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Epidemiological Epigenomics on Nutrition and Health

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

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 2380

Special Issue Editor


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Guest Editor
Director of Epigenomics in Endocrinology and Nutrition Group, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain
Interests: epigenomics; nutriepigenomics; mitoepigenetics; DNA methylation; epigenetic clock; nutrition; atlantic diet; ketogenic diet; ketone bodies; bioactive compounds; vitamins; antioxidants; cancer; obesity; oxidative stress; inflammation; adipokines; myokines; hepatokines; body composition; metabolism; biomarkers; liquid biopsia; adipose tissue; liver; muscle; blood leukocytes
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Special Issue Information

Dear Colleagues,

Human health is strongly determined by environmental factors such as dietary patterns, foods, nutrients, pollutants, toxics, or social stress, besides genetics. It is well established that the molecular mechanisms by means of which environmental factors alter biological processes are epigenetic mechanisms. These epigenetic mechanisms include DNA methylation marks, histone modifications, non-coding RNA (microRNA, long non-coding RNA) and sirtuin expression, epigenetic clock, mitochondrial DNA methylation, and telomere length. Epigenetics play a relevant role in physiological and pathological conditions by regulating gene expression. In this context, there has been growing interest in studying the associations between epigenetic variations and disease susceptibility. However, the elucidation of epigenetic biomarkers and the characterization of epigenetic therapeutic targets are still limited, which make the epidemiological epigenetics an emerging and fruitful field in clinical settings.

The purpose of this Special Issue is to add to the research which uses epigenetics only or in combination with other omic-technologies (genetics, transcriptomics, metabolomics, and microbiomics) in the identification of biomarkers of disease and exposure, or of susceptible populations, as well as in the characterization of modulators of epigenetic mechanisms. This could help to design methods for the prevention and treatment of non-communicable diseases such as obesity, diabetes, cardiovascular disease, fatty liver disease, neurological disorders, and cancer, and promote healthy aging.

Submissions may include population-based studies of variation in epigenetic marks, as well as studies regarding the effects of specific diets, dietary patterns, foods, nutrients, bioactive compounds, endocrine disruptors, or toxics (alcohol, tobacco, and abuse drugs) on changes in epigenomics parameters that could be associated with the biological responses and/or the risk of chronic non-communicable diseases and aging. The identification of epigenetic marks as biomarkers or drivers of disease could help to design more precise and personalized programs for disease prevention and management. This identification can be performed in body fluids (plasma, saliva, urine, and sperm) or tissues and at the nuclear or mitochondrial genome.

This Special Issue welcomes the submission of manuscripts describing original research or reviews of the scientific literature in humans (interventional, observational, or cohort studies).

I look forward to receiving your contributions.

Dr. Ana B. Crujeiras
Guest Editor

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Keywords

  • epigenetics
  • nutriepigenomics
  • mitoepigenetics
  • DNA methylation
  • microRNA
  • long non-coding RNA
  • inflammation
  • oxidative stress
  • dietary patterns
  • bioactive compounds
  • vitamins
  • antioxidants
  • disease
  • aging
  • longevity

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Published Papers (2 papers)

