Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY 10032, USA; Robert N Butler Columbia Aging Center, Columbia University Mailman School of Public Health, New York, NY 10032, USA.
Psychology Department, John Jay College, City University of New York, New York, USA; Graduate Center, City University of New York, New York, USA.
Psychoneuroendocrinology. 2022 Sep;143:105848. doi: 10.1016/j.psyneuen.2022.105848. Epub 2022 Jun 22.
Childhood adversity has been linked to many indicators of shorter healthy lifespan, including earlier onset of disease and disability as well as early mortality. These observations suggest the hypothesis that childhood maltreatment may accelerate aging.
To characterize the relationship between childhood maltreatment and accelerated biological aging in a prospective cohort of 357 individuals with documented cases of childhood maltreatment and 250 controls matched on demographic and socioeconomic factors.
Cases were drawn from juvenile and adult court records from the years 1967 through 1971 in a large Midwest metropolitan geographic area. Cases were defined as having court-substantiated cases of childhood physical or sexual abuse, or neglect occurring at age 11 or younger. Controls were selected from the same schools and hospitals of birth and matched on age, sex, race, and approximate socioeconomic status. We compared biological aging in these two groups using two blood-chemistry algorithms, the Klemera-Doubal method Biological Age (KDM BA) and the PhenoAge. Algorithms were developed and validated in data from the National Health and Nutrition Examination Surveys (NHANES) using published methods and publicly available software.
Participants (55% women, 49% non-White) had mean age of 41 years (SD=4). Those with court substantiated childhood maltreatment history exhibited more advanced biological aging as compared with matched controls, although this difference was statistically different for only the KDM BA measure (KDM BA Cohen's D=0.20, 95% CI=[0.03,0.36], p = 0.02; PhenoAge Cohen's D=0.09 95% CI=[-0.08,0.25], p = 0.296). In subgroup analyses, maltreatment effect sizes were larger for women as compared to men and for White participants as compared to non-White participants, although these differences were not statistically significant at the α= 0.05 level.
As of midlife, effects of childhood maltreatment on biological aging are small in magnitude but discernible. Interventions to treat psychological and behavioral sequelae of exposure to childhood maltreatment, including in midlife adults, have potential to protect survivors from excess burden of disease, disability, and mortality in later life.
童年逆境与许多健康寿命较短的指标有关，包括疾病和残疾的更早发作以及早逝。这些观察结果表明，童年期虐待可能会加速衰老。
在一个有记录的童年期虐待病例的 357 名个体和 250 名在人口统计学和社会经济因素上相匹配的对照组的前瞻性队列中，描述童年期虐待与加速生物学衰老之间的关系。
病例来自于中西部大城市地区 1967 年至 1971 年期间的少年和成人法庭记录。病例被定义为有法庭证实的 11 岁或以下的童年期身体或性虐待或忽视案件。对照组从同一学校和出生医院中选择，并按年龄、性别、种族和大致社会经济地位相匹配。我们使用两种血液化学算法 Klemera-Doubal 生物学年龄（KDM BA）和 PhenoAge 比较这两组的生物学衰老。算法是根据使用已发表方法和公开可用软件的国家健康和营养检查调查（NHANES）数据开发和验证的。
参与者（55%为女性，49%为非白人）的平均年龄为 41 岁（SD=4）。与匹配对照组相比，有法庭证实的童年期虐待史的人表现出更先进的生物学衰老，尽管这一差异仅在 KDM BA 测量上具有统计学意义（KDM BA Cohen's D=0.20，95%CI=[0.03，0.36]，p=0.02；PhenoAge Cohen's D=0.09，95%CI=[-0.08，0.25]，p=0.296）。在亚组分析中，与男性相比，女性的虐待效应大小更大，与非白人参与者相比，白人参与者的效应大小更大，但这些差异在α=0.05 水平上没有统计学意义。
截至中年，童年期虐待对生物学衰老的影响在数量上很小，但可以察觉。干预治疗接触童年期虐待的心理和行为后果，包括中年成年人，有可能保护幸存者免受晚年过度疾病、残疾和死亡的负担。
