Cited by 163Stress Responses and CortisolChild Abuse and TraumaBirth, Development, and Health

Timing matters: long term effects of adversities from prenatal period up to adolescence on adolescents' cortisol stress response. The TRAILS study

Open access
Bosch, Nienke M., Riese, Harriëtte, Reijneveld, Sijmen A., Bakker, Martin P., Verhulst, Frank C., Ormel, Johan, Oldehinkel, Albertine J.·2012·Psychoneuroendocrinology

Abstract

OBJECTIVE: Altered cortisol response is a vulnerability marker for a variety of stress-related diseases and psychiatric disorders. Childhood adversity has been shown to modify this response, but evidence is inconsistent. Effects may differ depending on the timing of exposure, or due to the interplay between pre/postnatal adversity and later adversities. The present study examined the influence of adversity during different timeframes (pre/postnatal, ages 0-5, 6-11, 12-13, 14-15 years), and the interaction between pre/postnatal and later adversity on adolescents' cortisol stress response. METHOD: Four salivary cortisol samples were collected before and after a social stress test in 471 16-year-old adolescents from the longitudinal study TRAILS. Data on pre/postnatal exposure to adversities were obtained from Preventive Child Healthcare records and parental reports, subsequent adversities from parental and self-reports. RESULTS: Pre/postnatal adversity was associated with increased cortisol reactivity. Adversities during ages 0-5 were not associated with cortisol outcomes. Adversities during ages 6-11 were associated with a high cortisol level, especially in those exposed to pre/postnatal adversity, while adversities during ages 12-13 and 14-15 were associated with a low cortisol level. CONCLUSIONS: Results highlight the importance to take the timing of stress exposure into account. In addition to programming effects, pre/postnatal adversity interacts with childhood adversity in producing deviant cortisol levels. Puberty may be marked by a transition in how adversities affect the HPA-axis, with cortisol hypersecretion before age 11 and hyposecretion after age 11.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.psyneuen.2012.01.013

Cites

42 of 42 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • ELS/CT in the first year of life, but not late childhood or adolescence, is related to higher cortisol reactivity in adult life.

    “Bosch et al. (125) confirmed this hypothesis showing a relation between ELS/CT in the first year of life, but not late childhood or adolescence, and higher cortisol reactivity in adult life.”

    From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [125]

    The Discussion and Figure 1 report higher cortisol reactivity after pre/postnatal adversity, but the response was measured in adolescents aged 16, not in adult life. The Discussion also reports no effect of childhood or adolescent adversity on cortisol reactivity. The exposure measure includes prenatal events and events shortly after birth, so it does not isolate adversity in the first year of life. (LLM, conf=0.90)

    Experimental — accuracy not yet measured
  • ELS/CT during childhood is associated with higher adult cortisol levels, while ELS/CT during adolescence is associated with lower cortisol output.

    “They could also show higher adult cortisol levels after ELS/CT experience during childhood, but lower cortisol output after experience of ELS/CT in adolescence.”

    From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [125]

    The Results (section 3.2) report higher overall cortisol after adversity at ages 6–11 and lower overall cortisol after adversity at ages 12–13 or chronic stress at ages 14–15. But cortisol was measured in 16-year-old adolescents, not adults, and the paper found no cortisol association for adversity at ages 0–5. The claim therefore overextends the findings to adult cortisol levels and childhood generally. (LLM, conf=0.89)

    Experimental — accuracy not yet measured
  • Alterations to the HPA axis functioning have been observed in humans exposed to childhood adversity, although variation in the timing, duration and type of adversity have led to differences in strength and direction of response.

    “Alterations to the HPA axis functioning have also been observed in humans exposed to childhood adversity, although variation in the timing, duration and type of adversity have led to differences in strength and direction of response (Nemeroff 2004; Bosch et al. 2012; McCrory et al. 2012).”

    From Childhood adversity, adult stress, and the risk of major depression or generalized anxiety disorder in US soldiers: a test of the stress sensitization hypothesis (2017) · cites this paper as Bosch et al. 2012

    The Introduction (section 1; page unavailable) reports altered HPA-axis reactivity after early-life stress, with variability in its degree and direction. The Results (section 3.2; page unavailable) link adversity at different ages, including chronic stress in middle adolescence, to different cortisol patterns. The passages support timing and address duration, but do not establish that differences in the type of adversity account for the variation claimed. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Bosch, N. M., Riese, H., Reijneveld, S. A., Bakker, M. P., Verhulst, F. C., Ormel, J., & Oldehinkel, A. J.
Affiliations
  • University Medical Center Groningen (NL)
  • Erasmus MC (NL)
Corresponding author
Bosch, Nienke M.
Venue
Psychoneuroendocrinology
Publisher
Elsevier BV
Published
2012-09
Volume
37
Issue
9
Pages
1439-1447
ISSN
0306-4530 (ISSN-L)
OpenAlex
W2047498990
Cited by
163
References
42
Citations by year
2026: 2 · 2025: 9 · 2024: 8 · 2023: 6 · 2022: 9 · 2021: 13 · 2020: 14 · 2019: 13 · 2018: 10 · 2017: 9 · 2016: 23 · 2015: 20 · 2014: 14 · 2013: 8 · 2012: 5
FWCI
6.24
Type
journal article
Language
en
Open access
Locations
  • Psychoneuroendocrinology (publishedVersion, other-oa)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
  • EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Keywords
cortisol stress response, childhood adversity, prenatal adversity, hypothalamic-pituitary-adrenal axis, adolescents, puberty, cortisol response, salivary cortisol, TRAILS study, developmental programming
MeSH terms
Adolescent, Child, Child, Preschool, Female, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Infant, Infant, Newborn, Life Change Events, Longitudinal Studies, Male, Pituitary-Adrenal System, Pregnancy, Prenatal Exposure Delayed Effects, Saliva, Stress, Psychological

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review