NI Elgesio medicinos laboratorija (11.14)

The psychiatrization of borderline personality disorder (BPD) has expanded beyond clinical contexts into identity formation, interpersonal regulation, and digital self-presentation. For individuals with BPD-whose psychopathology centrally involves identity diffusion-the diagnostic label may function not only as an explanatory framework but also as a stabilizing, defensive, or performative identity resource, particularly within online environments.

This article introduces a structured method for communication skills training within group schema therapy (GST) specifically tailored for individuals with borderline personality disorder (BPD). Patients with BPD often face relational difficulties due to intense emotional responses and maladaptive schema modes, thus creating a need for targeted communication training to promote healthier interpersonal relationships.

This work presents a policy analysis regarding Problematic Usage of the Internet (PUI) across seven countries (Netherlands, Spain, Hungary, Lithuania, Portugal, Estonia, and Switzerland) belonging to or associated with the European Union (EU). I It examines legislative instruments addressing PUI and its multifaceted impacts on society, including social, economic, and political dimensions. Despite the growing prevalence of PUI, particularly among adolescents, and its association with various mental health concerns, the study reveals a notable gap in direct policy interventions targeting PUI within these countries. Existing regulations largely focus on broader digital governance issues like data protection, cybersecurity, and market regulation, offering only indirect approaches to mitigating PUI's adverse effects. Our findings highlight a pressing need for innovative policy frameworks that incorporate mental health considerations into digital governance, promoting a balanced approach that fosters market innovation while ensuring robust public health protections. Building on the policy discourse examined in this study, future research should focus on developing targeted, multidimensional strategies to mitigate the risks associated with problematic internet use (PUI), with particular emphasis on safeguarding the well-being of vulnerable populations.

This work analyses policies related to the Problematic Usage of the Internet (PUI) and its relationships to adolescent mental health across the United Kingdom, France, Germany, Italy, Australia, Canada, the United States, and New Zealand. Using a policy path dependency framework, national legislation was examined to assess relationships with PUI. The study maps policy by reviewing governmental legislation and databases, analysing them on macro (societal), meso (market/intermediary organisations), and micro (citizen rights, duties, and protection) levels. It explores legal instruments related to PUI, including data protection, cybersecurity, content regulation, and harassment, offering both historical and comparative analyses across the eight countries. Findings indicate that while several countries have policies indirectly regulating PUI, significant legislative gaps persist relating to adolescent mental health. Most policies address broader internet concerns without specifically targeting PUI or its effects on mental health. Overall, the analysis highlights the need for more targeted public health policies to address the root causes of PUI, advocating for tailored interventions focused on adolescent well-being.

There is increasing global concern about the harms associated with problematic usage of the internet (PUI) affecting young people. Various risk factors have been proposed, but there is a scarcity of reliable evidence on the extent of the problem, who is most at risk of developing PUI and why, and how best to tackle it.

Background: Climate change is an urgent global challenge that affects mental health through multiple pathways, including trauma related to extreme weather events, ongoing psychological distress due to climate threats, and disruptions at the community level. Although awareness of these effects is increasing, research and clinical responses in Europe remain limited and fragmented.

Methods: To address this gap, the EU COST Action CliMent (CA23113) has developed a strategic roadmap to guide future research and practice in this emerging field.

Results: Drawing on a multidisciplinary network of experts, the roadmap identifies three key priorities: first, systematic assessment of mental health impacts, including the development of valid measures and identification of vulnerable populations; second, implementation of adaptive responses, such as evidence-based interventions tailored to climate-related stressors; and third, promotion of resilience through behavioural change, education, and integration of mental health into climate and environmental policies. This framework results from expert consensus within the CliMent network, reflecting both scientific evidence and contextual realities across Europe. It underscores the importance of collaboration among researchers, clinicians, policymakers, and community stakeholders to foster innovation and equitable access to care.

Conclusion: The roadmap highlights the urgency of involving early-career researchers and affected communities to ensure inclusive, sustainable progress. By consolidating efforts and addressing structural disparities, the initiative positions Europe to lead global efforts in protecting mental health in the face of environmental disruption, ultimately promoting both individual and collective well-being.

