Putting feelings into words (affect labeling) has long been thought to help manage negative emotional experiences; however, the mechanisms by which affect labeling produces this benefit remain largely unknown. Recent neuroimaging studies suggest a possible neurocognitive pathway for this process, but methodological limitations of previous studies have prevented strong inferences from being drawn. A functional magnetic resonance imaging study of affect labeling was conducted to remedy these limitations. The results indicated that affect labeling, relative to other forms of encoding, diminished the response of the amygdala and other limbic regions to negative emotional images. Additionally, affect labeling produced increased activity in a single brain region, right ventrolateral prefrontal cortex (RVLPFC). Finally, RVLPFC and amygdala activity during affect labeling were inversely correlated, a relationship that was mediated by activity in medial prefrontal cortex (MPFC). These results suggest that affect labeling may diminish emotional reactivity along a pathway from RVLPFC to MPFC to the amygdala.

Objective: Mindfulness is a process whereby one is aware and receptive to present moment experiences. Although mindfulnessenhancing interventions reduce pathological mental and physical health symptoms across a wide variety of conditions and diseases, the mechanisms underlying these effects remain unknown. Converging evidence from the mindfulness and neuroscience literature suggests that labeling affect may be one mechanism for these effects. Methods: Participants (n ϭ 27) indicated trait levels of mindfulness and then completed an affect labeling task while undergoing functional magnetic resonance imaging. The labeling task consisted of matching facial expressions to appropriate affect words (affect labeling) or to gender-appropriate names (gender labeling control task). Results: After controlling for multiple individual difference measures, dispositional mindfulness was associated with greater widespread prefrontal cortical activation, and reduced bilateral amygdala activity during affect labeling, compared with the gender labeling control task. Further, strong negative associations were found between areas of prefrontal cortex and right amygdala responses in participants high in mindfulness but not in participants low in mindfulness. Conclusions: The present findings with a dispositional measure of mindfulness suggest one potential neurocognitive mechanism for understanding how mindfulness meditation interventions reduce negative affect and improve health outcomes, showing that mindfulness is associated with enhanced prefrontal cortical regulation of affect through labeling of negative affective stimuli.

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Scientific understanding of social pain-the hurt feelings resulting from social rejection, separation, or loss-has been facilitated by the hypothesis that such feelings arise, in part, from some of the same neural and neurochemical systems that generate the unpleasant feelings resulting from physical pain. Accordingly, in animals, the painkiller morphine not only alleviates the distress of physical pain, but also the distress of social separation. Because morphine acts on the -opioid receptor, we examined whether variation in the -opioid receptor gene (OPRM1), as measured by the functional A118G polymorphism, was associated with individual differences in rejection sensitivity. Participants (n ‫؍‬ 122) completed a self-report inventory of dispositional sensitivity to social rejection and a subsample (n ‫؍‬ 31) completed a functional MRI session in which they were rejected from an online ball-tossing game played with two supposed others. The A118G polymorphism was associated with dispositional sensitivity to rejection in the entire sample and in the fMRI subsample. Consistent with these results, G allele carriers showed greater reactivity to social rejection in neural regions previously shown to be involved in processing social pain as well as the unpleasantness of physical pain, particularly the dorsal anterior cingulate cortex (dACC) and anterior insula. Furthermore, dACC activity mediated the relationship between the A118G polymorphism and dispositional sensitivity to rejection, suggesting that this is a critical site for -opioid-related influence on social pain. Taken together, these data suggest that the A118G polymorphism specifically, and the -opioid receptor more generally, are involved in social pain in addition to physical pain.anterior cingulate ͉ brain ͉ exclusion ͉ genetic ͉ social pain

