scholarly journals The heart as judge: Association of heart rate variability with moral judgment—A replication study

2021 ◽  
Author(s):  
Diana Armbruster ◽  
Alexander Strobel
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Activity ◽  
Vagal Tone ◽  
Moral Dilemmas ◽  
Total Sample ◽  
Hormonal Contraceptives ◽  
Cardiac Vagal Tone ◽  
Moral Decisions ◽  
Moral Judgements

There is growing research into contributing processes and biological correlates of differences in moral judgements with process dissociation procedures allowing independent quantifica-tion of utilitarian and deontic tendencies underlying moral decisions. Recently, Park et al. (2016) reported that estimated utilitarianism showed negative associations with heart rate variability (HRV) at rest. Resting HRV is an indicator of cardiac vagal tone and thus of para-sympathetic activity and has also been suggested to be a marker of neuro-visceral integra-tion. We aimed to replicate and extend these findings. Using the same set of moral dilemmas in N = 157 young adults, we found no such association in the total sample. However, when taking sex and the use of hormonal contraceptives into account, we found a positive associa-tion between HRV at rest and estimated deontology in women using combined oral contra-ceptives and men, while in free cycling women there was a negative association. While we did not replicate the original findings, our results partly indicate similar behavioral conse-quences of increased HRV, since both reduced utilitarianism (cf. Park et al., 2016) and in-creased deontology are linked to decreased endorsement of harmful actions. Furthermore, there were no associations between sympathetic activity (assessed via electro-dermal activi-ty) and moral judgements.

scholarly journals Circulating Inflammatory Markers Are Inversely Associated with Heart Rate Variability Measures in Type 1 Diabetes

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Anne-Marie L. Wegeberg ◽  
Tina Okdahl ◽  
Tina Fløyel ◽  
Christina Brock ◽  
Niels Ejskjaer ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Type 1 Diabetes ◽  
Adhesion Molecules ◽  
Autonomic Neuropathy ◽  
Vagal Tone ◽  
Cardiovascular Autonomic Neuropathy ◽  
Intercellular Adhesion Molecule ◽  
Cardiac Vagal Tone

Introduction. A neuroimmune communication exists, and compelling evidence suggests that diabetic neuropathy and systemic inflammation are linked. Our aims were (1) to investigate biomarkers of the ongoing inflammation processes including cytokines, adhesion molecules, and chemokines and (2) to associate the findings with cardiovascular autonomic neuropathy in type 1 diabetes by measuring heart rate variability and cardiac vagal tone. Materials and Methods. We included 104 adults with type 1 diabetes. Heart rate variability, time domain, and frequency domains were calculated from a 24-hour Holter electrocardiogram, while cardiac vagal tone was determined from a 5-minute electrocardiogram. Cytokines (interleukin- (IL-) 1α, IL-4, IL-12p70, IL-13, IL-17, and tumor necrosis factor- (TNF-) α), adhesion molecules (E-selectin, P-selectin, and intercellular adhesion molecule- (ICAM-) 1), and chemokines (chemokine (C-C motif) ligand (CCL)2, CCL3, CCL4, and C-X-C motif chemokine (CXCL)10) were assessed using a Luminex multiplexing technology. Associations between concentrations of inflammatory biomarkers and continuous variables of heart rate variability and cardiac vagal tone were estimated using multivariable linear regression adjusting for age, sex, disease duration, and smoking. Results. Participants with the presence of cardiovascular autonomic neuropathy had higher systemic levels of IL-1α, IL-4, CCL2, and E-selectin than those without cardiovascular autonomic neuropathy. IL-1α, IL-4, IL-12, TNF-α, and E-selectin were inversely associated with both sympathetic and parasympathetic heart rate variability measures (p>0.01). Discussion. Our results show that several pro- and anti-inflammatory factors, believed to be involved in the progression of diabetic polyneuropathy, are associated with cardiovascular autonomic neuropathy, suggesting that these factors may also contribute to the pathogenesis of cardiovascular autonomic neuropathy. Our findings emphasize the importance of the neuroimmune regulatory system in the pathogenesis of neuropathy in type 1 diabetes.

