Early-Life Stress: From Neuroendocrine Mechanisms to Stress-Related Disorders

Horm Res Paediatr. 2018;89(5):372-379. doi: 10.1159/000488468. Epub 2018 Jun 8.

Abstract

Stress exposure is highly prevalent in the general population; however, the experience of stress during vulnerable periods of development has substantial and permanent effects on brain structure and function and physical health in adulthood. Stress, the state of threatened homeostasis, is generally associated with a time-limited activation of the stress system, i.e., the hypothalamic-pituitary-adrenal axis and the arousal/sympathetic nervous system, tailored to the stressful stimulus also known as the stressor. On the other hand, chronic stress may be associated with lingering hyper- or hyposecretion of mediators of the stress system. This chronic condition is called dyshomeostasis, allostasis, or cacostasis and is associated with increased mental and physical morbidity in the long term. Stressful or traumatic experiences during fetal life, early childhood, and adolescence have been related to persistent neuroendocrine and epigenetic changes. Further, brain structures involved in the stress response, such as those of the stress system, the hippocampus, and the amygdala, may be programmed early on for a life of adversity.

Keywords: Allostasis; Catecholamines; Children; Cortisol; Early-life stress.

Publication types

  • Review

MeSH terms

  • Adolescent
  • Child
  • Child, Preschool
  • Chronic Disease
  • Endocrine System Diseases* / etiology
  • Endocrine System Diseases* / metabolism
  • Endocrine System Diseases* / pathology
  • Female
  • Humans
  • Hypothalamo-Hypophyseal System* / metabolism
  • Hypothalamo-Hypophyseal System* / pathology
  • Infant
  • Infant, Newborn
  • Male
  • Pituitary-Adrenal System* / pathology
  • Pregnancy
  • Prenatal Exposure Delayed Effects* / metabolism
  • Prenatal Exposure Delayed Effects* / pathology
  • Stress, Psychological* / complications
  • Stress, Psychological* / metabolism
  • Stress, Psychological* / pathology