Type 2 Diabetes Prevention and Management: An Update on Emerging Findings (Poster Theater Flash Session 10)

(PTFS10-05-25) Epigenetics of Social Stress and Metabolic Health in Boston Puerto Ricans

Monday, June 2, 2025

12:12 PM – 12:16 PM ET

Location: South Hall B (The Hub) - Poster Theater / Poster Board Number PT-3

Presenting Author(s)

Chao-Qiang Lai, Ph.D.

Molecular Biologist
USDA Agricultural Research Service, Nutrition and Genomics, Jean Mayer USDA Human Nutrition Research Center
Boston, Massachusetts, United States

Disclosure information not submitted.

Co-Author(s)

JM

Josiemer Mattei, PhD

Associate Professor
Harvard University
Boston, Massachusetts, United States
LP

Laurence Parnell, Ph. D.

USDA ARS, JM-USDA Human Nutrition Research Ctr on Aging @ Tufts
Boston, Massachusetts, United States
LF

Luis M. Falcon

Center for Population Health, University of Massachusetts Lowell
Boston, Massachusetts, United States
Katherine L. Tucker, PhD (she/her/hers)

Professor, Director of the Center for Population Health
University of Massachusetts Lowell
Zuckerberg College of Health Sciences
Lowell, Massachusetts, United States
Jose M. Ordovas, PhD

Director, Nutrition and Genomics
JM-USDA Human Nutrition Research Ctr on Aging @ Tufts
Boston, Massachusetts, United States

Objectives: To investigate how social stress contributes to biological aging and metabolic health disparities in Boston Puerto Ricans, an underrepresented minority group.

Methods: We conducted an epigenome-wide association study (EWAS) on 374 adults without type 2 diabetes over a 5-year period. Biological age was calculated using the Horvath DNAm age clock at baseline and follow-up. Social stress was quantified using a composite score based on income, perceived discrimination, social isolation, and external stress perception. Linear regression models assessed associations between biological aging, social stress, and metabolic health markers (e.g., insulin resistance, HbA1c), adjusting for key covariates.

Results: Biological aging was significantly accelerated by social stress (β = 0.082 ± 0.023, P = 0.0003), with each one-unit increase in stress score corresponding to an additional 0.082 years of aging. Elevated HbA1c was also linked to faster aging (β = 0.541 ± 0.244, P = 0.027). Significant epigenetic changes were identified, including cg2666527 in the BMP2 gene, associated with insulin resistance (P = 1.14E-08). Additional loci, such as cg4876028 near TCERG1L and cg26719314 on the X chromosome, were significant after FDR correction (P < 0.05).

Conclusions: Social stress accelerates biological aging and drives epigenetic changes linked to metabolic health, providing dynamic measures of health disparities. These findings underscore the importance of addressing social determinants of health—such as income inequality and discrimination—to mitigate metabolic disease risk and improve health equity.

Funding Sources: USDA and NIH