Internalising disorders - anxiety - research Flashcards
Miech and Shanahan (2000)
Numerous studies document lower levels of depression among adults with higher education, but little is known about the way in which the association varies over the life course. Do depression levels diverge or converge across educational strata with age? This study investigates how the association between education and depression changes with age and tests the extent to which these changes are accountedfor by physical health problems, widowed status, employment status, coping resources, household income, and financial strain. Data for this investigation come from the Work, Family, and Well-Being Study, 1990, a nationally representative sample of 2,031 adults aged 18 to 90 interviewed by telephone. Findings indicate that the association between depression and education strengthens with increasing age. Physical health problems among adults with lower education account for most of the diverging gap in depression. These results show that an integration of insights from the stress paradigm and the life course perspective can lead to a fuller understanding of socioeconomic inequality and its influence on psychological functioning.
Colman et al. (2007)
METHODS: A longitudinal latent variable analysis was conducted on measures of anxious and depressive symptoms at ages 13, 15, 36, 43, and 53 years among 4627 members of the Medical Research Council National Survey of Health & Development (the British 1946 birth cohort). Early life predictors of class membership were studied with ordinal logistic regression.
RESULTS:
We identified six distinct profiles up to age 53: absence of symptoms (44.8% of sample); repeated moderate symptoms (33.6%); adult-onset moderate symptoms (11.3%); adolescent symptoms with good adult outcome (5.8%); adult-onset severe symptoms (2.9%); and repeated severe symptoms over the life course (1.7%). Heavier babies had lower likelihood of depressive and anxious symptoms (odds ratio [OR] = .92; 95% confidence interval [CI] .85-.99), whereas delay in first standing (OR = 1.19; 95% CI 1.11-1.28) and walking (OR = 1.22; 95% CI 1.14-1.31) was associated with subsequent higher likelihood of symptoms, controlling for social circumstances and stressful life events during childhood.
CONCLUSIONS:
There was evidence of distinct profiles of depressive and anxious symptomatology over the life course and associations with markers of neurodevelopment. This suggests very early factors are associated with long-term experience of symptoms of depression and anxiety.
Colman et al. (2014)
BACKGROUND:
The aetiology of depression is multifactorial, with biological, cognitive and environmental factors across the life course influencing risk of a depressive episode. There is inconsistent evidence linking early life development and later depression. The aim of this study was to investigate relationships between low birthweight (LBW), infant neurodevelopment, and acute and chronic stress as components in pathways to depression in adulthood.
METHOD:
The sample included 4627 members of the National Survey of Health and Development (NSHD; the 1946 British birth cohort). Weight at birth, age of developmental milestones, economic deprivation in early childhood, acute stressors in childhood and adulthood, and socio-economic status (SES) in adulthood were assessed for their direct and indirect effects on adolescent (ages 13 and 15 years) and adult (ages 36, 43 and 53 years) measures of depressive symptoms in a structural equation modelling (SEM) framework. A structural equation model developed to incorporate all variables exhibited excellent model fit according to several indices.
RESULTS:
The path of prediction from birthweight to age of developmental milestones to adolescent depression/anxiety to adult depression/anxiety was significant (p < 0.001). Notably, direct paths from birthweight (p = 0.25) and age of developmental milestones (p = 0.23) to adult depression were not significant. Childhood deprivation and stressors had important direct and indirect effects on depression. Stressors in adulthood were strongly associated with adult depression.
CONCLUSIONS:
Depression in adulthood is influenced by an accumulation of stressors across the life course, including many that originate in the first years of life. Effects of early-life development on mental health appear by adolescence.
Andreescu et al. (2014)
Design and settings
Functional and structural MRI data were collected with subjects at rest. We analyzed the resting state functional connectivity patterns in the DMN for twenty-seven GAD participants and thirty-nine non-anxious comparison participants. Using a two-way ANOVA, we explored the interaction between age and GAD status on functional connectivity. In GAD participants we analyzed the correlation of functional connectivity indices with the duration of illness and worry severity.
Results
The age-by-anxiety interaction showed a greater anxiety effect on the functional connectivity between the posterior cingulate seed and the medial prefrontal cortex for the older group relative to the younger participants. Longer duration of illness was positively correlated with greater functional connectivity between the posterior cingulate cortex and the insula. Worry severity was inversely correlated with the functional connectivity between the PCC seed and the medial prefrontal cortex.
Conclusion
The presence of GAD, longer duration of illness and more severe worry exacerbate the effects of age on the functional connectivity in the Default Mode Network. These results support the need for tailored research and interventions in late-life anxiety.
