Protective and damaging effects of stress mediators: central role of the brain
By Bruce S. McEwen. Dialogues in Clinical Neuroscience, 2006
1,110 citations recorded by the source corpus.
The mind involves the whole body, and two-way communication between the brain and the cardiovascular, immune, and other systems via neural and endocrine mechanisms. Stress is a condition of the mind-body interaction, and a factor in the expression of disease that differs among individuals. It is not just the dramatic stressful events that exact their toll, but rather the many events of daily life that elevate and sustain activities of physiological systems and cause sleep deprivation, overeating, and other health-damaging behaviors, producing the feeling of being “stressed out.” Over time, this results in wear and tear on the body, which is called “allostatic load,” and it reflects not only the impact of life experiences but also of genetic load, individual lifestyle habits reflecting items such as diet, exercise, and substance abuse, and developmental experiences that set life-long patterns of behavior and physiological reactivity. Hormones associated with stress and allostatic load protect the body in the short run and promote adaptation by the process known as allostasis, but in the long run allostatic load causes changes in the body that can lead to disease. The brain is the key organ of stress, allostasis, and allostatic load, because it determines what is threatening and therefore stressful, and also determines the physiological and behavioral responses. Brain regions such as the hippocampus, amygdala, and prefrontal cortex respond to acute and chronic stress by undergoing structural remodeling, which alters behavioral and physiological responses. Translational studies in humans with structural and functional imaging reveal smaller hippocampal volume in stress-related conditions, such as mild cognitive impairment in aging and prolonged major depressive illness, as well as in individuals with low self-esteem. Alterations in amygdala and prefrontal cortex are also reported. Besides Pharmaceuticals, approaches to alleviate chronic stress and reduce allostatic load and the incidence of diseases of modern life include lifestyle change, and policies of government and business that would improve the ability of individuals to reduce their own chronic stress burden.
Subfields: Behavioral Neuroscience, Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/bfcf6f7e8aeea0388fa7bd7c870f36cc5e6fa449
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Behavioral Neuroscience
- Bruce S. McEwen
- M. Dickens
- Nicole E. Cyr
- Sonia J. Lupien
- R. Juster
- Peter J. Gianaros
- L. M. Romero
- Dennis S. Charney
In Cellular and Molecular Neuroscience
- Peter J. Gianaros
- L. M. Romero
- M. Dickens
- Nicole E. Cyr
- Sonia J. Lupien
- Jaak Panksepp
- D. Watt
- A. Danese
In Cognitive Neuroscience
- Peter J. Gianaros
- D. Watt
- L. M. Romero
- M. Dickens
- Nicole E. Cyr
- A. Danese
- Jaak Panksepp
- Sonia J. Lupien
Citations in the corpus
- The social determinants of health: coming of age. (2011, background): “The accumulated strain from trying, with inadequate resources, to cope with daily challenges may, over time, lead to more physiological damage than would a single dramatically stressful event (70).”
- Allostatic load biomarkers of chronic stress and impact on health and cognition. (2010, background): “At first, prolonged secretion of the stress hormones epinephrine, norepinephrine, and cortisol (antagonized by dehydroepiandosterone) can falter in their ability to protect the distressed individual and instead begin to damage the brain and body (McEwen, 2006a).”
- How does social support enhance resilience in the trauma-exposed individual? (2015, background): “…and neuroendocrine responses to stress among individuals with low social support compared to those with high social support (Southwick et al. 2005, McEwen 2006), and Eisenberger (2013a, b) reported that both the dorsal anterior cingulate and the dorso-medial prefrontal cortex are activated when…”
- The Reactive Scope Model - a new model integrating homeostasis, allostasis, and stress. (2009, positive): “The Allostatic Model has been used recently to explain why individuals are more susceptible to stress in humans of lower socioeconomic status (SES) (McEwen, 2000).”
- Depression: An Evolutionarily Conserved Mechanism to Terminate Separation Distress? A Review of Aminergic, Peptidergic, and Neural Network Perspectives (2009, background): “cortisol disrupts the hippocampus functionally, perhaps through impairing long-term potentiation (Pavlides, Nivón, & McEwen, 2002) potentially contributing to the mild amnestic syndrome seen in many depressions. Bremner (2000) found evidence that hippocampal volume loss is correlated with the durati”
- Exploring U.S. Shifts in Anti-Asian Sentiment with the Emergence of COVID-19 (2020, background): “Previous research shows that both short-term acute stress experiences as well as prolonged stress, particularly due to social identity threat, has lasting physiologic impacts [38,39].”
- The Lifelong Effects of Early Childhood Adversity and Toxic Stress (2012, background): “In addition to short-term changes in observable behavior, toxic stress in young children can lead to less outwardly visible yet permanent changes in brain structure and function.(39,46) The plasticity of the fetal, infant, and early childhood brain makes it particularly sensitive to chemical influen”
- Stress- and Allostasis-Induced Brain Plasticity (2011, positive): “, cortisol, sympathetic and parasympathetic transmitters, cytokines, metabolic hormones) operate within a nonlinear, dynamic, and interactive network in which mediators down- and upregulate each other, depending on such factors as their concentration, location in the body, and sequential temporal pa”
- Adverse childhood experiences, allostasis, allostatic load, and age-related disease. (2012, background): “Each of the mediators of allostasis interacts with other mediators in a complex non-linear fashion showing biphasic effects depending on the level and duration of activation [19].”