Search Results (181)

The citric acid cycle disruptions are implicated in the pathogenesis of chronic diseases, including diabetes, obesity, cancer, and cardiovascular conditions. Numerous publications link TCA cycle disorders to oncological, neurodegenerative, and osteoporotic diseases, and specific single-nucleotide polymorphisms have been proposed as potential markers. Nevertheless, lifestyle and diet have been strongly linked to risk factors for mitochondrial dysfunction; thus, preventive measures that minimize these risks are a relevant field of research. This review summarizes 45 years of relevant publications on the TCA cycle, its genetics and epigenetics, and the restorative potential of certain nutrients. The review includes articles in English and Russian, registered in PubMed, Elsevier, eLIBRARY.RU. The genes encoding the TCA cycle enzymes have been collected and presented. Information is provided that a number of changes in the expression of these genes, for example, Arg18Trp, Ser87Leu, Ala252Thr, and Leu357Val of the ACO2 gene, leads to the development of neurodegenerative diseases; mutations rs121913499, rs121913500 in the IDH1, IDH2 genes, rs1270341616 and the DLST gene lead to the development of cancer. There is evidence that through epigenetic modifications, nutrition affects the activity of the TCA cycle. Niacin, α-lipoic acid, succinic acid, resveratrol, curcumin, arginine, leucine, quercetin, ursolic acid, and alternol affect the regulation of the TCA cycle at the genetic level. Further research into the effects of plant metabolites, vitamins, and bioactive supplements on the TCA cycle may improve the existing preventative and therapeutic diets. Full article

Background/Objectives: Obesity and prediabetes are overlapping global epidemics. This systematic review synthesises evidence on gene-diet interactions in adults with obesity, prediabetes, or related cardiometabolic risks. It evaluates Mediterranean and DASH dietary patterns, macronutrient quality, and energy restriction across both single-variant and polygenic score approaches. Methods: PubMed was searched for English language papers published in the last 5 years (last run: 31 October 2025). Fewer than 200 studies were retained after excluding those lacking explicit statistical testing for gene-diet interactions or relevant endpoints. Results: Evidence supports restricting saturated fat and preserving carbohydrate quality as general baseline targets, with associations heterogeneous by genotype. Effect modification was observed: healthy dietary patterns were associated with lower risk in high polygenic-risk strata (OR~0.53) but little or no benefit in low-risk groups. TCF7L2 variants were associated with macronutrient thresholds (e.g., protein > 18%, carbohydrate < 48%) affecting visceral adiposity, while APOA2 variants showed genotype-dependent inflammation, including paradoxical increases in markers with higher dietary antioxidant capacity. Interpretation was limited by underpowered interaction tests, multiplicity, and uneven ancestry representation (e.g., unique SLC16A11 and CREBRF signals). Conclusions: While anti-inflammatory dietary substitutions improve biomarkers irrespective of some variants (e.g., TCF7L2), genotype-informed nutrition appears to yield the largest absolute risk reduction in high-risk populations. Clinical implementation should therefore combine baseline diet-quality guidance with targeted strategies for genotype-specific response patterns (e.g., APOA2 antioxidant heterogeneity and TCF7L2 carbohydrate thresholds), rather than rely on uniform recommendations alone. Future progress requires preregistered, genotype-stratified trials and locally trained polygenic scores to address ancestry-specific genetic architecture. Full article

