Depression, the Autonomic Nervous System, and Coronary Heart Disease

Carney, Robert M.; Freedland, Kenneth E.; Veith, Richard C.

doi:10.1097/01.psy.0000162254.61556.d5

Cited by 503 publications

(394 citation statements)

References 89 publications

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“…These results thus support models assuming that somatosensation (25,27) and embodiment (13,14) play critical roles in emotional processing. Unraveling the subjective bodily sensations associated with human emotions may help us to better understand mood disorders such as depression and anxiety, which are accompanied by altered emotional processing (30), ANS activity (31,32), and somatosensation (33). Topographical changes in emotion-triggered sensations in the body could thus provide a novel biomarker for emotional disorders.…”

Section: Resultsmentioning

confidence: 99%

Bodily maps of emotions

Nummenmaa

Glerean²,

Hari

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

674

583

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Emotions are often felt in the body, and somatosensory feedback has been proposed to trigger conscious emotional experiences. Here we reveal maps of bodily sensations associated with different emotions using a unique topographical self-report method. In five experiments, participants (n = 701) were shown two silhouettes of bodies alongside emotional words, stories, movies, or facial expressions. They were asked to color the bodily regions whose activity they felt increasing or decreasing while viewing each stimulus. Different emotions were consistently associated with statistically separable bodily sensation maps across experiments. These maps were concordant across West European and East Asian samples. Statistical classifiers distinguished emotion-specific activation maps accurately, confirming independence of topographies across emotions. We propose that emotions are represented in the somatosensory system as culturally universal categorical somatotopic maps. Perception of these emotion-triggered bodily changes may play a key role in generating consciously felt emotions.embodiment | feelings | somatosensation W e often experience emotions directly in the body. When strolling through the park to meet with our sweetheart we walk lightly with our hearts pounding with excitement, whereas anxiety might tighten our muscles and make our hands sweat and tremble before an important job interview. Numerous studies have established that emotion systems prepare us to meet challenges encountered in the environment by adjusting the activation of the cardiovascular, skeletomuscular, neuroendocrine, and autonomic nervous system (ANS) (1). This link between emotions and bodily states is also reflected in the way we speak of emotions (2): a young bride getting married next week may suddenly have "cold feet," severely disappointed lovers may be "heartbroken," and our favorite song may send "a shiver down our spine." Both classic (3) and more recent (4, 5) models of emotional processing assume that subjective emotional feelings are triggered by the perception of emotion-related bodily states that reflect changes in the skeletomuscular, neuroendocrine, and autonomic nervous systems (1). These conscious feelings help the individuals to voluntarily fine-tune their behavior to better match the challenges of the environment (6). Although emotions are associated with a broad range of physiological changes (1, 7), it is still hotly debated whether the bodily changes associated with different emotions are specific enough to serve as the basis for discrete emotional feelings, such as anger, fear, or happiness (8, 9), and the topographical distribution of the emotion-related bodily sensations has remained unknown.Here we reveal maps of bodily sensations associated with different emotions using a unique computer-based, topographical self-report method (emBODY, Fig. 1). Participants (n = 701) were shown two silhouettes of bodies alongside emotional words, stories, movies, or facial expressions, and they were asked to color the bodily regions...

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Section: Resultsmentioning

confidence: 99%

Bodily maps of emotions

Nummenmaa

Glerean²,

Hari

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

674

583

View full text Add to dashboard Cite

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“…For instance, stress in laboratory animals reduces BDNF synthesis, resulting in atrophy of CA3 pyramidal hippocampal neurons. 56 Further, BDNF knockout mice demonstrate impaired arousal responses 57 and increased anxiety-related behavior. 26 If our understanding of gene-environment interactions and their contribution to risk for depression and anxiety is to be improved beyond the phenomenological level, it is imperative that we understand these interactions in relation to their impact on brain structure and function.…”

