Innovative Nutrition Strategies for Aging and Chronic Disease Prevention: From Target Interventions to Population Health (Oral Session 22)

(OR22-04-25) Early-Life Nutrition Supplementation and Epigenetic Age in Middle-Adulthood Among Guatemalan Adults

Tuesday, June 3, 2025

10:36 AM – 10:48 AM ET

Location: S220 E-G

Presenting Author(s)

MC

Melissa Chapnick, RD, MS, MPH

Doctoral Student
Emory University
Decatur, Georgia, United States

Disclosure information not submitted.

Co-Author(s)

EY

Elaine A. Yu, PhD

Assistant Investigator
Vitalant Research Institute, UCSF
San Francisco, California, United States
AS

Alicia Smith

Emory University School of Medicine, United States
KC

Karen Conneely, PhD

Associate Professor, Department of Human Genetics
Emory University
Atlanta, Georgia, United States
MR

Manuel Ramirez-Zea, MD, PhD

Coordinator of the INCAP Research Center for the Prevention of Chronic Diseases -CIIPEC
Institute of Nutrition of Central America and Panama
Guatemala City, El Progreso, Guatemala
ZQ

Zhaohui Qin

Emory University Rollins School of Public Health, United States
LS

Lisa Staimez, MPH, PhD

Assistant Professor, Hubert Department of Global Health
Emory University
Atlanta, Georgia, United States
VV

Viola Vaccarino

Emory University
Atlanta, Georgia, United States
Aryeh D. Stein, PhD

Professor
Emory University
Atlanta, Georgia, United States

Objectives: Epigenetic clocks are biomarkers of aging. Associations of epigenetic clocks with early-life nutrition have been demonstrated following famine exposure. We investigated the impact of a cluster-randomized early-life nutrition intervention on epigenetic age among Guatemalan adults.

Methods: We analyzed follow-up data from participants in the INCAP Nutrition Supplementation Trial, conducted in 4 villages in eastern Guatemala. DNA methylation was measured in buffy coat samples using the Illumina EPIC V2 array and standard quality control procedures.

Epigenetic age was quantified using DunedinPACE and PhenoAge. We used intent-to-treat difference-in-difference modeling to assess the impact of atole, a protein-energy supplement, provided during the first 1,000 days of life (conception to age 2y), on epigenetic age. Covariates included sex, birth year, the trial supplement type (atole [intervention] vs. fresco [control]), exposure period of supplement (full first 1k days, partial first 1k days, other), and a random effect to account for sibships. The primary coefficient of interest is represented by the interaction between supplement type and exposure period.

Results: The analysis included 1079 participants (mean age 45.0 y (SD 4.3); 60.2 % female, 22.7% exposed to atole for the full 1000 days, mean DunedinPACE 1.2 (SD 0.1), Phenoage 39.7 y (SD 7.0). Individuals exposed to atole had lower DunedinPACE (-0.02; 95% CI –0.03, 0.00) and PhenoAge (-1.28y; 95% CI – 2.10, -0.45), compared to those exposed to fresco.

In difference-in-difference analyses, exposure to atole during the full first 1,000-day period was associated with lower DunedinPACE (- 0.02, 95% CI -0.05, 0.01) and PhenoAge (-1.16 y, 95% CI -2.90, 0.58), compared to other exposures. Partial exposure to atole during the first 1,000 days was associated with lower DunedinPACE (-0.04; 95% CI -0.07, 0.01) and PhenoAge (-2.17 y; 95% CI -3.95, 0.39), compared to other exposures.

Conclusions: Exposure to atole during the first 1,000 days was associated with modest reductions in epigenetic age as measured by both DunedinPACE and PhenoAge. These findings complement prior evidence suggesting that early-life nutrition supplementation reduces the risk of diabetes, which is associated with epigenetic age in this population.

Funding Sources: National Institutes of Health supported this research.