The Stress Response System in Supporting Health and Well-Being

2015 ◽  
Vol 27 (4pt2) ◽  
pp. 1461-1470 ◽  
Author(s):  
Melissa K. Peckins ◽  
Elizabeth J. Susman ◽  
Sonya Negriff ◽  
Jennie Noll ◽  
Penelope K. Trickett

AbstractThroughout the life span, exposure to chronic stress such as child maltreatment is thought to contribute to future dysfunction of the stress response system (SRS) through the process of adaptive calibration. Dysfunction of the SRS is associated with numerous health and behavior problems, so it is important to understand under what conditions and what time frame adaptive calibration occurs. The present study tested for adaptive calibration of the SRS in a sample of maltreated (n = 303) and nonmaltreated (n = 151) youth during the important developmental period of adolescence. Data were used from Waves 2, 3, and 4 of a larger study of the consequences of maltreatment on health and well-being. At each time point, participants underwent the Trier Social Stress Test for Children and provided a baseline and four poststressor saliva samples to measure cortisol reactivity. Adaptive calibration was tested by performing a latent profile analysis using the five samples of salivary cortisol provided at each time point, and testing whether maltreatment status predicted the likelihood of profile membership at Time 2, Time 3, and Time 4. Three cortisol profiles emerged from the data at each time point (blunted, moderate, and elevated), and results indicated that maltreated youth were more likely than nonmaltreated youth to present with the blunted cortisol profile compared to the moderate and elevated profiles at Time 2 and Time 3, even after controlling for recent exposure to violence and trauma. At Time 4, there was no longer a difference in profile membership between maltreated and nonmaltreated youth, suggesting adaptive calibration may be a lengthy process requiring a period of years to become evident. Overall, the findings provide support for adaptive calibration and offer insight into the conditions under which adaptive calibration occurs.


Author(s):  
André Korsloot ◽  
Cornelis A.M. van Gestel ◽  
Nico M. van Straalen

2017 ◽  
Vol 21 (4) ◽  
pp. 330-353 ◽  
Author(s):  
Michael P. Hengartner

The present work proposes an evolutionary model of externalizing personality that defines variation in this broad psychobiological phenotype resulting from genetic influences and a conditional adaptation to high-risk environments with high extrinsic morbidity-mortality. Due to shared selection pressure, externalizing personality is coadapted to fast life history strategies and maximizes inclusive fitness under adverse environmental conditions by governing the major trade-offs between reproductive versus somatic functions, current versus future reproduction, and mating versus parenting efforts. According to this model, externalizing personality is a regulatory device at the interface between the individual and its environment that is mediated by 2 overlapping psychobiological systems, that is, the attachment and the stress-response system. The attachment system coordinates interpersonal behavior and intimacy in close relationships and the stress-response system regulates the responsivity to environmental challenge and both physiological and behavioral reactions to stress. These proximate mechanisms allow for the integration of neuroendocrinological processes underlying interindividual differences in externalizing personality. Hereinafter I further discuss the model's major implications for personality psychology, psychiatry, and public health policy.


2008 ◽  
Vol 17 (2) ◽  
pp. 174-181 ◽  
Author(s):  
Harry van de Wiel ◽  
Erwin Geerts ◽  
Josette Hoekstra-Weebers

2013 ◽  
Vol 81 (5) ◽  
pp. 1450-1459 ◽  
Author(s):  
Irina Debnath ◽  
J. Paul Norton ◽  
Amelia E. Barber ◽  
Elizabeth M. Ott ◽  
Bijaya K. Dhakal ◽  
...  

ABSTRACTStrains of uropathogenicEscherichia coli(UPEC) are the primary cause of urinary tract infections, representing one of the most widespread and successful groups of pathogens on the planet. To colonize and persist within the urinary tract, UPEC must be able to sense and respond appropriately to environmental stresses, many of which can compromise the bacterial envelope. The Cpx two-component envelope stress response system is comprised of the inner membrane histidine kinase CpxA, the cytosolic response regulator CpxR, and the periplasmic auxiliary factor CpxP. Here, by using deletion mutants along with mouse and zebrafish infection models, we show that the Cpx system is critical to the fitness and virulence of two reference UPEC strains, the cystitis isolate UTI89 and the urosepsis isolate CFT073. Specifically, deletion of thecpxRAoperon impaired the ability of UTI89 to colonize the murine bladder and greatly reduced the virulence of CFT073 during both systemic and localized infections within zebrafish embryos. These defects coincided with diminished host cell invasion by UTI89 and increased sensitivity of both strains to complement-mediated killing and the aminoglycoside antibiotic amikacin. Results obtained with thecpxPdeletion mutants were more complicated, indicating variable strain-dependent and niche-specific requirements for this well-conserved auxiliary factor.


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