The stress response systems: Universality and adaptive individual differences☆

2006 ◽  
Vol 26 (2) ◽  
pp. 175-212 ◽  
Author(s):  
B ELLIS ◽  
J JACKSON ◽  
W BOYCE
Keyword(s):  
Individual Differences ◽  
Stress Response ◽  
Response Systems

Mechanism of the Immediate Capillary Stress Response

1957 ◽  
Vol 188 (2) ◽  
pp. 387-394 ◽  
Author(s):  
Jenö Kramár ◽  
William V. Meyers ◽  
Harry H. McCarthy ◽  
Nicholas Dietz ◽  
Margarete Simay-Kramár ◽  
...  
Keyword(s):  
Individual Differences ◽  
Stress Response ◽  
Potential Role ◽  
Primary Effect ◽  
Biphasic Response ◽  
Capillary Stress ◽  
Thyroid Glands ◽  
Capillary Resistance ◽  
Clinical Conditions ◽  
Capillary Response

Two possibilities may be considered for the mechanism of the immediate capillary stress response: the direct nervous origin, and the humoral. The latter was investigated in this study. Immediate capillary stress response was found in the absence of the adrenal, pituitary or thyroid glands, and after removal of both the adrenals and the pituitary. Among the 10 physiologic substances considered as playing a potential role in this phenomenon, three were found to possess capillary activity. Vasopressin as well as oxytocin increases capillary resistance. Histamine gives rise to a biphasic response, involving a decrease of capillary resistance (primary effect) followed by an increase (due to vasopressin elicited by histamine). By means of these substances it is possible to duplicate the immediate capillary stress response. During the immediate capillary response plasma has antidiuretic and chloruretic properties—a finding compatible with an increased vasopressin concentration and with the assumption that vasopressin is discharged rather regularly in the first phase of the stress response. The immediate capillary stress response seems to be the result of an interplay between vasopressin-oxytocin, and histamine. Species and individual differences in the sensitivity to these substances may account for the various patterns of the capillary response. The possible significance of the immediate capillary response and of the increased vasopressin activity in some clinical conditions is discussed.

Impact of stress response systems on forced choice recognition in an experimental trauma film paradigm

2018 ◽  
Vol 156 ◽  
pp. 45-52
Author(s):  
Felicitas Rombold-Bruehl ◽  
Christian Otte ◽  
Babette Renneberg ◽  
Julian Hellmann-Regen ◽  
Linda Bruch ◽  
...  
Keyword(s):  
Stress Response ◽  
Forced Choice ◽  
Experimental Trauma ◽  
Response Systems ◽  
Trauma Film Paradigm

Stress and Substance Misuse

2020 ◽  
pp. 101-118
Author(s):  
James M. Bjork ◽  
Nicholas D. Thomson
Keyword(s):  
Substance Use ◽  
Stress Response ◽  
Stress Responses ◽  
Acute Stress ◽  
Physiological Stress ◽  
Solution Space ◽  
Chronic Administration ◽  
Behavioral Repertoire ◽  
Physiological Stress Response ◽  
Response Systems

Stress is both a critical contributor and consequence of substance use disorder (SUD). First, exaggerated subjective stress responses are characteristic of affective symptomatology such as depression, bipolar disorder, generalized anxiety, and posttraumatic stress disorder (sometimes stemming from histories of abuse) that have been prognostic of development of addiction in longitudinal studies. Substance use is negatively reinforced in many at-risk and addicted individuals because it may acutely alleviate stress. Second, chronic administration of commonly abused substances alters physiological stress response systems, especially during acute withdrawal. Third, acute stress responses blunt the addicted individual’s frontocortically mediated behavioral repertoire (solution space) in favor of reflexive behavioral biases toward relief-based substance use. Therefore, acute stress responses are a strong trigger for relapse to substance use during extended recovery. These findings have collectively led to approaches to SUD relapse prevention that pharmacologically blunt components of the stress response, but these agents have not reliably shown success in human clinical trials. This chapter reviews these different relationships between stress and addiction and offers future avenues for additional research.

