Core Dimensions of Anxiety and Depression Change Independently During Adolescence

The developmental trajectories of emotional disorder symptoms during adolescence remain elusive, owing in part to a shortage of intensive longitudinal data. In the present study, we charted the temporal course of the tripartite model of anxiety and depression-which posits an overarching negative affect dimension and specific anhedonia and anxious arousal dimensions-over adolescence and emerging adulthood to construct a developmental map of the core dimensions of emotional disorders. We recruited 604 high school juniors, overselecting those at high risk for emotional disorders, and assessed the tripartite symptom domains 5 times annually. Latent curve modeling revealed that negative affect and anxious arousal declined over follow up, whereas anhedonia did not. Moreover, the correlation in rate of change varied across pairs of symptom domains. Change in negative affect was moderately correlated with change in anxious arousal, but change in anhedonia was not significantly related to change in any other domain. Symptom trajectories, and the pattern of covariation among trajectories, were equivalent across gender and comorbidity status. We discuss implications of these findings for developmental models of anxiety and depression, as well as transdiagnostic frameworks for emotional disorders

Pathological Personality Traits and the Naturalistic Course of Internalizing Disorders Among High-Risk Young Adults

BackgroundA personality disorder diagnosis signals a negative prognosis for depressive and anxiety disorders, but the precise abnormal personality traits that determine the temporal course of internalizing psychopathology are unknown. In the present study, we examined prospective associations between abnormal personality traits and the onset and recurrence of internalizing disorders. MethodsA sample of 371 young adults at high risk for internalizing problems completed the Schedule for Nonadaptive and Adaptive Personality-Second Editiona measure of 12 abnormal personality traits and three temperament dimensions (i.e., Negative Temperament, Positive Temperament, Disinhibition vs. Control)and underwent annual diagnostic interviews over 4 years of follow-up. ResultsIn multivariate survival analyses, Negative Temperament was a robust predictor of both new onsets and recurrences of internalizing disorder. Further, the Dependency and Self-Harm abnormal personality dimensions emerged as independent predictors of new onsets and recurrences, respectively, of internalizing disorders after statistically adjusting for variation in temperament. ConclusionsOur findings suggest that abnormal personality traits and temperament dimensions have complementary effects on the trajectory of internalizing pathology during young adulthood. In assessment and treatment settings, targeting the abnormal personality and temperament dimensions with the greatest prognostic value stands to improve the early detection of enduring internalizing psychopathology

Core Dimensions of Anxiety and Depression Change Independently During Adolescence

The developmental trajectories of emotional disorder symptoms during adolescence remain elusive, owing in part to a shortage of intensive longitudinal data. In the present study, we charted the temporal course of the tripartite model of anxiety and depression-which posits an overarching negative affect dimension and specific anhedonia and anxious arousal dimensions-over adolescence and emerging adulthood to construct a developmental map of the core dimensions of emotional disorders. We recruited 604 high school juniors, overselecting those at high risk for emotional disorders, and assessed the tripartite symptom domains 5 times annually. Latent curve modeling revealed that negative affect and anxious arousal declined over follow up, whereas anhedonia did not. Moreover, the correlation in rate of change varied across pairs of symptom domains. Change in negative affect was moderately correlated with change in anxious arousal, but change in anhedonia was not significantly related to change in any other domain. Symptom trajectories, and the pattern of covariation among trajectories, were equivalent across gender and comorbidity status. We discuss implications of these findings for developmental models of anxiety and depression, as well as transdiagnostic frameworks for emotional disorders

