BackgroundNeuroticism is frequently discussed as a risk factor for psychopathology. According to the maturity principle, neuroticism decreases over the course of life, but not uniformly across individuals. However, the implications of differences in personality maturation on mental health have not been well studied so far. Hence, we hypothesized that different forms of neuroticism development from adolescence to young adulthood are associated with differences in depression, anxiety and everyday emotional experience at the age of 25.MethodsA sample of 266 adolescents from the general population was examined three times over ten years (age at T0: 15, T1: 20 and T2: 25) using questionnaires, interviews and ecological momentary assessment (EMA). At all measurement points, neuroticism was assessed with the NEO inventory. At T2, diagnoses of major depression and anxiety disorders were captured with a structured clinical interview (M-CIDI). Phone-based EMA was used to assess emotional experience and affective instability over a two-week period at T2.ResultsThe best fitting model was a latent class growth analysis with two groups of neuroticism development. Most individuals (n = 205) showed moderate values whereas 61 participants were clustered into a group with elevated neuroticism levels. In both groups neuroticism significantly changed during the ten year period with a peak at the age of 20. Individuals with a higher absolute level were at 14-fold increased risk for depression and 7-fold risk for anxiety disorders at the age of 25. In EMA, increased negative affect and arousal as well as decreased positive emotions were found in this high group.ConclusionsOther than expected, personality did not mature in our sample. However, there was a significant change of neuroticism values from adolescence to young adulthood. Further, over 20% of our participants showed a neuroticism development which was associated with adverse outcomes such as negatively toned emotional experience and a heightened risk to suffer from depressive and anxiety disorders in young adulthood. These high-risk persons need to be identified early to provide interventions supporting continuous personality maturation.Electronic supplementary materialThe online version of this article (doi:10.1186/s12888-014-0210-2) contains supplementary material, which is available to authorized users.
Background/Aims: Maltreatment in childhood and adolescence is a risk factor for substance use disorders (SUDs) in adulthood. This association has rarely been investigated in the light of emotion dysregulation. To fill this gap, this study examines emotion dysregulation and SUDs among adults with a history of early maltreatment. Methods: Comparison of emotion dysregulation in adults with a history of early abuse and neglect who developed either an SUD (n = 105) or no mental disorder (n = 54). Further, a mediation model for the association between the severity of early maltreatment and SUDs was tested. Participants completed research diagnostic interviews for psychopathology, the Difficulties in Emotion Regulation Scale, and the Childhood Trauma Questionnaire. Results: By using hierarchical regression techniques and mediational analyses controlling for age and gender, it was possible to provide evidence for the mediating role of emotion dysregulation between early emotional and physical maltreatment and later SUDs. Conclusions: Emotion dysregulation is a potential mechanism underlying the relationship between early emotional and physical maltreatment and the development of SUDs. In light of these findings, focusing on the early training of adaptive emotion regulation strategies after childhood maltreatment might be of considerable relevance to prevent the development of SUDs.
Childhood abuse and neglect (CAN) is considered as a risk factor for substance use disorder (SUD). Based on the drinking to cope model, this study investigated the association of two trauma-relevant emotions (shame and sadness) and substance use. Using ecological momentary assessment we compared real-time emotion regulation in situations with high and low intensity of shame and sadness in currently abstinent patients with CAN and lifetime SUD (traumaSUD group), healthy controls with CAN (traumaHC group), and without CAN (nontraumaHC group). Multilevel analysis showed a positive linear relationship between high intensity of both emotions and substance use for all groups. The traumaSUD group showed heightened substance use in low, as well as in high, intensity of shame and sadness. In addition, we found an interaction between type of emotion, intensity, and group: the traumaHC group exhibited a fourfold increased risk for substance use in high intense shame situations relative to the traumaSUD group. Our findings provide evidence for the drinking to cope model. The traumaSUD group showed a reduced distress tolerance for variable intensity of negative emotions. The differential effect of intense shame for the traumaHC group emphazises its potential role in the development of SUD following CAN. In addition, shame can be considered a relevant focus for therapeutic preinterventions and interventions for SUD after CAN.
Background Factors contributing to the spread of SARS-CoV-2 outside the acute care hospital setting have been described in detail. However, data concerning risk factors for nosocomial SARS-CoV-2 infections in hospitalized patients remain scarce. To close this research gap and inform targeted measures for the prevention of nosocomial SARS-CoV-2 infections, we analyzed nosocomial SARS-CoV-2 cases in our hospital during a defined time period. Methods Data on nosocomial SARS-CoV-2 infections in hospitalized patients that occurred between May 2020 and January 2021 at Charité university hospital in Berlin, Germany, were retrospectively gathered. A SARS-CoV-2 infection was considered nosocomial if the patient was admitted with a negative SARS-CoV-2 reverse transcription polymerase chain reaction test and subsequently tested positive on day five or later. As the incubation period of SARS-CoV-2 can be longer than five days, we defined a subgroup of “definite” nosocomial SARS-CoV-2 cases, with a negative test on admission and a positive test after day 10, for which we conducted a matched case–control study with a one to one ratio of cases and controls. We employed a multivariable logistic regression model to identify factors significantly increasing the likelihood of nosocomial SARS-CoV-2 infections. Results A total of 170 patients with a nosocomial SARS-CoV-2 infection were identified. The majority of nosocomial SARS-CoV-2 patients (n = 157, 92%) had been treated at wards that reported an outbreak of nosocomial SARS-CoV-2 cases during their stay or up to 14 days later. For 76 patients with definite nosocomial SARS-CoV-2 infections, controls for the case–control study were matched. For this subgroup, the multivariable logistic regression analysis revealed documented contact to SARS-CoV-2 cases (odds ratio: 23.4 (95% confidence interval: 4.6–117.7)) and presence at a ward that experienced a SARS-CoV-2 outbreak (odds ratio: 15.9 (95% confidence interval: 2.5–100.8)) to be the principal risk factors for nosocomial SARS-CoV-2 infection. Conclusions With known contact to SARS-CoV-2 cases and outbreak association revealed as the primary risk factors, our findings confirm known causes of SARS-CoV-2 infections and demonstrate that these also apply to the acute care hospital setting. This underscores the importance of rapidly identifying exposed patients and taking adequate preventive measures.
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