The interaction between chrono-nutrition (dinner intake), glycemic index (GI), and the C358A variant of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), along with its impact on morning fasting insulin and glycemia, has not been previously explored. This study provides new insights into chronometabolic and nutrigenetic interactions. This study aims to analyze the association between the dinner GI and the C385A variant in the FAAH gene with respect to fasting glucose, insulin levels, and HOMA-IR in adults with obesity. It was hypothesized that the dinner GI, probably influenced by the FAAH variant, could be associated with glycemic homeostasis in adults with obesity. This is a secondary analysis of a cross-sectional study focused on 189 adults with obesity (129 women; mean age, 41 ± 12 years; mean BMI, 38.0 ± 5.2 kg/m²). Dietary intake was assessed through two 24 h food records, enabling the calculation of GI and macronutrient composition at each meal, especially dinner. Fasting-parameter setting and genotyping were done during the study. The lineal regression analyses were adjusted by age, sex, BMI, energy intake and dinner protein. Participants with lower fasting glucose levels had higher total GI and dinner GI values than those with higher fasting glucose levels, whereas no differences in dinner GI were observed across groups stratified by insulin or HOMA-IR levels. In fully adjusted regression models, dinner GI values remained inversely associated with fasting glucose levels (β = −0.172, 95%CI −0.298 to −0.045; p = 0.008). The FAAH C385A variant independently predicted lower insulin (β = −2.674, 95%CI −5.185 to −0.164; p = 0.037) and lower HOMA-IR (β = −0.731, 95%CI −1.364 to −0.099; p = 0.024) levels. No statistically significant interaction between dinner GI and the FAAH genotype was detected with respect to glycemia, insulin, and HOMA-IR. Overall, these findings indicate that the dinner GI influences fasting glucose levels in adults with obesity; the FAAH variant predicted lower insulin and HOMA-IR levels, supporting a plausible chrono-nutrigenetic interaction between carbohydrate quality, mealtime intake, and FAAH variation in metabolic regulation, which must be further studied. Full article

Background: Folate is essential for one-carbon metabolism, yet deficiency remains common in non-fortified populations. Bitter-taste-receptor genetics may influence vegetable intake and thus folate status, but the cumulative impact of sensory genetics, diet, and sociodemographic factors is unclear. This study aimed to investigate how taste-related genetic variants, aggregated into a polygenic score (PGS), together with dietary behavior and sociodemographic factors, modulate serum folate levels in a Hungarian adult population, including Roma ethnic minority participants. Methods: In a cross-sectional sample of 626 adults (312 from the Hungarian general population and 314 from the Roma ethnic minority), serum folate was quantified by chemiluminescent immunoassay, and eight taste-related single-nucleotide polymorphisms (SNPs) were genotyped. A four-SNP PGS (TAS2R19 rs10772420, OR10G4 rs1527483, TRPV1 rs8065080, and CD36 rs1761667) was optimized via the stepwise method (ΔR² criterion, FDR q < 0.05). Multivariable linear regression was used to assess associations with continuous folate, and logistic models were used to evaluate deficiency risk (≤13 µmol/L; area under the curve, AUC). Interaction terms were tested for effect modification by education and vegetable intake, and mediation pathways were examined by structural equation modeling with 1000 bootstrap replications. Results: TAS2R19 rs10772420 was found to be the strongest predictor of serum folate level. This effect remained significant even after adjusting for vegetable intake (β = 1.12 nmol/L; p = 0.003), suggesting a persistent genetic association independent of vegetable intake. The taste-related PGS exhibited a significant dose–response relationship with folate levels (p < 0.001) but had only modest discriminatory power for deficiency (AUC = 0.569). Higher educational attainment amplified the associations between the PGS and folate levels (p for interaction < 0.05), whereas vegetable intake did not mediate genetic effects. The associations were consistent across Hungarian general and Roma population subgroups. Conclusions: Bitter-taste-receptor genetics are associated with serum folate levels in a pattern not substantially mediated by self-reported vegetable intake, and this influence is further modified by education. These findings support the development of genome-informed, culturally tailored nutrition strategies for non-fortified populations. Full article

