The idea of psychological pain is an interesting one as it feels just as real as physical pain for the individual but it’s a lot harder to conceptualise. Considering how real psychological pain feels, it’s no surprise that both types of pain share similar neural circuitry.
Psychological pain is a commonly reported symptom in depression. While it’s not related with depression severity, it is associated with an increased risk of suicide. Despite the prevalence of “psychache” in depression, the relationship between this and physiological measures, beyond brain imaging, is not well known.
Oxytocin probably reaches the brain directly but it’s not necessary to influence social behavior and cognition
There are a myriad of studies indicating that intranasal oxytocin (OT) influences social behaviour and cognition. For instance, OT has been reported to improve emotion recognition, trust, social memory, altruism, generosity, and approachability. While not all of the reported improvements are “positive” (e.g., increasing schadenfraude1), there’s no doubt that OT modulates social behavior and cognition.
Most of these OT studies operate under the assumption that these observed effects are due to intranasally administered OT reaching the brain via pathways from the nasal cavity. As evidence, a cerebrospinal fluid (CSF) study by Jan Born and team2 is often cited. The idea here is that if a molecule can be detected in CSF, it’s also in the brain. However, this study didn’t actually use OT, instead reporting on vasopressin (neuropeptide that is structurally similar to OT).
Like it or not, the experience of negative emotions are a fact of life. Most people are able to effectively regulate their emotional responses but sometimes this can be hard, particularly for people with anxiety disorders.
One element of emotional reactions is the physiological response. For instance, when you’re speaking publicly your heart may begin to race. People with anxiety are particularly sensitive to these physiological cues, which leads to a vicious cycle as anxiety begets a physiological response, which begets anxiety, and so forth.
But what if you were better able to regulate your accelerating heart rate?
It’s a nice story. High frequency (HF) heart rate variability (HRV) represents parasympathetic nervous system (PNS) activity so it makes sense that low frequency (LF) HRV indexes the other branch of the autonomic nervous system (ANS), the sympathetic nervous system (SNS).
Understandably, a lot of papers have extended this idea to use LF HRV as a proxy for SNS activity stating things like “increased LF HRV in disorder x indicates higher SNS activity” or “activity x increases LF HRV thus SNS activity”
Unfortunately, this simply isn’t true.
Power spectrum analysis of heart rate fluctuation: a quantitative probe of beat-to-beat cardiovascular control
We almost take it for granted nowadays that high frequency (HF) heart rate variability (HRV) is a relatively pure measure of parasympathetic nervous system (PNS) function. But how was this first discovered?
In the early eighties, Akselrod and her team (1981) wanted to better understand the physiological mechanisms behind different oscillations in beat-to-beat heart rate fluctuation first observed by others the previous decade (e.g., Sayers, 1973).
I’ve uploaded the PDF to figshare. You can download a template to make your own preprint PDF here. Another benefit with iBooks Author is that you can upload your paper to Apple’s iBook store and add some great multimedia elements such as movies and interactive galleries, some really interesting possibilities here.
I just published a new paper in Psychophysiology.
Epidemiological literature indicates that the relationship between alcohol consumption and health outcomes reflects a J-shaped curve such that moderate alcohol consumption confers a protective effect in comparison to abstinence, while heavy consumption is associated with poorer health. While heart rate variability (HRV) may underpin the relationship between drinking and poor health in heavy drinkers, it is unclear whether HRV is increased in moderate, habitual drinkers relative to nonhabitual drinkers. HRV and drinking habits were assessed in 47 volunteers. Results supported hypotheses suggesting that moderate, habitual drinking increases HRV. Although not supported by a significant interaction between drinking group and sex, planned follow-up analysis also revealed that these findings may be specific to males. Regardless, results highlight HRV as a candidate mechanism for the findings reported in the epidemiological literature.
You can find the paper here
We just published a new paper in PLoS One.
This paper confirms that social anxiety disorder is associated with reduced heart rate variability. We conclude that resting state heart rate variability may be considered a marker for social approach-related motivation and capacity for social engagement. Additionally we suggest that heart rate variability may provide a useful biomarker to explain underlying difficulties with social approach, impaired stress regulation, and behavioral inhibition, especially in disorders associated with significant impairments in these domains.
You can find the paper here