Childhood adversities are associated with shorter leukocyte telomere length at adult age in a population-based study.


Journal

Psychoneuroendocrinology
ISSN: 1873-3360
Titre abrégé: Psychoneuroendocrinology
Pays: England
ID NLM: 7612148

Informations de publication

Date de publication:
08 2021
Historique:
received: 07 02 2021
revised: 20 04 2021
accepted: 16 05 2021
pubmed: 30 5 2021
medline: 19 2 2022
entrez: 29 5 2021
Statut: ppublish

Résumé

Telomeres are repeat sequences and an associated protein complex located at the end of the chromosomes. They shorten with every cell division and are regarded markers for cellular aging. Shorter leukocyte telomere length (LTL) has been observed in many complex diseases, including psychiatric disorders. However, analyses focusing on psychiatric disorders are mainly based on clinical samples and the significance of shorter LTL on the population level remains uncertain. We addressed this question in a population-based sample from Finland (N = 7142). The survey was performed and the blood samples were collected in 2000-2001 to assess major public health problems and their determinants. DSM-IV diagnoses of major psychiatric illnesses were obtained by interview using the Composite International Diagnostic Interview. Information regarding their risk factors, including the number of self-reported childhood adversities, recent psychological distress, and sleep difficulties was collected by questionnaires. LTL was measured by qPCR. None of the studied psychiatric illnesses, sleep difficulties, or recent psychological distress associated with LTL. However, individuals with three or more childhood adversities had shorter LTL at adult age (β = -0.006, P = 0.005). Also, current occupational status was associated with LTL (β = -0.03, P = 0.04). These effects remained significant after adjusting for known LTL-associated lifestyle or sociodemographic factors. In conclusion, relatively common childhood adversities were associated with shorter LTL at adult age in a nationally representative population-based cohort, implying that childhood adversities may cause accelerated telomere shortening. Our finding has potentially important implications as it supports the view that childhood adversities have an impact on psychological and somatic well-being later in life.

Identifiants

pubmed: 34051657
pii: S0306-4530(21)00150-5
doi: 10.1016/j.psyneuen.2021.105276
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

105276

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

Antti-Jussi Ämmälä (AJ)

Department of Genetics and Biomarkers, National Institute for Health and Welfare, Mannerheimintie 166, P.O. 30, 00271 Helsinki, Finland; Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. Electronic address: antti-jussi.ammala@helsinki.fi.

Jaana Suvisaari (J)

Mental Health and Substance Abuse Services, National Institute for Health and Welfare, Helsinki, Finland.

Laura Kananen (L)

Faculty of Medicine and Health Technology (MET), Tampere University, Tampere, Finland; Gerontology Research Center (GEREC), Finland; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Research Programs Unit, Molecular Neurology, Biomedicum-Helsinki, University of Helsinki, Finland.

Jouko Lönnqvist (J)

Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Mental Health and Substance Abuse Services, National Institute for Health and Welfare, Helsinki, Finland.

Samuli Ripatti (S)

Center of Excellence in Complex Disease Genetics, Institute of Molecular Medicine Finland (FIMM), University of Helsinki, Finland; Faculty of Medicine, University of Helsinki, Finland; Broad Institute of MIT and Harvard, Finland.

Sami Pirkola (S)

Faculty of Social Sciences, Tampere University, Tampere, Finland; Department of Adult Psychiatry, Tampere University Hospital, Pirkanmaa Hospital District, Tampere, Finland.

Tiina Paunio (T)

Department of Genetics and Biomarkers, National Institute for Health and Welfare, Mannerheimintie 166, P.O. 30, 00271 Helsinki, Finland; Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; SleepWell Research Program, Faculty of Medicine, University of Helsinki, P.O. Box 21, 00014, Finland.

Iiris Hovatta (I)

Research Programs Unit, Molecular Neurology, Biomedicum-Helsinki, University of Helsinki, Finland; SleepWell Research Program, Faculty of Medicine, University of Helsinki, P.O. Box 21, 00014, Finland; Department of Psychology and Logopedics, University of Helsinki, Finland; Neuroscience Center, Helsinki Institute of Life Science HiLIFE, University of Helsinki, Finland. Electronic address: iiris.hovatta@helsinki.fi.

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