Artificial intelligence (AI) is progressively transforming the field of nutrition, evolving from early applications focused on food recognition, dietary intake estimation, and malnutrition screening to more complex systems capable of integrating clinical, anthropometric, biochemical, dietary, functional, and contextual data. Within this emerging landscape, artificial intelligence agents, or agentic AI systems, represent a new generation of digital tools characterized by their ability to reason, plan, use external tools, maintain longitudinal memory, and coordinate tasks within predefined boundaries. This review analyzes the potential role of AI agents in nutrition based on some recent studies addressing their application in digital health, public nutrition, nutritional oncology, laboratory medicine, and personalized preventive programs. The available evidence suggests that AI agents may provide value in three major areas: automated and multimodal nutritional assessment, generation of personalized dietary recommendations, and longitudinal coordination of nutritional interventions in patients with chronic diseases, cancer, or cardiometabolic risk. In public health, agentic models may facilitate scalable precision nutrition strategies, particularly in communities with limited access to dietitians, nutrition specialists, or healthcare resources. In oncology, these systems could integrate malnutrition screening, body composition assessment, symptoms, oncological treatments, and dietary preferences in order to anticipate nutritional deterioration and activate early interventions. In laboratory medicine, AI agents may link biomarkers, omics data, and clinical outcomes to support more dynamic and individualized nutritional decision-making. Their implementation poses important challenges, including insufficient clinical validation, risk of errors or hallucinations, cultural and socioeconomic biases, privacy concerns, professional responsibility, interoperability, and the need for continuous human supervision. In conclusion, agentic AI represents a relevant evolution for both clinical and community nutrition. Nevertheless, its incorporation into practice should be gradual, regulated, explainable, prospectively evaluated, and subordinated to clinical judgment and patient values.

Metabolic hepatic steatosis (MetHS) is a clinically heterogeneous, multisystemic, dynamic, and complex disease, whose progression is one of the main causes of cirrhosis and hepatocarcinoma. This clinical practice guideline aims to respond to its main challenges, both in terms of disease burden and complexity. To this end, recommendations have been proposed to experts through the Delphi method. The consensus was optimal in recommendations regarding type 2 diabetes as a risk factor (1.5.1, 4.5.1), in which cases early detection of MetHS should be carried out (4.5.2). Its results also emphasize the importance of the use of non-invasive tests (FIB-4, NFS, HFS) for the exclusion of significant fibrosis in patients with suspected MetHS (2.3.1, 2.3.3). Diagnosis should be carried out through the sequential combination of non-invasive indices and transient elastography by FibroScan® for its risk stratification (2.3.3). A nearly unanimous consensus was reached regarding the role of early prevention in the impact on the quality of life and survival of patients (5.1.2), as well as on the effectiveness of the Mediterranean diet and physical exercise in relation to the improvement of steatosis, steatohepatitis and fibrosis in MetHS patients (5.2.2) and on the positive results offered by resmiterom and semaglutide in promoting fibrosis regression (5.4.1). Finally, a great consensus has been reached regarding the importance of multidisciplinary management in MetHS, for which it is essential to agree on multidisciplinary protocols for referral between levels in each health area (6.2.1), as well as ensuring that referrals to Hepatology/Digestive and Endocrinology or Internal Medicine services are effective and beneficial to prevent the risk of disease progression (6.2.3, 6.3.1).

BACKGROUND:meal replacement (MR) diets involve substituting one or more regular meals with specially formulated nutritional products. This 12-week intervention aimed to assess the impact of a hypocaloric meal replacement on body weight and metabolic parameters, emphasizing muscle mass evaluation by ultrasound Methods: a real-world study was conducted using a MR diet protocol, one daily meal was replaced with a nutritional formula. Anthropometric and biochemical parameters were assessed at baseline and after 12 weeks, along with ultrasound-based measurements of the rectus femoris and gastrocnemius medialis muscles to monitor changes in muscle mass. RESULTS:the study population had a mean age of 59.3 ± 9.1 years and included 18 males (28.1 %) and 46 females (71.9 %). After 12 weeks of intervention, significant reductions were observed in body weight, body mass index, fat mass, waist circumference, serum triglycerides, LDL cholesterol, fasting glucose, insulin, and HOMA-IR. Additionally, there was a notable decrease in the prevalence of metabolic syndrome, central obesity, hypertriglyceridemia, hypertension, and hyperglycemia. Ultrasound assessments revealed a significant increase in rectus femoris muscle area (RFMA) (4.40 ± 0.6 cm² to 5.86 ± 0.4 cm²; p = 0.04), and in rectus femoris muscle thickness (RFMT) (1.70 ± 0.3 cm to 2.32 ± 0.3 cm; p = 0.03), indicating a preserved or enhanced muscle morphology despite overall weight loss. CONCLUSIONS:this study shows that a structured MR program effectively reduces body weight and improves metabolic parameters in individuals with obesity. Notably, muscle mass -especially in the rectus femoris- was preserved or improved.

