Stress- and Allostasis-Induced Brain Plasticity
Open accessAbstract
The brain is the key organ of stress processes. It determines what individuals will experience as stressful, it orchestrates how individuals will cope with stressful experiences, and it changes both functionally and structurally as a result of stressful experiences. Within the brain, a distributed, dynamic, and plastic neural circuitry coordinates, monitors, and calibrates behavioral and physiological stress response systems to meet the demands imposed by particular stressors. These allodynamic processes can be adaptive in the short term (allostasis) and maladaptive in the long term (allostatic load). Critically, these processes involve bidirectional signaling between the brain and body. Consequently, allostasis and allostatic load can jointly affect vulnerability to brain-dependent and stress-related mental and physical health conditions. This review focuses on the role of brain plasticity in adaptation to, and pathophysiology resulting from, stressful experiences. It also considers interventions to prevent and treat chronic and prevalent health conditions via allodynamic brain mechanisms.
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Environmental conditions and interpersonal interactions, whether positive or negative, become biologically embedded and shape or canalize brain and behavioral development.
“environmental conditions and interpersonal interactions, both positive and negative, are embedded biologically, shaping or canalizing the development of brain and behavior”
From School Readiness and Self-Regulation: A Developmental Psychobiological Approach (2015) · cites this paper as McEwen & Gianaros 2011
The Introduction says environmental exposure interacts with genetic liability from in utero onward, and that stressful experiences can produce adaptive or maladaptive changes in brain plasticity and behavior. The Interventions section also discusses interpersonal relationships and social support. The paper does not establish the broader claim that positive and negative environmental conditions and interpersonal interactions generally become biologically embedded and canalize brain and behavioral development. (LLM, conf=0.83)
Experimental — accuracy not yet measuredExtensive literature links ELA to pervasive, quantifiable variation in brain structure and function.
“Extensive literature links ELA to pervasive, quantifiable variation in brain structure and function [15, 21, 24, 25].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
The section “Brain Systems Mediating and Targeted by Allodynamic Processes” reports measurable differences in brain structure and function associated with stress, including gray-matter volume and amygdala reactivity. The passages concern chronic or other stressful experiences generally, not specifically early-life adversity (ELA), so they do not establish the claim at that level of specificity. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredHPA hyper- and hypo-reactivity both represent prototypical patterns associated with excess allostatic load, and both predict human stress-related chronic illnesses including cardiovascular, metabolic, and psychiatric diseases linked epidemiologically to ELA.
“Importantly, HPA hyper- and hypo-reactivity both represent prototypical patterns associated with excess allostatic load, and both predict human stress-related chronic illnesses, including cardiovascular, metabolic, and psychiatric diseases linked epidemiologically to ELA [15, 29, 48].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAn aggregative approach to conceptualize early life adversity is supported by observed dose-response effects linking cumulative early adversity to later outcomes and by the allostatic load paradigm.
“Such an approach facilitates the synthesis of complex evidence for application, and is supported by observed dose–response effects linking cumulative early adversity to later outcomes [1, 3, 5], and by the “allostatic load” paradigm exploring pathogenic effects of cumulative all-cause stress [15].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
Chronic or excessive activation of stress-response systems contributes to the pathogenic physiological "wear and tear" described within the allostatic load paradigm.
“However, chronic or excessive activation contributes to the pathogenic physiological “wear and tear” described within the allostatic load paradigm [15, 29].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
Experience-dependent mechanisms regulate the sensitivity and plasticity of the central nervous system and act at several biological levels: cellular changes such as neurogenesis, pruning and sprouting of synapses, myelination of axons and alterations to the number of dendritic spines; subcellular changes, such as alterations to the cytoskeleton and the extracellular matrix and changes in the level
“These experience-dependent mechanisms regulate the sensitivity and plasticity of the central nervous system and act at several biological levels (likely partly in parallel with each other): i) cellular changes such as neurogenesis, pruning and sprouting of synapses, myelination of axons and alterations to the number of dendritic spines9, 10, ii) subcellular changes, such as alterations to the”
From Resilience in mental health: linking psychological and neurobiological perspectives. (2013) · cites this paper as [9]
The shape of the inverted U differs by sex, strain, and behavioral domain.
“The shape of the inverted U differs by many factors including sex, strain, and behavioral domain in question (Fig. 2).”
From Neurobiology of resilience (2012) · cites this paper as [50]
McEwen and colleagues found that stress affects most rat behavioral domains with an inverted U-shaped curve, where low and high stress impair behavior and intermediate stress promotes positive coping.
“McEwen and colleagues systematically measured the type, length, and quality of stress experience on multiple rat behaviors and found that stress affects most behavioral domains with an inverted U–shape curve, where low and high levels of stress both impair behavior, while intermediate levels actually promote positive coping responses (for review see50).”