Morbid obesity is a complex, multifactorial disorder characterized by metabolic and inflammatory dysregulation. The aim of this study was to observe changes in obese patients adhering to a personalized nutrition plan based on multi-omic data. This study included 14 adult patients with a body mass index (BMI) > 40 kg/m² who were consecutively recruited from those presenting to our outpatient clinic and who met the inclusion criteria. Clinical, biochemical, hormonal, and glycomic parameters were assessed, along with whole-genome sequencing (WGS) that included a focused analysis of obesity-associated genes and an extended analysis encompassing genes related to cardiometabolic disorders, hereditary cancer risk, and nutrigenetic profiles. Patients were stratified into nutrigenetic clusters using a patented unsupervised machine learning platform (German Patent Office, No. DE 20 2025 101 197 U1), which was employed to generate personalized nutrigenetic dietary recommendations for patients with morbid obesity to follow over a six-month period. At baseline, participants exhibited elevated glucose, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), triglycerides, and C-reactive protein (CRP) levels, consistent with insulin resistance and chronic low-grade inflammation. The majority of participants harbored risk alleles within the fat mass and obesity-associated gene (FTO) and the interleukin-6 gene (IL-6), together with multiple additional significant variants identified across more than 40 genes implicated in metabolic regulation and nutritional status. Using an AI-driven clustering model, these genetic polymorphisms delineated a uniform cluster of patients with morbid obesity. The mean GlycanAge index (56 ± 12.45 years) substantially exceeded chronological age (32 ± 9.62 years), indicating accelerated biological aging. Following a six-month personalized nutrigenetic dietary intervention, significant reductions were observed in both BMI (from 52.09 ± 7.41 to 34.6 ± 9.06 kg/m², p < 0.01) and GlycanAge index (from 56 ± 12.45 to 48 ± 14.83 years, p < 0.01). Morbid obesity is characterized by a pro-inflammatory and metabolically adverse molecular signature reflected in accelerated glycomic aging. Personalized nutrigenetic dietary interventions, derived from AI-driven analysis of whole-genome sequencing (WGS) data, effectively reduced both BMI and biological age markers, supporting integrative multi-omics and machine learning approaches as promising tools in precision-based obesity management. Full article

Bladder cancer (BC) is a biologically heterogeneous tumor affected by genetic, metabolic, environmental, and lifestyle factors. Recent research indicates that nutrition can change the way urothelial cancer forms by affecting inflammation, oxidative stress, cellular energy, and the epigenome. It can also change the risk of BC and how well treatment works. Simultaneous progress in precision nutrition (PN) and nutriomic profiling—encompassing nutrigenomics, nutrigenetics, nutriepigenetics, metabolomics, and microbiome science—presents novel options to tailor dietary regimens beyond universal guidelines. In this review, we consolidate existing knowledge regarding the nutritional factors influencing BC, outline pertinent principles of PN for BC prevention and survival, and explore how urine proteomics and molecular subtyping facilitate the integration of PN into precision oncology. Our review examines the methodological, bioinformatic, biomarker, and clinical translation challenges that impede the implementation of PN in BC management; these challenges include the need for validated nutritional biomarkers with mechanistic endpoints, interoperable data platforms, and rigorously designed clinical trials. Finally, we emphasize future prospects for PN-guided medical nutrition therapy and dietary models during and after systemic treatment recovery. We propose research priorities that will facilitate the integration of PN-informed individualized dietary plans with medical and surgical approaches in BC treatment, aiming to decrease the costs associated with expensive or excessively aggressive treatment methods, thereby supporting long-term survival care. This review seeks to establish a conceptual framework for the integration of PN into BC management by delineating the opportunities and challenges, hence promoting hypothesis-driven research in a promising yet underexplored domain. Full article

Background/Objectives: Chrononutrition—the temporal organization of food intake relative to circadian rhythms—has emerged as an important factor in cardiometabolic health. While meal timing is typically analyzed as an isolated variable, limited research has examined integrated meal timing patterns, and no study has systematically compared clustering approaches for their identification. This cross-sectional study compared four clustering techniques—traditional (K-means, Hierarchical) and non-traditional (Gaussian Mixture Models (GMM), Spectral)—to identify meal timing patterns from habitual breakfast, lunch, and dinner times. Methods: The sample included 388 Mexican university students (72.8% female). Patterns were characterized using sociodemographic, anthropometric, food intake quality, and chronotype data. Clustering method concordance was assessed via Adjusted Rand Index (ARI). Results: We identified five patterns (Early, Early–Intermediate, Late–Intermediate, Late, and Late with early breakfast). No differences were observed in BMI, waist circumference, or age among clusters. Chronotype aligned with patterns (morning types overrepresented in early clusters). Food intake quality differed significantly, with more early eaters showing healthy intake than late eaters. Concordance across clustering methods was moderate (mean ARI = 0.376), with the highest agreement between the traditional and non-traditional techniques (Hierarchical–Spectral = 0.485 and K-means-GMM = 0.408). Conclusions: These findings suggest that, while traditional and non-traditional clustering techniques did not identify identical patterns, they identified similar core structures, supporting complementary pattern detection across algorithmic families. These results highlight the importance of comparing multiple methods and transparently reporting clustering approaches in chrononutrition research. Future studies should generate meal timing patterns in university students from other contexts and investigate whether these patterns are associated with eating patterns and cardiometabolic outcomes. Full article

