Journal Article•
The stress-vulnerability model how does stress impact on mental illness at the level of the brain and what are the consequences?
TL;DR: The poster explores the interrelationship between all these factors, and the genetic component which in large part constitutes the ‘vulnerability’ part of the model, and shows that the effects of heightened cortisol levels are not confined to the brain but also cause metabolic problems including the ’Metabolic Syndrome’.
Abstract: SUMMARY Introduction: The stress -vulnerability model (Zubin et al. 1977) is an extremely useful model for identifying and treating relapses of mental illness. We accept that human persons carry genetic and other predisposition to mental illness. However, the question arises as to how stress impacts on a person in order to cause mental illness to develop. Furthermore there arises the issue as to what other effects such stress has on the human body beyond the human brain. Our aim was to research and integrate the current literature in order to establish how stress impacts on the brain at the cellular level, and to establish whether there are other consequences for the human body brought about by the impact of stress on the human brain. Method: Literature Search, using pubmed. Results: We have identified much literature on how stress affects biological mechanisms within the brain, and how it relates to biological vulnerabilities carried by different individuals. Conclusion: We have identified communalities in how the interplay between stress and vulnerability occurs in different disease processes.
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TL;DR: The authors reviewed existing literature on past epidemics, natural disasters, and COVID-19 with a focus on psychiatry and mental health to suggest numerous psychological effects following the pandemic.
Abstract: As cases of the coronavirus disease (COVID-19) continue to rise, psychological endurance is a challenge many people will face. For mental health, heightened stress responses to the pandemic, is likely to manifest in three ways: 1) development of a new episode of a disorder in those with a predisposition to a major psychiatric disorder or an acute exacerbation in those who already have such a disorder, 2) development of a trauma or stressor related disorder, such as acute stress disorder, Post Traumatic Stress Disorder (PTSD), or adjustment disorders, and 3) development of a symptomatic stress response that does not meet the diagnostic criteria of a psychiatric disorder. The authors reviewed existing literature on past epidemics, natural disasters, and COVID-19 with a focus on psychiatry and mental health. Psychological effects of past epidemics (Severe Acute Respiratory Syndrome CoV-1, Ebola, Middle East Respiratory Syndrome, the Anthrax threat), past natural disasters, and current COVID-19 data suggest numerous psychological effects following the pandemic. Alcohol use, PTSD, anxiety, anger, fear of contagion, perceived risk, uncertainty, and distrust are a few of the immediate and long-term effects that are likely to result from the COVID-19 pandemic. Identifying people in need of mental health care and determining the appropriate psychiatric services and therapy needed will be important. Increasing the use and availability of telehealth, group meetings, and online resources are some ways that health care workers can prepare for the increasing demand of psychiatric services during and following the pandemic.
161 citations
Cites background from "The stress-vulnerability model how ..."
...In other words, there is a genetic predisposition and intrinsic vulnerability that with the addition of psychosocial stressors leads to the development of a mental illness [11]....
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...Ultimately affecting neurogenesis and plasticity in the brain [11]....
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...Goh and Agius discuss how stress may lead to the development of disease at a cellular level [11]....
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TL;DR: Using available data on the association of AD and specific exposures and risk factors, the authors have conservatively estimated 423,000 new cases of AD in veterans by 2020, including 140,000 excess cases associated with specific military exposures.
Abstract: Delayed neurological health consequences of environmental exposures during military service have been generally underappreciated. The rapidly expanding understanding of Alzheimer's disease (AD) pathogenesis now makes it possible to quantitate some of the likely long-term health risks associated with military service. Military risk factors for AD include both factors elevated in military personnel such as tobacco use, traumatic brain injury (TBI), depression, and post-traumatic stress disorder (PTSD) and other nonspecific risk factors for AD including, vascular risk factors such as obesity and obesity-related diseases (e.g., metabolic syndrome), education and physical fitness. The degree of combat exposure, Vietnam era Agent Orange exposure and Gulf War Illness may also influence risk for AD. Using available data on the association of AD and specific exposures and risk factors, the authors have conservatively estimated 423,000 new cases of AD in veterans by 2020, including 140,000 excess cases associated with specific military exposures. The cost associated with these excess cases is approximately $5.8 billion to $7.8 billion. Mitigation of the potential impact of military exposures on the cognitive function of veterans and management of modifiable risk factors through specifically designed programs will be instrumental in minimizing the impact of AD in veterans in the future decades.