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Research

14 pages, 953 KiB  
Article
Maternal Vitamin D Deficiency Is a Risk Factor for Infants’ Epigenetic Gestational Age Acceleration at Birth in Japan: A Cohort Study
by Tomoko Kawai, Seung Chik Jwa, Kohei Ogawa, Hisako Tanaka, Saki Aoto, Hiromi Kamura, Naho Morisaki, Takeo Fujiwara and Kenichiro Hata
Nutrients 2025, 17(2), 368; https://doi.org/10.3390/nu17020368 - 20 Jan 2025
Viewed by 722
Abstract
Background/Objectives: The DNA methylation of neonatal cord blood can be used to accurately estimate gestational age. This is known as epigenetic gestational age. The greater the difference between epigenetic and chronological gestational age, the greater the association with an inappropriate perinatal fetal environment [...] Read more.
Background/Objectives: The DNA methylation of neonatal cord blood can be used to accurately estimate gestational age. This is known as epigenetic gestational age. The greater the difference between epigenetic and chronological gestational age, the greater the association with an inappropriate perinatal fetal environment and development. Maternal vitamin D deficiency is common in Japan. The aim of this study was to investigate the associations between maternal serum vitamin D levels and epigenetic gestational age acceleration at birth in Japan. Methods: The data were obtained from the hospital-based birth cohort study conducted at the National Center for Child Health and Development in Tokyo, Japan. Maternal blood was collected in the second trimester to measure the serum vitamin D concentration. Cord blood was collected at birth to measure serum vitamin D and to extract DNA. DNA methylation was assessed using an Illumina methylation EPIC array. Epigenetic gestational age was calculated using the “methylclock” R package. Linear regression analysis was performed to see associations. Results: Maternal serum vitamin D levels in the second trimester were negatively associated with epigenetic gestational age acceleration at birth when calculated by Bohlin’s method (regression coefficient [95% CI]: −0.022 [−0.039, −0.005], n = 157), which was still significant after considering infants’ sex (−0.022 [−0.039, −0.005]). Cord blood serum vitamin D levels were not associated with epigenetic age acceleration. Maternal age at delivery and birth height were associated in positive and negative ways with epigenetic gestational age acceleration, respectively (0.048 [0.012, 0.085] and −0.075 [−0.146, −0.003]). Conclusions: Maternal vitamin D deficiency was related to an infant’s epigenetic gestational age acceleration at birth. These findings suggest that the association between fetal development and maternal vitamin D levels may involve the fetal epigenetic regulation of the fetus. Full article
(This article belongs to the Special Issue Epidemiological Epigenomics on Nutrition and Health)
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12 pages, 484 KiB  
Article
A Novel Interaction between a 23-SNP Genetic Risk Score and Monounsaturated Fatty Acid Intake on HbA1c Levels in Southeast Asian Women
by Padmini Sekar, Arif S. Aji, Utami Ariyasra, Sri R. Sari, Nabila Tasrif, Finny F. Yani, Julie A. Lovegrove, Ikhwan R. Sudji, Nur I. Lipoeto and Karani S. Vimaleswaran
Nutrients 2024, 16(17), 3022; https://doi.org/10.3390/nu16173022 - 6 Sep 2024
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Abstract
Metabolic diseases result from interactions between genetic and lifestyle factors. Understanding the combined influences of single-nucleotide polymorphisms (SNPs) and lifestyle is crucial. This study employs genetic risk scores (GRS) to assess SNPs, providing insight beyond single gene/SNP studies by revealing synergistic effects. Here, [...] Read more.
Metabolic diseases result from interactions between genetic and lifestyle factors. Understanding the combined influences of single-nucleotide polymorphisms (SNPs) and lifestyle is crucial. This study employs genetic risk scores (GRS) to assess SNPs, providing insight beyond single gene/SNP studies by revealing synergistic effects. Here, we aim to investigate the association of a 23-SNP GRS with metabolic disease-related traits (obesity and type 2 diabetes) to understand if these associations are altered by lifestyle/dietary factors. For this study, 106 Minangkabau women were included and underwent physical, anthropometric, biochemical, dietary and genetic evaluations. The interaction of GRS with lifestyle factors was analyzed using linear regression models, adjusting for potential confounders. No statistically significant associations were observed between GRS and metabolic traits; however, this study demonstrates a novel interaction observed between 13-SNP GRS and monounsaturated fatty acid (MUFA) intake, and that it had an effect on HbA1c levels (p = 0.026). Minangkabau women with low MUFA intake (≤7.0 g/day) and >13 risk alleles had significantly higher HbA1c levels (p = 0.010). This finding has implications for public health, suggesting the need for large-scale studies to confirm our results before implementing dietary interventions in the Indonesian population. Identifying genetic influences on dietary response can inform personalized nutrition strategies to reduce the risk of metabolic disease. Full article
(This article belongs to the Special Issue Epidemiological Epigenomics on Nutrition and Health)
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