significantly influence statin pharmacokinetics and pharmacodynamics, thereby affecting both therapeutic response and susceptibility to adverse events. In addition, statin-induced lipid lowering may alter nutrition-related biomarkers, potentially leading to misclassification or overestimation of malnutrition. Conclusions: Although statins remain effective agents for lowering LDL-C, their prescription should be embedded within an individualized, patient-centered approach. Current guidelines provide a robust methodological framework for statin use; however, their application should be contextualized rather than automatic. Optimal effectiveness is achieved when pharmacological therapy is integrated with dietary patterns, nutritional status, and lifestyle factors. Incorporating nutritional assessment into statin management may improve tolerability, enhance clinical outcomes, and enable more accurate cardiovascular risk stratification beyond standardized cholesterol-lowering strategies. Full article

Gestational diabetes mellitus (GDM), one of the most common metabolic complications of gestation, affects approximately 10–15% of all pregnancies and represents a significant challenge for obstetricians and diabetologists aiming to reduce adverse feto-maternal outcomes. Medical nutrition therapy remains the cornerstone of GDM management, alongside lifestyle modification and pharmacological treatment in the presence of unmet glycemic targets. However, current dietary recommendations primarily emphasize nutrient composition and caloric intake, often without fully considering the temporal aspects of food intake. Chrono-nutrition is an emerging field that investigates the interaction between meal timing, circadian rhythms, and metabolic regulation. Increasing evidence indicates that glucose metabolism and insulin sensitivity exhibit marked diurnal variations, which may be further amplified in women with GDM, resulting in time-dependent differences in postprandial glycemic responses. This narrative review summarizes the current evidence on the role of chrono-nutrition in GDM by integrating mechanistic insights with findings from observational and interventional human studies. Although the available literature is limited by heterogeneity and a paucity of well-designed randomized controlled trials, the convergence of biological plausibility and emerging clinical data suggests that chrono-nutrition may represent a potential low-risk refinement of standard medical nutrition therapy. Incorporating temporal aspects of eating into dietary counseling may help frame glycemic management within a more physiologically aligned and personalized nutritional approach for pregnancies complicated by GDM. Full article

Introduction: Intensive chemotherapy protocols and hematopoietic stem cell transplantation (HSCT) in children with cancer frequently lead to severe complications, such as mucositis and immune dysfunction. A growing body of evidence indicates that these complications are closely associated with the patient’s nutritional status and the composition of the gut microbiome, which becomes profoundly destabilized as a result of cytotoxic therapy and antibiotic use. Background: The aim of this review is to critically evaluate the current state of knowledge on the interplay between gut dysbiosis, metabolomic profiles—with particular emphasis on short-chain fatty acids (SCFAs)—and treatment-related toxicity in pediatric patients, as well as to delineate pathways toward personalized nutritional therapy. Methods: A narrative review was conducted, including clinical and preclinical studies published between January 2015 and October 2025. PubMed/MEDLINE, Embase, Cochrane Library, and other databases were searched, focusing on changes in microbiome composition, correlations between gut-derived metabolites and the severity of complications (sepsis, graft-versus-host disease [GvHD], mucositis), and the effects of targeted nutritional interventions (probiotics, prebiotics, postbiotics, and fecal microbiota transplantation [FMT]) on microbiome modulation during anticancer therapy. Results: The analysis demonstrates that pediatric oncologic treatment leads to a marked reduction in microbial diversity, including the loss of protective Clostridiales taxa (e.g., Faecalibacterium), accompanied by an overgrowth of Proteobacteria pathobionts. Metabolomic profiling indicates that low SCFA levels (e.g., butyrate < 20–50 µmol/g) are a strong predictor of severe mucositis, prolonged neutropenia, and an increased risk of sepsis. Interventions aimed at restoring eubiosis and enhancing SCFA production show potential in strengthening the intestinal barrier, modulating immune responses, and enabling maintenance of the planned relative dose intensity (RDI) of chemotherapy by reducing treatment-related toxicity. Conclusions: Gut microbiome profiling and fecal metabolomics represent promising prognostic tools in pediatric oncology. There is an urgent need for further research employing “omics”-based approaches to develop precise, individually tailored nutritional protocols. Such strategies, including postbiotics and FMT, may minimize treatment-related adverse effects and improve long-term clinical outcomes in pediatric patients. Full article