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Related Experiment Videos

Glucocorticoid "programming" and PTSD risk.

Jonathan R Seckl1, Michael J Meaney

  • 1Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK. J.Seckl@ed.ac.uk

Annals of the New York Academy of Sciences
|August 8, 2006
PubMed
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Adverse fetal environments, like excess glucocorticoids, can program adult health risks. These effects, including altered stress responses and potential intergenerational impacts, highlight critical developmental programming.

Area of Science:

  • Developmental biology
  • Endocrinology
  • Neuroscience

Background:

  • Epidemiological studies link adverse fetal environments to adult cardiovascular, metabolic, neuroendocrine, and psychiatric disorders.
  • Prenatal stress and/or glucocorticoid excess are implicated as underlying factors in these developmental links.
  • Animal models demonstrate that prenatal stress or glucocorticoid exposure impacts birth weight, HPA axis activity, and behavior.

Purpose of the Study:

  • To investigate the link between adverse fetal environments, specifically glucocorticoid exposure, and long-term health outcomes in offspring.
  • To explore the role of 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD-2) in mediating these effects.
  • To examine potential intergenerational transmission of these programming effects.

Main Methods:

Related Experiment Videos

  • Review of epidemiological data and animal model studies.
  • Analysis of human studies on 11 beta-HSD-2 gene mutations and placental activity.
  • Examination of the impact of maternal stress, including PTSD, on offspring HPA axis and associated disorders.

Main Results:

  • Prenatal glucocorticoid excess or stress in animal models reduces birth weight and causes permanent hypertension, hyperglycemia, and anxiety-like behaviors.
  • In humans, low placental 11 beta-HSD-2 activity correlates with low birth weight and higher infant blood pressure, indicating HPA axis programming.
  • Maternal stress during pregnancy affects offspring HPA axis, with potential links to neuropsychiatric disorders and possible epigenetic transmission to subsequent generations.

Conclusions:

  • Prenatal exposure to excess glucocorticoids programs peripheral and central nervous system functions, predisposing to adult pathologies.
  • The enzyme 11 beta-HSD-2 plays a crucial role as a feto-placental barrier against maternal glucocorticoids.
  • Programming effects may be transmitted across generations, suggesting a role for epigenetic mechanisms.