Stress and Obesity: Are There More Susceptible Individuals?

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Abstract

Purpose of Review

Stress has long been suspected to be interrelated to (abdominal) obesity. However, interindividual differences in this complex relationship exist. We suggest that the extent of glucocorticoid action partly explains these interindividual differences. We provide latest insights with respect to multiple types of stressors.

Recent Findings

Increased long-term cortisol levels, as measured in scalp hair, are strongly related to abdominal obesity and to specific mental disorders. However, not all obese patients have elevated cortisol levels. Possibly, the interindividual variation in glucocorticoid sensitivity, which is partly genetically determined, may lead to higher vulnerability to mental or physical stressors. Other evidence for the important role for increased glucocorticoid action is provided by recent studies investigating associations between body composition and local and systemic corticosteroids.

Summary

Stress may play a major role in the development and maintenance of obesity in individuals who have an increased glucocorticoid exposure or sensitivity. These insights may lead to more effective and individualized obesity treatment strategies.

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Most cited references 104

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Stress and disorders of the stress system.

George P. Chrousos (2009)

All organisms must maintain a complex dynamic equilibrium, or homeostasis, which is constantly challenged by internal or external adverse forces termed stressors. Stress occurs when homeostasis is threatened or perceived to be so; homeostasis is re-established by various physiological and behavioral adaptive responses. Neuroendocrine hormones have major roles in the regulation of both basal homeostasis and responses to threats, and are involved in the pathogenesis of diseases characterized by dyshomeostasis or cacostasis. The stress response is mediated by the stress system, partly located in the central nervous system and partly in peripheral organs. The central, greatly interconnected effectors of this system include the hypothalamic hormones arginine vasopressin, corticotropin-releasing hormone and pro-opiomelanocortin-derived peptides, and the locus ceruleus and autonomic norepinephrine centers in the brainstem. Targets of these effectors include the executive and/or cognitive, reward and fear systems, the wake-sleep centers of the brain, the growth, reproductive and thyroid hormone axes, and the gastrointestinal, cardiorespiratory, metabolic, and immune systems. Optimal basal activity and responsiveness of the stress system is essential for a sense of well-being, successful performance of tasks, and appropriate social interactions. By contrast, excessive or inadequate basal activity and responsiveness of this system might impair development, growth and body composition, and lead to a host of behavioral and somatic pathological conditions.

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Regulation of the Hypothalamic-Pituitary-Adrenocortical Stress Response.

James P Herman, Jessica McKlveen, Sriparna Ghosal … (2016)

The hypothalamo-pituitary-adrenocortical (HPA) axis is required for stress adaptation. Activation of the HPA axis causes secretion of glucocorticoids, which act on multiple organ systems to redirect energy resources to meet real or anticipated demand. The HPA stress response is driven primarily by neural mechanisms, invoking corticotrophin releasing hormone (CRH) release from hypothalamic paraventricular nucleus (PVN) neurons. Pathways activating CRH release are stressor dependent: reactive responses to homeostatic disruption frequently involve direct noradrenergic or peptidergic drive of PVN neurons by sensory relays, whereas anticipatory responses use oligosynaptic pathways originating in upstream limbic structures. Anticipatory responses are driven largely by disinhibition, mediated by trans-synaptic silencing of tonic PVN inhibition via GABAergic neurons in the amygdala. Stress responses are inhibited by negative feedback mechanisms, whereby glucocorticoids act to diminish drive (brainstem) and promote transsynaptic inhibition by limbic structures (e.g., hippocampus). Glucocorticoids also act at the PVN to rapidly inhibit CRH neuronal activity via membrane glucocorticoid receptors. Chronic stress-induced activation of the HPA axis takes many forms (chronic basal hypersecretion, sensitized stress responses, and even adrenal exhaustion), with manifestation dependent upon factors such as stressor chronicity, intensity, frequency, and modality. Neural mechanisms driving chronic stress responses can be distinct from those controlling acute reactions, including recruitment of novel limbic, hypothalamic, and brainstem circuits. Importantly, an individual's response to acute or chronic stress is determined by numerous factors, including genetics, early life experience, environmental conditions, sex, and age. The context in which stressors occur will determine whether an individual's acute or chronic stress responses are adaptive or maladaptive (pathological).

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Endocrinology of the stress response.

Evangelia Charmandari, Constantine Tsigos, George Panagiotis Chrousos (2005)

The stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRH); arginine vasopressin; the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors.

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Author and article information

Contributors

Elisabeth F. C. van Rossum: e.vanrossum@erasmusmc.nl

Journal

Journal ID (nlm-ta): Curr Obes Rep

Journal ID (iso-abbrev): Curr Obes Rep

Title: Current Obesity Reports

Publisher: Springer US (New York )

ISSN (Electronic): 2162-4968

Publication date (Electronic): 16 April 2018

Publication date PMC-release: 16 April 2018

Publication date (Print): 2018

Volume: 7

Issue: 2

Pages: 193-203

Affiliations

[1 ]ISNI 000000040459992X, GRID grid.5645.2, Obesity Center CGG, Erasmus MC, , University Medical Center Rotterdam, ; Room D-428, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands

[2 ]ISNI 000000040459992X, GRID grid.5645.2, Department of Internal Medicine, division of Endocrinology, Erasmus MC, , University Medical Center Rotterdam, ; Rotterdam, The Netherlands

Article

Publisher ID: 306

DOI: 10.1007/s13679-018-0306-y

PMC ID: 5958156

PubMed ID: 29663153

SO-VID: a04787fb-9c32-416c-9045-6ee7eb1e1a98

License:

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Funding

Funded by: Erasmus University

Custom metadata

ScienceOpen disciplines: Health & Social care

Keywords: obesity,stress,cortisol,hair cortisol,glucocorticoid receptor,glucocorticoid receptor polymorphisms,corticosteroids

Data availability:

ScienceOpen disciplines: Health & Social care

Keywords: obesity, stress, cortisol, hair cortisol, glucocorticoid receptor, glucocorticoid receptor polymorphisms, corticosteroids

Stress and Obesity: Are There More Susceptible Individuals?

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Abstract

Purpose of Review

Recent Findings

Summary

Related collections

Stress signalling in stem cells

Most cited references 104

Stress and disorders of the stress system.

Regulation of the Hypothalamic-Pituitary-Adrenocortical Stress Response.

Endocrinology of the stress response.

Author and article information

Contributors

Journal

Affiliations

Article

History

Funding

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Custom metadata

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