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  Subjects -> NUTRITION AND DIETETICS (Total: 201 journals)
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Lifestyle Genomics
Journal Prestige (SJR): 0.614
Citation Impact (citeScore): 2
Number of Followers: 2  

  This is an Open Access Journal Open Access journal
ISSN (Print) 2504-3161 - ISSN (Online) 2504-3188
Published by Karger Homepage  [120 journals]
  • Vitamin D Metabolism Genes Are Differentially Methylated in Individuals
           with Chronic Knee Pain

    • Abstract: Introduction: Recent evidence suggests that vitamin D may interact with the epigenome and play a role in the pain experience. In order for proper functioning to occur, there must be an adequate level of vitamin D present, made possible by enzymatic reactions that allow vitamin D to be biologically active. The purpose of this study was to explore the epigenetic landscape of genes involved in vitamin D metabolism in individuals with and without chronic knee pain. Methods: Community-dwelling individuals recruited as part of a larger study focused on knee pain provided demographic, clinical, and pain-related information, as well as an intravenous blood sample to determine DNA methylation levels at CpG sites. Results: There were differences in DNA methylation between those with and without pain in genes that code for enzymes related to vitamin D metabolism: CYP27B1 (1-α-hydroxylase). There was also hypermethylation on the gene that codes for the vitamin D receptor (VDR). Conclusions: The presence of chronic pain is associated with epigenetic modifications in genes responsible for the expression of enzymes involved in vitamin D metabolism and cellular function. These results lay groundwork in understanding the mechanism underlying the association between vitamin D and chronic pain.
      Lifestyle Genomics 2023;16:98–105
      PubDate: Tue, 28 Feb 2023 09:16:55 +010
       
  • Discrimination Exposure and Polygenic Risk for Obesity in Adulthood:
           Testing Gene-Environment Correlations and Interactions

    • Abstract: Introduction: Exposure to discrimination has emerged as a risk factor for obesity. It remains unclear, however, whether the genotype of the individual can modulate the sensitivity or response to discrimination exposure (gene × environment interaction) or increase the likelihood of experiencing discrimination (gene-environment correlation). Methods: This was an observational study of 4,102 white/European Americans in the Health and Retirement Study with self-reported, biological assessments, and genotyped data from 2006 to 2014. Discrimination was operationalized using the average of nine Everyday Discrimination Scale items. Polygenic risk scores (PRSs) for body mass index (BMI) and waist circumference (WC) were calculated using the weighted sum of risk alleles based on studies conducted by the Genetic Investigation of Anthropometric Traits (GIANT) consortium. Results: We found that greater PRS-BMI was significantly associated with more reports of discrimination (β = 0.04 ± 0.02; p = 0.037). Further analysis showed that measured BMI partially mediated the association between PRS-BMI and discrimination. There was no evidence that the association between discrimination and BMI, or the association between discrimination and WC, differed by PRS-BMI or PRS-WC, respectively. Conclusion: Our findings suggest that individuals with genetic liability for obesity may experience greater discrimination in their lifetime, consistent with a gene-environment correlation hypothesis. There was no evidence of a gene-environment interaction. More genome-wide association studies in diverse populations are needed to improve generalizability of study findings. In the meantime, prevention and clinical intervention efforts that seek to reduce exposure to all forms of discrimination may help reduce obesity at the population level.
      Lifestyle Genomics 2023;16:90–97
      PubDate: Tue, 07 Feb 2023 18:33:48 +010
       
