The fear-defense system, emotions, and oxidative stress

Abstract

Psychosocial stress has a profound impact on well-being and health. The response to stress is associated mainly with the amygdala, a crucial structure of the fear-defense system, essential for social cognition and emotion regulation. Recent neuroimaging-studies demonstrated how an increased metabolic activity of the amygdala enhances inflammation, and leads to cardiometabolic disease. The development of therapeutic strategies depends on our understanding of both which factors activate the fear-defense system and the subsequent molecular mechanisms that translate emotional stress into cell damage. Fear of emotions as an aftermath of attachment trauma is the most important trigger of the maladaptive activation of the fear-defense system. The central molecular pathways are enhanced myelopoiesis and upregulated proinflammatory gene expression, glucocorticoid and insulin resistance, and oxidative stress. Therapeutic strategies may benefit from holistic approaches. Psychotherapy can reduce the maladaptively increased activation of the fear-defense system. Biological interventions can buffer the detrimental effects of oxidative stress in the organism.

Oxidative Dysregulation in Early Life Stress and Posttraumatic Stress Disorder: A Comprehensive Review

“…Lately, there has been an exponential knowledge growth concerning the effect of traumatic stress on oxidative components and redox-state homeostasis [20][21][22]. The neurobiological substrates of the redox system become activated under conditions of severe and chronic stress with excessive production of oxidative stress (OXS) and/or inadequacy of the organism's antioxidant capacity [23]. In this process, mitochondria become dysfunctional, and vital constituents of the cell such as protein, lipids, DNA end up degraded, finally leading the cell to an apoptotic state.…”

Novel Insights Into Molecular Mechanism of Mitochondria in Diabetic Cardiomyopathy

“…In the physiological state, only a very small amount of oxygen is reduced to ROS by single electron reduction ( Ghaemi Kerahrodi and Michal, 2020 ; Scialò et al, 2020 ). However, in diabetes, due to changes, such as high glucose, high lipid, insulin resistance, calcium signal disorder, and enhanced mitochondrial uncoupling, more nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) would flow to mitochondrial respiratory chain, causing hyperpolarization of the mitochondrial inner membrane, suppression of electron transfer in complex III, and excessive generation of ROS ( Shah and Brownlee, 2016 ; Zhang et al, 2020 ).…”

Stress und Psychobiologie bei kardiovaskulären Erkrankungen

“…Akuter emotionaler Stress (TSST) führt zu signifikanter oxidativer DNA-Schädigung, die im Zusammenhang mit dem individuellen 10-Jahres-Herzinfarktrisiko steht [11]. Als einer der zentralen molekularen Mechanismus für den Zusammenhang zwischen emotionalem Stress und kardiovaskulärer Zellschädigung wurde oxidativer Stress identifiziert [12].…”