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Among younger adults, the ability to willfully regulate negative affect, enabling effective responses to stressful experiences, engages regions of prefrontal cortex (PFC) and the amygdala. Because regions of PFC and the amygdala are known to influence the hypothalamic-pituitary-adrenal axis, here we test whether PFC and amygdala responses during emotion regulation predict the diurnal pattern of salivary cortisol secretion. We also test whether PFC and amygdala regions are engaged during emotion regulation in older (62- to 64-year-old) rather than younger individuals. We measured brain activity using functional magnetic resonance imaging as participants regulated (increased or decreased) their affective responses or attended to negative picture stimuli. We also collected saliva samples for 1 week at home for cortisol assay. Consistent with previous work in younger samples, increasing negative affect resulted in ventral lateral, dorsolateral, and dorsomedial regions of PFC and amygdala activation. In contrast to previous work, decreasing negative affect did not produce the predicted robust pattern of higher PFC and lower amygdala activation. Individuals demonstrating the predicted effect (decrease < attend in the amygdala), however, exhibited higher signal in ventromedial prefrontal cortex (VMPFC) for the same contrast. Furthermore, participants displaying higher VMPFC and lower amygdala signal when decreasing compared with the attention control condition evidenced steeper, more normative declines in cortisol over the course of the day. Individual differences yielded the predicted link between brain function while reducing negative affect in the laboratory and diurnal regulation of endocrine activity in the home environment.
Although depressed mood is a normal occurrence in response to adversity in all individuals, what distinguishes those who are vulnerable to major depressive disorder (MDD) is their inability to effectively regulate negative mood when it arises. Investigating the neural underpinnings of adaptive emotion regulation and the extent to which such processes are compromised in MDD may be helpful in understanding the pathophysiology of depression. We report results from a functional magnetic resonance imaging study demonstrating left-lateralized activation in the prefrontal cortex (PFC) when downregulating negative affect in nondepressed individuals, whereas depressed individuals showed bilateral PFC activation. Furthermore, during an effortful affective reappraisal task, nondepressed individuals showed an inverse relationship between activation in left ventrolateral PFC and the amygdala that is mediated by the ventromedial PFC (VMPFC). No such relationship was found for depressed individuals, who instead show a positive association between VMPFC and amygdala. Pupil dilation data suggest that those depressed patients who expend more effort to reappraise negative stimuli are characterized by accentuated activation in the amygdala, insula, and thalamus, whereas nondepressed individuals exhibit the opposite pattern. These findings indicate that a key feature underlying the pathophysiology of major depression is the counterproductive engagement of right prefrontal cortex and the lack of engagement of left lateral-ventromedial prefrontal circuitry important for the downregulation of amygdala responses to negative stimuli.
Recent studies have identified a distributed network of brain regions thought to support cognitive reappraisal processes underlying emotion regulation in response to affective images, including parieto-temporal regions and lateral/medial regions of prefrontal cortex (PFC). A number of these commonly activated regions are also known to underlie visuospatial attention and oculomotor control, which raises the possibility that people use attentional redeployment rather than, or in addition to, reappraisal as a strategy to regulate emotion. We predicted that a significant portion of the observed variance in brain activation during emotion regulation tasks would be associated with differences in how participants visually scan the images while regulating their emotions. We recorded brain activation using fMRI and quantified patterns of gaze fixation while participants increased or decreased their affective response to a set of affective images. fMRI results replicated previous findings on emotion regulation with regulation differences reflected in regions of PFC and the amygdala. In addition, our gaze fixation data revealed that when regulating, individuals changed their gaze patterns relative to a control condition. Furthermore, this variation in gaze fixation accounted for substantial amounts of variance in brain activation. These data point to the importance of controlling for gaze fixation in studies of emotion regulation that use visual stimuli.
Using functional magnetic resonance imaging, we examined whether individual differences in amygdala activation in response to negative relative to neutral information are related to differences in the speed with which such information is evaluated, the extent to which such differences are associated with medial prefrontal cortex function, and their relationship with measures of trait anxiety and psychological well-being (PWB). Results indicated that faster judgments of negative relative to neutral information were associated with increased left and right amygdala activation. In the prefrontal cortex, faster judgment time was associated with relative decreased activation in a cluster in the ventral anterior cingulate cortex (ACC, BA 24). Furthermore, people who were slower to evaluate negative versus neutral information reported higher PWB. Importantly, higher PWB was strongly associated with increased activation in the ventral ACC for negative relative to neutral information. Individual differences in trait anxiety did not predict variation in judgment time or in amygdala or ventral ACC activity. These findings suggest that people high in PWB effectively recruit the ventral ACC when confronted with potentially aversive stimuli, manifest reduced activity in subcortical regions such as the amygdala, and appraise such information as less salient as reflected in slower evaluative speed.