80 citations
TL;DR: The availability of a validated Persian PSS-10 would indicate a link between stress and chronic headache and the Cohen Perceived Stress Scale has good internal consistency and reliability.
57 citations
Cites background from "The stress-vulnerability model how ..."
...Today, the increase in stress-related diseases is a serious challenge for clinicians of different specialties in developed countries who are focused on the underlying psychological mechanisms (Gunnar and Quevedo 2007, Goh and Agius 2010)....
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TL;DR: In this article, a review summarizes the involvement of the HPA axis in the pathogenesis of neuropsychiatric disorders, focusing on major depression and schizophrenia, and highlights a possible correlation between these conditions.
Abstract: The hypothalamic-pituitary-adrenal (HPA) axis is involved in the pathophysiology of many neuropsychiatric disorders. Increased HPA axis activity can be observed during chronic stress, which plays a key role in the pathophysiology of depression. Overactivity of the HPA axis occurs in major depressive disorder (MDD), leading to cognitive dysfunction and reduced mood. There is also a correlation between the HPA axis activation and gut microbiota, which has a significant impact on the development of MDD. It is believed that the gut microbiota can influence the HPA axis function through the activity of cytokines, prostaglandins, or bacterial antigens of various microbial species. The activity of the HPA axis in schizophrenia varies and depends mainly on the severity of the disease. This review summarizes the involvement of the HPA axis in the pathogenesis of neuropsychiatric disorders, focusing on major depression and schizophrenia, and highlights a possible correlation between these conditions. Although many effective antidepressants are available, a large proportion of patients do not respond to initial treatment. This review also discusses new therapeutic strategies that affect the HPA axis, such as glucocorticoid receptor (GR) antagonists, vasopressin V1B receptor antagonists and non-psychoactive CB1 receptor agonists in depression and/or schizophrenia.
50 citations
TL;DR: The developed Greek version of PSS-14 seems to be a valid instrument for the assessment of perceived stress in the Greek adult population living in urban areas; a finding that supports its local use in research settings as an evaluation tool measuring perceived stress, mainly as a risk factor but without diagnostic properties.
Abstract: Aim: To evaluate validity of the Greek version of a global measure of perceived stress PSS-14 (Perceived Stress Scale - 14 item). Materials and Methods: The original PSS.14 (theoretical range 0.56) was translated into Greek and then back-translated. One hundred men and women (39±10 years old, 40 men) participated in the validation process. Firstly, participants completed the Greek PSS-14 and, then they were interviewed by a psychologist specializing in stress management. Cronbach's alpha (α) evaluated internal consistency of the measurement, whereas Kendall's tau-b and Bland & Altman methods assessed consistency with the clinical evaluation. Exploratory and Confirmatory Factor analyses were conducted to reveal hidden factors within the data and to confirm the two-dimensional character of the scale. Results: Mean (SD) PSS-14 score was 25(7.9). Strong internal consistency (Cronbach's α = 0.847) as well as moderate-to-good concordance between clinical assessment and PSS-14 (Kendall's tau-b = 0.43, p<0.01) were observed. Two factors were extracted. Factor one explained 34.7% of variability and was heavily laden by positive items, and factor two that explained 10.6% of the variability by negative items. Confirmatory factor analysis revealed that the model with 2 factors had chi-square equal to 241.23 (p<0.001), absolute fix indexes were good (i.e. GFI=0.733, AGFI=0.529), and incremental fix indexes were also adequate (i.e. NFI=0.89 and CFI=0.92). Conclusion: The developed Greek version of PSS-14 seems to be a valid instrument for the assessment of perceived stress in the Greek adult population living in urban areas; a finding that supports its local use in research settings as an evaluation tool measuring perceived stress, mainly as a risk factor but without diagnostic properties.
49 citations
References
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TL;DR: The short variant of the polymorphism reduces the transcriptional efficiency of the 5-HTT gene promoter, resulting in decreased 5HTT expression and 5HT uptake in lymphoblasts as discussed by the authors, which is the site of action of widely used uptake-inhibiting antidepressant and antianxiety drugs.
Abstract: Transporter-facilitated uptake of serotonin (5-hydroxytryptamine or 5-HT) has been implicated in anxiety in humans and animal models and is the site of action of widely used uptake-inhibiting antidepressant and antianxiety drugs. Human 5-HT transporter (5-HTT) gene transcription is modulated by a common polymorphism in its upstream regulatory region. The short variant of the polymorphism reduces the transcriptional efficiency of the 5-HTT gene promoter, resulting in decreased 5-HTT expression and 5-HT uptake in lymphoblasts. Association studies in two independent samples totaling 505 individuals revealed that the 5-HTT polymorphism accounts for 3 to 4 percent of total variation and 7 to 9 percent of inherited variance in anxiety-related personality traits in individuals as well as sibships.