Background: Although exposure to natural environments is generally associated with reduced stress, these effects are not universal and may vary depending on individual vulnerability (Olafsdottir G., 2020; Gatersleben B., 2013). The term weather sensitivity (WS) refers to a disruption in well-being and/or an exacerbation of physical symptoms triggered by weather changes (von Mackensen S, 2005), which may influence physiological stress regulation, particularly in individuals with coronary artery disease. Cortisol, a key marker of hypothalamic-pituitary-adrenal (HPA) axis activity, provides an objective indicator of stress reactivity and recovery (Miller WL, 2018; Nader N, 2010). Examining cortisol responses after outdoor versus indoor walking may therefore help clarify how environmental context shapes stress physiology in weather-sensitive cardiac patients. Aim: To examine cortisol stress responses in WS individuals with CAD after outdoor versus indoor walking. Subjects and methods. This randomized controlled trial included 90 weather-sensitive (WS) individuals with CAD (74.4% men and 25.6% women; mean age 59.4 years), all participating in a cardiac rehabilitation program. WS was assessed using a self-reported question ("Do you feel the weather changes?"), and participants who answered "YES" were classified as WS. Participants were randomly assigned to one of two walking conditions: outdoor walking in a natural environment (park) or indoor walking (gym on a treadmill). On the day of the experiment, participants completed a 20-minute walk according to their assigned condition. Acute physiological stress was subsequently induced using the cold pressor test (CPT). Salivary cortisol concentrations were assessed at three times: before walking (T1), after walking (T2), and 20 minutes after the CPT (T3). Within-group cortisol changes across measurement time points were analyzed using the Wilcoxon Signed Ranks Test. Results. Among weather-sensitive (WS) individuals, cortisol response patterns differed depending on the walking environment. In the indoor walking group (n = 48), no statistically significant overall differences in cortisol concentrations across measurement time points were observed (Friedman x2 = 3.487, p = 0.175, W = 0.04). Consistently, post-hoc pairwise comparisons did not reveal significant differences between T1, T2, and T3 measurements, indicating a stable cortisol profile throughout the procedure. In contrast, in the outdoor walking group (n = 42), pairwise comparisons indicated a significant increase in cortisol concentration from T1 to T3 (Z =- 2.177, p = 0.029, r= 0.34), as well as from T2 to T3 (Z =- 2.545, p = 0.011, r= 0.39). No significant change was observed between T1 and T2 (p=0.781). Conclusion. In WS individuals with CAD, physiological stress responses differ according to the walking environment. Outdoor walking was associated with a more pronounced cortisol response to subsequent stress, whereas indoor walking was followed by a relatively stable cortisol profile. These findings suggest that environmental context may play an important role in shaping stress reactivity in WS patients with CAD and highlight the need to consider individual environmental vulnerability when designing rehabilitation and stress-management strategies.

Background: Thyroid axis hormones, such as free triiodothyronine (fT3), free thyroxine (fT4), and thyrotropin (TSH) are associated with mental disorders, especially with depression and anxiety [1, 2]. These hormones have been associated with worse cognitive functioning in individuals with coronary artery disease [3]. Cognitive dysfunction is prevalent in individuals with anxiety and mood disorders (AMD) [4, 5], however, the associations between these variables have not been studied in individuals with AMD. Therefore, the aim of our study was to investigate the correlation between fT3, fT4, the fT3/fT4 ratio, TSH and cognitive functioning in individuals with AMD. Methods: One hundred and ninety-two (age 39±12 years; 21% men and 79% women) individuals attending a Stress-related disorders day care unit of the Palanga Hospital at Neuroscience Institute of the Lithuanian University of Health Sciences, took part in this cross-sectional study. Diagnoses of AMD were established using the Mini-International Neuropsychiatric Interview. Cognitive tests were completed in order to assess cognitive functioning. Participants completed Digit Span Test to assess auditory attention and Trail Making Test (TMT) A and B to assess their perceptual speed, task-switching and executive control characteristics. Venous blood samples were drawn for evaluation of fT3, fT4, and TSH. Blood was centrifuged and serum was stored frozen at -70˚C. Serum levels of fT3, fT4, and TSH were analysed using an automated enzyme immunoassay analyser. Depression symptoms were measured with the Patient Health Questionnaire-9 (PHQ-9), anxiety symptoms were measured with the Generalized Anxiety Disorder-7 (GAD-7). For statistical analyses, univariate regression analysis was used to examine unadjusted associations of fT3, fT4, TSH, and fT3/fT4 with scores on cognitive functioning tests. Then, multivariable regression analyses were performed to determine if fT3, fT4, TSH, and fT3/fT4 remained significantly associated with cognitive functioning after adjusting for age, sex, education, depression and anxiety symptoms, smoking, and current medication use. Results: In individuals with AMD, univariate regression analyses showed that fT3 had a negative correlation with TMT Part A (b=-0.206; p=0.004), and Part B (b=-0.145; p=0.046); however, these associations were not significant in multivariable analyses after adjusting for age, sex, education, depression and anxiety symptoms, smoking, and current medication use. A univariate regression analyses also showed a negative correlation between fT4 and TMT Part A (b=-0.210; p=0.004), as well as Part B (b=-0.152; p=0.036). These associations were significant even after controlling them for aforementioned confounding factors (b=-0.192; p=0.006; b=-0.151; p=0.036 respectively). Conclusions: Overall, in individuals with AMD, lower fT4 concentrations were associated with slower perceptual speed and worsened task-switching abilities independent of socio-demographic characteristics, clinical factors as well as depression and anxiety symptoms. The results show the importance of thyroid hormones on cognitive functions in individuals with AMD. Particularly lower fT4 could be a potential biomarker of impaired cognitive functioning in individuals with AMD.

