Hypothalamic-Pituitary-Adrenal axis dysfunction by early life stress

Neurosci Lett. 2021 Aug 10:759:136037. doi: 10.1016/j.neulet.2021.136037. Epub 2021 Jun 8.

Abstract

Evidence indicates that early life stress (ELS) may act as a risk factor for the development and maintenance of adulthood severe mental health disorders due to persistent dysregulation within the hypothalamic-pituitary-adrenal (HPA) axis. It is now broadly accepted that psychological stress may change the internal homeostatic state of an individual. The dysregulation seems to be a byproduct of changes noted in the HPA axis hormone's ability to bind to the glucocorticoid and mineralocorticoid receptors, crucial in maintaining homeostasis. Whenever there is an acute interruption of this balance, illness may result. The social and physical environments have an enormous impact on our physiology and behavior, and they influence the process of adaptation or 'allostasis'. The HPA axis response to stress can be thought of as a mirror of the organism's response to stress: acute responses are generally adaptive, but excessive or prolonged responses can lead to deleterious effects. Evidence indicates that early-life stress can induce persistent changes in the ability of the HPA axis to respond to stress in adulthood This review aims to examine and summarise the existing literature exploring the relationship between ELS with regards specifically to HPA axis functioning. The maintenance of the internal homeostatic state of an individual is proposed to be based on the ability of circulating glucocorticoids to exert negative feedback on the secretion of HPA hormones through binding to mineralocorticoid (MR) and glucocorticoid (GR) receptors limiting the vulnerability to diseases related to psychological stress in genetically predisposed individuals.

Keywords: Corticosteroid; Early life stress; Glucocorticoid receptor; Hypothalamic-Pituitary-Adrenal axis; Mineralocorticoid receptor; Stress.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adverse Childhood Experiences*
  • Animals
  • Humans
  • Hypothalamo-Hypophyseal System / physiopathology*