5,072 citations
"The stress-vulnerability model how ..." refers background in this paper
...Polymorphisms in the SERT gene have been shown to influence different individual responses to stress (Lesch et al. 1996), an example of a direct stress-vulnerability interaction....
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TL;DR: Findings translate previous results from rat to humans and suggest a common effect of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression.
Abstract: Maternal care influences hypothalamic-pituitary-adrenal (HPA) function in the rat through epigenetic programming of glucocorticoid receptor expression. In humans, childhood abuse alters HPA stress responses and increases the risk of suicide. We examined epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history of childhood abuse and those from either suicide victims with no childhood abuse or controls. We found decreased levels of glucocorticoid receptor mRNA, as well as mRNA transcripts bearing the glucocorticoid receptor 1F splice variant and increased cytosine methylation of an NR3C1 promoter. Patch-methylated NR3C1 promoter constructs that mimicked the methylation state in samples from abused suicide victims showed decreased NGFI-A transcription factor binding and NGFI-A–inducible gene transcription. These findings translate previous results from rat to humans and suggest a common effect of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression.
3,087 citations
TL;DR: A neurobiologic understanding of depression also requires identification of the genes that make individuals vulnerable or resistant to the syndrome, and advances will fundamentally improve the treatment and prevention of depression.
2,768 citations
"The stress-vulnerability model how ..." refers background in this paper
...The link between the hypothalamo-pituitary-adrenal (HPA) axis and the development of mental illnesses like depression (Nestler et al. 2002), psychosis (Pariante et al. 2004, Garner et al. 2005), bipolar mania and anxiety disorders is well documented in the literature....
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TL;DR: These findings constitute the framework for an updated molecular and cellular hypothesis of depression, which posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, neurotrophic factors necessary for the survival and function of particular neurons.
Abstract: Recent studies have begun to characterize the actions of stress and antidepressant treatments beyond the neurotransmitter and receptor level. This work has demonstrated that long-term antidepressant treatments result in the sustained activation of the cyclic adenosine 3',5'-monophosphate system in specific brain regions, including the increased function and expression of the transcription factor cyclic adenosine monophosphate response element-binding protein. The activated cyclic adenosine 3',5'-monophosphate system leads to the regulation of specific target genes, including the increased expression of brain-derived neurotrophic factor in certain populations of neurons in the hippocampus and cerebral cortex. The importance of these changes is highlighted by the discovery that stress can decrease the expression of brain-derived neurotrophic factor and lead to atrophy of these same populations of stress-vulnerable hippocampal neurons. The possibility that the decreased size and impaired function of these neurons may be involved in depression is supported by recent clinical imaging studies, which demonstrate a decreased volume of certain brain structures. These findings constitute the framework for an updated molecular and cellular hypothesis of depression, which posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, neurotrophic factors necessary for the survival and function of particular neurons. This hypothesis also explains how stress and other types of neuronal insult can lead to depression in vulnerable individuals and it outlines novel targets for the rational design of fundamentally new therapeutic agents.
2,029 citations
"The stress-vulnerability model how ..." refers background in this paper
...Other monoamine neurotransmitters may well be involved in similar mechanisms to affect down-stream BDNF production (Duman et al. 1997)....
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TL;DR: In this article, a second-order model, vulnerability, is proposed as the common denominator, and methods for finding markers of vulnerability are suggested in the hope of revitalizing the field.
Abstract: Although descriptive and etiological approaches to psychopathology have made notable advances, they seem to have reached a plateau. After reviewing the six approaches to etiology that now preempt the field—ecological, developmental, learning, genetic, internal environment, and neurophysiological models—a second-order model, vulnerability, is proposed as the common denominator, and methods for finding markers of vulnerability are suggested in the hope of revitalizing the field. It is assumed that exogenous and/or endogenous challengers elicit a crisis in all humans, but depending on the intensity of the elicited stress and the threshold for tolerating it, that is, one's vulnerability, the crisis will either be contained homeostatically or lead to an episode of disorder. Vulnerability and episode stand in a trait-state relation, and markers for each must be provided to distinguish between them.
2,022 citations