Children exposed to extreme stress are at heightened risk for developing mental and physical disorders. However, little is known about mechanisms underlying these associations in humans. An emerging insight is that children's social environments change gene expression, which contributes to biological vulnerabilities for behavioral problems. Epigenetic changes in the glucocorticoid receptor gene, a critical component of stress regulation, were examined in whole blood from 56 children aged 11–14 years. Children exposed to physical maltreatment had greater methylation within exon 1F in the NR3C1 promoter region of the gene compared to nonmaltreated children, including the putative NGFI-A (nerve growth factor) binding site. These results highlight molecular mechanisms linking childhood stress with biological changes that may lead to mental and physical disorders.
Background Child maltreatment is associated with heightened risk for depression; however, not all individuals who experience maltreatment develop depression. Previous research indicates that maltreatment contributes to an attention bias for emotional cues, and that depressed individuals show attention bias for sad cues. Method The present study examined attention patterns for sad, depression-relevant cues in children with and without experience of maltreatment. We also explored whether individual differences in physiological reactivity and emotion regulation in response to a sad emotional state predict heightened attention to sad cues associated with depression. Results Children who experienced high levels of maltreatment showed an increase in attention bias for sad faces throughout the course of the study, such that they showed biased attention for sad faces following the initiation of a sad emotional state. Maltreated children who had high levels of trait rumination showed an attention bias toward sad faces across all time points. Conclusions These data suggest that maltreated children show heightened attention for depression-relevant cues in certain contexts (e.g., after experience of a sad emotional state). Additionally, maltreated children who tend to engage in rumination show a relatively stable pattern of heightened attention for depression-relevant cues. These patterns may identify which maltreated children are most likely to exhibit biased attention for sad cues and be at heightened risk for depression.
Background Children who experience socioeconomic disadvantage are at heightened risk for developing depression; however, little is known about neurobiological mechanisms underlying this association. Low socioeconomic status (SES) during childhood may confer risk for depression through its stress-related effects on the neural circuitry associated with processing monetary rewards. Methods In a prospective study, we examined the relationships among the number of years of household receipt of public assistance from age 5–16 years, neural activation during monetary reward anticipation and receipt at age 16, and depression symptoms at age 16 in 123 girls. Results Number of years of household receipt of public assistance was positively associated with heightened response in the medial prefrontal cortex during reward anticipation, and this heightened neural response mediated the relationship between socioeconomic disadvantage and current depression symptoms, controlling for past depression. Conclusions Chronic exposure to socioeconomic disadvantage in childhood may alter neural circuitry involved in reward anticipation in adolescence, which in turn may confer risk for depression.
Negative cognitive styles are an important cognitive vulnerability for depression, but stability of high cognitive risk, once developed, is unclear. The current study examined stability of cognitive vulnerability to depression in individuals at high and low cognitive risk (extreme scores on both the CSQ and DAS) over a 7-year period from late adolescence through early adulthood. Cognitive vulnerability showed high relative stability, as evidenced by the moderate to high correlation (r s = . 62) between cognitive risk status at study onset and at final assessment 7 years later. Consistent with stability, subgroups were identified using growth mixture modeling, and most cognitively high-risk (62.22% for CSQ, 68.89% for DAS) and low-risk (55.05% for CSQ, 57.96% for DAS) participants showed stable trajectories of cognitive vulnerability. Despite this overall pattern of stability, small mean group changes were found, and a minority of participants showed changing trajectories, consistent with regression toward the mean. Predictors of change and implications for risk for depression in high-and low-risk individuals are discussed. Keywords cognitive vulnerability; depression; trajectory; stabilityOnce an individual develops vulnerability to depression, can it change without intervention? According to cognitive theories of depression (Abramson, Metalsky, & Alloy, 1989;Beck, 1967), some individuals have a characteristic way of negatively interpreting life events that provides risk for depression, and this vulnerability appears to coalesce and become fully operational during adolescence (Gibb & Alloy, 2006;Hankin & Abramson, 2001;Hyde, Mezulis, & Abramson, 2008). The current study examines stability of cognitive vulnerability to depression in individuals at high and low cognitive risk during the transition from late adolescence, when this vulnerability already has developed, to early adulthood, a critical developmental period (Arnett, 2000). Cognitive Theories of DepressionHopelessness theory (Abramson, Metalsky, & Alloy, 1989) and Beck's (1967) theory of depression are both vulnerability-stress models in which a cognitive pattern serves as a vulnerability that interacts with negative events to predict depression. In hopelessness theory, the cognitive vulnerability is a negative cognitive style, or the tendency to make inferences that negative life events have stable and global causes, have significant negative consequences for the future, and are indicative of negative self-characteristics. This negative cognitive style interacts with the experience of negative life events to predict hopelessness, the proximal cause of depression in hopelessness theory. NIH Public Access Author ManuscriptCognit Ther Res. Author manuscript; available in PMC 2010 March 8. In Beck's theory of depression, the cognitive vulnerability is a negative self-schema containing dysfunctional attitudes involving themes of loss, failure, worthlessness, and inadequacy. When this self-schema is activated by negative life events, it leads to specif...
Individuals with negative cognitive style are at high risk for depressive disorders; however, the mechanisms linking cognitive vulnerability to depression are not fully understood. Here, we use an attentional blink task to test whether stimuli associated with negative attributions are especially salient to individuals with high negative cognitive style. We found that individuals high in negative cognitive style were able to attend to negative attribution words during a period of time when attentional resources would ordinarily be depleted. These individuals were not more likely than those with low or moderate negative cognitive style to detect neutral and negative non-self-relevant words during this period. These data suggest that cognitive style modulates the saliency of material that is relevant to negative attributions, and these alterations in information processing may link cognitive style to development of depression.
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