Psychological resources-optimism, mastery, and self-esteem-buffer the deleterious effects of stress and are predictors of neurophysiological and psychological health-related outcomes. These resources have been shown to be highly heritable, yet the genetic basis for this heritability remains unknown. Here, we report a link between the oxytocin receptor (OXTR) SNP rs53576 and psychological resources, such that carriers of the "A" allele have lower levels of optimism, mastery, and self-esteem, relative to G/G homozygotes. OXTR was also associated with depressive symptomatology. Mediation analysis indicates that the effects of OXTR on depressive symptoms may be largely mediated by the influence of OXTR on psychological resources. P sychological resources refer to individual differences that are directly predictive of physical and psychological health (1-3). The most well-studied of these resources are optimism, mastery, and self-esteem (4-6). Optimism refers to the extent to which people hold favorable expectations about the future (4, 7); as a dispositional variable, it reflects positive expectations across a broad array of outcomes. Mastery involves the belief that one can determine one's own behavior, influence one's environment, and bring about desired outcomes; it also has a strong dispositional component (8). Self-esteem is a dispositional concept that refers to a person's overall evaluation of self-worth (9). Previous research has established that these three resources are closely interrelated (4, 6, 10) and, both independently and as a cluster, they are known to buffer the effects of stressful life events and experimentally manipulated stressors on physiological stress responses (for reviews, see refs. 2 and 5). Moreover, considerable research demonstrates that susceptibility to depression and other forms of psychological distress is lower among individuals high in optimism (4, 11, 12), mastery (13, 14), and self-esteem (15)(16)(17).The model guiding the present research attributes the origins of psychological resources to developmental and genetic factors (2, 5). Aspects of the early environment that affect the development of these resources include family socioeconomic status (15,18,19), childhood adversities (20), and parental practices (18,20). Psychological resources may continue to be influenced by life experiences in adolescence, young adulthood, and beyond (18), but less research is available on this question. Although we acknowledge the importance of these environmental factors in the developmental origins of psychological resources, the present research is primarily concerned with the second primary source: human genetics.Twin studies have shown that a large proportion of the variance in psychological resources is heritable (21-25). The extant research suggests a narrow range for the heritability of optimism, with independent reports ranging from 20% (21) to 36% (24). Estimates for the heritability of self-esteem range more widely, from a low of 29% (23) to a high of 73% (22). Research on the behav...

Adversity in childhood has effects on mental and physical health, not only in childhood but across the lifespan. A chief task of our research has been to define the pathways by which childhood experience has these surprising health outcomes, often decades later. The concept of allostatic load, which refers to dysregulations across major biological regulatory systems that have cumulative interacting adverse effects over time, provides a mechanism for understanding these relations and defining specific pathways. To chart these pathways, we examine early childhood socioeconomic status, family environment, and genetic predispositions as antecedents to socioemotional functioning/psychological distress; and neural responses to threat that have downstream effects on major stress regulatory systems, ultimately culminating in risks to mental and physical health outcomes. This integrative approach to investigating the impact of childhood experience on adult health outcomes illustrates the significance of multilevel integrative approaches to understanding developmental psychopathology more generally.

Background: Mindfulness meditation training interventions have been shown to improve markers of health, but the underlying neurobiological mechanisms are not known. Building on initial cross-sectional research showing that mindfulness meditation may increase default mode network (DMN) resting state functional connectivity (rsFC) with regions important in top-down executive control (dorsolateral prefrontal cortex, dlPFC), here we test whether mindfulness meditation training increases DMN-dlPFC rsFC, and whether these rsFC alterations prospectively explain improvements in interleukin-6 (IL-6) in a randomized controlled trial.

Although stress-induced increases in inflammation have been implicated in several major disorders, including cardiovascular disease and depression, the neurocognitive pathways that underlie inflammatory responses to stress remain largely unknown. To examine these processes, we recruited 124 healthy young adult participants to complete a laboratory-based social stressor while markers of inflammatory activity were obtained from oral fluids. A subset of participants (n = 31) later completed an fMRI session in which their neural responses to social rejection were assessed. As predicted, exposure to the laboratory-based social stressor was associated with significant increases in two markers of inflammatory activity, namely a soluble receptor for tumor necrosis factor-α (sTNFαRII) and interleukin-6 (IL-6). In the neuroimaging subsample, greater increases in sTNFαRII (but not IL-6) were associated with greater activity in the dorsal anterior cingulate cortex and anterior insula, brain regions that have previously been associated with processing rejectionrelated distress and negative affect. These data thus elucidate a neurocognitive pathway that may be involved in potentiated inflammatory responses to acute social stress. As such, they have implications for understanding how social stressors may promote susceptibility to diseases with an inflammatory component.P sychological stress is intimately related to human health and well-being. It increases susceptibility to the common cold (1), elevates risk for several major diseases (2), and is a strong, independent predictor of morbidity and mortality. In a recent epidemiological study, for example, males experiencing high levels of stress were 32% more likely to die during a 22-y assessment period than were those experiencing low levels of stress (3).