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Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrigenetics and Nutrigenomics".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 32358

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Special Issue Editor

Dr. Stavroula Kanoni

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Guest Editor

William Harvey Research Institude, Clinical Pharmacology, Barts and the London School of Medicine and Dentistry, Queen Mary University London, London, UK
Interests: cardiovascular genetics; cardiometabolic traits; gene–diet interactions; nutrigenetics; nutrigenomics; causality; precision medicine; risk prediction; polygenicity; environment

Special Issue Information

Dear Colleagues,

Recent advances in genomic research have greatly enhanced our knowledge of disease-related metabolic pathways, highlighting at the same time potential new intervention targets. Complex diseases including cardiovascular, hypertension, type 2 diabetes (T2D), metabolic syndrome, obesity, nonalcoholic fatty liver disease (NAFLD), and cancer have been linked, through epidemiological studies, to lifestyle and diet, with a substantial body of evidence showing that gene–nutrient interactions impact molecular mechanisms.

In order to better tailor treatment to the individual and/or improve prevention strategies for complex diseases, it is essential to establish people’s metabotypes though the combined application of nutritional and genetic epidemiology with metabolite and molecular profiling at the gene, transcriptome, proteome, and metabolome level. An additional level of complexity that needs to be considered when establishing metabotypes is the individual’s gut microbiome.

The purpose of this Special Issue is to collect original research reports and review articles that highlight recent advances in the field of nutritional genomics and metagenomics in complex diseases. We welcome studies with various experimental designs, functional studies, clinical trials, epidemiological studies, and meta-analyses.

Dr. Stavroula Kanoni
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

nutrigenetics
nutrigenomics
gene–diet interactions
precision nutrition
omics
microbiota
complex diseases
biomarkers
metabotypes
genetic studies

Published Papers (7 papers)

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Research

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11 pages, 529 KiB

Open AccessArticle

TM6SF2-rs58542926 Genetic Variant Modifies the Protective Effect of a “Prudent” Dietary Pattern on Serum Triglyceride Levels

by Ioanna Panagiota Kalafati, Maria Dimitriou, Konstantinos Revenas, Alexander Kokkinos, Panos Deloukas and George V. Dedoussis

Nutrients 2023, 15(5), 1112; https://doi.org/10.3390/nu15051112 - 23 Feb 2023

Cited by 1 | Viewed by 1536

Abstract

The epidemic prevalence of non-alcoholic fatty liver disease (NAFLD), despite extensive research in the field, underlines the importance of focusing on personalized therapeutic approaches. However, nutrigenetic effects on NAFLD are poorly investigated. To this end, we aimed to explore potential gene-dietary pattern interactions in a NAFLD case–control study. The disease was diagnosed with liver ultrasound and blood collection was performed after an overnight fast. Adherence to four a posteriori, data-driven, dietary patterns was used to investigate interactions with PNPLA3-rs738409, TM6SF2-rs58542926, MBOAT7-rs641738, and GCKR-rs738409 in disease and related traits. IBM SPSS Statistics/v21.0 and Plink/v1.07 were used for statistical analyses. The sample consisted of 351 Caucasian individuals. PNPLA3-rs738409 was positively associated with disease odds (OR = 1.575, p = 0.012) and GCKR-rs738409 with lnC-reactive protein (CRP) (beta = 0.098, p = 0.003) and Fatty Liver Index (FLI) levels (beta = 5.011, p = 0.007). The protective effect of a “Prudent” dietary pattern on serum triglyceride (TG) levels in this sample was significantly modified by TM6SF2-rs58542926 (p_interaction = 0.007). TM6SF2-rs58542926 carriers may not benefit from a diet rich in unsaturated fatty acids and carbohydrates in regard to TG levels, a commonly elevated feature in NAFLD patients. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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11 pages, 1717 KiB

Open AccessArticle

Causal Associations between Vitamin D Levels and Psoriasis, Atopic Dermatitis, and Vitiligo: A Bidirectional Two-Sample Mendelian Randomization Analysis

by Yunqing Ren, Jipeng Liu, Wei Li, Huiwen Zheng, Huatuo Dai, Guiying Qiu, Dianhe Yu, Dianyi Yao and Xianyong Yin

