Dataset Information

Brooding rumination and heart rate variability in women at high and low risk for depression: group differences and moderation by COMT genotype.

ABSTRACT: There is growing evidence that rumination, perhaps specifically brooding rumination, is a core feature of depression and that it contributes to the development and maintenance of the disorder. A separate line of research has highlighted the role played by heart rate variability (HRV). Both brooding rumination and HRV appear to be driven by disruption in the same neural circuit, heightened amygdala reactivity combined with decreased prefrontal control, and both are highlighted in different units of analysis as reflecting the Research Domain Criteria (RDoC) construct of Loss. However, little is known about the relation among these variables. In the current study, we predicted that higher levels of brooding rumination would be associated with lower levels of HRV and that women at high risk for future depression (i.e., those with a history of past major depressive disorder [MDD]) would exhibit higher levels of brooding and lower levels of HRV. We also examined genetic influences on the variables in this model. We predicted that COMT Val158Met genotype, which has been linked to heightened amygdala reactivity and deficits in prefrontal functioning, would be associated with brooding rumination and HRV, particularly among women with a history of past MDD. The results largely supported our hypotheses, providing additional support for relations among the different units of analysis for the Loss construct.

SUBMITTER: Woody ML

PROVIDER: S-EPMC4107362 | biostudies-literature | 2014 Feb

REPOSITORIES: biostudies-literature

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Brooding rumination and heart rate variability in women at high and low risk for depression: group differences and moderation by COMT genotype.

Woody Mary L ML McGeary John E JE Gibb Brandon E BE

Journal of abnormal psychology 20140201 1

There is growing evidence that rumination, perhaps specifically brooding rumination, is a core feature of depression and that it contributes to the development and maintenance of the disorder. A separate line of research has highlighted the role played by heart rate variability (HRV). Both brooding rumination and HRV appear to be driven by disruption in the same neural circuit, heightened amygdala reactivity combined with decreased prefrontal control, and both are highlighted in different units ...[more]

PMID: 24661160

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Project description:The analysis of brain signal variability is a promising approach to understand pathological brain function related to chronic pain. This study investigates whether blood-oxygen-level-dependent signal variability (BOLDSV) in specific frequency bands is altered in temporomandibular disorder (TMD) and correlated to its clinical features. Twelve patients with chronic myofascial TMD and 24 healthy controls (HCs) underwent resting-state functional magnetic resonance imaging. The BOLDSV was measured as the standard deviation of the BOLD time series at each voxel and compared between groups. We also examined the potential relationship between the BOLDSV and the catechol-O-methyltransferase (COMT) Val158Met polymorphism. We assessed sensory-discriminative pain in the craniofacial region, pain sensitivity to sustained masseteric pain challenge, and TMD pain frequency for clinical correlation. Patients displayed reduced BOLDSV in the dorsolateral prefrontal cortex (dlPFC) as compared with HC in all frequency bands. In the slow-3 band, patients also showed reduced BOLDSV in the medial dorsal thalamus, primary motor cortex (M1), and primary somatosensory cortex (S1) and heightened BOLDSV in the temporal pole. Notably, we found a significant correlation between lower BOLDSV (slow-3) in the orofacial M1/S1 regions and higher clinical pain (intensity/area) and higher sensitivity of the masseter muscle pain. Moreover, lower BOLDSV (slow-3) in the dlPFC and ventrolateral PFC was associated with a higher TMD pain frequency. Participants who had the COMT 158Met substitution exhibited lower BOLDSV in the dlPFC and higher BOLDSV in the temporal pole as compared with participants without the COMT 158Met substitution. An increasing number of Met alleles was associated with lower dlPFC and greater temporal pole BOLDSV in both HC and TMD groups. Together, we demonstrated that chronic TMD patients exhibit aberrant BOLDSV in the top-down pain modulatory and sensorimotor circuits associated with their pain frequency and severity. COMT Val158Met polymorphism might affect clinical symptoms in association with regional brain signal variability, specifically involved in cognitive and emotional regulation of pain.

Project description:The endocannabinoid system has been implicated in stress adaptation and the regulation of mood in rodent studies, but few human association studies have examined these links and replications are limited.To examine whether a synonymous polymorphism, rs1049353, in exon 4 of the gene encoding the human endocannabinoid receptor (CNR1) moderates the effect of self-reported childhood physical abuse on lifetime anhedonia and depression and to replicate this interaction in an independent sample.Genetic association study in 1041 young US women with replication in an independent Australian sample of 1428 heroin-dependent individuals as cases and 506 participants as neighborhood controls.Self-reported anhedonia and depression (with anhedonia).In both samples, individuals who experienced childhood physical abuse were considerably more likely to report lifetime anhedonia. However, in those with 1 or more copies of the minor allele of rs1049353, this pathogenic effect of childhood physical abuse was attenuated. Thus, in participants reporting childhood physical abuse, although 57.1% of those homozygous for the major allele reported anhedonia, only 28.6% of those who were carriers of the minor allele reported it (P=.01). The rs1049353 polymorphism also buffered the effects of childhood physical abuse on major depressive disorder; however, this influence was largely attributable to anhedonic depression. These effects were also noted in an independent sample, in which minor allele carriers were at decreased risk for anhedonia even when exposed to physical abuse.Consistent with preclinical findings, a synonymous CNR1 polymorphism, rs1049353, is linked to the effects of stress attributable to childhood physical abuse on anhedonia and anhedonic depression. This polymorphism reportedly resides in the neighborhood of an exon splice enhancer; hence, future studies should carefully examine its effect on expression and conformational variation in CNR1, particularly in relation to stress adaptation.

Dataset Information

Brooding rumination and heart rate variability in women at high and low risk for depression: group differences and moderation by COMT genotype.

Publications

Brooding rumination and heart rate variability in women at high and low risk for depression: group differences and moderation by COMT genotype.

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