Section: -51mentioning

confidence: 99%

Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety

et al. 2009

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The Brain Resource International Database and Brain Resource, Sydney, NSW, Australia and San Francisco, CA, USA Individual risk markers for depression and anxiety disorders have been identified but the explicit pathways that link genes and environment to these markers remain unknown. Here we examined the explicit interactions between the brain-derived neurotrophic factor (BDNF) Val66Met gene and early life stress (ELS) exposure in brain (amygdala-hippocampalprefrontal gray matter volume), body (heart rate), temperament and cognition in 374 healthy European volunteers assessed for depression and anxiety symptoms. Brain imaging data were based on a subset of 89 participants. Multiple regression analysis revealed main effects of ELS for body arousal (resting heart rate, P = 0.005) and symptoms (depression and anxiety, P < 0.001) in the absence of main effects for BDNF. In addition, significant BDNF-ELS interactions indicated that BDNF Met carriers exposed to greater ELS have smaller hippocampal and amygdala volumes (P = 0.013), heart rate elevations (P = 0.0002) and a decline in working memory (P = 0.022). Structural equation path modeling was used to determine if this interaction predicts anxiety and depression by mediating effects on the brain, body and cognitive measures. The combination of Met carrier status and exposure to ELS predicted reduced gray matter in hippocampus (P < 0.001), and associated lateral prefrontal cortex (P < 0.001) and, in turn, higher depression (P = 0.005). Higher depression was associated with poorer working memory (P = 0.005), and slowed response speed. The BDNF Met-ELS interaction also predicted elevated neuroticism and higher depression and anxiety by elevations in body arousal (P < 0.001). In contrast, the combination of BDNF V/V genotype and ELS predicted increases in gray matter of the amygdala (P = 0.003) and associated medial prefrontal cortex (P < 0.001), which in turn predicted startle-elicited heart rate variability (P = 0.026) and higher anxiety (P = 0.026). Higher anxiety was linked to verbal memory, and to impulsivity. These effects were specific to the BDNF gene and were not evident for the related 5HTT-LPR polymorphism. Overall, these findings are consistent with the correlation of depression and anxiety, yet suggest that partially differentiated gene-brain cognition pathways to these syndromes can be identified, even in a nonclinical sample. Such findings may aid establishing an evidence base for more tailored intervention strategies.

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“…28,29 Depression may contribute to dysregulation of the autonomic system, with reduction in the parasympathetic and increase in the sympathetic tone and its attendant increase in heart rate, reduction in heart rate variability and lower threshold for myocardial ischaemia and adverse cardiac events in patients with CVD. 30,31 The heightened sympathetic tone is associated with increased levels of cortisol, coagulant phase by increasing platelet activation 32,33 and inhibiting the synthesis of protective eicosanoids in response to the increased haemodynamic stress on the vascular wall. 34 Reduced inhibition of macrophage activation via the cholinergic anti-inflammatory pathway contributes to the elevation of pro-inflammatory markers, such as C-reactive protein and cytokines, such as interleukin-1beta, interleukin-6 and tumour necrosis factor alpha (TNF-alpha), in depression.…”

Section: Pathophysiological Implications Of Depression In Cardiovascumentioning

confidence: 99%

Depression in Patients with Heart Failure: Is Enough Being Done?

Mbakwem¹,

Aina²,

Amadi³

2016

Cardiac Failure Review

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Depression is a major issue in heart failure (HF). Depression is present in about one in five HF patients, with about 48 % of these individuals having significant depression. There is a wide variation in reported prevalences because of differences in the cohorts studied and methodologies. There are shared pathophysiological mechanisms between HF and depression. The adverse effects of depression on the outcomes in HF include reduced quality of life, reduced healthcare use, rehospitalisation and increased mortality. Results from metaanalysis suggest a twofold increase in mortality in HF patients with compared to those without depression. Pharmacological management of depression in HF has not been shown to improve major outcomes. No demonstrable benefits over cognitive behavioural therapy and psychotherapy have been demonstrated.

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Depression, the Autonomic Nervous System, and Coronary Heart Disease

Cited by 503 publications

References 89 publications

Bodily maps of emotions

Bodily maps of emotions

Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety

Depression in Patients with Heart Failure: Is Enough Being Done?

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