  • Precision Nutrition for Cardiovascular Disease Prevention

    • Abstract: Background: Cardiovascular diseases (CVDs) are the leading cause of death globally, making their prevention a major challenge for modern society. For decades, treatments aimed at reducing CVD risk factors through nutritional recommendations and medications have had variable success. One of the main reasons behind this is the interindividual variability in response to drugs and nutritional interventions. The development of genomics has allowed the discovery of genetic variants influencing drug and food response, leading to more personalized treatments in the form of precision medicine and precision nutrition. The latter is founded on the principle that one diet does not fit all and the need to stratify individuals into subgroups based on their response to food and nutrients. Despite showing great promise in pushing forward the field of nutrition, health professionals have very little knowledge of precision nutrition, even though the general population is showing interest in more personalized nutritional guidance. Summary: This review aimed to provide an overview of key sources of interindividual variability observed in CVD risk factors in response to nutritional interventions. Despite some limitations, genetic testing is a mature predictive tool that should be at the forefront of tailored nutrition recommendations for CVD prevention. Although the epigenome-diet relationship shows great promise, it is still too early in its development to allow for its clinical deployment. Metabolomics has the potential to enhance genetic testing by complementing traditional self-reported dietary intake instruments as well as a very promising metabotyping method. Microbiome phenotyping, despite its complexity, provides a wealth of information on the health status of the host and its response to food and nutrients. Finally, current applications are discussed and an outline of the required steps for a successful implementation of precision nutrition in clinical practice as a tool for CVD prevention is presented. Key Messages: Precision nutrition is the cornerstone of a promising approach offering targeted nutritional recommendations for CVD prevention.
      Lifestyle Genomics 2023;16:73–82
      PubDate: Mon, 30 Jan 2023 10:20:37 +010
       
  • Abdominal Obesity, Excessive Adiposity, and the Taq1B CETP Variant Are
           Positively Associated with Serum Lipid Levels in Mexican Women

    • Abstract: Introduction: Obesity is a prevalent multifactorial disease whose main complication is dyslipidemia. Serum lipid levels also depend on genetic factors including the Taq1B variant of the CETP gene, which is suggested to be influenced by environmental factors and adiposity. Therefore, this study aimed to determine the effect of the Taq1B CETP variant on serum lipid levels associated with anthropometrical variables. Methods: 165 women from western Mexico were enrolled in this cross-sectional study. Weight and body fat were measured by bioimpedance and waist circumference with a measuring tape. Serum lipid levels were determined by dry chemistry. The Taq1B CETP variant was analyzed by allelic discrimination. Results: Women with abdominal obesity and the B1B2/B2B2 genotype had significantly higher total cholesterol levels (195.17 [185.95–204.39] vs. 183 mg/dL [169.83–196.16], p = 0.007) and low density lipoprotein (118.84 [110.65–127.03] vs. 113.84 mg/dL [102.37–125.31], p = 0.037) than carriers of the B1B1 genotype. Likewise, subjects with excessive adiposity and the B1B2/B2B2 genotype showed significantly higher total cholesterol levels (195.05 [186.04–204.06] vs. 182.40 mg/dL [169.03–195.76], p = 0.003) than those with the B1B1 genotype. Conclusion: Women with abdominal obesity or excessive adiposity, who are also carriers of the B1B2/B2B2 genotype, have higher serum lipid levels than women with the B1B1 genotype.
      Lifestyle Genomics 2023;16:83–89
      PubDate: Wed, 18 Jan 2023 13:41:36 +010
       
  • A Nutrigenetic Approach to Investigate ApoB EcoR1 Polymorphism-Dietary
           Acid Load Interactions on Lipid and Anthropometric-Related Outcomes in
           Adults with Dyslipidemic Type 2 Diabetes

    • Abstract: Introduction: Despite multiple studies having considered the role of dietary acid load (DAL) or the apolipoprotein B (ApoB) EcoR1 rs1042031 polymorphism in diabetes, none have assessed their interplay effect on metabolic markers. Therefore, this study aimed to determine the interaction of EcoR1 rs1042031 and DAL on metabolic markers among adults with type 2 diabetes mellitus (T2DM). Methods: 492 randomly selected individuals with T2DM were recruited for this cross-sectional study. Dietary intake was evaluated by a validated food frequency questionnaire. DAL was assessed as net-endogenous acid production (NEAP) and potential renal acid load (PRAL). Real-time-PCR was used to genotype the EcoR1 rs1042031 polymorphism. Metabolic markers were also assessed. The interaction effect of the polymorphism and DAL indexes was analyzed by analysis of covariance (ANCOVA). Result: The frequency of EcoR1 rs1042031 genotypes was not different between dyslipidemic and normolipidemic participants (p #x3e; 0.05). Among participants with dyslipidemia, those with the GG genotype and who consumed a higher level of NEAP had higher body mass index (BMI) (p = 0.03) and waist circumference (WC; p = 0.02). Moreover, triglyceride (TG) concentration (p = 0.007), the LDL/HDL ratio (p = 0.03), and the TG/HDL (p = 0.03) ratio were significantly higher in A allele carriers with higher than the median intake of NEAP, in comparison with GG homozygotes. Finally, GA/AA carriers who had a higher intake of PRAL had a higher TG concentration (p = 0.006) and TG/HDL ratio (p = 0.01) compared to lower median intake in the dyslipidemia group. Discussion: In the dyslipidemic group, there was a higher TG concentration among individuals with the GA/AA genotype and a higher intake of NEAP/PRAL. Also, in this group, a higher intake of NEAP may be considered as a risk factor for increased levels of BMI and WC among participants with the GG genotype.
      Lifestyle Genomics 2023;16:61–72
      PubDate: Wed, 14 Dec 2022 18:12:17 +010
       
