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Chronic liver disease is a global health issue. Patients with chronic liver disease require a fresh approach that focuses on the genetic and environmental factors that contribute to disease initiation and progression. Emerging knowledge in the fields of Genomic Medicine and Genomic Nutrition demonstrates differences between countries in terms of genetics and lifestyle risk factors such as diet, physical activity, and mental health in chronic liver disease, which serves as the foundation for the implementation of Personalized Medicine and Nutrition (PerMed-Nut) strategies. Most of the world's populations have descended from various ethnic groupings. Mexico's population has a tripartite ancestral background, consisting of Amerindian, European, and African lineages, which is common across Latin America's regional countries. The purpose of this review is to discuss the genetic and environmental components that could be incorporated into a PerMed-Nut model for metabolic-associated liver disease, viral hepatitis B and C, and hepatocellular carcinoma in Mexico. Additionally, the implementation of the PerMed-Nut approach will require updated medicine and nutrition education curricula. Training and equipping future health professionals and researchers with new clinical and investigative abilities focused on preventing liver illnesses in the field of genomic hepatology globally is a vision that clinicians and nutritionists should be concerned about.

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INTRODUCTION: It has been suggested that capsaicin (CAP), a major pungent component in chili peppers, can be used as an anti-obesity ingredient due to effects on energy metabolism, but evidence is not consistent. Genetics may account for differences in CAP tolerance and its impact on adiposity status. The aim of this study was to systematically review current evidence concerning the role of genetic polymorphisms influencing CAP tolerance. METHODS: The present systematic review analyzed and synthesized available evidence concerning associations between genetic polymorphisms and CAP tolerance following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) guidelines. Databases such as PubMed/MEDLINE, Cochrane, Scopus, Google Scholar, SciELO, and LILACS were screened. Out of 228 publications identified, only 6 meet inclusion criteria and were finally included in the final report. RESULTS: Overall, a total of 28 single nucleotide polymorphisms were associated with several CAP tolerance traits including sensitivity to burning/stinging, heat pain, and cough reactions, and detection of bitter taste thresholds. These genetic variants were located within 6 genes involved in key physiological processes such synthesis of tetrahydrobiopterin and nitric oxide production (GCH1), CAP uptake and transduction of thermal stimuli (TRPV1), and bitter taste perception (TAS2R38, TAS2R3, TAS2R4, and TAS2R5). CONCLUSION: There is evidence about the influence of genetic polymorphisms on CAP tolerance by affecting nociceptive signaling, CAP binding, and bitter tasting. This knowledge may facilitate the design and implementation of innovative CAP-based nutrigenetic strategies for a more precise clinical management of obesity.

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BACKGROUND: Betaine, an osmolyte derivative of the metabolite choline and the amino acid glycine, acts as a methyl donor in the conversion of homocysteine to methionine and is involved in the maintenance of adequate lipid metabolism. There is growing evidence for the role of betaine in the development of various lipid-related diseases, including dyslipidemia and cardiovascular risk. This study aimed to analyze associations between betaine intake and blood lipid profiles in Mexican subjects. METHODS: A total of 212 adults were randomly recruited in the city of Tijuana, Baja California, Mexico. Betaine intake was estimated using Nutritionist Pro software. Body composition and metabolic measurements were obtained by conventional methods. In the total sample, the average intake of betaine was 14.32 mg/d. Individuals were categorized into three groups according to tertiles of betaine consumption: tertile/group 1 (<4.16 mg/d), tertile/group 2 (4.16-12.02 mg/d), and tertile/group 3 (>12.02 mg/d). RESULTS: Compared to group 3, subjects within group 1 had higher serum levels of total cholesterol (p = 0.001), LDL-c (p = 0.026), and non-HDL-c (p = 0.021). In addition, significant negative Pearson correlations were found between betaine intake and the serum levels of total cholesterol (r = -0.432, 95% CI, -0.684, -0.185, p = 0.001), LDL-c (r = -0.370, 95% CI, -0.606, -0.134, p = 0.002), and non-HDL-c (r = -0.351, 95%CI, -0.604, -0.098, p = 0.007). CONCLUSIONS: Our results show that a low intake of betaine is associated with elevated blood cholesterol levels in Mexican subjects. On this basis, betaine consumption could be used as an additional dietary measure for cardiovascular care. However, additional studies are required to confirm our results in other Mexican regions as well as in other populations worldwide.

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Globally, type 2 diabetes mellitus (T2DM) is one of the most common metabolic disorders. T2DM physiopathology is influenced by complex interrelationships between genetic, metabolic and lifestyle factors (including diet), which differ between populations and geographic regions. In fact, excessive consumptions of high fat/high sugar foods generally increase the risk of developing T2DM, whereas habitual intakes of plant-based healthy diets usually exert a protective effect. Moreover, genomic studies have allowed the characterization of sequence DNA variants across the human genome, some of which may affect gene expression and protein functions relevant for glucose homeostasis. This comprehensive literature review covers the impact of gene-diet interactions on T2DM susceptibility and disease progression, some of which have demonstrated a value as biomarkers of personal responses to certain nutritional interventions. Also, novel genotype-based dietary strategies have been developed for improving T2DM control in comparison to general lifestyle recommendations. Furthermore, progresses in other omics areas (epigenomics, metagenomics, proteomics, and metabolomics) are improving current understanding of genetic insights in T2DM clinical outcomes. Although more investigation is still needed, the analysis of the genetic make-up may help to decipher new paradigms in the pathophysiology of T2DM as well as offer further opportunities to personalize the screening, prevention, diagnosis, management, and prognosis of T2DM through precision nutrition.