In animals and humans, nutrients influence signaling cascades, transcriptional programs, chromatin dynamics, and mitochondrial function, collectively shaping traits related to growth, immunity, reproduction, and stress resilience. This review synthesizes evidence supporting nutrient-mediated regulation of DNA methylation, histone modifications, non-coding RNAs, and mitochondrial biogenesis, and emphasizes their integration within metabolic and developmental pathways. Recent advances in epigenome-wide association studies (EWAS), single-cell multi-omics, and systems biology approaches have revealed how diet composition and timing can reprogram gene networks, sometimes across generations. Particular attention is given to central metabolic regulators (e.g., PPARs, mTOR) and to interactions among methyl donors, fatty acids, vitamins, and trace elements that maintain genomic stability and metabolic homeostasis. Nutrigenetic evidence further shows how genetic polymorphisms (SNPs) in loci such as IGF-1, MSTN, PPARs, and FASN alter nutrient responsiveness and influence traits like feed efficiency, body composition, and egg quality, information that can be exploited via marker-assisted or genomic selection. Mitochondrial DNA integrity and oxidative capacity are key determinants of feed conversion and energy efficiency, while dietary antioxidants and mitochondria-targeted nutrients help preserve bioenergetic function. The gut microbiome acts as a co-regulator of host gene expression through metabolite-mediated epigenetic effects, linking diet, microbial metabolites (e.g., SCFAs), and host genomic responses via the gut–liver axis. Emerging tools such as whole-genome and transcriptome sequencing, EWAS, integrated multi-omics, and CRISPR-based functional studies are transforming the field and enabling DNA-informed precision nutrition. Integrating genetic, epigenetic, and molecular data will enable genotype-specific feeding strategies, maternal and early-life programming, and predictive models that enhance productivity, health, and sustainability in poultry production. Translating these molecular insights into practice offers pathways to enhance animal welfare, reduce environmental impact, and shift nutrition from empirical feeding toward mechanistically informed precision approaches. Full article

Obesity is a highly complex, multifactorial disease influenced by dynamic interactions among genetic, epigenetic, environmental, and behavioral determinants that explicitly position genetics as the core. While advances in multi-omic integration have revolutionized our understanding of adiposity pathways, translation into personalized clinical nutrition remains a critical challenge. This review systematically consolidates emerging insights into the molecular and nutrigenomic architecture of obesity by integrating data from large-scale GWAS, functional epigenomics, nutrigenetic interactions, and microbiome-mediated metabolic programming. The primary aim is to systematically organize and synthesize recent genetic and genomic findings in obesity, while also highlighting how these discoveries can be contextualized within precision nutrition frameworks. A comprehensive literature search was conducted across PubMed, Scopus, and Web of Science up to July 2024 using MeSH terms, nutrigenomic-specific queries, and multi-omics filters. Eligible studies were classified into five domains: monogenic obesity, polygenic GWAS findings, epigenomic regulation, nutrigenomic signatures, and gut microbiome contributions. Over 127 candidate genes and 253 QTLs have been implicated in obesity susceptibility. Monogenic variants (e.g., LEP, LEPR, MC4R, POMC, PCSK1) explain rare, early-onset phenotypes, while FTO (polygenic) and MC4R (monogenic mutations as well as common polygenic variants) represent major loci across populations. Epigenetic mechanisms, dietary composition, physical activity, and microbial diversity significantly recalibrate obesity trajectories. Integration of genomics, functional epigenomics, precision nutrigenomics, and microbiome science presents transformative opportunities for personalized obesity interventions. However, translation into evidence-based clinical nutrition remains limited, emphasizing the need for functional validation, cross-ancestry mapping, and AI-driven precision frameworks. Specifically, this review systematically identifies and integrates evidence from genomics, epigenomics, nutrigenomics, and microbiome studies published between 2000 and 2024, applying structured inclusion/exclusion criteria and narrative synthesis to highlight translational pathways for precision nutrition. Full article