scholarly journals Changes in cardiac vagal tone as measured by heart rate variability during naloxone-induced opioid withdrawal

2019 ◽  
Vol 204 ◽  
pp. 107538
Author(s):  
Charles J. Levin ◽  
Jonathan M. Wai ◽  
Jermaine D. Jones ◽  
Sandra D. Comer
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Vagal Tone ◽  
Opioid Withdrawal ◽  
Cardiac Vagal Tone

Accuracy of assessment of cardiac vagal tone by heart rate variability in normal subjects

1991 ◽  
Vol 67 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Junichiro Hayano ◽  
Yusaku Sakakibara ◽  
Akira Yamada ◽  
Masami Yamada ◽  
Seiji Mukai ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Vagal Tone ◽  
Normal Subjects ◽  
Cardiac Vagal Tone

Low cardiac vagal tone index by heart rate variability differentiates bipolar from major depression

2017 ◽  
Vol 20 (5) ◽  
pp. 359-367 ◽  
Author(s):  
Brandon Hage ◽  
Briana Britton ◽  
David Daniels ◽  
Keri Heilman ◽  
Stephen W. Porges ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Major Depression ◽  
Vagal Tone ◽  
Cardiac Vagal Tone

scholarly journals Circulating Inflammatory Markers are Inversely Associated with Heart Rate Variability Measures in type 1 Diabetes

2020 ◽  
Author(s):  
Anne-Marie Langmach Wegeberg ◽  
Tina Okdahl ◽  
Tina Fløyel ◽  
Christina Brock ◽  
Niels Ejskjaer ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Type 1 Diabetes ◽  
Adhesion Molecules ◽  
Autonomic Neuropathy ◽  
Vagal Tone ◽  
Cardiovascular Autonomic Neuropathy ◽  
Cardiac Vagal Tone ◽  
Tnf Α

Abstract Background A neuro-immune communication exists, and compiling evidence suggests that diabetic neuropathy and systemic inflammation are linked. Our aims were 1) to investigate biomarkers of the ongoing inflammation processes including cytokines, adhesion molecules and chemokines, and 2) to associate the findings with cardiovascular autonomic neuropathy in type 1 diabetes by measuring heart rate variability and cardiac vagal tone.Methods We included 104 adults with type 1 diabetes. Heart rate variability, time- and frequency domains, were calculated from a 24-hour Holter electrocardiogram, while cardiac vagal tone was determined from a 5-minute electrocardiogram. Cytokines (interleukin (IL)-1α, IL-4, IL-12p70, IL-13, IL-17 and tumor necrosis factor (TNF)-α), adhesion molecules (E-selectin, P-selectin and intercellular adhesion molecule (ICAM)-1) and chemokines (chemokine (C-C motif) ligand (CCL)2, CCL3, CCL4 and C-X-C motif chemokine (CXCL)10) were assessed using a Luminex multiplexing technology. Associations between concentrations of inflammatory biomarkers and continuous variables of heart rate variability and cardiac vagal tone were estimated using multivariable linear regression adjusting for age, sex, disease duration and smoking.Results Participants with the presence of cardiovascular autonomic neuropathy had higher systemic levels of IL-1α, IL-4, CCL2 and E-selectin, than those without cardiovascular autonomic neuropathy. IL-1α, IL-4, IL-12, TNF-α and E-selectin were inversely associated with both sympathetic and parasympathetic heart rate variability measures (p>0.01).Conclusion Our results show that several pro- and anti-inflammatory factors, believed to be involved in the progression of diabetic polyneuropathy are associated with cardiovascular autonomic neuropathy, suggesting that these factors may also contribute to the pathogenesis of cardiovascular autonomic neuropathy. Our findings emphasize the importance of the neuro-immune regulatory system in the pathogenesis of neuropathy in type 1 diabetes.Trial registration: The study was approved by the North Denmark Regional Committee on Health Research Ethics (N2013-0077 and N2017-0045) and registered in public databases (Eudra CT 2013-004375-12 and clinicaltrials.gov NCT02138045.

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