TY - JOUR PY - 2016// TI - Crack cocaine addiction, early life stress and accelerated cellular aging among women JO - Progress in neuro-psychopharmacology and biological psychiatry A1 - Levandowski, Mateus Luz A1 - Tractenberg, Saulo Gantes A1 - de Azeredo, Lucas Araújo A1 - De Nardi, Tatiana A1 - Rovaris, Diego Luiz A1 - Bau, Claiton H. D. A1 - Rizzo, Lucas B. A1 - Maurya, Pawan Kumar A1 - Brietzke, Elisa A1 - Tyrka, Audrey R. A1 - Grassi-Oliveira, Rodrigo SP - 83 EP - 89 VL - 71 IS - N2 - BACKGROUND: Early life stress (ELS) and addiction are related to age-related diseases and telomere shortening. However, the role of telomere length (TL) in crack cocaine addiction remains unknown. The purpose of this study was to investigate the TL in a sample of crack cocaine dependent-women who reported an ELS history and in a community-based sample of elderly women as a reference group for senescence.

METHODS: This study included treatment seeking crack cocaine dependents women (n=127) and elderly women without a psychiatric diagnosis (ELD, n=49). The crack cocaine sample was divided in two groups according to their Childhood Trauma Questionnaire (CTQ) scores: presence of history of childhood abuse and neglect (CRACK-ELS) and absence of ELS history (CRACK). TL was assessed by T/S ratio obtained from peripheral blood DNA using quantitative PCR assay.

RESULTS: CRACK and CRACK-ELS subjects exhibited shortened TL in comparison to the ELD group, despite their younger age. Among crack cocaine sample, CRACK-ELS group had significantly shorter telomeres than the CRACK group. Correlation analysis within crack cocaine group indicated that TL was negatively correlated with emotional abuse scores.

CONCLUSIONS: These results support previous findings associating telomere shortening with both ELS and drug addiction. This study suggests new evidence of a distinct biological phenotype for drug-dependent women with ELS. The results support the biological senescence hypothesis underpinning ELS experience.

Copyright © 2016. Published by Elsevier Inc.

Language: en

LA - en SN - 0278-5846 UR - http://dx.doi.org/10.1016/j.pnpbp.2016.06.009 ID - ref1 ER -