Dimensions of Depression and Anxiety and the Hypothalamo-Pituitary-Adrenal Axis

Wardenaar, Klaas J.; Vreeburg, Sophie A.; Veen, Tineke van; Giltay, Erik J.; Veen, Gerthe; Penninx, Brenda W. J. H.; Zitman, Frans G.

doi:10.1016/j.biopsych.2010.09.005

Cited by 87 publications

(65 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Non-linear associations with an inverted U-shape were observed during anticipatory anxiety to pain for the anterior cingulate cortex (Straube et al 2009). In a study assessing a large sample of patients with lifetime anxiety disorder, anxious arousal showed a similar non-linear association with cortisol awakening response (Wardenaar et al 2011), which is of interest given that our analysis also implicated the hypothalamus. An earlier study in healthy volunteers observed the inverted U-shaped relationship between anxiety and both cerebral blood flow and cerebral metabolic rates for glucose (Gur et al 1987).…”

Section: Discussionmentioning

confidence: 57%

Neural response to the observable self in social anxiety disorder

et al. 2012

View full text Add to dashboard Cite

Background. Distorted images of the observable self are considered crucial in the development and maintenance of social anxiety. We generated an experimental situation in which participants viewed themselves from an observer's perspective when exposed to scrutiny and evaluation by others.Method. Twenty patients with social anxiety disorder (SAD) and 20 control subjects were assessed using functional magnetic resonance imaging (fMRI) during the public exposure of pre-recorded videos in which they were each shown performing a verbal task. The examiners acted as the audience in the experiment and rated performance. Whole-brain functional maps were computed using Statistical Parametric Mapping.Results. Robust activation was observed in regions related to self-face recognition, emotional response and general arousal in both study groups. Patients showed significantly greater activation only in the primary visual cortex. By contrast, they showed significant deactivation or smaller activation in dorsal frontoparietal and anterior cingulate cortices relevant to the cognitive control of negative emotion. Task-related anxiety ratings revealed a pattern of negative correlation with activation in this frontoparietal/cingulate network. Importantly, the relationship between social anxiety scores and neural response showed an inverted-U function with positive correlations in the lower score range and negative correlations in the higher range.Conclusions. Our findings suggest that exposure to scrutiny and evaluation in SAD may be associated with changes in cortical systems mediating the cognitive components of anxiety. Disorder severity seems to be relevant in shaping the neural response pattern, which is distinctively characterized by a reduced cortical response in the most severe cases.

show abstract

Section: Discussionmentioning

confidence: 57%

Neural response to the observable self in social anxiety disorder

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Complex interactions between genetic susceptibility to serotonergic and noradrenergic system dysfunction and stress-related changes in the HPA axis have been implicated in the etiology of depression (Firk, Markus, Firk, & Markus, 2007;Porter et al, 2004), and psychopharmacological treatment studies support the role of reduced neurotransmission of serotonin and norepinephrine in the pathophysiology of GAD (Nutt, Argyropoulos, Hood, & Potokar, 2006). Despite the extensive body of research linking corticotrophin-releasing factor and the HPA axis to depression (Hankin, Badanes, Abela, & Watamura, 2010;Nemeroff & Vale, 2005;Wardenaar, et al, 2011), almost 24 no research has investigated the role of the HPA axis in the etiology of GAD separate from the INT-FA anxiety disorders. Although findings of associations between the HPA axis functioning and anxiety disorders in general have been mixed (Risbrough & Stein, 2006), evidence from a study of HPA functioning in GAD patients showed significant changes in plasma cortisol following cognitive treatment (Tafet, Feder, Abulafia, & Roffman, 2005).…”

mentioning

confidence: 99%

An Integrative Common Liabilities Model for the Comorbidity of Substance Use Disorders with Externalizing and Internalizing Disorders

Tully

Iacono

2014

Oxford Handbooks Online

View full text Add to dashboard Cite

This paper presents an integrative research-derived model to explain comorbidity among SUDs, externalizing disorders, and internalizing disorders. This hierarchical model is based on phenotypic covariance among the disorders and latent common genetic liability. At the highest level of the hierarchy, general genetically-influenced biological dispositions to negative emotionality and behavioral disinhibition each give rise to spectra of related personality traits, cognitive processes, behavioral tendencies, and psychopathology that account for the pattern of co-occurrence among mental disorders. At the lowest level of the hierarchy, disorder-specific genetic and environmental effects explain the presence of some and not other disorders associated with a given general liability. Interplay between the general liabilities and both other genes and environmental factors throughout development affect the likelihood of developing specific mental disorders.

