Impact of paternal education on epigenetic ageing in adolescence and mid-adulthood: a multi-cohort study in the USA and Mexico.
DNA methylation
ageing
epidemiology
epigenetics
health disparities
Journal
International journal of epidemiology
ISSN: 1464-3685
Titre abrégé: Int J Epidemiol
Pays: England
ID NLM: 7802871
Informations de publication
Date de publication:
13 06 2022
13 06 2022
Historique:
accepted:
26
08
2021
pubmed:
18
9
2021
medline:
15
6
2022
entrez:
17
9
2021
Statut:
ppublish
Résumé
Both parental and neighbourhood socio-economic status (SES) are linked to poorer health independently of personal SES measures, but the biological mechanisms are unclear. Our objective was to examine these influences via epigenetic age acceleration (EAA)-the discrepancy between chronological and epigenetic ages. We examined three USA-based [Coronary Artery Risk Disease in Adults (CARDIA) study, Fragile Families and Child Wellbeing Study (FFCWS) and Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS)] and one Mexico-based (Project Viva) cohort. DNA methylation was measured using Illumina arrays, personal/parental SES by questionnaire and neighbourhood disadvantage from geocoded address. In CARDIA, we examined the most strongly associated personal, parental and neighbourhood SES measures with EAA (Hannum's method) at study years 15 and 20 separately and combined using a generalized estimating equation (GEE) and compared with other EAA measures (Horvath's EAA, PhenoAge and GrimAge calculators, and DunedinPoAm). EAA was associated with paternal education in CARDIA [GEEs: βsome college = -1.01 years (-1.91, -0.11) and β<high school = 1.05 (0.09, 2.01) vs college graduates] and FFCWS [GEEs: β<high school = 0.62 (0.00, 1.24)]. We found stronger associations for some paternal education categories among White adults (for GEE, βsome college = -1.39 (-2.41, -0.38)], men (βsome college = -1.76 (-3.16, -0.35)] and women [β<high school = 1.77 (0.42, 3.11)]. These findings suggest that EAA captures epigenetic impacts of paternal education independently of personal SES later in life. Longitudinal studies should explore these associations at different life stages and link them to health outcomes. EAA could be a useful biomarker of SES-associated health and provide important insight into the pathogenesis and prevention of chronic disease.
Sections du résumé
BACKGROUND
Both parental and neighbourhood socio-economic status (SES) are linked to poorer health independently of personal SES measures, but the biological mechanisms are unclear. Our objective was to examine these influences via epigenetic age acceleration (EAA)-the discrepancy between chronological and epigenetic ages.
METHODS
We examined three USA-based [Coronary Artery Risk Disease in Adults (CARDIA) study, Fragile Families and Child Wellbeing Study (FFCWS) and Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS)] and one Mexico-based (Project Viva) cohort. DNA methylation was measured using Illumina arrays, personal/parental SES by questionnaire and neighbourhood disadvantage from geocoded address. In CARDIA, we examined the most strongly associated personal, parental and neighbourhood SES measures with EAA (Hannum's method) at study years 15 and 20 separately and combined using a generalized estimating equation (GEE) and compared with other EAA measures (Horvath's EAA, PhenoAge and GrimAge calculators, and DunedinPoAm).
RESULTS
EAA was associated with paternal education in CARDIA [GEEs: βsome college = -1.01 years (-1.91, -0.11) and β<high school = 1.05 (0.09, 2.01) vs college graduates] and FFCWS [GEEs: β<high school = 0.62 (0.00, 1.24)]. We found stronger associations for some paternal education categories among White adults (for GEE, βsome college = -1.39 (-2.41, -0.38)], men (βsome college = -1.76 (-3.16, -0.35)] and women [β<high school = 1.77 (0.42, 3.11)].
CONCLUSIONS
These findings suggest that EAA captures epigenetic impacts of paternal education independently of personal SES later in life. Longitudinal studies should explore these associations at different life stages and link them to health outcomes. EAA could be a useful biomarker of SES-associated health and provide important insight into the pathogenesis and prevention of chronic disease.
Identifiants
pubmed: 34534313
pii: 6371914
doi: 10.1093/ije/dyab196
pmc: PMC9189973
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
870-884Subventions
Organisme : NICHD NIH HHS
ID : R25 HD074544
Pays : United States
Organisme : NIMHD NIH HHS
ID : R01 MD011716
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES013744
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201800003I
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201800007I
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD076592
Pays : United States
Organisme : NIEHS NIH HHS
ID : K99 ES020346
Pays : United States
Organisme : NICHD NIH HHS
ID : P2C HD050924
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201800006I
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI102960
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201800004I
Pays : United States
Informations de copyright
© The Author(s) 2021; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
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