BackgroundLife course factors play an important role in the multifactorial etiology of obesity, yet quantitative analysis of patient-originated, unstructured weight gain cause narratives remains a challenge. This study automated the thematic labeling of such narratives with a large language model to assess the clinical relevance of patient-reported weight gain cause data in weight loss prediction and patient phenotyping.Subjects and methodsA total of 2,463 patients with overweight or obesity shared open weight gain cause narratives prior to starting a multidisciplinary medical-nutritional weight loss treatment, followed until reaching a pre-defined weight loss target or dropout. Narratives were labeled using 12 thematic categories in a GPT4.1 large language model. Associations of reported causal themes with age, sex, BMI class and treatment outcomes were evaluated using group-wise statistical comparisons and a Random Forest classifier. Weight gain cause co-occurrence patterns were modeled with a direct association network and pairwise risk ratio analyses. A partitional unsupervised clustering model integrating age, sex, baseline BMI and weight gain cause themes was designed to elucidate patient phenotypes defined by reported weight gain trajectories. Cluster-specific outcomes were compared using descriptive tests and linear mixed models.ResultsMean weight loss was 9.2 ± 6.8% over 108.6 ± 111.6 days. Automated weight gain narrative categorization achieved precision and recall of 0.906 and 0.897 against a reference sample. Reported weight gain causes were associated with age and sex but not BMI class. Associations between attributed causes and treatment outcomes were moderate, while between individual causes, strong associations were found. Disrupted schedules, mental health and external circumstances increased the risk ratio of unhealthy eating habits [3.65 (2.63–5.65), 2.16 (1.89–2.48), 1.51 (1.25–1.81) respectively], while medical issues and external circumstances increased physical inactivity risk [1.58 (1.31–1.90), 1.49 (1.23–1.82)]. Based on weight gain cause reports, age, sex and BMI class, seven clusters were identified with different demographic, clinical, treatment outcome and adherence characteristics.ConclusionPatient-reported weight gain narrative analysis can be accurately automated using large language models, providing clinically relevant insights into obesity heterogeneity. While individual causes show modest associations with weight loss, their combined patterns allow the identification of distinct behavioral phenotypes with differential treatment responses. Integrating patient narratives into data-driven frameworks supports a more precise, person-centered obesity management.

Introduction:Aims: this study aimed to identify the threshold values of TyG index-related parameters for diagnosing metabolic syndrome (MetS) in elderly Caucasian individuals with obesity, and to evaluate the predictive performance of the TyG index in comparison to HOMA-IR. Methods: a cross-sectional study was conducted including 465 elderly individuals with obesity. The triglyceride-glucose (TyG) index was computed using the formula: Ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)] / 2. Based on this index, additional TyG-derived parameters were calculated: TyG-BMI, defined as TyG×body mass index (BMI); TyG-WC, defined as TyG×waist circumference (WC); and TyG-WHtR, defined as TyG×waist-to-height ratio (WHtR). Results: the study population consisted of 465 elderly individuals, including 105 men (22.6 %) and 360 women (77.4 %), mean age of 73.4 ± 6.8 years. MetS was identified in 303 participants, representing 65.2 % of the cohort. The area under the curve (AUC) of TyG index based on the ATPIII criteria was 0.743 (95 % CI: 0.695-0.791; p = 0.001). The optimal cut-off point was 4.74. For HOMA-IR, the AUC was 0.681 (95 % CI: 0.621-0.741, p = 0.01, with a cutoff point of 2.49. AUCs of the TyG index-related parameters (TyGBMI: 0.715 (95 % CI: 0.661-0.762), TyGWC: 0.765 (95 % CI: 0.714-0.813), TyGWHtR: 0.757 (95 % CI: 0.707-0.807)) were similar to TyG and superior to HOMA-IR. Conclusions: TyG-related parameters serve as dependable indicators for detecting MetS in elderly individuals with obesity.

