From Allostatic Load to Allostatic State—An Endogenous Sympathetic Strategy to Deal With Chronic Anxiety and Stress?

Ullmann, Enrico; Perry, Seth W.; Licinio, Júlio; Wong, Ma Li; Dremencov, Eliyahu; Zavjalov, Evgenii L.; Shevelev, Oleg B.; Khotskin, Nikita V.; Koncevaya, Galina V.; Khotshkina, Anna S.; Мошкин, М. П.; Lapshin, Maxim; Komelkova, Maria; Feklicheva, Inna; Tseilikman, Olga; Черкасова, О. П.; Bhui, Kamaldeep; Jones, Edgar; Kirschbaum, Clemens; Bornstein, Stefan R.; Tseĭlikman, Vadim

doi:10.3389/fnbeh.2019.00047

Cited by 25 publications

(31 citation statements)

References 48 publications

(56 reference statements)

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“…Chronic emotional stress results in hyperalgesia that correlates with altered CNS glutamate processing (Greenwood-Van Meerveld and Johnson, 2017). Allostasis (from allostatic load to allostatic states) leads to decreased glutamate levels, an effect also observed in overstressed rats (Ullmann et al, 2019). This research shows that allostasis may be a protective mechanism in rats for adapting to chronic stress (Ullmann et al, 2019).…”

Section: Overview Of Existing Literaturesupporting

confidence: 55%

“…Allostasis (from allostatic load to allostatic states) leads to decreased glutamate levels, an effect also observed in overstressed rats (Ullmann et al, 2019). This research shows that allostasis may be a protective mechanism in rats for adapting to chronic stress (Ullmann et al, 2019). A recent study (Greenwood-Van Meerveld and Johnson, 2017) employed a rodent neuropathic pain model to assess the long-term impact of chronic pain on the hypothalamic pituitary adrenal (HPA) axis and limbic system.…”

Section: Overview Of Existing Literaturementioning

confidence: 84%

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Walking the Tightrope: A Proposed Model of Chronic Pain and Stress

Lunde

Sieberg

2020

Front. Neurosci.

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Pain and stress are both phenomena that challenge an individual's homeostasis and have significant overlap in conceptual and physiological processes. Allostasis is the ability to adapt to pain and stress and maintain homeostasis; however, if either process becomes chronic, it may result in negative long-term outcomes. The negative effects of stress on health outcomes on physiology and behavior, including pain, have been well documented; however, the specific mechanisms of how stress and what quantity of stress contributes to the maintenance and exacerbation of pain have not been identified, and thus pharmacological interventions are lacking. The objective of this brief review is to: 1. identify the gaps in the literature on the impact of acute and chronic stress on chronic pain, 2. highlight future directions for stress and chronic pain research; and 3. introduce the Pain-Stress Model in the context of the current literature on stress and chronic pain. A better understanding of the connection between stress and chronic pain could provide greater insight into the neurobiology of these processes and contribute to individualized treatment for pain rehabilitation and drug development for these often comorbid conditions.

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Section: Overview Of Existing Literaturesupporting

confidence: 55%

Section: Overview Of Existing Literaturementioning

confidence: 84%

Walking the Tightrope: A Proposed Model of Chronic Pain and Stress

Lunde

Sieberg

2020

Front. Neurosci.

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“…Interestingly, low levels of basal corticosterone [16] and low levels of cerebral MAO without distinguishing the isoforms of MAO linked to physical activity were shown in rats, three days after traumatic stress [17]. And, in more physical active offensive rats we found a reduction of anxiety, corticosteroids and glutamate as well as higher concentrations of lactate in the amygdala region compared to the hippocampal region by using our model of chronic and extensive predator stress, indicating a limbic triggered HPA activity with different oxidative processes [18].…”

Section: Mao Metabolism In Ptsdmentioning

confidence: 59%

Post-Traumatic Stress Disorder Chronification via Monoaminooxidase and Cortisol Metabolism

et al. 2019

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“…On the other hand, stress effects may lead to changes in the circulating concentrations of cortisol, insulin, ghrelin, and leptin, which may influence eating behavior [12][13][14] . As a possible psychophysiological mechanism of high/low glucocorticoid response to stress, the active offensive or passive defensive calming response mechanisms with different levels of physical activity were described in a chronic stress paradigm, regarding different allostatic set points 15 .…”

Section: Stress and Eating Behaviormentioning

confidence: 99%

High/low cortisol reactivity and food intake in people with obesity and healthy weight

et al. 2020

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Increased food intake, termed "comfort eating", is a pathologic coping mechanism in chronic stress. Cortisol reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, cortisol reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low cortisol reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age-and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high cortisol reactors (HCR) and low cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR (t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls (p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR (t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the cortisol reactivity to stress predicts stressinduced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.

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From Allostatic Load to Allostatic State—An Endogenous Sympathetic Strategy to Deal With Chronic Anxiety and Stress?

Cited by 25 publications

References 48 publications

Walking the Tightrope: A Proposed Model of Chronic Pain and Stress

Walking the Tightrope: A Proposed Model of Chronic Pain and Stress

Post-Traumatic Stress Disorder Chronification via Monoaminooxidase and Cortisol Metabolism

High/low cortisol reactivity and food intake in people with obesity and healthy weight

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