Associations between exposure to adverse childhood experiences and biological aging: Evidence from the Canadian Longitudinal Study on Aging

被引:13
作者
Mian, Oxana [1 ]
Belsky, Daniel W. [3 ,9 ]
Cohen, Alan A. [4 ]
Anderson, Laura N. [2 ]
Gonzalez, Andrea [5 ]
Ma, Jinhui [2 ]
Sloboda, Deborah M. [6 ]
Bowdish, Dawn Me [7 ,10 ,11 ]
Verschoor, Chris P. [1 ,2 ,8 ]
机构
[1] Hlth Sci North Res Inst, 41 Ramsey Lake Rd,Rm 32033, Sudbury, ON P3E 5J1, Canada
[2] McMaster Univ, Dept Hlth Res Methods Evidence & Impact, Hamilton, ON, Canada
[3] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10027 USA
[4] Univ Sherbrooke, Dept Family Med, Grp Rech PRIMUS, Sherbrooke, PQ, Canada
[5] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada
[6] McMaster Univ, Farncombe Family Digest Hlth Res Inst, Dept Biochem & Biomed Sci, Pediat & Obstet & Gynecol, Hamilton, ON, Canada
[7] McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada
[8] Northern Ontario Sch Med Univ, Sudbury, ON, Canada
[9] Columbia Univ, Robert N Butler Columbia Aging Ctr, New York, NY 10027 USA
[10] St Josephs Healthcare, Firestone Inst Resp Hlth, Hamilton, ON, Canada
[11] McMaster Univ, Hamilton, ON, Canada
基金
加拿大创新基金会; 加拿大健康研究院;
关键词
Childhood maltreatment; Klemera-Doubal; Phenotypic age; Homeostatic dysregulation; CLSA; EARLY-LIFE ADVERSITY; AGE; MORTALITY; NEGLECT; HEALTH; SPAN; RISK;
D O I
10.1016/j.psyneuen.2022.105821
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
People exposed to adverse childhood experiences (ACEs) suffer from an increased risk of chronic disease and shorter lifespan. These individuals also tend to exhibit accelerated reproductive development and show signs of advanced cellular aging as early as childhood. These observations suggest that ACEs may accelerate biological processes of aging through direct or indirect mechanisms; however, few population-based studies have data to test this hypothesis. We analysed ACEs and biological aging data from the Canadian Longitudinal Study on Aging (CLSA; n = 23,354 adults aged 45-85) and used the BioAge R package to compute three indices of biological aging from blood-chemistry and organ-function data: Klemera-Doubal method (KDM) biological age, phenotypic age (PA), and homeostatic dysregulation (HD). Adults with ACEs tended to be biologically older than those with no ACEs, although the observed effect-sizes were small (Cohen's d<0.15), with the exception of neglect (d=0.35 for KDM and PA). Associations were similar for men and women and tended to be smaller for older as compared to midlife participants. Subtypes of ACEs perceived as being more severe (e.g., being pushed or kicked, experiencing forced sexual activity, witnessing physical violence) and more frequent and diverse exposures were associated with relatively larger effect-sizes. These findings support the hypothesis that ACEs contribute to accelerated biological aging, although replication is needed in studies with access to prospective records of ACEs and cellular-level measurements of biological aging. Furthermore, future work to better understand the degree to which associations between ACEs and biological aging are moderated by specific life-course pathways, and mediated by lifestyle and socioeconomic factors is warranted.
引用
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页数:7
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