The influence of affective empathy and autism spectrum traits on empathic accuracy

Autism spectrum disorder is characterized by interpersonal deficits and has been associated with limited cognitive empathy, which includes perspective taking, theory of mind, and empathic accuracy (EA). The capacity for affective empathy may also be impaired. In the present study we aimed to determine if EA in normally developing individuals with varying levels of autism spectrum traits is moderated by trait affective empathy. Fifty male and fifty female participants ('perceivers') completed the Autism-Spectrum Quotient and the Balanced Emotional Empathy Scale to assess autism spectrum traits and trait affective empathy, respectively. EA was assessed using a Dutch-language version of a previously developed task and involved rating the feelings of others ('targets') verbally recounting autobiographical emotional events. Targets varied in trait emotional expressivity, assessed using the Berkeley Expressivity Questionnaire. Perceivers with more autism spectrum traits performed worse on the EA task, particularly when their trait affective empathy was relatively low. Interpersonal deficits in autism spectrum disorder may be partially explained by low cognitive empathy. Further, they might be aggravated by a limited capacity for affective empathy

Understanding the effects of sleep deprivation and acute social stress on cognitive performance using a comprehensive approach

Different professionals (e.g. in the military) have to perform cognitive challenging tasks in multi-stressor environments. However, our understanding how combined stressors interact and affect cognitive performance is limited (Van Dongen & Belenky, 2009). This study examined how sleep deprivation (SD) and acute social stress affect cognitive performance in isolation and in combination, and used a comprehensive approach to find evidence for a (shared) mechanism. Recent research suggests that SD leads to higher amounts of proinflammatory markers (i.e. cytokines) in the blood, which assumedly contribute to a decline in cognitive performance (Irwin, 2019; Shields et al., 2017). In addition, acute social stressors have also been shown to elicit an immune response, as reflected by circulating cytokines in blood (Marsland et al., 2017; Prather et al., 2014). These findings suggest that different stressors may affect cognitive performance through an effect on the immune system. We therefore hypothesize that individuals showing a high proinflammatory response to a combination of two stressors (SD and acute social stress) are more vulnerable to cognitive decline compared to individuals showing a lower proinflammatory response. To test this hypothesis, we measured not only cognitive performance, but also the physiological response and biochemical determinants of metabolism and inflammation at baseline and after SD, but also in response to an acute social stressor (Tkacheenko & Dinges, 2018)

Understanding the combined effects of sleep deprivation and acute social stress on cognitive performance using a comprehensive approach

Background: Sleep deprivation (SD) and acute social stress are common, often unavoidable, and frequently co-occurring stressors in high-risk professions. Both stressors are known to acutely induce inflammatory responses and an increasing body of literature suggests this may lead to cognitive impairment. This study examined the combined effects of total SD and acute social stress on cognitive performance and took a comprehensive approach to explore their (shared) underlying mechanism leading to cognitive decline. Method: We recorded cognitive performance on a response inhibition task and a multitask and monitored a range of inflammatory, psychophysiological and self-reported markers in 101 participants, both before and after one night of either sleep (control group: N = 48) or SD (N = 53), and both before and after a social stressor (Trier Social Stress Test). Results: SD decreased cognitive performance. The social stress test also results in cognitive performance decline in the control group on the response inhibition task, but improved rather than decreased performance of sleep deprived participants on both tasks. The subjective ratings of mental effort also reflect this antagonistic interaction, indicating that the social stressor when sleep-deprived also reduced mental effort. In the inflammatory and physiological measures, this pattern was only reflected by IL-22 in blood. SD reduced blood IL-22 concentrations, and the social stress reduced IL-22 in the control group as well, but not in sleep-deprived participants. There were no interactive effects of SD and social stress on any other inflammatory or psychophysiological measures. The effects of the social stress test on autonomic measures and subjective results suggest that increased arousal may have benefited sleep-deprived participants’ cognitive performance. Discussion: SD generally decreased cognitive performance and increased required mental effort. By contrast, the isolated effects of a social stressor were not generic, showing a positive effect on cognitive performance when sleep deprived. Our study is the first that studied combined effects of sleep deprivation and acute social stress on cognitive performance and inflammatory markers. It provides a comprehensive overview of effects of these stressors on a range of variables. We did not show unequivocal evidence of an underlying physiological mechanism explaining changes in performance due to (the combination of) sleep deprivation and social stress, but consider IL-22 as a possible cytokine involved in this mechanism and certainly worth following up on in future research.</p

Empathic accuracy and oxytocin after tryptophan depletion in adults at risk for depression

Contains fulltext : 172451.pdf (Publisher’s version ) (Open Access

Serotonin manipulations and social behavior: Studies in individuals at familial risk for depression

Interactions with others affect our mood, and vice versa. Unsurprisingly, people with a mood disorder such as depression often have difficulties in their social relationships. Depression is often thought to be associated with a decreased availability of serotonin, a signaling molecule in the brain which enables the processing of social and emotional information. Therefore a decreased availability of serotonin could also have an adverse effect on social behavior and mood during interactions with others. However, Hogenelst and colleagues showed that a temporary decrease of serotonin (over several hours) has little impact on mood or social behavior as measured in the lab. The results were similar in study participants with and without an elevated depression risk. In a second study in people with an elevated depression risk, the researchers increased the availability of serotonin over several days. They examined the effects on mood and social behavior in everyday life. As expected, mood improved. Unexpectedly, however, the participants also became less friendly. This behavioral effect was only seen during interactions at home. It is possible that, when serotonin availability was increased, participants stood up for themselves more. This in line with the idea that people prone to depression experience little control over their social lives. As most medications for depression aim to increase the availability of serotonin, an important next question is how these medications affect the social behavior of depressed people