scholarly journals Consequences of Chronic Stress on the PINE Network

2021 ◽  
Author(s):  
Verena Nold ◽  
Kelly Allers
Keyword(s):  
Risk Factor ◽  
Individual Differences ◽  
Chronic Stress ◽  
Energy Status ◽  
Coping With Stress ◽  
Gene Environment ◽  
Glucocorticoid Signaling ◽  
Response To Stress ◽  
Survival Of The Fittest ◽  
Ultradian Rhythmicity

Stress is a risk factor for the development and progression of a variety of disorders. At the same time stress is essential to initiate adaptation to the current situation and to promote survival of the fittest. Thus, responses to stress evolved to be fast and efficient. This is implemented by a tight networking of the psycho-immune-neuro-energy (PINE) system. Within the PINE network, glucocorticoids are the universal messengers that regulate overall physiology jointly with cytokines, neurotransmitters and energy status. While the secretion of glucocorticoids in response to stress is itself a rather unspecific reaction to any kind of stressor, complexity of the outcome is encoded by lifetime, recent and present events. Together, these individual experiences modulate the diurnal and ultradian rhythmicity of glucocorticoid levels. Given the time- and dose-dependency of glucocorticoid signaling, this rhythmicity allows for flexibility in the coping with stress. In a chronic stress setting, the interaction of PINE network components is altered. While stress-resilient individuals retain adaptive capacity, vulnerable individuals lose flexibility in their responsiveness. Gene × environment interactions could explain individual differences. To better elucidate the molecular underpinnings of risk and resiliency, models that allow studying the consequences of chronic stress on the PINE network are required.

Individual Differences in Cellular Immune Response to Stress

1991 ◽  
Vol 2 (2) ◽  
pp. 111-115 ◽  
Author(s):  
Stephen B. Manuck ◽  
Sheldon Cohen ◽  
Bruce S. Rabin ◽  
Matthew F. Muldoon ◽  
Elizabeth A. Bachen
Keyword(s):  
Immune Response ◽  
Individual Differences ◽  
Cellular Immune Response ◽  
Response To Stress ◽  
Cellular Immune

scholarly journals Impact of chronic stress on periodontal health

2018 ◽  
Vol 24 (1) ◽  
pp. 44-50 ◽  
Author(s):  
Mathieu Gunepin ◽  
Florence Derache ◽  
Marion Trousselard ◽  
Bruno Salsou ◽  
Jean-Jacques Risso
Keyword(s):  
Periodontal Disease ◽  
Chronic Stress ◽  
Negative Impact ◽  
Periodontal Diseases ◽  
Behavioral Changes ◽  
Educational Objective ◽  
Pathogenic Microorganisms ◽  
Periodontal Health ◽  
Response To Stress ◽  
The Impact

Introduction: Periodontal diseases are caused by pathogenic microorganisms that induce increases in of local and systemic proinflammatory cytokines, resulting in periodontal damage. The onset and evolution of periodontal diseases are influenced by many local and systemic risk factors. Educational objective: In this article, we aim to review the results of the research on the impact of chronic stress on the occurrence, development, and response to periodontal disease treatments and on the pathophysiological mechanisms of periodontal disease. Conclusion: Chronic stress has a negative impact on the occurrence, development, and response to the treatment of periodontal disease via indirect actions on the periodontium. This can result from behavioral changes caused by stress (poor dental hygiene, smoking, etc.) and a direct neuroimmunoendocrinological action related to the consequences (particularly immunological) of the secretion of certain chemicals (e.g., cortisol) induced by the activation of the hypothalamus and the autonomic nervous system in response to stress. These factors necessitate multidisciplinary management (e.g., physician, oral surgeon, and psychologist) of patients to identify subjects with chronic stress and to employ countermeasures to decrease the impact of stress on the periodontium.

Hair cortisol and its potential value as a physiological measure of stress response in human and non-human animals

2017 ◽  
Vol 57 (3) ◽  
pp. 401 ◽  
Author(s):  
C. Burnard ◽  
C. Ralph ◽  
P. Hynd ◽  
J. Hocking Edwards ◽  
A. Tilbrook
Keyword(s):  
Chronic Stress ◽  
Stress Responses ◽  
Sampling Site ◽  
Future Research ◽  
Hair Cortisol ◽  
Hair Sampling ◽  
Acute And Chronic Stress ◽  
Lack Of Information ◽  
Technical Validation ◽  
Response To Stress

There is considerable interest in the potential for measuring cortisol in hair as a means of quantifying stress responses in human and non-human animals. This review updates the rapid advancement in our knowledge of hair cortisol, methods for its measurement, its relationship to acute and chronic stress, and its repeatability and heritability. The advantages of measuring cortisol in hair compared with other matrices such as blood, saliva and excreta and the current theories of the mechanisms of cortisol incorporation into the fibre are described. Hair cortisol as a measure of the physiological response to stress in a variety of species is presented, including correlations with other sample matrices, the relationship between hair cortisol and psychosocial stress and the repeatability and heritability of hair cortisol concentrations. Current standards for the quantification of hair cortisol are critically reviewed in detail for the first time and gaps in technical validation of these methods highlighted. The known effects of a variety of sources of hair cortisol variation are also reviewed, including hair sampling site, sex, age and adiposity. There is currently insufficient evidence to conclude that cortisol concentration in hair accurately reflects long-term blood cortisol concentrations. Similarly, there is a lack of information surrounding the mechanisms of cortisol incorporation into the hair. This review highlights several directions for future research to more fully validate the use of hair cortisol as an indicator of chronic stress.

