ArticleClinical epigenetics2020
Genetic and environmental causes of variation in epigenetic aging across the lifespan.
Article in Clinical epigenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 67 citations in OpenAlex.
- Assessing differences in epigenetic aging markers between sexual or gender minority and straight cisgender adults using the Coronary Artery Risk Development in Young Adults cohort.Social science & medicine (1982) · 2026Article
- Genetic and epigenetic underpinnings of biological aging: a multi-omics study integrating Mendelian randomization, spatial transcriptomics, and drug target discovery.Clinical epigenetics · 2026Article
- Mental health across the lifecourse as predictors of epigenetic aging from a longitudinal birth cohort in the United States.Journal of affective disorders · 2026Article
- Analysis of ocular biometry in Korean using swept-source optical coherence tomography.Scientific reports · 2025Article
- Climate-related disasters and biological aging based on DNA methylation: a twin and family study in Australian women.International journal of epidemiology · 2025Article
- The Aging Lung: Exploring Multimorbidity Patterns and Their Clinical Implications: A Narrative Review.Current issues in molecular biology · 2025Review
- Article
- Perinatal Exposure to Lead or Diethylhexyl Phthalate in Mice: Sex-Specific Effects on Cardiac DNA Methylation and Gene Expression across Time.Environmental health perspectives · 2025Article
- Genetic and environmental contributions to epigenetic aging across adolescence and young adulthood.Clinical epigenetics · 2025Article
- Epigenetics and ultraviolet radiation: Implications for skin ageing and carcinogenesis.Skin health and disease · 2024Review
- Neuroinflammaging: A Tight Line Between Normal Aging and Age-Related Neurodegenerative Disorders.Aging and disease · 2024Review
- Sociodemographic and Lifestyle Factors and Epigenetic Aging in US Young Adults: NIMHD Social Epigenomics Program.JAMA network open · 2024Article
- Mother adversity and co-residence time impact mother-child similarity in genome-wide and gene-specific methylation profiles.Clinical epigenetics · 2024Article
- Curcumin improves atrial fibrillation susceptibility by regulating tsRNA expression in aging mouse atrium.PeerJ · 2024Article
- Host fecal DNA specific methylation signatures mark gut dysbiosis and inflammation in children affected by autism spectrum disorder.Scientific reports · 2023Article
- Variance of age-specific log incidence decomposition (VALID): a unifying model of measured and unmeasured genetic and non-genetic risks.International journal of epidemiology · 2023Article
- Association between the epigenetic lifespan predictor GrimAge and history of suicide attempt in bipolar disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Forensic Age Estimation through a DNA Methylation-Based Age Prediction Model in the Italian Population: A Pilot Study.International journal of molecular sciences · 2023Article
- Low birthweight is associated with epigenetic age acceleration in the first 3 years of life.Evolution, medicine, and public health · 2023Article
- The Heritability of Kidney Function Using an Older Australian Twin Population.Kidney international reports · 2022Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDNA methylation-based biological age (DNAm age) is an important biomarker for adult health. Studies in specific age ranges have found widely varying results about its genetic and environmental causes of variation. However, these studies are not able to provide a comprehensive view of the causes of variation over the lifespan.
resultsIn order to investigate the genetic and environmental causes of DNAm age variation across the lifespan, we pooled genome-wide DNA methylation data for 4217 people aged 0-92 years from 1871 families. DNAm age was calculated using the Horvath epigenetic clock. We estimated familial correlations in DNAm age for monozygotic (MZ) twin, dizygotic (DZ) twin, sibling, parent-offspring, and spouse pairs by cohabitation status. Genetic and environmental variance components models were fitted and compared. We found that twin pair correlations were - 0.12 to 0.18 around birth, not different from zero (all P > 0.29). For all pairs of relatives, their correlations increased with time spent living together (all P < 0.02) at different rates (MZ > DZ and siblings > parent-offspring; P < 0.001) and decreased with time spent living apart (P = 0.02) at similar rates. These correlation patterns were best explained by cohabitation-dependent shared environmental factors, the effects of which were 1.41 (95% confidence interval [CI] 1.16 to 1.66) times greater for MZ pairs than for DZ and sibling pairs, and the latter were 2.03 (95% CI 1.13 to 9.47) times greater than for parent-offspring pairs. Genetic factors explained 13% (95% CI - 10 to 35%) of variation (P = 0.27). Similar results were found for another two epigenetic clocks, suggesting that our observations are robust to how DNAm age is measured. In addition, results for the other clocks were consistent with there also being a role for prenatal environmental factors in determining their variation.
conclusionsVariation in DNAm age is mostly caused by environmental factors, including those shared to different extents by relatives while living together and whose effects persist into old age. The equal environment assumption of the classic twin study might not hold for epigenetic aging.
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