Cortisol stress response in psychosis from the high-risk to the chronic stage: a systematic review

2019 ◽  
Vol 36 (4) ◽  
pp. 305-315 ◽  
Author(s):  
M. R. Dauvermann ◽  
G. Donohoe

Objectives:We review studies of whether cortisol levels following psychosocial stress exposure differ between patients with psychosis and healthy control subjects.Methods:Original research published between 1993 and February 2019 was included in the literature search. Studies that used experimentally induced psychosocial stress and reported stress response measures of plasma or saliva cortisol levels in patients at any stage of illness (i.e. high risk, first episode and chronic phase) were included.Results:A total of 17 studies were included. Although there was evidence of inconsistencies in measures, we observed moderate evidence of an association with stress-induced cortisol blunting response across studies.Conclusions:This review highlights recent evidence of blunting of cortisol response following experimentally induced psychosocial stress. While there was some evidence of this blunted response across illness types and stages, the strongest evidence was observed for those with chronic schizophrenia. Due to the low number of studies, in particular in bipolar disorder, much work is still needed to accurately characterise the biological effects of stress in psychosis.

2021 ◽  
Vol 12 ◽  
Author(s):  
Rodrigo R. Nieto ◽  
Andrea Carrasco ◽  
Sebastian Corral ◽  
Rolando Castillo ◽  
Pablo A. Gaspar ◽  
...  

Brain Derived Neurotrophic Factor (BDNF) has been linked to cognitive symptoms of schizophrenia, which has been documented in previous reviews by several authors. However, a trend has recently emerged in this field moving from studying schizophrenia as a disease to studying psychosis as a group. This review article focuses on recent BDNF studies in relation to cognition in human subjects during different stages of the psychotic process, including subjects at high risk of developing psychosis, patients at their first episode of psychosis, and patients with chronic schizophrenia. We aim to provide an update of BDNF as a biomarker of cognitive function on human subjects with schizophrenia or earlier stages of psychosis, covering new trends, controversies, current research gaps, and suggest potential future developments in the field. We found that most of current research regarding BDNF and cognitive symptoms in psychosis is done around schizophrenia as a disease. Therefore, it is necessary to expand the study of the relationship between BDNF and cognitive symptoms to psychotic illnesses of different stages and origins.


2021 ◽  
pp. 100930
Author(s):  
Błażej Misiak ◽  
Marita Pruessner ◽  
Jerzy Samochowiec ◽  
Michał Wiśniewski ◽  
Artur Reginia ◽  
...  

2011 ◽  
Vol 23 (11) ◽  
pp. 3218-3227 ◽  
Author(s):  
Franziska Plessow ◽  
Rico Fischer ◽  
Clemens Kirschbaum ◽  
Thomas Goschke

Dynamically adjusting the right amount of goal shielding to varying situational demands is associated with the flexibility of cognitive control, typically linked with pFC functioning. Although stress hormones are found to also bind to prefrontal receptors, the link between stress and cognitive control remains elusive. Based on that, we aimed at investigating effects of acute psychosocial stress on dynamic control adjustments. Forty-eight healthy volunteers were exposed to either a well-established stress induction protocol (the Trier Social Stress Test, TSST) or a standardized control situation before a selective attention (Simon) task involving response conflicts. The individual physiological stress response was monitored by analyzing levels of free cortisol and α-amylase activity in saliva samples showing that the TSST reliably induced an increase of endogenous stress hormone levels. Acute stress did not inevitably impair cognitive functioning, however, as stressed participants showed tonically increased goal shielding (to reduce interference) at the expense of decreased cognitive flexibility. Importantly, as a novel finding in humans, stress effects on cognitive functions were not present immediately after the stress experience but developed gradually over time and, therefore, paralleled the time course of the hypothalamus–pituitary–adrenal (HPA) stress response. In addition, the total increase of individual cortisol levels reflecting HPA activity, but not the total changes in α-amylase activity associated with sympathetic activity, was reversely related to the amount of cognitive flexibility in the final block of testing. Our study provides evidence for a stress-induced time-dependent decrease of cognitive flexibility that might be related to changes in cortisol levels.


2017 ◽  
Vol 43 (suppl_1) ◽  
pp. S175-S176
Author(s):  
Jordan Meyers ◽  
Robert Smith ◽  
Renrong Wu ◽  
Yi Liu ◽  
Jijun Wang ◽  
...  

