Neurobiology of Early Life Stress in Women

Abstract

Early life stress can have lasting effects on neurobiology and cognition in women that can lead to an array of negative physical and mental health outcomes. Early life stress can lead to chronic posttraumatic stress disorder (PTSD) in adulthood, as well as other mental health disorders like depression and substance abuse. In addition, changes in neurobiology, acting either directly or through associated mental disorders, can have an effect on physical health function. One area that is infl uenced by stress-induced changes in neurobiology and that is a focus of this chapter is cardiovascular disease. Lasting changes in stress-responsive neurohormonal systems, including the hypothalamic-pituitary-adrenal (HPA) axis and noradrenergic systems, are associated with exposure to chronic stress. Childhood abuse also has long-term effects on brain areas involved in memory and emotion, including the hippocampus, amygdala, and medial prefrontal cortex. These brain areas have outputs to peripheral sympathetic and hormonal systems that activate the cardiovascular response to stress. We review in this chapter mechanisms by which early life stress affects neurobiology and in turn can have a deleterious effect on cardiovascular disease outcomes for women in adulthood. Keywords The Effects of Early Life Stress on WomenEarly life stress can have lasting effects on cognitive and neurobiological function in women. As many as one in fi ve or more girls are affected by some form of childhood abuse, whether sexual, physical, or emotional abuse (MacMillan et al. 1997 ;

Behavioral, emotional and neurobiological determinants of coronary heart disease risk in women

“…Studies in women with early life stress and stress-spectrum disorders like depression and PTSD have corroborated the changes in brain and neurobiology found in preclinical studies (Bremner, 2005; Bremner and Vaccarino, 2015). Girls with early life stress with associated PTSD and/or depression show increased cortisol levels and/or blunted ACTH response to CRF (which indicates down-regulation due to chronic hypercortisolemia) (Cicchetti and Rogosch, 2001; De Bellis et al, 1994, 1999; Gunnar et al, 2001) as well as increased cortisol response to stress (Luby et al, 2003).…”

“…Girls with early life stress with associated PTSD and/or depression show increased cortisol levels and/or blunted ACTH response to CRF (which indicates down-regulation due to chronic hypercortisolemia) (Cicchetti and Rogosch, 2001; De Bellis et al, 1994, 1999; Gunnar et al, 2001) as well as increased cortisol response to stress (Luby et al, 2003). Notably, these changes in neurobiology persist into adulthood especially if there is PTSD (Bremner, 2005; Bremner et al, 2008; Bremner and Vaccarino, 2015). Women with PTSD secondary to childhood sexual abuse show decreased baseline cortisol based on 24-hour diurnal assessments, with flattening of the normal diurnal cortisol curve and increased pulsatility of cortisol reflecting dysregulation of CRF release (Bremner et al, 2007a).…”

Chronic corticosterone administration in adolescence enhances dorsolateral striatum-dependent learning in adulthood

“…Therefore, ELS-induced changes to memory systems that lead to 10.3389/fnbeh.2022.970304 enhanced habit memory in adulthood may partially account for the habit-like symptoms observed in these adult psychiatric disorders (e.g., avoidance symptoms in PTSD, drug-seeking and relapse, compulsive behaviors, repetitive and stereotyped behaviors, etc.). It is important to emphasize that ELS has a dramatic impact on multiple brain areas and circuits that may be related to adult psychopathology (Gutman and Nemeroff, 2002;Heim and Nemeroff, 2002;Bremner and Vaccarino, 2015;Agorastos et al, 2019;Kirsch et al, 2020), and enhanced DLS habit memory represents only one of the many neurobehavioral outcomes of ELS. Nevertheless, considering how ELS-induced enhancements of habit memory could critically explain some of the hallmark features of adult human psychopathology, this effect and its underlying mechanisms warrant further investigation in future research.…”