Ordinary Origins of Psychological Problems

2021 ◽  
pp. 187-214
Author(s):  
Benjamin B. Lahey
Keyword(s):  
Individual Differences ◽  
Racial Discrimination ◽  
Race And Ethnicity ◽  
Environmental Influences ◽  
Psychological Problems ◽  
Stressful Events ◽  
Stress Generation ◽  
The People ◽  
Gene Environment

This chapter delves deeper into the role of environmental influences, without forgetting that environmental influences always play their role in the context of gene–environment correlations and interactions. The environments (i.e., experiences) that, on average, are statistically correlated with a higher risk are easy to identify in studies. They include stressful events, including trauma and economic hardship, maladaptive family and neighborhood environments, racial discrimination, and some characteristics of family environments. Environments do not passively shape behavior into psychological problems, however. People actively transact with their environments, meaning that their environments influence their behavior, their behavior and other characteristics influence their environments, and their characteristics moderate the extent to which their experiences influence their behavior. Many characteristics influence people’s transactions with the environment, including age, sex, race, and ethnicity. It is also useful to examine broad individual differences in cognitive and emotional traits, termed dispositions, which play key roles in people’s transactions with the environment that result in psychological problems. One important aspect of this is that many people engage in stress generation, in which their behavior actively creates stressful events such as conflicts with others that in turn stress the people who engage in the stress generation.

scholarly journals The role of the genome in experience-dependent plasticity: Extending the analogy of the genomic action potential

2019 ◽  
Vol 117 (38) ◽  
pp. 23252-23260 ◽  
Author(s):  
David F. Clayton ◽  
Ina Anreiter ◽  
Maria Aristizabal ◽  
Paul W. Frankland ◽  
Elisabeth B. Binder ◽  
...  
Keyword(s):  
Individual Differences ◽  
Action Potential ◽  
Neural Circuits ◽  
Early Gene ◽  
Long Term Memory ◽  
Starting Point ◽  
Contemporary Work ◽  
Response To Stress ◽  
Dependent Modification ◽  
Past Experiences

Our past experiences shape our current and future behavior. These experiences must leave some enduring imprint on our brains, altering neural circuits that mediate behavior and contributing to our individual differences. As a framework for understanding how experiences might produce lasting changes in neural circuits, Clayton [D. F. Clayton,Neurobiol. Learn. Mem.74, 185–216 (2000)] introduced the concept of the genomic action potential (gAP)—a structured genomic response in the brain to acute experience. Similar to the familiar electrophysiological action potential (eAP), the gAP also provides a means for integrating afferent patterns of activity but on a slower timescale and with longer-lasting effects. We revisit this concept in light of contemporary work on experience-dependent modification of neural circuits. We review the “Immediate Early Gene” (IEG) response, the starting point for understanding the gAP. We discuss evidence for its involvement in the encoding of experience to long-term memory across time and biological levels of organization ranging from individual cells to cell ensembles and whole organisms. We explore distinctions between memory encoding and homeostatic functions and consider the potential for perpetuation of the imprint of experience through epigenetic mechanisms. We describe a specific example of a gAP in humans linked to individual differences in the response to stress. Finally, we identify key objectives and new tools for continuing research in this area.

scholarly journals Chronic stress: a critical risk factor for atherosclerosis

2019 ◽  
Vol 47 (4) ◽  
pp. 1429-1440 ◽  
Author(s):  
Bo-chen Yao ◽  
Ling-bing Meng ◽  
Meng-lei Hao ◽  
Yuan-meng Zhang ◽  
Tao Gong ◽  
...  
Keyword(s):  
Risk Factor ◽  
Chronic Stress ◽  
Vascular System ◽  
Foam Cell ◽  
Cell Formation ◽  
Systemic Reaction ◽  
Epidemiological Studies ◽  
The Body ◽  
Foam Cell Formation ◽  
Signal Pathways

Chronic stress refers to the non-specific systemic reaction that occurs when the body is stimulated by various internal and external negative factors over a long time. The physiological response to chronic stress exposure has long been recognized as a potent modulator in the occurrence of atherosclerosis. Furthermore, research has confirmed the correlation between atherosclerosis and cardiovascular events. Chronic stress is pervasive during negative life events and may lead to the formation of plaque. Several epidemiological studies have shown that chronic stress is an independent risk factor for the development of vascular disease and for increased morbidity and mortality in patients with pre-existing coronary artery disease. One possible mechanism for this process is that chronic stress causes endothelial injury, directly activating macrophages, promoting foam cell formation and generating the formation of atherosclerotic plaque. This mechanism involves numerous variables, including inflammation, signal pathways, lipid metabolism and endothelial function. The mechanism of chronic stress in atherosclerosis should be further investigated to provide a theoretical basis for efforts to eliminate the effect of chronic stress on the cardiocerebral vascular system.

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