Background/Objectives: Despite the growing understanding of the relationship between the genome and nutrition, clearly defined and evidence-based clinical guidelines remain insufficient. The objective of this review was to identify and compile all available European guidelines related to the impact of genetic predisposition on nutritional recommendations in the field of gastroenterology. Methods: A review of guidelines and position papers issued by four European organisations [the European Crohn’s and Colitis Organisation (ECCO), the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN), the European Society for Clinical Nutrition and Metabolism (ESPEN), and United European Gastroenterology (UEG)] was conducted for the past ten years. Results: Out of 5196 recommendations and statements extracted from 124 manuscripts, only 13 highlighted a link between genetic predisposition and dietary factors in clinical gastroenterology. From the available guidelines, there is no clear trend indicating an increased focus on genetic background and its association with nutrition in recent years. Conclusions: There is a critical opportunity for European organisations to develop an evidence-based information framework, guided by clinical protocols, in order to integrate the large volume of genetic data into clinical practice and personalised care of individuals with gastrointestinal disorders. Full article

Background/Objectives: This study evaluated whether personalized nutrition (PN) advice combined with disclosure of genetic information leads to a greater reduction in caffeine consumption than PN advice alone in slow caffeine metabolizers in the short and long terms. Additionally, Ecological Momentary Assessment (EMA) was considered for its potential to improve dietary intake assessment. Methods: In 2019–2021, 94 adults (aged 18–60 years, C allele carriers of rs762551 CYP1A2, consuming ≥ 200 mg/day caffeine), 63% of whom were women, participated in a twenty-week intervention. Participants were randomized to receive PN with genotype information (the intervention group, n = 55) or without it (the control group, n = 39). All participants were advised to limit caffeine intake to 100 mg/day. Caffeine intake was assessed using a food frequency questionnaire and a smartphones application. After three years caffeine intake was reassessed. Results: After the intervention, caffeine consumption decreased (intervention group: 380.69 ± 217.58 to 153.73 ± 98.19 mg/day; control group: 394.44 ± 256.29 to 169.87 ± 85.70 mg/day; p < 0.01), with no group differences (p = 0.41). Three years later, a reduction (p < 0.01) was still observed in the intervention group, but the effect of time x group was insignificant. In total, 63% of the intervention group and 51% of the control group responded to at least three EMA prompts per day for at least three days. Conclusions: PN seems to affect caffeine intake in the long term. However, including genotype information in PN is no more effective than receiving PN recommendations without genetic information. EMA’s effectiveness in large-scale nutritional research may be limited due to the relatively low response rate. Full article

Genetic variants in nutrition-related genes exhibit variable functional consequences; however, systematic characterization across different nutritional domains remains limited. This highlights the need for detailed exploration of variant distribution and functional effects across nutritional gene categories. Therefore, the main objective of this computational study is to delve deeper into the distribution and functional impact of missense variants in nutrition-related genes. We analyzed Genetic polymoRphism variants using Personalized Medicine (GRPM) dataset, focusing on ten groups of nutrition-related genes. Missense variants were characterized using ProtVar for functional/structural impact, Pharos for functional classification, network analysis for pathway identification, and Gene Ontology enrichment for biological process annotation. The analysis of 63,581 Single Nucleotide Polymorphisms (SNP) revealed 27,683 missense variants across 1589 genes. Food intolerance (0.23) and food allergy (0.15) groups showed the highest missense/SNP ratio, while obesity-related genes showed the lowest (0.04). Enzymes predominated in xenobiotic and vitamin metabolism groups, while G-protein-coupled receptors were enriched in eating behavior genes. The vitamin metabolism group had the highest proportion of pathogenic variants. Network analysis identified apolipoproteins as central hubs in metabolic groups and inflammatory proteins in allergy-related groups. These findings offer insights into personalized nutrition approaches and underscore the utility of computational variant analysis in elucidating gene-diet interactions. Full article