Background: Chronic low-grade inflammation has been strongly implicated in the pathogenesis of major depressive disorder (MDD) [1]. In particular, cytokines interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α), have been associated with diagnosis of MDD and depressive symptoms in a subset of patients. Preclinical studies have demonstrated that administration of lipopolysaccharide (LPS), a pro-inflammatory component of gram-negative bacterial membranes, induces inflammation and depressive-like behaviours in animal models [2,3]. While these findings provide strong experimental support for an inflammatory component in depression, clinical data on circulating LPS levels in individuals with MDD remain limited. This study aimed to investigate whether plasma concentrations of LPS, IL-6, and TNF-α differ between patients with MDD and healthy controls. Methods: This cross-sectional study included patients with MDD and a control group of subjects without psychiatric history. MDD diagnoses were based on ICD-10 diagnostic criteria and verified by experienced psychiatrists. Participants with unstable medical comorbidities or current anti-inflammatory treatment were excluded. Each study participant completed a sociodemographic questionnaire. Fasting venous blood samples were assayed for plasma LPS, IL-6 and TNF- α using commercial ELISA kits. Descriptive statistics were used to summarize sociodemographic and clinical characteristics. Continuous variables were presented as medians with interquartile ranges (IQR), assessed by the Shapiro-Wilk test. Between-group comparisons for continuous variables were conducted using the Mann-Whitney U test, as data did not meet the assumptions of normality. The Z-score and p-value were reported for each comparison. Results: A total of 143 participants were included in the analysis – 97 subjects with MDD and 46 controls. Demographic and clinical characteristics were comparable between MDD groups and controls with respect to age (Z= –0.801, p=0.423), female proportion (Z= –0.807, p=0.931), and body mass index (BMI) (Z= –0.713, p=0.476). Smoking prevalence was significantly higher in MDD group (Z= –3.513, p<0.001). Somatic comorbidities did not differ between two groups (Z= –0.701, p=0.483). Blood plasma LPS levels were significantly elevated in all the participants with MDD (median: 148.0 pg/ml, IQR: 81.1–245.3) compared to controls (median: 95.6 pg/ml, IQR: 57.5–132.3), with a statistical result of Z = –3.525 and p<0.001. In contrast, IL-6 levels did not differ significantly between the groups (Z = –0.145, p = 0.884), with median values of 1.31 pg/ml (IQR: 0.55–3.20) for the MDD group and 1.25 pg/mL (IQR: 0.59–3.13) for the controls. TNF-α levels were mostly undetectable in both groups; however, a slight but statistically significant difference was noted (Z = –1.98, p = 0.048). Most participants in both the MDD and control groups had undetectable TNF-α levels, which may be attributed to the limited sensitivity of the immunoassay used. Conclusion: Elevated plasma LPS, but not IL-6 and TNF-α differentiates MDD patients from healthy controls. These findings support LPS as a potential biomarker and therapeutic target in MDD.