Association of persistent and severe postnatal depression with child outcomes

IMPORTANCE Maternal postnatal depression (PND) is common and associated with adverse child outcomes. These effects are not inevitable, and it is critical to identify those most at risk. Previous work suggests that the risks of adverse outcomes are increased when PND is severe and persistent, but this has not been systematically studied. OBJECTIVE To examine the association between differing levels of persistence and severity of PND and long-term child outcomes. DESIGN, SETTING, AND PARTICIPANTS The sample for this observational study comprised participants in the Avon Longitudinal Study of Parents and Children in the United Kingdom. Three thresholds of PND severity—moderate, marked, and severe—were defined using the self-rated Edinburgh Postnatal Depression Scale (EPDS). Depression was defined as persistent when the EPDS score was above the threshold level at both 2 and 8 months after childbirth. For each of these severity and persistence categories, the following were examined: (1) the trajectories of later EPDS scores (6 time points between 21 months and 11 years after childbirth) and (2) child outcomes—behavioral problems at 3.5 years of age, school-leaving mathematics grades at 16 years of age, and depression at 18 years of age. Data analysis was conducted from July 12, 2016, to February 8, 2017. MAIN OUTCOMES AND MEASURES Child behavioral problems at 3.5 years of age using the Rutter total problems scale, school-leaving mathematics grades at 16 years of age extracted from records of external national public examinations, and offspring depression at 18 years of age using the Clinical Interview Schedule–Revised. RESULTS For the 9848 mothers in the sample, the mean (SD) age at delivery was 28.5 (4.7) years. Of the 8287 children, 4227 (51%) were boys and 4060 (49%) were girls. Compared with women with PND that was not persistent and women who did not score above the EPDS threshold, for all 3 severity levels, women with persistent PND showed elevated depressive symptoms up to 11 years after childbirth. Whether persistent or not, PND doubled the risk of child behavior disturbance. The odds ratio (OR) for child behavioral disturbance for mothers with moderate PND was 2.22 (95% CI, 1.74-2.83), for mothers with marked PND was 1.91 (95% CI, 1.36-2.68), and for mothers with severe PND was 2.39 (95% CI, 1.78-3.22). Persistence of severe PND was particularly important to child development, substantially increasing the risk for behavioral problems at 3.5 years of age (OR, 4.84; 95% CI, 2.94-7.98), lower mathematics grades at 16 years of age (OR, 2.65; 95% CI, 1.26-5.57), and higher prevalence of depression at 18 years of age (OR, 7.44; 95% CI, 2.89-19.11). CONCLUSIONS AND RELEVANCE Persistent and severe PND substantially raises the risk for adverse outcome on all child measures. Meeting criteria for depression both early and late in the postnatal year, especially when the mood disturbance is severe, should alert health care professionals to a depression that is likely to be persistent and to be associated with an especially elevated risk of multiple adverse child outcomes. Treatment for this group should be prioritized

Preliminary Evidence That CD38 Moderates the Association of Neuroticism on Amygdala-Subgenual Cingulate Connectivity.

CD38 genetic variation has been associated with autism spectrum disorders and social anxiety disorder, which may result from CD38's regulation of oxytocin secretion. Converging evidence has found that the rs3796863 A-allele contributes to increased social sensitivity compared to the CC genotype. The current study examined the moderating role of CD38 genetic variants (rs3796863 and rs6449182) that have been associated with enhanced (or reduced) social sensitivity on neural activation related to neuroticism, which is commonly elevated in individuals with social anxiety and depression. Adults (n = 72) with varying levels of social anxiety and depression provided biological samples for DNA extraction, completed a measure of neuroticism, and participated in a standardized emotion processing task (affect matching) while undergoing fMRI. A significant interaction effect was found for rs3796863 x neuroticism that predicted right amygdala-subgenual anterior cingulate cortex (sgACC) functional connectivity. Simple slopes analyses showed a positive association between neuroticism and right amygdala-sgACC connectivity among rs3796863 A-allele carriers. Findings suggest that the more socially sensitive rs3796863 A-allele may partially explain the relationship between a known risk factor (i.e. neuroticism) and promising biomarker (i.e. amygdala-sgACC connectivity) in the development and maintenance of social anxiety and depression