From Neurobiology of resilience (2012) · cites this paper as [50]
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Self-citationThe stressed synapse: the impact of stress and glucocorticoids on glutamate transmission
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Self-citationSchool Readiness and Self-Regulation: A Developmental Psychobiological Approach
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Brain on stress: how the social environment gets under the skin
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Self-citationMore than a feeling: A unified view of stress measurement for population science
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“This latter finding is important because the hippocampus is replete with glucocorticoid receptors and thus renders the hippocampus at risk for atrophy when exposed to the high doses of glucocorticoids observed in response to prolonged stress in animal models (McEwen, 1999; Sapolsky, 1999), as well as excitatory amino…”
BackgroundThe Brain on Stress: Vulnerability and Plasticity of the Prefrontal Cortex over the Life Course
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Self-citationChild Development in the Context of Disaster, War, and Terrorism: Pathways of Risk and Resilience
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The neuroendocrinology of social isolation
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Social influences on neuroplasticity: stress and interventions to promote well-being
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Self-citationSex differences in stress-related psychiatric disorders: neurobiological perspectives
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“However, chronic or excessive activation contributes to the pathogenic physiological “wear and tear” described within the allostatic load paradigm [15, 29].”
BackgroundInfluentialUncertainty and stress: Why it causes diseases and how it is mastered by the brain
Peters, A., McEwen, B. S., & Friston, K. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2017.05.004 · Cited by 652 · see citing works
Self-citationThe Functional and Clinical Significance of the 24-Hour Rhythm of Circulating Glucocorticoids
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A Systematic Review of Allostatic Load, Health, and Health Disparities
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Self-citationResilience in mental health: linking psychological and neurobiological perspectives.
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Self-citationEpigenetics of Stress-Related Psychiatric Disorders and Gene × Environment Interactions
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Pregnenolone Can Protect the Brain from Cannabis Intoxication
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Psychological Stress and Mitochondria: A Conceptual Framework
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Self-citationCurrent Psychosomatic Practice
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Child and Family Resilience: A Call for Integrated Science, Practice, and Professional Training
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In pursuit of resilience: stress, epigenetics, and brain plasticity
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Self-citationToxic Stress in Children and Adolescents
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Recognizing resilience: Learning from the effects of stress on the brain
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High anxiety trait: A vulnerable phenotype for stress‐induced depression
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Naturalistic rodent models of chronic early‐life stress
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Self-citationHow the brain connects in response to acute stress: A review at the human brain systems level
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Hippocampal gene expression changes underlying stress sensitization and recovery
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Self-citationThe Brain on Stress: Toward an Integrative Approach to Brain, Body, and Behavior
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Self-citationLactate Shuttles in Neuroenergetics—Homeostasis, Allostasis and Beyond
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Self-citationResilience in Development: Progress and Transformation
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Self-citationGenomic and epigenomic mechanisms of glucocorticoids in the brain
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Self-citationFrom Receptor Balance to Rational Glucocorticoid Therapy
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A culture-brain link: negative age stereotypes predict Alzheimer's disease biomarkers
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Resilience as a focus of suicide research and prevention
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Stress-induced changes in human decision-making are reversible
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Environmental effects on fish neural plasticity and cognition
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Cognitive Aging and the Promise of Physical Activity
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Self-citationDisrupted default mode network connectivity in migraine without aura
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Common hippocampal structural and functional changes in migraine
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Self-citationPeriodization Theory: Confronting an Inconvenient Truth
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The complex neurobiology of resilient functioning after childhood maltreatment
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- Authors
- McEwen, B. S., & Gianaros, P. J.
- Affiliations
- Rockefeller University (US)
- University of Pittsburgh (US)
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 2011-02-18
- Volume
- 62
- Issue
- 1
- Pages
- 431-445
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- PMC
- PMC4251716
- OpenAlex
- W2116769635
- Cited by
- 1,171
- References
- 74
- Citations by year
- 2026: 96 · 2025: 100 · 2024: 78 · 2023: 55 · 2022: 98 · 2021: 81 · 2020: 81 · 2019: 86 · 2018: 60 · 2017: 83 · 2016: 79 · 2015: 64 · 2014: 73 · 2013: 54 · 2012: 58
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL089850)
- National Institute of Mental Health (5P01 MH58911, K01MH070616, R01 MH41256, P50MH058911, R01MH041256)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- allostasis, allostatic load, neuroplasticity, stress response, stress-related disorders, stress adaptation, stress coping
- MeSH terms
- Adaptation, Physiological, Adaptation, Psychological, Animals, Brain, Female, Humans, Male, Neuronal Plasticity, Stress, Physiological, Stress, Psychological, Mice, Rats, Allostasis
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