Wolitzky-Taylor et al. (2010)
This review aims to address issues unique to older adults with anxiety disorders in order to inform potential changes in the DSM‐V. Prevalence and symptom expression of anxiety disorders in late life, as well as risk factors, comorbidity, cognitive decline, age of onset, and treatment efficacy for older adults are reviewed. Overall, the current literature suggests: (a) anxiety disorders are common among older age individuals, but less common than in younger adults; (b) overlap exists between anxiety symptoms of younger and older adults, although there are some differences as well as limitations to the assessment of symptoms among older adults; (c) anxiety disorders are highly comorbid with depression in older adults; (d) anxiety disorders are highly comorbid with a number of medical illnesses; (e) associations between cognitive decline and anxiety have been observed; (f) late age of onset is infrequent; and (g) both pharmacotherapy and CBT have demonstrated efficacy for older adults with anxiety. The implications of these findings are discussed and recommendations for the DSM‐V are provided, including extending the text section on age‐specific features of anxiety disorders in late life and providing information about the complexities of diagnosing anxiety disorders in older adults.
Nilsson et al. (2018)
Method
Semistructured psychiatric examinations were performed in population‐based samples of 70‐ (n = 562), 75‐ (n = 770), 79/80‐ (n = 603), and 85‐year‐olds (n = 433). Individuals with dementia were excluded. GAD was diagnosed according to DSM‐5 (DSM5 GAD) and ICD‐10 (ICD10 GAD) criteria. Individual symptoms were assessed according to severity and frequency. Functioning was measured with Global Assessment of Functioning (GAF).
Results
The prevalence of clinical anxiety, autonomic arousal, muscle tension, and irritability decreased with age, while that of worry and fatigue increased. Concentration difficulties and sleep disturbances remained stable. The prevalence of ICD10 GAD tended to decrease, while that of DSM5 GAD did not change with age. Core symptoms and diagnoses of GAD were related to lower GAF scores. However, in those with autonomic arousal and ICD10 GAD, GAF scores increased with age.
Conclusions
The prevalence of ICD10 GAD tended to decrease with increasing age while the prevalence of DSM5 GAD remained stable. This difference was partly due to a decreased frequency of severe anxiety and autonomic arousal symptoms, and that worries increased, suggesting changes in the expression of GAD with increasing age.
Lavallee and Schnieder (2019)
earliest and most common in children
attachment related stress
BI and attachment are risk factors
highly comorbid with other anxiety disorders .
Cho et al. (2019)
A number of revisions were proposed for the DSM-5 criteria for GAD, yet the following DSM-IV criteria have been retained without modification: Excessive anxiety and worry occurring more days than not about a number of events or activities for at least 6 months (Criterion A); Worry is difficult to control (Criterion B); Anxiety and worry are associated with at least one of the following six symptoms for children (these symptoms were present for more days than not for the past 6 months): restlessness, being easily fatigued, concentration difficulties, irritability, muscle tension, sleep disturbance (Criterion C); The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion D). With the exception of the minimum number of associated symptoms required for Criterion C, the current version of the DSM applies identical symptom criteria to adults and children. Guidelines are available, however, for developmentally-informed clinical decision-making with very young children. For example, the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood: Revised Edition (DC:05; ZERO TO THREE, 2016) offers descriptive information about the ways in which the DSM-5 symptoms of GAD commonly manifest in children ages 5 years and younger. During early childhood, symptoms of GAD are likely to occur in the context of caregiverchild interaction. Cognitive symptoms such as uncontrollable worries are often expressed behaviorally during young
children’s interaction with their caregivers (e.g., excessive verbal reassurance seeking that does not decrease with repetition). Similarly, impairment is likely to be observed at the dyadic level, with caregivers’ accommodation of children’s excessive worries being a common form of impairment associated with GAD in early childhood.
GAD is a highly prevalent anxiety disorder that is accompanied by elevated rates of comorbidity and impairment. Although worry and emotional distress that characterize GAD occur across all anxiety disorders, findings that document the distinctive patterns of
developmental trajectories and unique correlates of GAD provide compelling evidence for its status as a meaningful, stand-alone childhood disorder. Multiple lines of research consistently demonstrate that cognitive, social, and neurobiological correlates of GAD are linked to heightened affective reactivity and emotional dysfunction. Therefore, consistent with contemporary theoretical models of GAD that are based on the adult GAD population, accumulating evidence indicates the centrality of affective dysfunction in GAD in children and youths. In an attempt to integrate the distinct etiological factors that are implicated in childhood GAD, we reviewed the Contrast Avoidance Model of Worry as a conceptual framework that outlines the transactional processes by which developmental, biological, and socialization experiences lead to chronic worry and sustained negative affect. Although treatment mechanisms of pediatric GAD remain to be understood, decades of research on treatment of pediatric GAD indicates that youths with GAD tend to respond favorably to CBT and emphasizes the value of incorporating exposure to worryeliciting situations and post-exposure processing. Future research examining personalized approaches to treatment and exposure-oriented approaches that target affective dysfunction (e.g., fear of increased negative affect) may inform efforts to augment the efficacy of
CBT for GAD. Recent advances in assessment of early childhood also offer exciting new opportunities to explore the etiological processes that begin early in life and underscore the importance of developing intervention and prevention for early-onset GAD.