Interoceptive Anxiety and Body Representation in Anorexia Nervosa

Individuals with anorexia nervosa (AN) typically display anxious traits prior to the onset of food avoidance and weight loss that characterize the disorder. Meal associated anxiety is an especially common clinical feature in these patients, and heightened sensitivity to sympathetically mediated interoceptive sensations has also been observed. However, it remains unclear how heightened interoceptive sensitivity relates to experiences of anxiety before and after meals. To investigate this relationship, we experimentally induced anxiety and panic symptoms with isoproterenol, a peripheral sympathetic agonist similar to adrenaline, across several different conditions: during panic provocation, during anticipation of a 1,000 Calorie meal, and after meal consumption. Fifteen AN and 15 age- and sex-matched healthy comparisons received bolus infusions of isoproterenol and saline in a double-blinded, randomized design. Participants rated anxiety symptoms after each infusion, completed panic rating scales, and traced the location of perceived palpitations on a manikin to index interoceptive “body map” representation. The AN group reported significantly elevated anxiety relative to healthy comparisons during infusions before and after the meal, but surprisingly, not during panic provocation. These symptoms were accompanied by geographical differences in patterns of perceived heartbeat sensations across each condition. In particular, the AN group localized heartbeat sensations disproportionately to the chest during meal related saline infusions, when no cardiorespiratory modulation actually occurred. The AN group also showed a trend toward higher panic attack rates during the meal anticipation period. Correcting for anxiety levels reported during saline infusions abolished group differences in anxiety change across all conditions, suggesting a significant contribution of anxious traits in AN. The observation of meal related “visceral illusions” provides further evidence that AN is associated with abnormal interoceptive representation of the heartbeat and suggests that meal consumption, particularly when anticipated, preferentially alters the processing of interoception related signals in AN

Chronic and episodic interpersonal stress as statistically unique predictors of depression in two samples of emerging adults.

Few studies comprehensively evaluate which types of life stress are most strongly associated with depressive episode onsets, over and above other forms of stress, and comparisons between acute and chronic stress are particularly lacking. Past research implicates major (moderate to severe) stressful life events (SLEs), and to a lesser extent, interpersonal forms of stress; research conflicts on whether dependent or independent SLEs are more potent, but theory favors dependent SLEs. The present study used 5 years of annual diagnostic and life stress interviews of chronic stress and SLEs from 2 separate samples (Sample 1 N = 432; Sample 2 N = 146) transitioning into emerging adulthood; 1 sample also collected early adversity interviews. Multivariate analyses simultaneously examined multiple forms of life stress to test hypotheses that all major SLEs, then particularly interpersonal forms of stress, and then dependent SLEs would contribute unique variance to major depressive episode (MDE) onsets. Person-month survival analysis consistently implicated chronic interpersonal stress and major interpersonal SLEs as statistically unique predictors of risk for MDE onset. In addition, follow-up analyses demonstrated temporal precedence for chronic stress; tested differences by gender; showed that recent chronic stress mediates the relationship between adolescent adversity and later MDE onsets; and revealed interactions of several forms of stress with socioeconomic status (SES). Specifically, as SES declined, there was an increasing role for noninterpersonal chronic stress and noninterpersonal major SLEs, coupled with a decreasing role for interpersonal chronic stress. Implications for future etiological research were discussed

Altered emotion regulation capacity in social phobia as a function of comorbidity

Social phobia (SP) has been associated with amygdala hyperreactivity to fear-relevant stimuli. However, little is known about the neural basis of SP individuals capacity to downregulate their responses to such stimuli and how such regulation varies as a function of comorbid depression and anxiety. We completed an functional magnetic resonance imaging (fMRI) study wherein SP participants without comorbidity (n ¼ 30), with comorbid depression (n ¼ 18) and with comorbid anxiety (n ¼ 19) and healthy controls (n ¼ 15) were scanned while completing an affect labeling emotion regulation task. Individuals with SP as a whole exhibited a reversal of the pattern observed in healthy controls in that they showed upregulation of amygdala activity during affect labeling. However, subsequent analyses revealed a more complex picture based on comorbidity type. Although none of the SP subgroups showed the normative pattern of amygdala downregulation, it was those with comorbid depression specifically who showed significant upregulation. Effects could not be attributed to differences in task performance, amygdala reactivity or right ventral lateral prefrontal cortex (RVLPFC) engagement, but may stem from dysfunctional communication between amygdala and RVLPFC. Furthermore, the particularly altered emotion regulation seen in those with comorbid depression could not be fully explained by symptom severity or state anxiety. Results reveal altered emotion regulation in SP, especially when comorbid with depression