People with childhood trauma are likely to be aging faster by mid life

Embargoed until: Publicly released: 2023-06-13 01:00

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People with childhood trauma are likely to have a higher biological age than their peers by mid-life, according to international research. Your biological or epigenetic age can be different to your chronological age, which can impact the development of health problems experienced by older people. The researchers tested DNA from the blood of nearly 900 participants, mostly in their 40s, and compared the amount of adverse events like violence, neglect, emotional abuse and household drug abuse the participants had experienced as children. They say those with four or more adverse childhood events were likely to have older biological ages regardless of their socioeconomic status.

Media release

From: JAMA

About The Study: Adverse childhood experiences were associated with epigenetic age acceleration, a biomarker associated with various health outcomes in middle-age adults, after controlling for demographics, behavior, and socioeconomic status. These findings of the associations between early life experience and the biological aging process in midlife may contribute to health promotion in a life course perspective.

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Journal/
conference: JAMA Network Open

Research:Paper

Organisation/s: Northwestern University Feinberg School of Medicine, USA

Funder: The Coronary Artery Risk Development in Young Adults Study (CARDIA) was conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the University of Alabama at Birmingham, Northwestern University, University of Minnesota, and Kaiser Foundation Research Institute, with grants HHSN268201800005I and HHSN268201800007I to the University of Alabama at Birmingham, HHSN268201800003I to Northwestern University, HHSN268201800006I to the University of Minnesota, and HHSN268201800004I to the Kaiser Foundation Research Institute from the NHLBI. CARDIA was also partially supported by the Intramural Research Program of the National Institute on Aging (NIA) and intraagency agreement AG0005 between the NIA and NHLBI. Laboratory work and analytical components were funded by grants 17SFRN33700278 and 14SFRN20790000 from the American Heart Association to Northwestern University, with principal investigator Dr Hou. Research reported in this publication was partially supported by grants R01AG081244 to Drs Hou, Zhang, and Liu and R01AG069120 to Dr Hou from the NIA and K23HL145101 to Dr Perak and K08HL159350 to Dr Nagata from the NHLBI.

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