Title: “Labels Matter: Is it stress or is it Trauma?”

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Abstract

In neuroscience, the term ‘Stress’ has a negative connotation because of its potential to trigger or exacerbate psychopathologies. Yet in the face of exposure to stress, the more common reaction to stress is resilience, indicating that resilience is the rule and stress-related pathology the exception. This is critical because neural mechanisms associated with stress-related psychopathology are expected to differ significantly from those associated with resilience.

Research labels and terminology affect research directions, conclusions drawn from the results, and the way we think about a topic, while choice of labels is often influenced by biases and hidden assumptions. It is therefore important to adopt a terminology that differentiates between stress conditions, leading to different outcomes.

Here, we propose to conceptually associate the term ‘stress’/‘stressful experience’ with ‘stress resilience’, while restricting the use of the term ‘trauma’ only in reference to exposures that lead to pathology. We acknowledge that there are as yet no ideal ways for addressing the murkiness of the border between stressful and traumatic experiences. Yet ignoring these differences hampers our ability to elucidate the mechanisms of trauma-related pathologies on the one hand, and of stress resilience on the other. Accordingly, we discuss how to translate such conceptual terminology into research practice.

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Most cited references 151

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Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication.

Ronald C Kessler, Patricia Berglund, Olga Demler … (2005)

Little is known about lifetime prevalence or age of onset of DSM-IV disorders. To estimate lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the recently completed National Comorbidity Survey Replication. Nationally representative face-to-face household survey conducted between February 2001 and April 2003 using the fully structured World Health Organization World Mental Health Survey version of the Composite International Diagnostic Interview. Nine thousand two hundred eighty-two English-speaking respondents aged 18 years and older. Lifetime DSM-IV anxiety, mood, impulse-control, and substance use disorders. Lifetime prevalence estimates are as follows: anxiety disorders, 28.8%; mood disorders, 20.8%; impulse-control disorders, 24.8%; substance use disorders, 14.6%; any disorder, 46.4%. Median age of onset is much earlier for anxiety (11 years) and impulse-control (11 years) disorders than for substance use (20 years) and mood (30 years) disorders. Half of all lifetime cases start by age 14 years and three fourths by age 24 years. Later onsets are mostly of comorbid conditions, with estimated lifetime risk of any disorder at age 75 years (50.8%) only slightly higher than observed lifetime prevalence (46.4%). Lifetime prevalence estimates are higher in recent cohorts than in earlier cohorts and have fairly stable intercohort differences across the life course that vary in substantively plausible ways among sociodemographic subgroups. About half of Americans will meet the criteria for a DSM-IV disorder sometime in their life, with first onset usually in childhood or adolescence. Interventions aimed at prevention or early treatment need to focus on youth.

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Physiology and neurobiology of stress and adaptation: central role of the brain.

Bruce McEwen (2007)

The brain is the key organ of the response to stress because it determines what is threatening and, therefore, potentially stressful, as well as the physiological and behavioral responses which can be either adaptive or damaging. Stress involves two-way communication between the brain and the cardiovascular, immune, and other systems via neural and endocrine mechanisms. Beyond the "flight-or-fight" response to acute stress, there are events in daily life that produce a type of chronic stress and lead over time to wear and tear on the body ("allostatic load"). Yet, hormones associated with stress protect the body in the short-run and promote adaptation ("allostasis"). The brain is a target of stress, and the hippocampus was the first brain region, besides the hypothalamus, to be recognized as a target of glucocorticoids. Stress and stress hormones produce both adaptive and maladaptive effects on this brain region throughout the life course. Early life events influence life-long patterns of emotionality and stress responsiveness and alter the rate of brain and body aging. The hippocampus, amygdala, and prefrontal cortex undergo stress-induced structural remodeling, which alters behavioral and physiological responses. As an adjunct to pharmaceutical therapy, social and behavioral interventions such as regular physical activity and social support reduce the chronic stress burden and benefit brain and body health and resilience.

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Stress and the individual. Mechanisms leading to disease.

B S McEwen, E STELLAR (1993)

This article presents a new formulation of the relationship between stress and the processes leading to disease. It emphasizes the hidden cost of chronic stress to the body over long time periods, which act as a predisposing factor for the effects of acute, stressful life events. It also presents a model showing how individual differences in the susceptibility to stress are tied to individual behavioral responses to environmental challenges that are coupled to physiologic and pathophysiologic responses. Published original articles from human and animal studies and selected reviews. Literature was surveyed using MEDLINE. Independent extraction and cross-referencing by us. Stress is frequently seen as a significant contributor to disease, and clinical evidence is mounting for specific effects of stress on immune and cardiovascular systems. Yet, until recently, aspects of stress that precipitate disease have been obscure. The concept of homeostasis has failed to help us understand the hidden toll of chronic stress on the body. Rather than maintaining constancy, the physiologic systems within the body fluctuate to meet demands from external forces, a state termed allostasis. In this article, we extend the concept of allostasis over the dimension of time and we define allostatic load as the cost of chronic exposure to fluctuating or heightened neural or neuroendocrine response resulting from repeated or chronic environmental challenge that an individual reacts to as being particularly stressful. This new formulation emphasizes the cascading relationships, beginning early in life, between environmental factors and genetic predispositions that lead to large individual differences in susceptibility to stress and, in some cases, to disease. There are now empirical studies based on this formulation, as well as new insights into mechanisms involving specific changes in neural, neuroendocrine, and immune systems. The practical implications of this formulation for clinical practice and further research are discussed.

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Author and article information

Contributors

Gal Richter-Levin:

ORCID: http://orcid.org/0000-0001-7980-5212

galrichterlevin@gmail.com

Journal

Journal ID (nlm-ta): Transl Psychiatry

Journal ID (iso-abbrev): Transl Psychiatry

Title: Translational Psychiatry

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2158-3188

Publication date (Electronic): 10 July 2021

Publication date PMC-release: 10 July 2021

Publication date Collection: 2021

Volume: 11

Electronic Location Identifier: 385

Affiliations

[1 ]GRID grid.18098.38, ISNI 0000 0004 1937 0562, Sagol Department of Neurobiology, , University of Haifa, ; Haifa, Israel

[2 ]GRID grid.18098.38, ISNI 0000 0004 1937 0562, Psychology Department, , University of Haifa, ; Haifa, Israel

[3 ]GRID grid.18098.38, ISNI 0000 0004 1937 0562, The Integrated Brain and Behavior Research Center (IBBR), , University of Haifa, ; Haifa, Israel

[4 ]GRID grid.5333.6, ISNI 0000000121839049, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), ; Lausanne, Switzerland

Author information

Gal Richter-Levin http://orcid.org/0000-0001-7980-5212

Carmen Sandi http://orcid.org/0000-0001-7713-8321

Article

Publisher ID: 1514

DOI: 10.1038/s41398-021-01514-4

PMC ID: 8272714

PubMed ID: 34247187

SO-VID: 71a1329a-ddbb-42dc-9af2-7b7ae83b859e

License:

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