Momentary gustative-olfactory sensitivity and tonic heart rate variability are independently associated with motivational behavior.

Deficits in motivational functioning including impairments in reward learning or reward sensitivity are common in psychiatric disorders characterized by anhedonia. Recently, anhedonic symptoms have been exacerbated by the pandemic caused by the Coronavirus disease 2019 (COVID-19) in the general population. The present study examined the putative associations between loss of smell (anosmia) and taste (ageusia) sensitivity, irrespective of COVID-19 infection, and anhedonia, measured by a signal-detection task probing the ability to modify behavior as a function of rewards (Probabilistic Reward Task; PRT). Tonic heart rate variability (HRV) was included in the model, due to its association with both smell and taste sensitivity as well as motivational functioning. The sample included 114 healthy individuals (81 females; mean age 22.2 years), who underwent a laboratory session in which dispositional traits, resting HRV and PRT performance were assessed, followed by a 4-days ecological momentary assessment to obtain daily measures of anosmia and ageusia. Lower levels of tonic HRV and lower momentary levels of smell and taste sensitivity were associated with impaired reward responsiveness and ability to shape future behavioral choices based on prior reinforcement experiences. Overall, the current results provide initial correlational evidence that could be fruitfully used to inform future experimental investigations aimed at elucidating the disruptive worldwide mental health consequences triggered by the pandemic.

Post-acute sequelae of COVID-19: Evidence of mood & cognitive impairment.

Acute health consequences associated with coronavirus disease 2019 (COVID-19) infection have been thoroughly characterized; however, long-term impacts are not yet understood. Post-acute sequelae of COVID-19 (PASC), also known as Long COVID syndrome, is the persistence of COVID-19 symptoms long after viral infection. In addition to physical symptoms, those with PASC experience changes in mental health, but few studies have empirically examined these effects. The current study investigated mood and cognitive functioning in individuals who have recovered from COVID-19 infection. We recruited 100 male and female adults (M â€‹= â€‹30 years old) with no history of mood or cognitive impairment prior to the COVID-19 pandemic (Jan. 2020). Half of the subjects were healthy controls (i.e., no prior COVID-19 infection) and half had received a past COVID-19 diagnosis (ascertained by PCR or antibody test) but were no longer infectious. Participants completed self-reported measures of stress, depression, and anhedonia, as well as the Attention Network Test (ANT), a behavioural measure of attentional alerting, orienting and executive functioning. Relative to controls, depression and anhedonia were significantly higher in the past-COVID group. Selective impairment in attention was observed in the past-COVID group, marked by deficits in executive functioning while alerting and orienting abilities remained intact. Effects were most pronounced among individuals diagnosed 1-4 months prior to assessment. There were no group differences in pandemic-related experiences with respect to social interaction, social distancing, or isolation. The past-COVID group scored significantly higher on perceived stress; however, this did not moderate any effects observed on mood or cognition. These findings implicate a protracted reaction to the virus, possibly via prolonged inflammation, contributing to sustained mood dysregulation and cognitive impairment. Future research should examine the neural and physiological underpinnings of PASC, particularly mechanisms that promote psychiatric sequelae 1-4 months following diagnosis.

Does inflammation link stress to poor COVID-19 outcome?

Coronavirus disease 2019 (COVID-19) continues to ravage communities across the world. Despite its primary effect on the respiratory system, the virus does not solely impact those with underlying lung conditions as initially predicted. Indeed, prognosis is worsened (often fatal) in patients with pre-existing hyperinflammatory responses (e.g., hypertension, obesity and diabetes), yet the mechanisms by which this occurs are unknown. A number of psychological conditions are associated with inflammation, suggesting that these may also be significant risk factors for negative outcomes of COVID-19. In this review, we evaluate preclinical and clinical literature suggesting that chronic stress-induced hyperinflammation interacts synergistically with COVID-19-related inflammation, contributing to a potentially fatal cytokine storm syndrome. In particular, we hypothesize that both chronic stress and COVID-19-related hyperinflammation are a product of glucocorticoid insufficiency. We discuss the devastating effects of SARS-CoV-2 on structural and functional aspects of the biological stress response and how these induce exaggerated inflammatory responses, particularly interleukin (IL)-6 hypersecretion. We postulate that chronic stress should be considered a significant risk factor for adverse COVID-19-related health outcomes, given overlapping peripheral and central immune dysregulation in both conditions. We conclude by discussing how people with a history of chronic stress could mitigate their risk for COVID-19 complications, identifying specific strategies that can be implemented during self-isolation.