Background/Objectives: Obesity is increasing worldwide, driven by unhealthy dietary habits and sedentary lifestyles. Genetic variations in taste receptor genes, particularly TAS1R2 and TAS2R38, may influence taste preferences, dietary intake, and obesity risk. This study examined associations between TAS1R2 and TAS2R38 polymorphisms, sugar-sweetened beverage (SSB) intake, and obesity risk in Kuwaiti adolescents. Methods: A cross-sectional study was conducted among 260 adolescents aged 11–14 years recruited from public schools in Kuwait. Genotyping of five single-nucleotide polymorphisms (SNPs) was performed using TaqMan assays. Associations between SNPs, SSB intake, and obesity parameters were evaluated using multinomial logistic regression and non-parametric tests, adjusted for age, sex, nationality, BMI z-scores, basal metabolic rate, and physical activity. p-values were corrected using the Benjamini–Hochberg method. Results: The rs713598 SNP in TAS2R38 showed a marginal association with BMI percentiles and z-scores. Adolescents carrying the CC genotype of rs10246939 SNP in TAS2R38 had significantly lower odds of high SSB consumption (>3 servings/week) compared with T-allele carriers (p = 0.018, OR= 0.24, 95% CI = 0.08–0.79). No significant associations were detected for TAS1R2 SNPs. Conclusions: Variations in TAS2R38 were linked to obesity measures and beverage intake in Kuwaiti adolescents, supporting a potential genetic contribution to dietary behaviors. These findings highlight the importance of taste receptor genetics in obesity research, though replication in larger and more diverse populations is required. Full article

Breast cancer is the most common malignant tumor among women. It is a significant health and social issue affecting 2.3 million women worldwide. Breast cancer is caused by various factors, including gender, age, race, genetics, hormonal balance, obesity, alcohol and many others. A crucial issue related to breast cancer is the impact of diet on the development of the disease. Dietary fats play a key role. Saturated fatty acids and trans fatty acids increase the risk of breast cancer, while polyunsaturated fatty acids have a protective effect. A high-protein diet reduces the risk of breast cancer and improves prognosis among patients. The role of carbohydrates remains unclear, but women may benefit from reducing their intake of high glycemic index foods. Among the macronutrients influencing the development and progression of breast cancer are calcium and magnesium. Adopting a Mediterranean diet may offer benefits. Among the factors influencing the development of breast cancer, the gastrointestinal microbiota is also noteworthy. Regular physical activity can reduce the risk of developing breast cancer, support treatment, reduce side effects and improve patients’ quality of life. Chronic stress also contributes to the development of breast cancer by affecting the nervous, hormonal and immune systems, disrupting the body’s homeostasis. Full article

Background/Objectives: Nutrigenetics has emerged as a promising tool to advance personalized nutrition strategies. This study aimed to analyze the scope and perception of Mexican dietitians regarding nutritional genomics with an emphasis on nutrigenetics’ use in clinical practice. Methods: A survey was conducted online among dietitians in Mexico to assess their educational background, awareness of nutrigenetic testing, use in practice, and interest in further training through 33 questions. Results: One hundred and thirty participants from states across six Mexican regions completed the survey, and most of respondents had a bachelor’s degree. The analysis showed that while most respondents were familiar with the concepts of nutrigenomics and nutrigenetics, 92.3% did not incorporate genetic testing into their practice; the main barriers of their use were misinformation, limited access to reliable resources, and ethical concerns surrounding genetic testing. Although 86.2% expressed interest in learning about nutrigenetics, only 31.5% were willing to invest in further training. Social media and non-academic sources were important sources of information, raising concerns about their inaccurate content and highlighting their importance in completing the curricula. Patients’ demand for genetic testing is limited and directed by disease prevention interests. Conclusions: Nutrigenetics is currently an area with limited practical application among Mexican dietitians; however, it is perceived as a valuable tool for future daily practice. The gap between perception and application underscores the need to integrate nutrigenetics into undergraduate curricula and to provide accessible, evidence-based professional development; these are essential to promote the ethical and effective use of nutrigenetics and support the transition toward personalized nutrition. Full article