Family-centered prevention ameliorates the longitudinal association between risky family processes and epigenetic aging

被引:106
作者
Brody, Gene H. [1 ]
Yu, Tianyi [1 ]
Chen, Edith [2 ,3 ]
Beach, Steven R. H. [4 ]
Miller, Gregory E. [2 ]
机构
[1] Univ Georgia, Ctr Family Res, 1095 Coll Stn Rd, Athens, GA 30602 USA
[2] Northwestern Univ, Dept Psychol, Evanston, IL USA
[3] Northwestern Univ, Dept Med Social Sci, Evanston, IL USA
[4] Univ Georgia, Owens Inst Behav Res, Athens, GA 30602 USA
关键词
Depression; epigenetics; epigenetic clock; health; intervention; parenting; prevention; DNA METHYLATION AGE; DEPRESSION; CHILDHOOD; STRESS; HEALTH; WOMEN; PREVALENCE; POSTPARTUM; DISEASES; LIFE;
D O I
10.1111/jcpp.12495
中图分类号
B844 [发展心理学(人类心理学)];
学科分类号
040202 ;
摘要
Background: Research has suggested that 'risky' family processes have unforeseen negative consequences for health later in life. The purpose of this study was to further understanding of risky family environments and development of health vulnerabilities by (a) examining the likelihood that elevated levels of parental depressive symptoms when children are age 11 forecast accelerated epigenetic aging 9 years later at age 20; (b) determining whether participation in an efficacious family-centered prevention program focused on enhancing supportive parenting and strengthening family relationships will ameliorate this association; and (c) testing a moderation-mediation hypothesis that prevention-induced reductions in harsh parenting across adolescence will account for prevention effects in reducing accelerated epigenetic aging. Methods: In the rural southeastern United States, parents and 11-year-old children from 399 families participated in the Strong African American Families (SAAF) program or a control condition. Parents reported their own depressive symptoms when their children were 11, and both youths and parents reported youth exposure to harsh parenting at ages 11 and 16. Blood was drawn from youths at age 20 to measure accelerated epigenetic aging using a marker derived from the DNA methylation of cells. Results: Elevated parental depressive symptoms forecast accelerated epigenetic aging among youths in the control condition, but not among SAAF participants. Moderated-mediation analyses confirmed that reductions in harsh parenting accounted for SAAF's protective effects on epigenetic aging. Subsequent exploratory analyses indicated that accelerated epigenetic aging forecast emotional distress among young adults in the control condition but not among those who participated in SAAF. Conclusions: This study is unique in using a randomized prevention trial to test hypotheses about the ways risky family processes contribute to accelerated epigenetic aging. The results suggest that developmentally appropriate family-centered interventions designed to enhance parenting and strengthen families can buffer the biological residue of life in a risky family.
引用
收藏
页码:566 / 574
页数:9
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