Beyond allostatic load: Rethinking the role of stress in regulating human development

2013 ◽  
Vol 26 (1) ◽  
pp. 1-20 ◽  
Author(s):  
Bruce J. Ellis ◽  
Marco Del Giudice
Keyword(s):  
Life History ◽  
Stress Response ◽  
Allostatic Load ◽  
Life History Theory ◽  
Calibration Model ◽  
Load Model ◽  
Adaptive Calibration ◽  
Trade Offs ◽  
Response Systems

AbstractHow do exposures to stress affect biobehavioral development and, through it, psychiatric and biomedical disorder? In the health sciences, the allostatic load model provides a widely accepted answer to this question: stress responses, while essential for survival, have negative long-term effects that promote illness. Thus, the benefits of mounting repeated biological responses to threat are traded off against costs to mental and physical health. The adaptive calibration model, an evolutionary–developmental theory of stress–health relations, extends this logic by conceptualizing these trade-offs as decision nodes in allocation of resources. Each decision node influences the next in a chain of resource allocations that become instantiated in the regulatory parameters of stress response systems. Over development, these parameters filter and embed information about key dimensions of environmental stress and support, mediating the organism's openness to environmental inputs, and function to regulate life history strategies to match those dimensions. Drawing on the adaptive calibration model, we propose that consideration of biological fitness trade-offs, as delineated by life history theory, is needed to more fully explain the complex relations between developmental exposures to stress, stress responsivity, behavioral strategies, and health. We conclude that the adaptive calibration model and allostatic load model are only partially complementary and, in some cases, support different approaches to intervention. In the long run, the field may be better served by a model informed by life history theory that addresses the adaptive role of stress response systems in regulating alternative developmental pathways.

The interaction between perinatal factors and childhood abuse in the risk of developing anorexia nervosa

2009 ◽  
Vol 40 (4) ◽  
pp. 657-665 ◽  
Author(s):  
A. Favaro ◽  
E. Tenconi ◽  
P. Santonastaso
Keyword(s):  
Anorexia Nervosa ◽  
Stress Response ◽  
Childhood Abuse ◽  
Low Birthweight ◽  
Stressful Events ◽  
Stressful Event ◽  
Perinatal Complications ◽  
Perinatal Factors ◽  
Additive Interaction ◽  
Response Systems

BackgroundPerinatal factors seem to be implicated in the pathogenesis of anorexia nervosa (AN) and may be involved in the programming of stress response systems in humans. Our aim was to explore one of the possible pathways to explain the association between perinatal complications and a psychiatric disorder. In particular, we tested the hypothesis that neonatal immaturity may confer an enhanced vulnerability to AN after exposure to a severe stressful event, such as childhood abuse.MethodThe sample was composed of subjects who took part in a prevalence study carried out on a representative sample of the general population and cases of AN referred to an out-patient specialist unit. All subjects (n=663) were born in the two obstetric wards of Padua Hospital between 1971 and 1979. We analysed data using both a case-control and a cohort design.ResultsWe found that functional signs of neonatal dysmaturity, but not a low birthweight or prematurity, had a significant additive interaction with childhood abuse in determining the risk for this illness. In normal subjects, but not in subjects with AN, neonatal dysmaturity was associated with being small, short or thin for gestational age at birth.ConclusionsThe synergistic effect of neonatal dysmaturity and childhood abuse in increasing the risk for AN provides evidence for the hypothesis that a prenatal programming of stress response systems can result in an impairment of the individual's resilience to severe stressful events.

scholarly journals Ethanol-induced stress response of Staphylococcus aureus

2017 ◽  
Vol 63 (9) ◽  
pp. 745-757 ◽  
Author(s):  
Jasmine M. Pando ◽  
Richard F. Pfeltz ◽  
Jesus A. Cuaron ◽  
Vijayaraj Nagarajan ◽  
Mukti N. Mishra ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Stress Response ◽  
Protein Quality ◽  
Transcriptional Profiling ◽  
Stress Protein ◽  
Nucleotide Biosynthesis ◽  
Induced Stress ◽  
Stress Functions ◽  
Response Systems ◽  
Mrsa Strains

Transcriptional profiles of 2 unrelated clinical methicillin-resistant Staphylococcus aureus (MRSA) isolates were analyzed following 10% (v/v) ethanol challenge (15 min), which arrested growth but did not reduce viability. Ethanol-induced stress (EIS) resulted in differential gene expression of 1091 genes, 600 common to both strains, of which 291 were upregulated. With the exception of the downregulation of genes involved with osmotic stress functions, EIS resulted in the upregulation of genes that contribute to stress response networks, notably those altered by oxidative stress, protein quality control in general, and heat shock in particular. In addition, genes involved with transcription, translation, and nucleotide biosynthesis were downregulated. relP, which encodes a small alarmone synthetase (RelP), was highly upregulated in both MRSA strains following ethanol challenge, and relP inactivation experiments indicated that this gene contributed to EIS growth arrest. A number of persistence-associated genes were also upregulated during EIS, including those that encode toxin–antitoxin systems. Overall, transcriptional profiling indicated that the MRSA investigated responded to EIS by entering a state of dormancy and by altering the expression of elements from cross protective stress response systems in an effort to protect preexisting proteins.

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