The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies

The notion that chronic stress fosters disease by activating the hypothalamic-pituitary-adrenocortical (HPA) axis is featured prominently in many theories. The research linking chronic stress and HPA function is contradictory, however, with some studies reporting increased activation, and others reporting the opposite. This meta-analysis showed that much of the variability is attributable to stressor and person features. Timing is an especially critical element, as hormonal activity is elevated at stressor onset but reduces as time passes. Stressors that threaten physical integrity, involve trauma, and are uncontrollable elicit a high, flat diurnal profile of cortisol secretion. Finally, HPA activity is shaped by a person's response to the situation; it increases with subjective distress but is lower in persons with posttraumatic stress disorder.

If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans.

The estimated lifetime prevalence of bipolar disorder (BPD) in population surveys using structured diagnostic interviews and standardized criteria averages approximately 0.8% for BP-I and 1.1% for BP-II.1-8 Despite this comparatively low prevalence, BPD is a leading cause of premature mortality due to suicide and associated medical conditions such as diabetes and cardiovascular disease.9, 10 BPD also causes widespread role impairment.11, 12 The recurrent nature of manic and depressive episodes often leads to high direct as well as high indirect health care costs.13, 14

BPD might be even more burdensome from a societal perspective due to the fact that sub-threshold bipolar spectrum disorder has seldom been taken into consideration in examining the epidemiology of BPD. Bipolar spectrum disorder includes hypomania without major depression and hypomania of lesser severity or briefer duration than specified in the DSM and ICD criteria. Although the precise definitions are as yet unclear, recent studies suggest that bipolar spectrum disorder might affect as many as 6% of the general population.15, 16 However, bipolar spectrum disorder has not been studied previously in a nationally representative survey of the US. The purpose of the current report is to present the results of such a study based on analysis of the National Comorbidity Survey Replication (NCS-R).17 We estimate prevalence and clinical features of sub-threshold BPD in comparison to BP-I and BP-II.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/482285/yoa60082_543_552.pdf

Lifetime and 12-Month Prevalence of Bipolar Spectrum Disorder in the National Comorbidity Survey Replication

Estimates of 12-month and lifetime prevalence and of lifetime morbid risk (LMR) of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) anxiety and mood disorders are presented based on US epidemiological surveys among people aged 13+. The presentation is designed for use in the upcoming DSM-5 manual to provide more coherent estimates than would otherwise be available. Prevalence estimates are presented for the age groups proposed by DSM-5 workgroups as the most useful to consider for policy planning purposes. The LMR/12-month prevalence estimates ranked by frequency are as follows: major depressive episode: 29.9%/8.6%; specific phobia: 18.4/12.1%; social phobia: 13.0/7.4%; post-traumatic stress disorder: 10.1/3.7%; generalized anxiety disorder: 9.0/2.0%; separation anxiety disorder: 8.7/1.2%; panic disorder: 6.8%/2.4%; bipolar disorder: 4.1/1.8%; agoraphobia: 3.7/1.7%; obsessive-compulsive disorder: 2.7/1.2. Four broad patterns of results are most noteworthy: first, that the most common (lifetime prevalence/morbid risk) lifetime anxiety-mood disorders in the United States are major depression (16.6/29.9%), specific phobia (15.6/18.4%), and social phobia (10.7/13.0%) and the least common are agoraphobia (2.5/3.7%) and obsessive-compulsive disorder (2.3/2.7%); second, that the anxiety-mood disorders with the earlier median ages-of-onset are phobias and separation anxiety disorder (ages 15-17) and those with the latest are panic disorder, major depression, and generalized anxiety disorder (ages 23-30); third, that LMR is considerably higher than lifetime prevalence for most anxiety-mood disorders, although the magnitude of this difference is much higher for disorders with later than earlier ages-of-onset; and fourth, that the ratio of 12-month to lifetime prevalence, roughly characterizing persistence, varies meaningfully in ways consistent with independent evidence about differential persistence of these disorders.

Twelve‐month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States.

Stress is a part of every life to varying degrees, but individuals differ in their stress vulnerability. Stress is usefully viewed from a biological perspective; accordingly, it involves activation of neurobiological systems that preserve viability through change or allostasis. Although they are necessary for survival, frequent neurobiological stress responses increase the risk of physical and mental health problems, perhaps particularly when experienced during periods of rapid brain development. Recently, advances in noninvasive measurement techniques have resulted in a burgeoning of human developmental stress research. Here we review the anatomy and physiology of stress responding, discuss the relevant animal literature, and briefly outline what is currently known about the psychobiology of stress in human development, the critical role of social regulation of stress neurobiology, and the importance of individual differences as a lens through which to approach questions about stress experiences during development and child outcomes.

https://sites.oxy.edu/clint/physio/article/neurobiologyofstressanddevelopment.pdf

The neurobiology of stress and development.

Objective To describe the psychometric properties of the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime version (K-SADS-PL) interview, which surveys additional disorders not assessed in prior K-SADS, contains improved probes and anchor points, includes diagnosis-specific impairment ratings, generates DSM-III-R and DSM-IV diagnoses, and divides symptoms surveyed into a screening interview and five diagnostic supplements. Method Subjects were 55 psychiatric outpatients and 11 normal controls (aged 7 through 17 years). Both parents and children were used as informants. Concurrent validity of the screen criteria and the K-SADS-PL diagnoses was assessed against standard self-report scales. Interrater ( n = 15) and test-retest ( n = 20) reliability data were also collected (mean retest interval: 18 days; range: 2 to 38 days). Results Rating scale data support the concurrent validity of screens and K-SADS-PL diagnoses. Interrater agreement in scoring screens and diagnoses was high (range: 93% to 100%). Test-retest reliability κ coefficients were in the excellent range for present and/or lifetime diagnoses of major depression, any bipolar, generalized anxiety, conduct, and oppositional defiant disorder (.77 to 1.00) and in the good range for present diagnoses of posttraumatic stress disorder and attention-deficit hyperactivity disorder (.63 to .67). Conclusion Results suggest the K-SADS-PL generates reliable and valid child psychiatric diagnoses. J. Am. Acad. Child Adolesc. Psychiatry , 1997, 36(7): 980–988.

Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (K-SADS-PL): Initial Reliability and Validity Data

Paula Moreci

Papers

Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (K-SADS-PL): Initial Reliability and Validity Data

Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version

The corticotropin-releasing hormone challenge in depressed abused, depressed nonabused, and normal control children.