The present study investigated the premise that individual differences in autonomic physiology could be used to specify the nature and consequences of information processing taking place in medial prefrontal regions during cognitive reappraisal of unpleasant pictures. Neural (blood oxygenation level-dependent functional magnetic resonance imaging) and autonomic (electrodermal [EDA], pupil diameter, cardiac acceleration) signals were recorded simultaneously as twenty-six older people (ages 64-66 years) used reappraisal to increase, maintain, or decrease their responses to unpleasant pictures. EDA was higher when increasing and lower when decreasing compared to maintaining. This suggested modulation of emotional arousal by reappraisal. By contrast, pupil diameter and cardiac acceleration were higher when increasing and decreasing compared to maintaining. This suggested modulation of cognitive demand. Importantly, reappraisal-related activation (increase, decrease>maintain) in two medial prefrontal regions (dorsal medial frontal gyrus and dorsal cingulate gyrus) was correlated with greater cardiac acceleration (increase, decrease>maintain) and monotonic changes in EDA (increase>maintain>decrease). These data indicate that these two medial prefrontal regions are involved in the allocation of cognitive resources to regulate unpleasant emotion, and that they modulate emotional arousal in accordance with the regulatory goal. The emotional arousal effects were mediated by the right amygdala. Reappraisal-related activation in a third medial prefrontal region (subgenual anterior cingulate cortex) was not associated with similar patterns of change in any of the autonomic measures, thus highlighting regional specificity in the degree to which cognitive demand is reflected in medial prefrontal activation during reappraisal.
Despite the vast literature that has implicated asymmetric activation of the prefrontal cortex in approach-withdrawal motivation and emotion, no published reports have directly explored the neural correlates of well-being. Eighty-four right-handed adults (ages 57-60) completed self-report measures of eudaimonic well-being, hedonic well-being, and positive affect prior to resting electroencephalography. As hypothesized, greater left than right superior frontal activation was associated with higher levels of both forms of well-being. Hemisphere-specific analyses documented the importance of goal-directed approach tendencies beyond those captured by approach-related positive affect for eudaimonic but not for hedonic well-being. Appropriately engaging sources of appetitive motivation, characteristic of higher left than right baseline levels of prefrontal activation, may encourage the experience of well-being.
BACKGROUND: Increasingly, researchers attend to both positive and negative aspects of mental health. Such distinctions call for clarification of whether psychological well-being and ill-being comprise opposite ends of a bipolar continuum, or are best construed as separate, independent dimensions of mental health. Biology can help resolve this query--bipolarity predicts 'mirrored' biological correlates (i.e. well-being and ill-being correlate similarly with biomarkers, but show opposite directional signs), whereas independence predicts 'distinct' biological correlates (i.e. well-being and ill-being have different biological signatures). METHODS: Multiple aspects of psychological well-being (eudaimonic, hedonic) and ill-being (depression, anxiety, anger) were assessed in a sample of aging women (n = 135, mean age = 74) on whom diverse neuroendocrine (salivary cortisol, epinephrine, norepinephrine, DHEA-S) and cardiovascular factors (weight, waist-hip ratio, systolic and diastolic blood pressure, HDL cholesterol, total/HDL cholesterol, glycosylated hemoglobin) were also measured. RESULTS: Measures of psychological well-being and ill-being were significantly linked with numerous biomarkers, with some associations being more strongly evident for respondents aged 75+. Outcomes for seven biomarkers supported the distinct hypothesis, while findings for only two biomarkers supported the mirrored hypothesis. CONCLUSION: This research adds to the growing literature on how psychological well-being and mental maladjustment are instantiated in biology. Population-based inquiries and challenge studies constitute important future directions.
This study examined the interplay of social engagement, sleep quality, and plasma levels of interleukin-6 (IL-6) in a sample of aging women (n = 74, aged 61-90, M age = 73.4). Social engagement was assessed by questionnaire, sleep was assessed by using the NightCap in-home sleep monitoring system and the Pittsburgh Sleep Quality Index, and blood samples were obtained for analysis of plasma levels of IL-6. Regarding subjective assessment, poorer sleep (higher scores on the Pittsburgh Sleep Quality Index) was associated with lower positive social relations scores. Multivariate regression analyses showed that lower levels of plasma IL-6 were predicted by greater sleep efficiency (P < 0.001), measured objectively and by more positive social relations (P < 0.05). A significant interaction showed that women with the highest IL-6 levels were those with both poor sleep efficiency and poor social relations (P < 0.05). However, those with low sleep efficiency but compensating good relationships as well as women with poor relationships but compensating high sleep efficiency had IL-6 levels comparable to those with the protective influences of both good social ties and good sleep.
OBJECTIVE: To test the hypothesis that socioeconomic status (SES) would be associated with sleep quality measured objectively, even after controlling for related covariates (health status, psychosocial characteristics). Epidemiological studies linking SES and sleep quality have traditionally relied on self-reported assessments of sleep. METHODS: Ninety-four women, 61 to 90 years of age, participated in this study. SES was determined by pretax household income and years of education. Objective and subjective assessments of sleep quality were obtained using the NightCap sleep system and the Pittsburgh Sleep Quality Index (PSQI), respectively. Health status was determined by subjective health ratings and objective measures of recent and chronic illnesses. Depressive symptoms and neuroticism were quantified using the Center for Epidemiological Studies Depression Scale and the Neuroticism subscale of the NEO Personality Inventory, respectively. RESULTS: Household income significantly predicted sleep latency and sleep efficiency even after adjusting for demographic factors, health status, and psychosocial characteristics. Income also predicted PSQI scores, although this association was significantly attenuated by inclusion of neuroticism in multivariate analyses. Education predicted both sleep latency and sleep efficiency, but the latter association was partially reduced after health status and psychosocial measures were included in analyses. Education predicted PSQI sleep efficiency component scores, but not global scores. CONCLUSIONS: These results suggest that SES is robustly linked to both subjective and objective sleep quality, and that health status and psychosocial characteristics partially explain these associations.