Epigenetic aging in newborns: role of maternal diet.


Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
01 03 2020
Historique:
received: 16 08 2019
accepted: 09 12 2019
pubmed: 17 1 2020
medline: 6 5 2020
entrez: 17 1 2020
Statut: ppublish

Résumé

Epigenetic aging is associated with higher risk of cardiovascular disease, cancer, and all-cause mortality and may be a mechanistic link between early-life exposures, such as maternal dietary characteristics during pregnancy, and risk of adult disease. We sought to determine the early-life risk factors for newborn epigenetic aging, specifically maternal dietary macronutrient intake, and whether epigenetic aging is associated with cardiovascular health markers in the newborn. Epigenetic age acceleration of 169 newborns was measured from saliva using the Horvath age calculator. Maternal diet during pregnancy was assessed using food-frequency questionnaires. Newborns with positive age acceleration were more likely to be female and have greater body fatness. Maternal intakes of saturated fat [6.2 wk epigenetic age acceleration (95% CI: 1.0, 11.3) per 5% of energy; P = 0.02] and monounsaturated fat [12.4 wk (95% CI: 4.2, 20.5) per 5% of energy; P = 0.003] were associated with higher epigenetic age acceleration in the newborn. The strongest association of individual fatty acids were for palmitoleic acid (25.3 wk; 95% CI: 11.4, 39.2; P = 0.0004), oleic acid (2.2 wk; 95% CI: 0.8, 3.6; P = 0.002), and palmitic acid (2.9 wk; 95% CI: 1.0, 4.9; P = 0.004) per 1% of energy intake. Vitamin D supplementation was associated with lower epigenetic age acceleration (-8.1 wk; 95% CI: -14.5, -1.7; P = 0.01). Epigenetic age acceleration was associated with aortic intima-media thickness in preterm infants [1.0 µm (95% CI: 0.2, 1.8) per week of epigenetic age acceleration; P = 0.01], but not among those born at term (P = 0.78). Epigenetic age acceleration was not associated with heart rate variability in either preterm or term born infants (both P > 0.2). This study provides evidence of maternal dietary characteristics that are associated with epigenetic aging in the offspring. Prospective intervention studies are required to determine whether such associations are causal.

Sections du résumé

BACKGROUND
Epigenetic aging is associated with higher risk of cardiovascular disease, cancer, and all-cause mortality and may be a mechanistic link between early-life exposures, such as maternal dietary characteristics during pregnancy, and risk of adult disease.
OBJECTIVES
We sought to determine the early-life risk factors for newborn epigenetic aging, specifically maternal dietary macronutrient intake, and whether epigenetic aging is associated with cardiovascular health markers in the newborn.
METHODS
Epigenetic age acceleration of 169 newborns was measured from saliva using the Horvath age calculator. Maternal diet during pregnancy was assessed using food-frequency questionnaires.
RESULTS
Newborns with positive age acceleration were more likely to be female and have greater body fatness. Maternal intakes of saturated fat [6.2 wk epigenetic age acceleration (95% CI: 1.0, 11.3) per 5% of energy; P = 0.02] and monounsaturated fat [12.4 wk (95% CI: 4.2, 20.5) per 5% of energy; P = 0.003] were associated with higher epigenetic age acceleration in the newborn. The strongest association of individual fatty acids were for palmitoleic acid (25.3 wk; 95% CI: 11.4, 39.2; P = 0.0004), oleic acid (2.2 wk; 95% CI: 0.8, 3.6; P = 0.002), and palmitic acid (2.9 wk; 95% CI: 1.0, 4.9; P = 0.004) per 1% of energy intake. Vitamin D supplementation was associated with lower epigenetic age acceleration (-8.1 wk; 95% CI: -14.5, -1.7; P = 0.01). Epigenetic age acceleration was associated with aortic intima-media thickness in preterm infants [1.0 µm (95% CI: 0.2, 1.8) per week of epigenetic age acceleration; P = 0.01], but not among those born at term (P = 0.78). Epigenetic age acceleration was not associated with heart rate variability in either preterm or term born infants (both P > 0.2).
CONCLUSIONS
This study provides evidence of maternal dietary characteristics that are associated with epigenetic aging in the offspring. Prospective intervention studies are required to determine whether such associations are causal.

Identifiants

pubmed: 31942922
pii: S0002-9165(22)01037-1
doi: 10.1093/ajcn/nqz326
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

555-561

Informations de copyright

Copyright © The Author(s) 2020.

Auteurs

Melinda Phang (M)

Boden Collaboration for Obesity, Nutrition, Exercise, and Eating Disorders, University of Sydney, Sydney, Australia.
Sydney Medical School, University of Sydney, Sydney, Australia.

Jason Ross (J)

CSIRO Health and Biosecurity, Sydney, Australia.

Jineel H Raythatha (JH)

Boden Collaboration for Obesity, Nutrition, Exercise, and Eating Disorders, University of Sydney, Sydney, Australia.
Sydney Medical School, University of Sydney, Sydney, Australia.

Hasthi U Dissanayake (HU)

Boden Collaboration for Obesity, Nutrition, Exercise, and Eating Disorders, University of Sydney, Sydney, Australia.
Sydney Medical School, University of Sydney, Sydney, Australia.
Sleep Research Group, University of Sydney, Sydney, Australia.

Rowena L McMullan (RL)

Boden Collaboration for Obesity, Nutrition, Exercise, and Eating Disorders, University of Sydney, Sydney, Australia.
Sydney Medical School, University of Sydney, Sydney, Australia.
Royal Prince Alfred Hospital, Sydney, Australia.

Yang Kong (Y)

Boden Collaboration for Obesity, Nutrition, Exercise, and Eating Disorders, University of Sydney, Sydney, Australia.
Sydney Medical School, University of Sydney, Sydney, Australia.

Jon Hyett (J)

Royal Prince Alfred Hospital, Sydney, Australia.

Adrienne Gordon (A)

Sydney Medical School, University of Sydney, Sydney, Australia.
Royal Prince Alfred Hospital, Sydney, Australia.

Peter Molloy (P)

CSIRO Health and Biosecurity, Sydney, Australia.

Michael R Skilton (MR)

Boden Collaboration for Obesity, Nutrition, Exercise, and Eating Disorders, University of Sydney, Sydney, Australia.
Sydney Medical School, University of Sydney, Sydney, Australia.

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