BACKGROUND & AIMS:A significant association has been confirmed between the rs10811661 polymorphism in the CDKN2 gene, and increased susceptibility to type 2 diabetes. The present study aimed to investigate the association of the rs10811661 polymorphism with metabolic syndrome (MS) in individuals with obesity and impaired fasting glucose (IFG). METHODS:This research was conducted on 110 individuals diagnosed with obesity and IFG. Data collection included anthropometric measurements, arterial blood pressure, biochemical profiles, and the assessment of the prevalence of MS among participants. In addition, the study examined the genotypic distribution of the CDKN2 gene polymorphism (rs10811661) RESULTS: There were 73 women (66.4%) and 37 men (33.6%) with an average body mass index of 40.1 ± 1.9 kg/m2 (range: 35.7-42.4). When comparing the two genotype groups under a recessive model framework (CC + CT versus TT), several differences emerged. Specifically, individuals carrying both T alleles exhibited higher systolic blood pressure levels, waist circumference, fasting glucose, triglycerides, low-density lipoprotein cholesterol, hemoglobin A1c, insulin, and HOMA-IR. Logistic regression analysis showed an increased risk of MS in TT subjects (OR = 2.99, 95% CI = 1.08-18.11; p = 0.03) after adjusting. CONCLUSIONS:The CDKN2A/B rs10811661 TT genotype is associated with a higher prevalence of MS and adverse metabolic traits in individuals with obesity and IFG.

INTRODUCTION:the syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of chronic hyponatremia. Persistent hyponatremia has been associated with multiple long-term complications. Consequently, there is increasing interest in identifying safe and effective strategies for the long-term management of this condition. CASE REPORT:we report the case of a middle-aged woman with underlying pulmonary disease and multiple hospital admissions during the previous year, who presented with moderate chronic hyponatremia meeting the diagnostic criteria for SIADH, as well as disease-related malnutrition. DISCUSSION:given her history of cancer treatment-related sequelae, outpatient treatment with oral urea was initiated. During follow-up, the patient achieved sustained eunatremia without adverse effects, and showed no deterioration in nutritional status, as assessed by bioelectrical impedance analysis.

Objectives Oncostatin-M (OSM) and leukemia inhibitor factor (LIF) have shown relationship with muscle catabolism in Disease Related Malnutrition (DRM). We aimed to investigate the role of OSM and LIF in sarcopenia among patients with cancer and DRM. Design and methods 33 cancer patients with DRM were included. Muscle mass assessment via ultrasound at the rectus femoris (RF) level, bioimpedance (skeletal muscle mass (SMM), appendicular SMM (aSMM), and the aSMM index (aSMMI)), and circulating OSM and LIF levels were evaluated. Confirmed sarcopenia was diagnosed based on the criteria of low muscle strength combined with an abnormal aSMMI. Results The average age was 66.5±15.5 years. The gender distribution was 16 females (48.5%) and 17 males (51.5%). Sixteen patients (48.5%) were diagnosed with sarcopenia. Patients with sarcopenia showed worse values: phase angle (−0.4±0.1°; p=0.01), reactance (−4.9±1.8Ω; p=0.03), SMM (−2.0±0.3kg; p=0.03), aSMM (−1.6±0.2kg; p=0.03), aSMMI (−0.6±0.2kg/m2; p=0.02), muscle area RF (−0.7±0.2cm2; p=0.04), Y-axis RF (−0.4±0.1cm; p=0.03), muscle strength (−8.1±1.5kg; p=0.01) and albumin levels (−0.3±0.1g/dl; p=0.03). Circulating levels of OSM and LIF were elevated in patients with sarcopenia, with values of 10.6±1.3pg/ml (p=0.01) and 6.4±2.3pg/ml (p=0.02), respectively. Logistic regression analysis indicated a significant OR (odds ratio) of sarcopenia associated with elevated median levels of OSM (OR=3.6, 95% CI=1.4–9.9; p=0.01) and LIF-1 (OR=3.3, 95% CI=1.3–10.1; p=0.01) Conclusion High levels of serum OSM and LIF-1 were closely associated with sarcopenia in patients with cancer and DRM.