show abstract

“…Curiously, the most replicated finding is that PTSD is associated with lower cortisol levels (319,322), which is somewhat unexpected, and may be explained specifically by symptoms of emotional numbing which are unrelated to depression (322,323). In addition, PTSD involves all three components of anxious arousal, dysphoria (which includes anhedonia) and non-specific distress/negative affectivity (314); with the components which feature most prominently differing greatly across patients and changing across the course of the disorder (324,325); and with these components in addition to emotional numbing found differently associated with HPA activity (315,316,323). These dynamics, in addition to the numerous confounding factors which impact the expression of PTSD (e.g., levels of social support, cognitive appraisal of the trauma and genetic factors), may explain the inconsistent results regarding PTSD and HPA activity (326).…”

Section: Major Findings Fetal Development and Psychopathologymentioning

confidence: 94%

“…Chapter two outlined the case that IUGR may be indicative of altered development, which includes permanent reprogramming of the offspring HPA axis that leaves the individual more susceptible to later psychopathology (17). While animal models lack the ability to differentiate behaviours by specific characteristics of human disorders, human biological studies somewhat support the idea that HPA activity is differently related to specific psychiatric disorders, as studies have found that HPA dysregulation is more strongly associated with anhedonia and distress (characteristic of MDD, GAD and PTSD) than anxious arousal (characteristic of phobias and panic) (315,316). These studies suggest that anhedonia and distress may be associated with chronic HPA dysregulation, while anxious arousal could be associated with more temporal elevations in HPA activity.…”

Section: Major Findings Fetal Development and Psychopathologymentioning

confidence: 99%

Early life course determinants of psychopathology

Betts¹

View full text Add to dashboard Cite

Background: Mental health problems are associated with a range of adverse outcomes as well as increased risk of later morbidity and premature mortality. Help seeking is uncommon at the early stages of mental health problems. Rather, treatment is often sought by patients after illnesses have already caused considerable distress or had substantial adverse personal, social and economic impacts. The purpose of the current work is to investigate the role of a number of early life course risk factors in the development of later psychopathology, using advanced statistical and epidemiological approaches applied to longitudinal data to ascertain predictive and causal pathways. The overall scope of this thesis is to provide the evidence necessary for developing primary and secondary prevention programs aimed at reducing the burden of mental illness on society. Aim 1:To investigate the role of intrauterine growth restriction in increasing the risk of psychiatric disorders characterised by negative affectivity. Aim 2:To investigate the potential for a transmission of maternal psychopathology to offspring. Aim 3:To assess whether maternal prenatal infection and exposure to stressful life events predict positive psychotic experiences in the offspring directly, or indirectly via postnatal risks and antecedents of psychosis. Aim 4:To investigate potential risk factors for the increased rates of female post-traumatic stress disorders, including gender-specific vulnerability resulting from physical assault and cognitive ability. Methods:The data came from the Mater University Study of Pregnancy (MUSP), a prospective pre-birth cohort study which began in 1981 at the Mater Hospital in Brisbane, Australia. The baseline sample consisted of 7,223 pregnant women attending their first obstetric visit for that pregnancy. Since then follow-ups over 21 years have prospectively ascertained a range of health related data on both mother and child. The current work uses predictor variables and covariates from every measurement period, and behaviour and mental health measures ascertained from the offspring at ages 14 and 21 years. A number of statistical and methodological approaches were applied to estimate the longitudinal association between a number of early life course risk factors and later psychopathology, and to account for attrition. Key findings:The relationship between birth weight and later psychopathology was specific to particular psychiatric diagnoses, namely Post-Traumatic Stress Disorders, and comorbid Major Depression and Generalised Anxiety Disorders. The combination of maternal prenatal depressive, anxious and stress symptoms predicted increased internalising and externalising behaviour problems in adolescent and adult offspring. Prenatal maternal infections and stressful life events predicted later offspring psychotic experiences via the intermediaries of early infant illness iii susceptibility and child behaviour problems respectively. The risk of Post-Traumatic Stress Disorder associated with physical assault and ...

show abstract

Dimensions of Depression and Anxiety and the Hypothalamo-Pituitary-Adrenal Axis

Cited by 87 publications

References 47 publications

Neural response to the observable self in social anxiety disorder

Neural response to the observable self in social anxiety disorder

An Integrative Common Liabilities Model for the Comorbidity of Substance Use Disorders with Externalizing and Internalizing Disorders

Early life course determinants of psychopathology

Contact Info

Product

Resources

About