Nutrients 2022, 14(24), 5284; https://doi.org/10.3390/nu14245284 - 11 Dec 2022

Cited by 6 | Viewed by 5176

Abstract

Background: Vitamin D level has been reported to be associated with psoriasis, atopic dermatitis, and vitiligo. However, its causal relationship with the risk of these three diseases remains unclear. Methods: We obtained genome-wide association statistics for three measures of circulating vitamin D levels (25(OH)D in 120,618 individuals, and 25(OH)D3 and epimeric form C3-epi-25(OH)D3 in 40,562 individuals) and for the diseases psoriasis (3871 cases and 333,288 controls), atopic dermatitis (21,399 cases and 95,464 controls), and vitiligo (4680 cases and 39,586 controls). We performed Mendelian randomization using inverse-variance weighted, weighted median, MR-Egger, and MR-pleiotropy residual sum and outlier methods. We carried out sensitivity analyses to evaluate the robustness of the results. Results: We showed that elevated vitamin D levels protected individuals from developing psoriasis (OR = 0.995, p = 8.84 × 10⁻⁴ for 25(OH)D; OR = 0.997, p = 1.81 × 10⁻³ for 25(OH)D₃; and OR = 0.998, p = 0.044 for C3-epi-25(OH)D₃). Genetically predicted risk of atopic dermatitis increased the levels of 25(OH)D (OR = 1.040, p = 7.14 × 10⁻⁴) and 25(OH)D₃ (OR = 1.208, p = 0.048). A sensitivity analysis suggested the robustness of these causal associations. Conclusions: This study reported causal relationships between circulating vitamin D levels and the risk of psoriasis, atopic dermatitis, and vitiligo. These findings provide potential disease intervention and monitoring targets. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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13 pages, 950 KiB

Open AccessArticle

Obesity, Fat Distribution and Risk of Cancer in Women and Men: A Mendelian Randomisation Study

by Nellie Y. Loh, Wenyi Wang, Raymond Noordam and Constantinos Christodoulides

Nutrients 2022, 14(24), 5259; https://doi.org/10.3390/nu14245259 - 9 Dec 2022

Cited by 8 | Viewed by 3447

Abstract

Obesity and upper-body fat distribution are independent, cardiometabolic risk factors but whether they also display comparable associations with cancer risk is unknown. We investigated the causal relationships between body mass index (BMI) and BMI-adjusted waist-to-hip ratio (WHRadjBMI) and cancer risk and searched for potential drivers linking these traits to carcinogenesis using two-sample and multivariable Mendelian randomisation. In women, genetically instrumented higher BMI was associated with lower breast (OR = 0.87, 95% CI 0.81–0.93) and higher endometrial (OR = 1.75, 95% CI 1.55–1.96) cancer risk whilst WHRadjBMI was associated with higher colon cancer risk (OR = 1.22, 95% CI 1.07–1.42). In men, elevated BMI was associated with lower prostate cancer risk (OR = 0.91, 95% CI 0.85–0.98). Mechanistically, testosterone and insulin mediated 21% and 35%, respectively of the total, genetically determined association of BMI with endometrial cancer risk whilst HDL cholesterol and IGF-1 mediated 40% and 22%, respectively of the association between BMI and breast cancer risk. In men, testosterone mediated 21% of the association between BMI and prostate cancer risk. Colon cancer aside, the total amount of body fat might be more important than its location in modulating cancer susceptibility due to differential effects of obesity and fat distribution on adiposity-associated cancer drivers. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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12 pages, 1019 KiB

Open AccessArticle

Novel Insights into the Effects of Genetic Variants on Serum Urate Response to an Acute Fructose Challenge: A Pilot Study

by Xinruo Zhang, Baba B. Mass, Valentina Talevi, Ruixue Hou, Kari E. North and Venkata Saroja Voruganti

Nutrients 2022, 14(19), 4030; https://doi.org/10.3390/nu14194030 - 28 Sep 2022

Cited by 1 | Viewed by 1638

Abstract

Studies have shown that genetic variations can influence metabolic response to nutrient intake, and that diets rich in fructose contribute to hyperuricemia. In this pilot study, our aim was to determine the variability of serum urate in response to an acute fructose challenge and to investigate if genetic variants would affect this response in young to middle-aged adults who self-reported as Black or White. Fifty-seven participants consumed a fructose-rich beverage after an overnight fast. Blood was drawn at five time points (baseline, 30, 60, 120, and 180 min after consumption). Thirty urate-related single nucleotide polymorphisms (SNPs) were analyzed for their associations with baseline serum urate and its percent changes, using a two-step modeling approach followed by meta-analysis. At baseline, serum urate (mg/dL, mean ± SD) was higher in Whites (5.60 ± 1.01 vs. 5.37 ± 0.96), men (6.17 ± 1.14 vs. 5.24 ± 0.79), and those with obesity (5.69 ± 1.08 vs. 5.42 ± 1.06 vs. 5.34 ± 0.80). Three SNPs were significantly associated with baseline serum urate or its percent changes, and six SNPs were nominally associated with percent changes in serum urate. In summary, our results showed that genetic variants could play a role in short-term urate metabolism. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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Review