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S64-S64
Author(s):  
Raktima Datta ◽  
Gregory Strauss ◽  
Nina Kraguljac ◽  
Sydney Howie ◽  
Adrienne Lahti

Abstract Background Prior studies indicate that chronic schizophrenia (SZ) is associated with a specific profile of reinforcement learning abnormalities. These impairments are characterized by: 1) reductions in learning rate, and 2) impaired Go learning and intact NoGo learning. Furthermore, each of these deficits are associated with greater severity of negative symptoms, consistent with theoretical perspectives positing that avolition and anhedonia are associated with deficits in generating, updating, and maintaining mental representations of reward value hat are needed to guide decision-making. However, it is unclear whether these deficits extend to earlier phases of psychotic illness and when individuals are unmedicated. Methods Two studies were conducted to examine reinforcement learning deficits in earlier phases of psychosis. In study 1, participants included 35 participants with first episode psychosis (FEP) and 25 healthy controls (HC). Study 2 included 17 antipsychotic naïve individuals who met criteria for attenuated psychosis syndrome (APS) (i.e., those with a prodromal syndrome) and 18 matched healthy controls (HC). In both studies, participants completed the Temporal Utility Integration Task, a measure of probabilistic reinforcement learning that contained Go and NoGo learning blocks. Participants in the clinical groups also completed neuropsychological testing and standard clinical interviews designed to determine symptom severity and diagnosis. Results FEP displayed impaired Go learning and intact NoGo learning. In contrast, APS did not display impairments in Go or NoGo learning at the group level. Negative symptoms were not significantly associated with reinforcement learning in APS participants. However, greater impairments in Go learning were associated with increased cross-sectional risk for conversion on the NAPLS risk calculator score in the APS group. Discussion Findings provide new evidence for areas of spared and impaired reinforcement learning in early phases of psychosis. Similar to chronic SZ, FEP was associated with impaired Go learning, and intact NoGo learning. Reinforcement learning is more spared in those at clinical high-risk, except those at greatest risk for conversion, where Go learning deficits are more pronounced. These findings suggest that reinforcement learning deficits may emerge early among those who are at clinical high risk for developing psychosis and that they are already pronounced by illness onset in the first episode. Importantly, these reinforcement learning deficits do not appear to be a byproduct of illness chronicity or antipsychotic medication use, but rather a consequence of the illness itself.


2021 ◽  
Vol 22 (13) ◽  
pp. 6881
Author(s):  
Ariel Frajerman ◽  
Linda Scoriels ◽  
Oussama Kebir ◽  
Boris Chaumette

Schizophrenia typically emerges during adolescence, with progression from an ultra-high risk state (UHR) to the first episode of psychosis (FEP) followed by a chronic phase. The detailed pathophysiology of schizophrenia and the factors leading to progression across these stages remain relatively unknown. The current treatment relies on antipsychotics, which are effective for FEP and chronic schizophrenia but ineffective for UHR patients. Antipsychotics modulate dopaminergic and glutamatergic neurotransmission, inflammation, oxidative stress, and membrane lipids pathways. Many of these biological pathways intercommunicate and play a role in schizophrenia pathophysiology. In this context, research of preventive treatment in early stages has explored the antipsychotic effects of omega-3 supplementation in UHR and FEP patients. This review summarizes the action of omega-3 in various biological systems involved in schizophrenia. Similar to antipsychotics, omega-3 supplementation reduces inflammation and oxidative stress, improves myelination, modifies the properties of cell membranes, and influences dopamine and glutamate pathways. Omega-3 supplementation also modulates one-carbon metabolism, the endocannabinoid system, and appears to present neuroprotective properties. Omega-3 has little side effects compared to antipsychotics and may be safely prescribed for UHR patients and as an add-on for FEP patients. This could to lead to more efficacious individualised treatments, thus contributing to precision medicine in psychiatry.


2021 ◽  
Vol 12 ◽  
Author(s):  
Emily E. Carol ◽  
Robert L. Spencer ◽  
Vijay A. Mittal

Deficits in stress-response systems are a characteristic of schizophrenia and psychosis spectrum illnesses, and recent evidence suggests that this impairment may be evident in those at clinical high-risk (CHR) for the development of a psychotic disorder. However, there is limited research specifically investigating biological and subjective stress reactivity in CHR individuals. In the present study, 38 CHR individuals and group of 38 control individuals participated in the Trier Social Stress Test (TSST), an experimentally induced psychosocial stressor. Changes in salivary cortisol and alpha amylase, as well as self-reported units of distress (SUDS), were evaluated. Interestingly, the TSST did not induce a change in cortisol levels in either group, though the CHR group did show higher overall cortisol levels throughout the TSST (pre-anticipation period through recovery period). However, indicative of an effective task manipulation, the TSST did illicit an increase in alpha amylase in both groups. CHR participants exhibited higher levels of subjective stress prior to the stressor compared to the control group and CHR SUDs did not significantly increase in response to the stressor. In contrast, the control group showed an increase in SUDS in response to the stressor. Notably, SUDS for the control group post task mirrored the levels CHR youth endorsed prior to the stressor. Taken together, these findings suggest that there may be a functional relationship between persistently elevated cortisol and chronic high levels of subjective distress in CHR individuals.


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