Introduction:Background: the body roundness index (BRI) has recently been proposed as a potential marker of obesity. The objective was to evaluate the relationship between BRI and metabolic syndrome (MS) in Caucasian patients with obesity and type 2 diabetes mellitus. Methods: adiposity parameters, blood pressure, fasting glucose, insulin concentration, insulin resistance (HOMA-IR), lipid profile, C-reactive protein, adipokines, and the prevalence of MS were evaluated in 358 patients. Results: among the participants, 258 (72.1 %) were diagnosed with MS. The risk of developing MS in the high BRI group was OR: 3.61 (95 % CI: 2.15-6.07; p = 0.02). The area under the curve (AUC) for HOMA-IR to detect MS was 0.67 (0.59-0.78; p = 0.01), with a cut-off value of 3.37 based on the Youden index (sensitivity 74.9 % and specificity 64.7 %). For BRI, the AUC was 0.78 (0.68-0.85; p = 0.001). The Youden index determined a cut-off value of 10.31 (sensitivity 84.6 % and specificity 72.9 %). Conclusions: BRI demonstrates the ability to correlate with adiposity parameters and biomarkers in patients with type 2 diabetes mellitus and obesity, showing a capacity to detect MS.

Introduction Malnutrition is a highly prevalent chronic condition that contributes to higher morbidity and mortality in patients with multiple comorbidities. While positive effects of nutritional therapy in the in-hospital setting have recently been demonstrated, the benefits of long-term nutritional therapy after hospital discharge remain uncertain. Herein, we outline the design and rationale of the EFFORTII trial, the largest nutritional trial to date to assess the effects of continued nutritional support after hospital discharge in medical patients, with particular attention to key design decisions regarding nutritional strategy, patient selection criteria and study endpoints.Methods and analysis The Effect of Continued Nutritional Support at Hospital Discharge on Mortality, Frailty, Functional Outcomes and Recovery (EFFORTII) is an investigator-initiated, non-commercial randomised controlled trial designed to evaluate whether ongoing, individualised nutritional therapy after hospital discharge—targeted to meet specific energy and protein requirements—offers a cost-effective approach to lowering mortality, minimising complications and maintaining functional status compared with standard care. Eligible participants are adult, chronically ill medical inpatients at risk of malnutrition. Patients in the intervention group receive individualised nutritional therapy delivered by an experienced dietitian through a combination of telemedicine and in-person consultations. The intervention aims to meet personalised nutritional targets, supported by a trained dietitian. Control group patients receive nutritional counselling at discharge, but no structured nutritional management during follow-up. We designed the trial as an event-driven trial with a target of 247 mortality events (primary endpoint), which will be assessed over approximately 5 years until event-driven endpoint is met. The minimum total sample size is at least 802 participants, based on the assumed treatment HR of 0.70. The main trial is enrolling patients across multiple sites in Switzerland. During the trial, additional sites in Spain joined the study, and their data will be analysed using a patient-level pooled approach.Ethics and dissemination This study involves human participants and was first granted ethical approval by the Ethics Committee Northwest- and Central Switzerland and then by all participating local ethics committees. Written informed consent will be obtained from all participants. Findings will be disseminated in peer-reviewed journals and academic conferences.Trial registration number NCT04926597.

