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Associating Flexible Regulation of Emotional Expression With Psychopathological Symptoms

ABSTRACT: Background: Stressful situations and psychopathology symptoms (e.g., depression and anxiety) shape how individuals regulate and respond to others’ emotions. However, how emotional expressions influence mental health and impact intrapersonal and interpersonal experiences is still unclear. Objective: Here, we used the Flexible Regulation of Emotional Expression (FREE) scale to explore the relationship between emotional expression abilities with affective symptoms and mental health markers. Methods: From a sample of 351 participants, we firstly validate a German version of the FREE scale on a final sample of 222 participants located in Germany, recruited through an online platform. Following this, we performed confirmatory factor analyses to assess the model structure of the FREE-scale. We then utilize a LASSO regression to determine which indicators of psychopathology symptoms and mental health are related to emotional expressive regulation and determine their particular interactions through the general linear model. Results: We replicated the FREE scale’s four latent factors (i.e., ability to enhance and suppress positive as well as negative emotional expressions). After the selection of relevant instruments through LASSO regression, the suppress ability showed specific negative associations with depression (r = 0.2) and stress symptoms (r = 0.16) and positive associations with readiness to confront distressing situations (r = 0.25), self-support (r = 0.2), and tolerance of emotions (r = 0.2). Both, emotional expressions enhance and suppress abilities positively associated with coping markers (resilience) and emotion regulation skills. Finally, the interaction effects between emotional flexibility abilities and stress, depression, and anxiety symptoms evidenced that consistent with the flexibility theory, enhancing and suppressing abilities may predict psychopathological symptoms. Conclusions: These findings emphasize the importance of considering the flexibility to express emotions as a relevant factor for preserved mental health or the development of psychopathological symptoms and indicate that online surveys may serve as a reliable indicator of mental health.

SUBMITTER: Gonzalez-Escamilla G

PROVIDER: S-EPMC9272006 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:HIV-infection is associated with neuroinflammation and greater psychopathological symptoms, which may be mediated by imbalances in the kynurenic pathway (KP). Two key KP enzymes that catabolize kynurenine include kynurenine-aminotransferase II (KATII), which yields antioxidative kynurenine acid [KYNA] in astrocytes, and kynurenine-3-monooxygenase (KMO), which produces neurotoxic metabolites in microglia. The relationships between polymorphisms in KMO and KATII, psychopathological symptoms, and cerebrospinal fluid (CSF) [KYNA] were evaluated in subjects with and without HIV-infection. Seventy-two HIV-positive and 72-seronegative (SN) participants were genotyped for KATII-rs1480544 and KMO-rs1053230. Although our participants were not currently diagnosed with depression or anxiety, they were assessed for psychopathological distress with Center for Epidemiologic Studies-Depression scale and Symptom Checklist-90-Revised. CSF-[KYNA] was also measured in 100 subjects (49 HIV/51 SN). HIV-participants had more psychopathological distress than SN, especially for anxiety. KATII-by-HIV interactions were found on anxiety, interpersonal sensitivity and obsessive compulsivity; KATII-C-carriers had lower scores than TT-carriers in SN but not in HIV. In contrast, the KMO-polymorphism had no influence on psychopathological symptoms in both groups. Overall, CSF-[KYNA] increased with age independently of HIV-serostatus, except KATII-TT-carriers tended to show no age-dependent variations. Therefore, the C-allele in KATII-rs1480544 appears to be protective against psychopathological distress in SN but not in HIV individuals, who had more psychopathological symptoms and likely greater neuroinflammation. The age-dependent increase in CSF-[KYNA] may reflect a compensatory response to age-related inflammation, which may be deficient in KATII-TT-carriers. Targeted treatments that decrease neuroinflammation and increase KYNA in at risk KATII-TT-carriers may reduce psychopathological symptoms in HIV.

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Associating Flexible Regulation of Emotional Expression With Psychopathological Symptoms

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