Abstract
Smoking-associated DNA methylation (DNAm) signatures are reproducible among studies of mostly European descent, with mixed evidence if smoking accelerates epigenetic aging and its relationship to longevity. We evaluated smoking-associated DNAm signatures in the Costa Rican Study on Longevity and Healthy Aging (CRELES), including participants from the high longevity region of Nicoya. We measured genome-wide DNAm in leukocytes, tested Epigenetic Age Acceleration (EAA) from five clocks and estimates of telomere length (DNAmTL), and examined effect modification by the high longevity region. 489 participants had a mean (SD) age of 79.4 (10.8) years, and 18% were from Nicoya. Overall, 7.6% reported currently smoking, 35% were former smokers, and 57.4% never smoked. 46 CpGs and five regions (e.g. AHRR, SCARNA6/SNORD39, SNORA20, and F2RL3) were differentially methylated for current smokers. Former smokers had increased Horvath’s EAA (1.69-years; 95% CI 0.72, 2.67), Hannum’s EAA (0.77-years; 95% CI 0.01, 1.52), GrimAge (2.34-years; 95% CI1.66, 3.02), extrinsic EAA (1.27-years; 95% CI 0.34, 2.21), intrinsic EAA (1.03-years; 95% CI 0.12, 1.94) and shorter DNAmTL (− 0.04-kb; 95% CI − 0.08, − 0.01) relative to non-smokers. There was no evidence of effect modification among residents of Nicoya. Our findings recapitulate previously reported and novel smoking-associated DNAm changes in a Latino cohort.
Highlights
Smoking-associated DNA methylation (DNAm) signatures are reproducible among studies of mostly European descent, with mixed evidence if smoking accelerates epigenetic aging and its relationship to longevity
In this study of a Latino adult population living in Costa Rica, including residents from the high longevity region of the Nicoya Peninsula, we investigated associations between current, former, and never smoking status with DNA methylation signatures and epigenetic age acceleration
Our findings replicated previously reported associations within the AHRR, PRSS23, SIN3B, and F2RL3 genes and found 5 novel signatures, which annotated to the mitogen-activated protein kinase 4 (MAPK4), heterogeneous nuclear ribonucleoprotein M (HNRNPM), prostaglandin I2 receptor (PTGIR), and thioredoxin reductase 1 (TXNRD1) genes
Summary
Smoking-associated DNA methylation (DNAm) signatures are reproducible among studies of mostly European descent, with mixed evidence if smoking accelerates epigenetic aging and its relationship to longevity. Studies (EWAS) conducted in blood samples have shown that adult cigarette smoking is associated with altered DNA methylation patterns of leukocytes across cohorts of mostly European d escent[12–18]. These smoking-associated changes in DNA methylation may contribute to an increased risk for poor health outcomes among smokers. Several epigenetic clocks have been developed in order to include epigenetic markers in specific or multiple tissues and improve predictive performance for specific aging measures, morbidity, or mortality. Cigarette smoking has recently been shown to be associated with increased age acceleration in respiratory tissues, which may be reversed by smoking c essation[34]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