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BACKGROUND: It has been suggested that the dysfunction of the gut microbiome can have deleterious effects on the regulation of body weight and adiposity by affecting energy metabolism. In this context, gut bacterial profiling studies have contributed to characterize specific bacteria associated with obesity. This review covers the information driven by gut bacterial profiling analyses and emphasizes the potential application of this knowledge in precision nutrition strategies for obesity understanding and weight loss management. SUMMARY: Gut bacterial profiling studies have identified bacterial families that are more abundant in obese than in nonobese individuals (i.e., Prevotellaeae, Ruminococcaceae, and Veillonellaceae) as well as other families that have been repeatedly found more abundant in nonobese people (i.e., Christensenellaceae and Coriobacteriaceae), suggesting that an increase in their relative amount could be an interesting target in weight-loss treatments. Also, some gut-derived metabolites have been related to the regulation of body weight, including short-chain fatty acids, trimethylamine-N-oxide, and branched-chain and aromatic amino acids. Moreover, gut microbiota profiles may play a role in determining weight loss responses to specific nutritional treatments for the precise management of obesity. Thus, incorporating gut microbiota features may improve the performance of integrative models to predict weight loss outcomes. KEY MESSAGES: The application of gut bacterial profiling information is of great value for precision nutrition in metabolic diseases since it contributes to the understanding of the role of the gut microbiota in obesity onset and progression, facilitates the identification of potential microorganism targets, and allows the personalization of tailored weight loss diets as well as the prediction of adiposity outcomes based on the gut bacterial profiling of each individual. Integrating microbiota information with other omics knowledge (genetics, epigenetics, transcriptomics, proteomics, and metabolomics) may provide a more comprehensive understanding of the molecular and physiological events underlying obesity and adiposity outcomes for precision nutrition.

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Background: Capsaicin (CAP) is the main chemical component responsible for the pungency (burning pain) of the chili plant (capsicum spp.), whose metabolic functions include energy balance and fatty acid oxidation. The aim of this study is to analyze the association of dietary capsaicin consumption with markers of adiposity and fatty liver in a Mexican adult population. Methods: This cross-sectional/analytical study recruited 221 subjects aged 18 to 65 years who were resident in the city of Tijuana, Baja California, Mexico. The daily CAP intake was analyzed through a validated chili/CAP consumption questionnaire. Anthropometric and biochemical measurements were performed following standardized protocols. Adjusted Pearson's correlations were applied to analyze the association of CAP with adiposity and fatty liver markers. Results: In this study, the daily average consumption of CAP was 152.44 mg. The dietary CAP consumption positively correlated with BMI (r = 0.179, p = 0.003), hip circumference (r = 0.176, p = 0.004) and body adiposity index (r = 0.181, p = 0.001. Likewise, the daily CAP intake positively correlated with hepatic steatosis index (r = 0.158, p = 0.004), fatty liver index (r = 0.141, p = 0.003) and lactate dehydrogenase (r = 0.194, p = 0.016) after statistical settings. Conclusions: The results of this study suggest positive associations between dietary CAP consumption and the markers of body adiposity and fatty liver in a Mexican adult population.

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The pathogenesis of obesity and dyslipidemia involves genetic factors, such as polymorphisms related to lipid metabolism alterations predisposing their development. This study aimed to evaluate the effect of a nutrigenetic intervention on the blood lipid levels, body composition, and inflammation markers of adults with obesity and overweight. Eleven genetic variants associated with dyslipidemias in Mexicans were selected, and specific nutrigenetic recommendations for these polymorphisms were found. One hundred and one adults were recruited and assigned to follow either a standard or nutrigenetic diet for eight weeks. Anthropometric, biochemical, body composition, and inflammation markers were evaluated through standardized methods. Weighted genetic risk scores (wGRSs) were computed using the study polymorphisms. After intervention, both diets significantly decreased the anthropometric parameters and body composition (p < 0.05). Only the nutrigenetic diet group showed significant reductions in VLDL-c (p = 0.001), triglycerides (p = 0.002), TG:HDL (p = 0.002), IL-6 (p = 0.002), and TNF-α (p = 0.04). wGRSs had a high impact on the ΔTGs and ΔVLDL-c of both groups (standard diet: ΔTGs: Adj R2 = 0.69, p = 0.03; ΔVLDL-c: Adj R2 = 0.71, p = 0.02; nutrigenetic diet: ΔTGs: Adj R2 = 0.49, p = 0.03 and ΔVLDL-c: R2 = 0.29, p = 0.04). This nutrigenetic intervention improved lipid abnormalities in patients with excessive body weight. Hence, nutrigenetic strategies could be coadjuvant tools and enhance the standard dietary treatment for cardiometabolic diseases.

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Studies have examined the possible utility of epigenetic phenomena (DNA methylation changes, covalent histone modifications, and miRNA expression patterns) in predicting individual responses to different lifestyle programs. Nonetheless, most available evidence is focused on identifying epigenetic marks eventually associated with body composition and adiposity outcomes, whereas their roles in metabolic endings remain less explored. This document comprehensively reviewed the evidence regarding the use of epigenetic signatures as putative biomarkers of metabolic outcomes (glycemic, lipid, blood pressure, and inflammatory/oxidative stress features) in response to different lifestyle interventions in humans. Although more investigation is still necessary in order to translate this knowledge in clinical practice, these scientific insights are contributing to the design of advanced strategies for the precise management of cardiometabolic risk, gaining understanding on metabolic heterogeneity, allowing for the prediction of metabolic outcomes, and facilitating the design of epigenome-based nutritional strategies for a more customized approach for metabolic alterations treatment under the scope of precision nutrition.

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