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48 pages, 1563 KiB

Open AccessEditor’s ChoiceReview

Short Chain Fatty Acid Metabolism in Relation to Gut Microbiota and Genetic Variability

by Guilherme Ramos Meyers, Hanen Samouda and Torsten Bohn

Nutrients 2022, 14(24), 5361; https://doi.org/10.3390/nu14245361 - 16 Dec 2022

Cited by 27 | Viewed by 5427

Abstract

It is widely accepted that the gut microbiota plays a significant role in modulating inflammatory and immune responses of their host. In recent years, the host-microbiota interface has gained relevance in understanding the development of many non-communicable chronic conditions, including cardiovascular disease, cancer, autoimmunity and neurodegeneration. Importantly, dietary fibre (DF) and associated compounds digested by the microbiota and their resulting metabolites, especially short-chain fatty acids (SCFA), were significantly associated with health beneficial effects, such as via proposed anti-inflammatory mechanisms. However, SCFA metabolic pathways are not fully understood. Major steps include production of SCFA by microbiota, uptake in the colonic epithelium, first-pass effects at the liver, followed by biodistribution and metabolism at the host’s cellular level. As dietary patterns do not affect all individuals equally, the host genetic makeup may play a role in the metabolic fate of these metabolites, in addition to other factors that might influence the microbiota, such as age, birth through caesarean, medication intake, alcohol and tobacco consumption, pathogen exposure and physical activity. In this article, we review the metabolic pathways of DF, from intake to the intracellular metabolism of fibre-derived products, and identify possible sources of inter-individual variability related to genetic variation. Such variability may be indicative of the phenotypic flexibility in response to diet, and may be predictive of long-term adaptations to dietary factors, including maladaptation and tissue damage, which may develop into disease in individuals with specific predispositions, thus allowing for a better prediction of potential health effects following personalized intervention with DF. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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38 pages, 2020 KiB

Open AccessReview

Chrononutrition—When We Eat Is of the Essence in Tackling Obesity

by Maninder Kaur Ahluwalia

Nutrients 2022, 14(23), 5080; https://doi.org/10.3390/nu14235080 - 29 Nov 2022

Cited by 9 | Viewed by 6523

Abstract

Obesity is a chronic and relapsing public health problem with an extensive list of associated comorbidities. The worldwide prevalence of obesity has nearly tripled over the last five decades and continues to pose a serious threat to wider society and the wellbeing of future generations. The pathogenesis of obesity is complex but diet plays a key role in the onset and progression of the disease. The human diet has changed drastically across the globe, with an estimate that approximately 72% of the calories consumed today come from foods that were not part of our ancestral diets and are not compatible with our metabolism. Additionally, multiple nutrient-independent factors, e.g., cost, accessibility, behaviours, culture, education, work commitments, knowledge and societal set-up, influence our food choices and eating patterns. Much research has been focused on ‘what to eat’ or ‘how much to eat’ to reduce the obesity burden, but increasingly evidence indicates that ‘when to eat’ is fundamental to human metabolism. Aligning feeding patterns to the 24-h circadian clock that regulates a wide range of physiological and behavioural processes has multiple health-promoting effects with anti-obesity being a major part. This article explores the current understanding of the interactions between the body clocks, bioactive dietary components and the less appreciated role of meal timings in energy homeostasis and obesity. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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16 pages, 1664 KiB

Open AccessReview

Genetic Biomarkers of Metabolic Detoxification for Personalized Lifestyle Medicine

by Lucia Aronica, Jose M. Ordovas, Andrey Volkov, Joseph J. Lamb, Peter Michael Stone, Deanna Minich, Michelle Leary, Monique Class, Dina Metti, Ilona A. Larson, Nikhat Contractor, Brent Eck and Jeffrey S. Bland

Nutrients 2022, 14(4), 768; https://doi.org/10.3390/nu14040768 - 11 Feb 2022

Cited by 9 | Viewed by 6978

Abstract

Metabolic detoxification (detox)—or biotransformation—is a physiological function that removes toxic substances from our body. Genetic variability and dietary factors may affect the function of detox enzymes, thus impacting the body’s sensitivity to toxic substances of endogenous and exogenous origin. From a genetic perspective, most of the current knowledge relies on observational studies in humans or experimental models in vivo and in vitro, with very limited proof of causality and clinical value. This review provides health practitioners with a list of single nucleotide polymorphisms (SNPs) located within genes involved in Phase I and Phase II detoxification reactions, for which evidence of clinical utility does exist. We have selected these SNPs based on their association with interindividual variability of detox metabolism in response to certain nutrients in the context of human clinical trials. In order to facilitate clinical interpretation and usage of these SNPs, we provide, for each of them, a strength of evidence score based on recent guidelines for genotype-based dietary advice. We also present the association of these SNPs with functional biomarkers of detox metabolism in a pragmatic clinical trial, the LIFEHOUSE study. Full article

(This article belongs to the Special Issue Nutrigenetics, Nutrigenomics, and Precision Nutrition in Complex Diseases)

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