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J Epidemiol Community Health 2008;62:e5 doi:10.1136/jech.2007.060350
  • Research report
    • Electronic pages

Chernobyl exposure as stressor during pregnancy and hormone levels in adolescent offspring

  1. A C Huizink1,
  2. M Bartels2,
  3. R J Rose3,6,
  4. L Pulkkinen4,
  5. C J P Eriksson5,
  6. J Kaprio5,6
  1. 1
    Department of Child and Adolescent Psychiatry, Erasmus Medical Center, Rotterdam, The Netherlands
  2. 2
    Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands
  3. 3
    Department of Psychology, Indiana University, Bloomington, Indiana, USA
  4. 4
    Department of Psychology, University of Jyväskylä, Finland
  5. 5
    Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland
  6. 6
    Department of Public Health, University of Helsinki, Finland
  1. Anja C Huizink, Erasmus Medical Center Rotterdam/Sophia Children’s Hospital, Department of Child and Adolescent Psychiatry, PO Box 2060, 3000 CB Rotterdam, The Netherlands; a.c.huizink{at}erasmusmc.nl
  • Accepted 23 October 2007

Abstract

Background: Animal research suggests a programming effect of prenatal stress in the fetal period, resulting in disruptions in behavioural and neuromotor development. Physiological changes that mediate these effects include alterations in the hypothalamic-pituitary-adrenal axis and in testosterone levels. This human study focuses on changes related to these physiological systems after prenatal stress exposure.

Methods: We examined the potential effect of prenatal stress associated with the Chernobyl disaster in an ongoing genetic epidemiological study in Finland. One birth cohort of twins (n = 121 twin pairs) was exposed in utero to maternal stress, and their saliva cortisol and testosterone levels at age 14 were compared with twins (n = 157 twin pairs) born one year later.

Results: Cortisol levels in both sexes and testosterone levels among females were significantly elevated after prenatal exposure to maternal stress from the second trimester onwards, compared to reference groups of non-exposed adolescents. Exposure explains 3% of variance (p<0.05) in cortisol levels and 18% of variance in testosterone levels (p<0.001). No significant differences were found for exposure from either first or third trimester onwards.

Conclusion: Our results suggest that prenatal exposure to maternal stress in the second trimester of pregnancy may have resulted in prenatal programming of physiological systems relating to cortisol and testosterone levels.

Footnotes

  • Funding: Data collection in the FinnTwin12 study has been supported by the National Institute on Alcohol Abuse and Alcoholism (grants R01 AA-09203 and R37 AA-12502) to RJR and by awards from the Academy of Finland (grant 100499, 204690, 205585) to JK. Data analysis was also part of the GENOMEUTWIN project, which is supported by the European Union Contract No QLG2-CT-2002-01254, and was financially supported by the Exchange Programme of ZonMW in The Netherlands and the Finnish Research Council for Medicine (grant 20-00413-98-04-004 to ACH). JK is supported by the Academy of Finland Centre of Excellence in Complex Disease Genetics.

  • Competing interests: None.

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