La esteatosis hepática metabólica (EHmet) es una enfermedad clínicamente heterogénea, multisistémica, dinámica y compleja, cuyo progreso es una de las causas principales de cirrosis y hepatocarcinoma. La presente guía de práctica clínica pretende dar respuesta a los principales desafíos que presenta, tanto en su carga de enfermedad como en su complejidad. Para ello se han propuesto una serie de recomendaciones consensuadas mediante el método Delphi. El consenso resultó óptimo en las recomendaciones relativas a la diabetes mellitus tipo 2 (DM2) como factor de riesgo (1.5.1, 4.5.1), en cuyos casos se debe llevar a cabo una detección precoz de EHmet (4.5.2). Destaca la importancia del uso de pruebas no invasivas (FIB-4, NFS, HFS) para la exclusión de fibrosis significativa en pacientes con sospecha de EHmet (2.3.1, 2.3.3). El diagnóstico debe ser llevado a cabo a través de la combinación secuencial de índices no invasivos y elastografía transitoria (ET) mediante FibroScan® para una correcta estratificación del riesgo (2.3.3). Se ha alcanzado un consenso casi unánime en el papel de la prevención precoz en el impacto en la calidad de vida y supervivencia de los pacientes (5.1.2), así como en la efectividad de la dieta mediterránea y el ejercicio físico en relación con la mejoría de la esteatosis, la esteatohepatitis y la fibrosis en pacientes con EHmet (5.2.2) y en los resultados positivos ofrecidos por resmiterom y semaglutida para promover la regresión de la fibrosis (5.4.1). Finalmente, se ha alcanzado un gran consenso en la importancia del manejo multidisciplinar de EHmet, para el cual es esencial consensuar protocolos multidisciplinares de derivación entre niveles en cada área sanitaria (6.2.1), así como que las derivaciones a los servicios de hepatología/digestivo y endocrinología o medicina interna resulten efectivas y beneficiosas para prevenir el riesgo de progresión de la enfermedad (6.2.3, 6.3.1).

Introduction:Introduction: FGF21 has potential functions as a key regulator in coordinating the metabolic response to protein deficiency. Objective: the aim of our design is to explore the role of circulating FGF21 in patients with disease-related-malnutrition (DRM) and its relationship with protein dietary intake. Material and methods: 108 DRM patients were included. Bioelectrical impedance analysis was conducted to assess skeletal muscle mass (SMM), appendicular skeletal muscle mass (aSMM), and the appendicular skeletal muscle mass index (aSMMI). Muscle mass was evaluated using ultrasound at the rectus femoris quadriceps (RFQ) level, too. Handgrip strength, biochemical parameters, dietary intake, and circulating FGF21 levels were also measured. Results: mean age was 61.3 ± 1.1 years. A negative correlation between FGF21 levels and some parameters of rectus femoris quality (RFQ) such as dominant muscle area, reactance, SMM, aSMM and albumin levels were reported. Protein intake was negatively correlated (r = -0.55; p = 0.02), too. Patients with higher protein intake (median intake 53.7 g/day) had higher dominant muscle area RQF (0.6 ± 0.2 cm2; p = 0.03), reactance (7.5 ± 0.3; p = 0.03), SMM (2.6 ± 0.3 kg; p = 0.03), aSMM (2.3 ± 0.8 kg; p = 0.03), albumin (0.7 ± 0.2 mg/dL; p = 0.04), prealbumin (10.1 ± 0.8 mg/dL; p = 0.02) and lower levels of FGF21 (86.5 ± 9.8 ng/dL; p = 0.01). Patients with FGF21 levels above the median cut-off point (61.3 ng/mL) had a significantly higher risk of low protein intake (OR = 2.47, 95 % CI = 1.14-5.35; p = 0.02). Conclusion: a significant association between increased serum FGF21 levels and low protein dietary intake is reported in patients with DRM.

