Authors
Mariana Rodrigues, Adolfo G Cuevas, Alisha A Crump, Zoe Lindenfeld, Saba Rouhani, Jemar R Bather
Published in
Neuroscience and biobehavioral reviews. Pages 106942. Sep 03, 2026. Epub Sep 03, 2026.
Abstract
Contact with the criminal legal system (CLS) is a prevalent and socially patterned exposure in the United States (U.S.) with well-documented health consequences. Growing research suggests that CLS contact may be associated with biological aging, but evidence remains variable across biomarker domains, forms of exposure, and study designs. This systematic review synthesized literature on CLS contact and biomarkers relevant to biological aging in the U.S.
We systematically searched seven electronic databases and Google Scholar. Eligible studies examined direct or vicarious CLS contact in relation to at least one biomarker domain relevant to biological aging, including epigenetic measures, telomere length, inflammatory markers, or allostatic load. Retrieved references were imported into Covidence for deduplication and screening. Data were extracted using a standardized form and evidence quality was assessed using an adapted Newcastle-Ottawa Scale.
Twenty-two studies met inclusion criteria. Sixteen studies (72.7%) reported findings consistent with accelerated biological aging in association to CLS contact. The most consistent evidence was observed for epigenetic outcomes, with all seven studies reporting significant accelerated epigenetic aging in association with CLS contact. Evidence for inflammatory markers, allostatic load, and telomere length were less consistent, although several studies linked CLS contact with elevated inflammation, greater multisystem physiological dysregulation, and shorter telomere length. Associations varied by form of CLS contact, timing, and context, including violence during incarceration and racialized exposure to policing.
CLS contact may be associated with multiple biological systems relevant to biological aging. More research is needed to clarify temporality, heterogeneity, and underlying pathways.
PMID:
42692381
Bibliographic data and abstract were imported from PubMed on 04 Sep 2026.
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