The early-life exposome and epigenetic age acceleration in children

Prado-Bert, Paula de; Ruiz‐Arenas, Carlos; Vives-Usano, Marta; Andrušaitytė, Sandra; Cadiou, Solène; Carracedo, Ángel; Casas, Maribel; Chatzi, Leda; Dadvand, Payam; González, Juan R.; Gützkow, Kristine B.; Haug, Line Småstuen; Hernández-Ferrer, Carles; Keun, Hector C.; Lepeule, Johanna; Maitre, Léa; McEachan, Rosemary; Nieuwenhuijsen, Mark; Pelegrí, Dolors; Robinson, Oliver; Slama, Rémy; Vafeiadi, Marina; Sunyer, Jordi; Vrijheid, Martine; Bustamante, Mariona

doi:10.1016/j.envint.2021.106683

Cited by 64 publications

(47 citation statements)

References 85 publications

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“…Conversely, dietary intake of methyl donors appears to be beneficially associated with methylation of CpG sites linked to inflammation in children with asthma [ 86 ]. This variation in the effects of nutrient supplementation may be partially explained by the wide degree of environmental, psychological, and social exposures that vary across children, or the distinct differences in methylation outcomes [ 87 , 88 ].…”

Section: Resultsmentioning

confidence: 99%

Epigenetic Aging in Early Life: Role of Maternal and Early Childhood Nutrition

Koemel

Skilton

2022

Curr Nutr Rep

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Purpose of Review Early life presents a pivotal period during which nutritional exposures are more likely to cause epigenetic modifications, which may impact an individual’s health during adulthood. This article reviews the current evidence regarding maternal and early childhood nutritional exposures and their role in epigenetic aging. Recent Findings Maternal and early life consumption of diets higher in fiber, antioxidants, polyphenols, B vitamins, vitamin D, and ω-3 fatty acids is associated with slower epigenetic aging. Conversely, diets higher in glycemic load, fat, saturated fat, and ω-6 fatty acids demonstrate a positive association with epigenetic aging. Summary Maternal and early life nutrition directly and indirectly influences epigenetic aging via changes in one-carbon metabolism, cardiometabolic health, and the microbiome. Clinical trials are warranted to determine the specific foods, dietary patterns, and dietary supplements that will normalize or lower epigenetic aging across the life course.

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Section: Resultsmentioning

confidence: 99%

Epigenetic Aging in Early Life: Role of Maternal and Early Childhood Nutrition

Koemel

Skilton

2022

Curr Nutr Rep

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“…A recent exposome-wide association study highlighted the association between early life environmental exposures and epigenetic age acceleration or deceleration in children utilizing the Horvath Skin and Blood clock ( de Prado-Bert et al, 2021 ). Several cohort studies in adult populations have reported exposure to ambient PM associated with epigenetic aging using the Horvath, Hannum and Levine epigenetic clocks ( Nwanaji-Enwerem et al, 2016 ; Ward-Caviness et al, 2016 ; White et al, 2019 ; Ward-Caviness et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…Epigenetic age acceleration, having an estimated epigenetic age that exceeds actual chronological age, has been studied in association with health outcomes and age-related conditions ( Marioni et al, 2015 ; Chen et al, 2016 ; Perna et al, 2016 ; Levine et al, 2018 ). Emerging evidence suggests that epigenetic age acceleration or deceleration can be moderated by lifestyle and environmental factors such as cigarette smoking, socioeconomic status, body mass index, and air pollution ( Horvath et al, 2014 ; Quach et al, 2017 ; Simpkin et al, 2017 ; Lu et al, 2019 ; Ward-Caviness et al, 2020 ; de Prado-Bert et al, 2021 ). A recent study by de Pardo-Bert et al investigated the association between more than 100 exposures and epigenetic age acceleration during childhood using an exposome-wide approach; but no significant associations were observed between prenatal air pollution and epigenetic aging in childhood ( de Prado-Bert et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

“…Emerging evidence suggests that epigenetic age acceleration or deceleration can be moderated by lifestyle and environmental factors such as cigarette smoking, socioeconomic status, body mass index, and air pollution ( Horvath et al, 2014 ; Quach et al, 2017 ; Simpkin et al, 2017 ; Lu et al, 2019 ; Ward-Caviness et al, 2020 ; de Prado-Bert et al, 2021 ). A recent study by de Pardo-Bert et al investigated the association between more than 100 exposures and epigenetic age acceleration during childhood using an exposome-wide approach; but no significant associations were observed between prenatal air pollution and epigenetic aging in childhood ( de Prado-Bert et al, 2021 ). Epigenetic clocks for gestational age at birth ( Bohlin et al, 2016 ; Knight et al, 2016 ; Lee et al, 2019 ), estimated using cord blood and placenta DNAm data, were developed to reflect the fetal developmental age and to capture the fetal programming progress.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal Exposure to Ambient Air Pollution and Epigenetic Aging at Birth in Newborns

Song

Feinberg²,

Bakulski³

et al. 2022

Front. Genet.

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In utero air pollution exposure has been associated with adverse birth outcomes, yet effects of air pollutants on regulatory mechanisms in fetal growth and critical windows of vulnerability during pregnancy are not well understood. There is evidence that epigenetic alterations may contribute to these effects. DNA methylation (DNAm) based age estimators have been developed and studied extensively with health outcomes in recent years. Growing literature suggests environmental factors, such as air pollution and smoking, can influence epigenetic aging. However, little is known about the effect of prenatal air pollution exposure on epigenetic aging. In this study, we leveraged existing data on prenatal air pollution exposure and cord blood DNAm from 332 mother-child pairs in the Early Autism Risk Longitudinal Investigation (EARLI) and Markers of Autism Risk in Babies-Learning Early Signs (MARBLES), two pregnancy cohorts enrolling women who had a previous child diagnosed with autism spectrum disorder, to assess the relationship of prenatal exposure to air pollution and epigenetic aging at birth. DNAm age was computed using existing epigenetic clock algorithms for cord blood tissue—Knight and Bohlin. Epigenetic age acceleration was defined as the residual of regressing chronological gestational age on DNAm age, accounting for cell type proportions. Multivariable linear regression models and distributed lag models (DLMs), adjusting for child sex, maternal race/ethnicity, study sites, year of birth, maternal education, were completed. In the single-pollutant analysis, we observed exposure to PM2.5, PM10, and O3 during preconception period and pregnancy period were associated with decelerated epigenetic aging at birth. For example, pregnancy average PM10 exposure (per 10 unit increase) was associated with epigenetic age deceleration at birth (weeks) for both Knight and Bohlin clocks (β = −0.62, 95% CI: −1.17, −0.06; β = −0.32, 95% CI: −0.63, −0.01, respectively). Weekly DLMs revealed that increasing PM2.5 during the first trimester and second trimester were associated with decelerated epigenetic aging and that increasing PM10 during the preconception period was associated with decelerated epigenetic aging, using the Bohlin clock estimate. Prenatal ambient air pollution exposure, particularly in early and mid-pregnancy, was associated with decelerated epigenetic aging at birth.

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“…Another study observed this same association in early childhood and found that the difference in HorvathAA became larger as the children aged into adolescence ( Simpkin et al, 2016 ). Another study found that exposure to maternal tobacco use during pregnancy and parental tobacco use during childhood (neither parent vs. both parents) were associated with the offspring’s HorvathAA in childhood ( de Prado-Bert et al, 2021 ). To our knowledge, no studies have evaluated maternal and paternal effects of alcohol use during childhood on offspring epigenetic age.…”

Section: Introductionmentioning

confidence: 99%