Several investigations have documented relationships between body mass index (BMI) and gut microbiota composition in the context of inflammation. However, the precise interaction between BMI and gut microbiota influencing inflammatory markers is still unclear, presenting a challenge for personalized interventions. This study aimed to analyze anthropometric, biochemical and inflammatory variables of participants with systemic lupus erythematosus (SLE) compared to those with low-grade metabolic inflammation (MI), as well as to elucidate the impact of gut microbiota composition, particularly Alistipes, in relation to adiposity, as assessed by BMI, on inflammatory markers within the METAINFLAMATION cohort. A total of 127 adults diagnosed with both diseases, categorized according to the WHO definition of obesity (BMI ≥ 30 kg/m2) and phenotypically analyzed by 16S sequencing of fecal samples. The results showed that patients with low-grade MI had higher anthropometric values, glycosylated hemoglobin and triglyceride levels. On the other hand, patients with SLE and high BMI showed elevated insulin, CRP, and fibrinogen levels, alongside significant changes in Alistipes abundance. Notably, CRP levels were influenced by both BMI and Alistipes, particularly in lupus individuals with higher BMI, and elevated IL-6 was associated with higher CRP in this subgroup. CRP levels are influenced by BMI and Alistipes shahii abundance, especially in lupus individuals with higher BMI. In addition, elevated IL-6 concentrations are significantly associated with more elevated CRP levels in SLE individuals with higher BMI. These findings showed that CRP levels are influenced by BMI and Alistipes, particularly in lupus individuals with higher BMI and highlight the need for personalized approaches based on body composition, inflammatory markers and gut microbiota in patients with lupus and obesity for improving clinical management and outcomes.

BACKGROUND AND AIMS:Few studies have evaluated the effect of rs490683 on weight loss. The objective of our study was to evaluate the role of this variant of GHSR gene on body weight loss and cardiovascular risk factors secondary to a partial meal replacement (pMR) hypocaloric diet. METHODS:96 individuals with a body mass index (BMI > 35 kg/m2) were enrolled. Participants consumed a normocaloric, hyperproteic formula twice daily (12-w). Measurements were taken for body weight, BMI, fat mass, waist circumference, blood pressure, lipid profile, fasting insulin levels and HOMA-IR. RESULTS:The genotype was 70 patients (72.9 %) CC genotype, 19 patients(19.8 %) CG genotype, and 7 patients(7.3 %) GG genotype. The intake of calories, grams of carbohydrates, fats and proteins was higher at 12w in patients carrying the G allele. BMI (-3.5 ± 0.4 kg/m2 vs -1.0 ± 0.2 kg/m2 (p = 0.01)), body weight (-8.5 ± 1.0 kg vs -2.6 ± 1.1 kg (p = 0.01)), fat mass (-7.7 ± 0.3 kg vs -2.6 ± 0.2 kg (p = 0.01)), waist circumference (-7.2 ± 0.3 cm vs -2.9 ± 0.1 cm (p = 0.01)), glucose levels (-12.1 ± 1.4 mg/dl vs -3.1 ± 1.8 mg/dl, p = 0.01), insulin (-10.8 ± 1.2 UI/L vs -3.9 ± 1.1 UI/L, p = 0.01), HOMA-IR (-2.1 ± 1.0 units vs -0.58 ± 0.2 units, p = 0.01), CRP (-1.2 ± 0.1 mg/dl vs -0.7 ± 0.2 mg/dl, p = 0.01), triglycerides (-22.1 ± 4.1 mg/dl vs -5.1 ± 3.2 mg/dl, p = 0.01), total-cholesterol (-22.2 ± 1.3 mg/dl vs -8.8 ± 1.9 mg/dl, p = 0.01), LDL-cholesterol (-15.2 ± 1.1 mg/dl vs -4.7 ± 1.2 mg/dl, p = 0.01), and HDL-cholesterol (6.2 ± 0.4 mg/dl vs -2.9 ± 1.2 mg/dl, p = 0.01) modifications were better in non-G allele carriers. After intervention, the odds ratio (OR) of MS in non-carrier of G allele improved OR 0.48 (95%CI: 0.31-0.73; p = 0.02). CONCLUSIONS:G allele of rs490683 have a deleterious effect on dietary restrictions, body weight and metabolic response after a pMR diet.