  • 15th Congress of the International Society of Nutrigenetics &
           Nutrigenomics (ISNN)

    • Abstract:
      Lifestyle Genomics
      PubDate: Tue, 15 Nov 2022 10:58:10 +010
       
  • Genome Tectonics: Linking Dynamic Genome Organization with Cellular
           Nutrients

    • Abstract: Background: Our daily intake of food provides nutrients for the maintenance of health, growth, and development. The field of nutrigenomics aims to link dietary intake/nutrients to changes in epigenetic status and gene expression. Summary: Although the relationship between our diet and our genes in under intense investigation, there is still a significant aspect of our genome that has received little attention with regard to this. In the past 15 years, the importance of genome organization has become increasingly evident, with research identifying small-scale local changes to large segments of the genome dynamically repositioning within the nucleus in response to/or mediating change in gene expression. The discovery of these dynamic processes and organization maybe as significant as dynamic plate tectonics is to geology, there is little information tying genome organization to specific nutrients or dietary intake. Key Messages: Here, we detail key principles of genome organization and structure, with emphasis on genome folding and organization, and link how these contribute to our future understand of nutrigenomics.
      Lifestyle Genomics 2023;16:21–34
      PubDate: Mon, 14 Nov 2022 08:28:52 +010
       
  • Nutrigenomics: Perceptions of South African Dietitians and General
           Practitioners

    • Abstract: Introduction: Although investigations into the emerging field of nutrigenomics are relatively limited and more research in this field is required, experts agree that there is potential for it to be incorporated into health care practice. If health care professionals can promote healthy dietary behavior based on nutrigenomic testing, it can assist in addressing the health consequences of poor diet and lightning the strain on the South African health care system. Methods: Registered dietitians (RDs) and general practitioners (GPs) registered with the Health Professions Council of South Africa (HPCSA) who obtained their qualification in South Africa (SA) were eligible to participate in this cross-sectional study. Participants were identified using convenience and snowball sampling. A self-administered electronic survey using EvaSys Software® was completed by those that agreed to participate. Results: Nearly all RDs (97.3%), but less than a third of GPs (30.4%), had heard of the term nutrigenomics. Approximately three-quarters of RDs (74.7%) and GPs (73.9%) had or would personally consider undergoing genetic testing. More than 40% (43.5%) of RDs ranked direct-to-consumer genetic testing companies as the most equipped, while 31.8% of GPs ranked RDs as the most equipped to provide patients with nutrigenomic services. Both RDs and GPs ranked similar reasons as “strongly agree” for why consumers were motivated to make use of nutrigenomic services, which included “motivated by a desire to prevent or manage disease” (56.7%), “prevent a disease based on family history” (65.9%), “control health outcomes based on family history” (54.9%), and “improve overall health-related quality of life” (48.6%). Cost concerns were reported as the greatest barrier to implementing nutrigenomic services (75.7%). Other barriers included confidentiality issues (47.8%) and moral concerns (37.3%). Greater individualization of diet prescription (66.5%), stronger foundations for nutrition recommendations (62.4%), and dietary prescriptions that would manage or prevent certain diseases more effectively (59.0%) were all perceived as benefits of including nutrigenomics in practice. Conclusion: This study identified perceived consumer motivators and barriers that might affect the willingness to seek nutrigenomic services in SA. In addition, the need for more nutrigenomic training opportunities, including the planning of personalized diets based on genetic testing results and interpretation of results, was confirmed. However, both RDs and GPs felt that the emerging field of nutrigenomics needs further development before it can be applied effectively in routine private and public health care in SA.
      Lifestyle Genomics 2023;16:11–20
      PubDate: Tue, 01 Nov 2022 12:31:38 +010
       
