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Developmental change in amygdala reactivity during adolescence: effects of family history of depression and stressful life events.

ABSTRACT: Although heightened amygdala reactivity is observed in patients with major depression, two critical gaps in our knowledge remain. First, it is unclear whether heightened amygdala reactivity is a premorbid vulnerability or a consequence of the disorder. Second, it is unknown how and when this neural phenotype develops. The authors sought to address these gaps by evaluating developmental change in threat-related amygdala reactivity in adolescents at high or low risk for depression based on family history, before onset of disorder.At baseline and again 2 years later, adolescents (initially 11-15 years of age) participated in a functional MRI paradigm that elicited threat-related amygdala reactivity. After quality control, data were available for 232 adolescents at wave 1 and 197 adolescents at wave 2; longitudinal data meeting quality control at both waves were available for 157 of these participants. Change in amygdala reactivity was assessed as a function of family history of depression and severity of stressful life events.Threat-related amygdala reactivity increased with age in participants with a positive family history regardless of the severity of life stress reported, and it increased in adolescents with a negative family history who reported relatively severe life stress. These changes in amygdala reactivity with age occurred in the absence of clinical disorder or increases in depressive symptoms.These results suggest that heightened amygdala reactivity emerges during adolescence, prior to the development of depression, as a function of familial risk or, in the absence of familial risk, stressful life events.

SUBMITTER: Swartz JR

PROVIDER: S-EPMC4452289 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

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Developmental change in amygdala reactivity during adolescence: effects of family history of depression and stressful life events.

Swartz Johnna R JR Williamson Douglas E DE Hariri Ahmad R AR

The American journal of psychiatry 20141219 3

<h4>Objective</h4>Although heightened amygdala reactivity is observed in patients with major depression, two critical gaps in our knowledge remain. First, it is unclear whether heightened amygdala reactivity is a premorbid vulnerability or a consequence of the disorder. Second, it is unknown how and when this neural phenotype develops. The authors sought to address these gaps by evaluating developmental change in threat-related amygdala reactivity in adolescents at high or low risk for depressio ...[more]

PMID: 25526599

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Project description:Introduction: Borderline personality disorder (BPD) in adolescents is characterized by emotional dysregulation, insecure attachment, a history of stressful life events (SLEs) as well as dysfunctional parent-child interactions. The respective contribution of each of these factors on BPD affective symptoms is not yet clear. The purpose of this study is to assess the distinct impact of parental adversity and SLEs on BPD affective symptoms and the role of attachment and alexithymia in such emotional processes. Method: This study explored parental dysfunction and SLEs as predictors of affective symptoms of BPD and of attachment insecurity in BPD adolescents (n = 85) and healthy controls (n = 84) aged 13-19 years from the European Research Network on BPD. The links between adversity and BPD symptoms were also investigated by emotional dysregulation assessment, as measured by alexithymia and hopelessness. Results: Dysfunctional parental interactions were linked to affective symptoms, hopelessness, and anxious attachment in healthy controls but not in BPD. Cumulative SLEs were positively correlated with affective symptoms and avoidant attachment in the control group but negatively correlated with both these variables in BPD. Multivariate regression analysis revealed that, in BPD, affective symptoms were independent of dysfunctional parenting but depended on attachment, whereas in controls, a maternal affectionless control style directly predicted affective symptoms. Moreover, increasing numbers of SLEs reduced affective symptoms in BPD, independently of parental interactions or attachment, and were associated with growing use of operative thinking. Discussion: BPD patients showed paradoxical emotional reactions: there was no increase of hopelessness and affective symptoms with an increased parental dysfunction, but a decrease in affective symptoms and hopelessness with cumulative SLE. Two pathways arose, one involving attachment as an emotional dysregulation process for parent-child interactions and a second one for SLE, with a more direct pathway to affective symptoms, independent of attachment but dependent on early interactions, and involving alexithymia. In summary, adversity factors have distinct effects in BPD, and attachment is partly accountable for affective symptoms independently of adversity. Our results suggest that in highly insecure conditions, cumulative adversity may produce paradoxical effects, including a lesser expression of affective symptoms and hopelessness.

Project description:BackgroundScientific enthusiasm about gene × environment interactions, spurred by the 5-HTTLPR (serotonin transporter-linked polymorphic region) × SLEs (stressful life events) interaction predicting depression, have recently been tempered by sober realizations of small effects and meta-analyses reaching opposing conclusions. These mixed findings highlight the need for further research. Converging evidence suggests that the effects of 5-HTTLPR genotype may be neurodevelopmental in origin, but we are not aware of empirical studies that have investigated whether the 5-HTTLPR genotype × SLE interaction predicts preschool-onset depression (PO-MDD), the earliest validated form of depression.MethodsChildren (n = 234) aged 3-5 were recruited for a longitudinal study designed to examine PO-MDD. In a comprehensive baseline assessment, the child's primary caregivers completed questionnaires and were interviewed about their child's behaviors, psychiatric symptoms, and exposure to SLEs.ResultsA 5-HTTLPR × SLEs interaction emerged, such that children homozygous for the short allele were more susceptible to depression in the context of elevated SLE than long allele carriers. In contrast, at low SLE exposure, short allele homozygotes had fewer depressive symptoms. The data were best fit by a plasticity model with a substantial reduction in fit by diathesis-stress models.ConclusionsExtending studies in adult and adolescent populations, these data suggest that 5-HTTLPR genotype may provide plasticity to environmental influence, for better or worse. Specifically, children homozygous for the short allele were more susceptible to the depressogenic effects of SLEs but benefitted, in the form of reduced depressive symptoms, in the context of relatively benign environmental conditions (i.e. relatively low SLE exposure). These data highlight the importance of examining gene × environment interactions across development, environment, and outcome but should be interpreted cautiously given the small sample size.

Dataset Information

Developmental change in amygdala reactivity during adolescence: effects of family history of depression and stressful life events.

Publications

Developmental change in amygdala reactivity during adolescence: effects of family history of depression and stressful life events.

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