Kertz and Woodruff-Borden (2011)
Although childhood generalized anxiety disorder is generally understudied, worry, the cardinal feature of GAD, appears to be relatively common in youth. Despite its prevalence, there are few conceptual models of the development of clinical worry in children. The current review provides a framework for integrating the developmental psychopathology perspective, models of worry in adults, and data available on worry in children. General risk factors for the development of worry are considered, as well as potential pathways including genetics, temperament, cognitive, emotional and parenting influences, as well as the influence of cognitive development. Based on this review, it appears unlikely that main effects models will be able to explain the development of GAD or clinical worry in children and that a broad, complex model incorporating a number of factors and their interactions will best describe etiological and maintaining factors. With this perspective in mind, a number of suggestions for future work are offered.
NCBI
table comparing DSM-IV to V
Meier and Deckert (2019)
In this brief review, we have examined the current evidence for heritability of anxiety disorders with a particular focus on large-scale, unbiased GWAS results. We also reviewed first EWAS attempts aiming to identify differential DNA methylation patterns associated with anxiety risk. Although both GWAS and EWAS studies report genome-wide significant findings, most of these loci are not consistently replicated. Further, most studies still lack sufficient power to unravel the complex genetic architecture of anxiety disorders. These conclusions immediately suggest directions for future research to satisfy the need for an enhanced prediction of disease
risk, course, and responsiveness to clinical interventions.
There is need for very large, well-characterized samples and even larger meta-analyses to be conducted by large consortia before unambiguous findings will be available. Second, leveraging of genetic covariance with other disorders is necessary in such a highly comorbid disorder as anxiety. And finally, as anxiety disorder, like most mental disorders, and certainly PTSD, is a result of both environmental risk and biological risk, more emphasis should be given to efforts integrating both risk types. As the field evolves, genetic research might enable us to utilize more effective strategies for the prevention and treatment of anxiety disorders in the future.
Meier et al. (2019)
anxiety conditions are complex heritable phenotypes with varying genetic correlations
Ersoy (2019)
BI is involved in the aetiology of early emerging anxiety traits in toddlers at risk of ASD.
Brujnen et al. (2019)
Background: Social anxiety disorder (SAD) is one of the most prevalent psychiatric disorders in South Africa. Previous studies have linked childhood trauma with the development of SAD. The behavioural inhibition system (BIS) and the behavioural activation system (BAS), two dimensions of personality related to anxiety and impulsivity, respectively, are said to influence the development of psychopathology, including SAD. Both SAD and childhood trauma have an impact on quality of life. This study investigated the relationship between BIS, BAS and quality of life in patients with SAD with and without exposure to childhood trauma, compared to healthy controls.
Method: Data were collected for 102 adults. A total of 76 participants met SAD criteria, of which 51 were exposed to childhood trauma and 25 were not. The remaining 26 participants were demographically matched healthy controls. Measures of anxiety, impulsivity and quality of life were obtained by administering Carver and White’s BIS/BAS scales and the Quality of Life Enjoyment and Satisfaction Questionnaire – Self Report.
Results: A positive correlation was found between the severity of SAD symptoms and the amount of childhood trauma exposure. No significant differences in impulsivity were found across the three groups. Healthy controls reported significantly lower anxiety and a better quality of life than both groups with SAD, while no differences were found between patients with SAD and childhood trauma and those without childhood trauma.
Conclusion: More childhood trauma exposure appears to be associated with greater SAD severity. The lack of differences in BIS, BAS and quality of life in patients with SAD with or without childhood trauma requires further investigation.
Trask (2019)
This study explored the relationship between anxiety and the social information processing (SIP) model. Children’s responses to several stages of the SIP model were assessed after children had undergone anxious mood induction procedures, and similarities and differences between anxious and aggressive children were examined. Furthermore, temperament and heritability were investigated in relation to anxiety and stages of the SIP model. Data were collected from 45 families within the Southern Illinois Twins/Triplets and Siblings Study
(SITSS). Results showed that children’s anxiety was related to generating avoidant responses in one stage of the SIP model, whereas children’s aggression was not significantly associated with any SIP stage. Children’s worried and angry mood states predicted avoidant and aggressive
responses, respectively. Temperament was not significantly related to anxiety or stages of the SIP model. Lastly, there was evidence of heritability for child-rated anxiety, but not for parentrated anxiety or stages of the SIP model. Overall, this study provides important information about possible contributors to children’s maladaptive social behavior.
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