  • Mechanism of Glycitein in the Treatment of Colon Cancer Based on Network
           Pharmacology and Molecular Docking

    • Abstract: Introduction: The prevalence of colon cancer remains high across the world. The early diagnosis of colon cancer is challenging. Moreover, patients with colon cancer frequently suffer from poor prognoses. Methods: Differentially expressed genes (DEGs) in colon cancer were acquired based on TCGA-COAD dataset screening. DEGs were input into the Connectivity Map (CMap) database to screen small molecule compounds with the potential to reverse colon cancer pathological function. Glycitein ranked first among the screened small-molecule compounds. We downloaded the main targets of glycitein from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database and constructed protein-protein interaction (PPI) networks of those which were closely related to targets by the Search Tool for the Retrieval of Interaction Gene/Proteins (STRING). Five potential targets of glycitein for treating colon cancer were identified (CCNA2, ESR1, ESR2, MAPK14, and PTGS2). These targets were used as seeds for random walk with restart (RWR) analysis of PPI networks. Then, the interaction network of glycitein-colon cancer-related genes was constructed based on the top 50 genes in affinity coefficients. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted on the potential genes targeted by glycitein in colon cancer treatment and those that were closely bound up with targets. Results: GO analysis demonstrated that the enrichment of these genes was primarily discovered in biological functions including regulation of fibroblast proliferation, response to oxygen levels, and epithelial cell proliferation. The KEGG analysis results illustrated that the signaling pathways where these genes were mostly involved consisted of the mitogen-activated protein kinase signaling pathway, the phosphatidylinositol-3-kinase-Akt signaling pathway, and the p53 signaling pathway. Finally, stable binding of glycitein to five potential targets in colon cancer was verified by molecular docking. Conclusion: This study elucidated the key targets and main pathways of glycitein on the basis of network pharmacology and preliminarily analyzed molecular mechanisms in the treatment of colon cancer. A scientific basis is provided for glycitein application in treating colon cancer.
      Lifestyle Genomics 2023;16:1–10
      PubDate: Fri, 30 Sep 2022 11:38:11 +020
       
  • Quantile-Specific Heritability of Mean Platelet Volume, Leukocyte Count,
           and Other Blood Cell Phenotypes

    • Abstract: Introduction: “Quantile-dependent expressivity” occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., mean platelet volume, MPV) is high or low relative to its distribution. Methods: Offspring-parent regression slopes (βOP) were estimated by quantile regression, from which quantile-specific heritabilities (h2) were calculated (h2 = 2βOP/[1 + rspouse]) for blood cell phenotypes in 3,929 parent-offspring pairs from the Framingham Heart Study. Results: Quantile-specific h2 (±SE) increased with increasing percentiles of the offspring’s age- and sex-adjusted MPV distribution (plinear = 0.0001): 0.48 ± 0.09 at the 10th, 0.53 ± 0.04 at the 25th, 0.70 ± 0.06 at the 50th, 0.74 ± 0.06 at the 75th, and 0.90 ± 0.12 at the 90th percentile. Quantile-specific h2 also increased with increasing percentiles of the offspring’s white blood cell (WBC, plinear = 0.002), monocyte (plinear = 0.01), and eosinophil distributions (plinear = 0.0005). In contrast, heritibilities of red blood cell (RBC) count, hematocrit (HCT), and hemoglobin (HGB) showed little evidence of quantile dependence. Quantile-dependent expressivity is consistent with gene-environment interactions reported by others, including (1) greater increases in WBC and PLT concentrations in subjects who are glutathione-S-transferase Mu1 (GSTM1) null homozygotes than GSTM1 sufficient when exposed to endotoxin; (2) significantly higher WBC count in AA homozygotes than carriers of the G-allele of the glutathione S-transferase P1 (GSTP1) rs1695 polymorphism at low but not high benzene exposure in shoe factory workers; (3) higher WBC counts in TT homozygotes than C-allele carriers of the interleukin-1β (IL1B) c.315C#x3e;T polymorphism after undergoing surgery for infective endocarditis but not before surgery. Discussion/Conclusion: Quantile-dependent expressivity may explain several purported gene-environment interactions involving blood cell phenotypes.
      Lifestyle Genomics 2022;15:111–123
      PubDate: Thu, 22 Sep 2022 07:46:21 +020
       
 
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