OBJECTIVES:The objective of this study was to evaluate the prognostic value of albumin-myosteatosis gauge (AMG) in Caucasian patients with non-metastatic colorectal cancer and to relate AMG with classic bioimpedancemetry (BIA) parameters. MATERIAL AND METHODS:This study involved 130 Caucasian patients diagnosed with non-metastasic colorectal cancer. CT scans were analysed at the L3 vertebral level to determine the cross-sectional area of skeletal muscle, skeletal muscle index (SMI), skeletal muscle density(SMD). Bioelectrical impedance analysis (BIA) was employed. Albumin and prealbumin were measured. The albumin-myosteatosis gauge (AMG) was calculated: serum albumin (g/dL) × skeletal muscle density (SMD) in Hounsfield Units (HU). RESULTS:The median age was 69.7 ± 9.7 years, with a range of 57-90 years. Patients with AMG values below the median had significantly reduced serum albumin levels, L3-SMI, SMD, SMI-BIA and phase angle. The patients who died during the follow-up of these 5 years had lower levels of serum albumin, body weight, BMI, SMD, phase angle, reactance, AMG and a higher percentage of low muscle mass according to CT and hospital readmissions. The AMG values were negatively correlated with age and positively with albumin, SMD, L3-SMI, phase angle and reactance. Significant differences in 5-year survival between the AMG groups (low median AMG vs High median AMG) (HR 3.83, IC95 % = 1.10-13.42 and the SMD groups (HR 3.57, IC95 % = 1.01-12.58) were observed. AMG was identified as an independent prognostic factor for survival (HR 4.83, 95%CI = 1.21-19.17) CONCLUSION: AMG may function as an independent prognostic marker in Caucasian patients with non-metastatic CRC.

Scientific evidence demonstrates that a very low-calorie ketogenic diet (VLCKD) is effective and beneficial in the treatment of obesity, capable of reversing the methylome associated with obesity and has immunomodulatory capacity. This effect is in part promoted by nutritional ketosis and could be involved in counteracting obesity-related cancer. The aim of this study was to evaluate the effect of nutritional ketosis on the methylation of genes related to tumor processes in patients with obesity and in breast cancer cells. Based on methylome data (Infinium MethylationEPIC BeadChip, Illumina) from patients with obesity treated with a VLCKD for weight loss (n = 10; n = 5 women, age = 48.8 ± 9.20 years, BMI = 32.9 ± 1.4 kg/m2), genes belonging to cancer-related pathways were specifically evaluated and further validated in vitro in MDA-MB-231 (triple negative) and MCF7 (RE positive) breast tumor cells pretreated for 72 h with βOHB, the main ketone body, secretome from visceral (VATs) or subcutaneous (SATs) adipose tissue of patients with obesity. The cell tumoral phenotype was evaluated by proliferation assay and expression of cancer-related genes. VLCKD-induced nutritional ketosis promoted changes in the methylation of 18 genes (20 CpGs; 17 hypomethylated, 3 hypermethylated) belonged to cancer-related pathways with MAPK10, CCN1, CTNNA2, LAMC3 and GLI2 being the most representative genes. A similar pattern was observed in the MDA-MB-231 cells treated with β-OHB, without changes in MCF7. These epigenetic changes paralleled the tumoral phenotype modulated by the treatments. Taking together these results highlight the potential role of VLCKD as an adjuvant to anticancer treatment in groups more susceptible to the development of cancer such as patients with obesity, exerting epigenetic regulation through nutritional ketosis and weight loss.

Plant-based, low-fat, and carbohydrate-restricted diets have been linked to a reduced risk of chronic diseases such as type 2 diabetes mellitus, cardiovascular diseases, neurodegenerative disorders, and cancer. However, recent trends emphasize the need for precision nutrition approaches, a field leveraging genomics, microbiome data, and other phenotypic factors to tailor dietary recommendations to individual needs. This manuscript aimed to provide an updated perspective on how nutrigenetics and gut microbiota contribute to improving the effectiveness and individual response to different dietary patterns. Key findings reveal that plant-based diets, especially Mediterranean dietary patterns, improve metabolic biomarkers and modulate gut microbiota composition in a healthy manner. On the other hand, low-fat diets have been shown to improve insulin sensitivity and circulating lipid profiles, with SNPs and other genetic markers influencing individual responses. Moreover, carbohydrate-restricted diets promote fat metabolism and weight loss, with genetic and microbiome variations modulating individual outcomes. While the genus Dorea decreased on the Mediterranean and carbohydrate-restricted diets, Bifidobacterium increased on the plant-based and low-fat diets. In conclusion, precision nutrition offers a promising framework to optimize dietary interventions by considering both genetic and gut microbiota profiles. These complementary approaches highlight the potential of personalized dietary strategies to enhance adherence and improve health outcomes.