Accumulation of stress is a prognostic trigger for cardiovascular disease. Classical scores for cardiovascular risk estimation typically do not consider psychosocial stress. The aim of this study was to develop a global stress index (GSI) from healthy participants by combining individual measures of acute and chronic stress from childhood to adult life. One-hundred and ninety-two female and male soldiers completed the Perceived Stress Scale (PSS4), Trier Inventory for Chronic Stress (TICS), Hospital Anxiety and Depression Scale (HADS), Childhood Trauma Questionnaire (CTQ), Posttraumatic Diagnostic Scale Checklist (PDS), and the Deployment Risk and Resilience Inventory (DRRI-2). The underlying structure for the GSI was examined through structural equation modeling. The final hierarchical multilevel model revealed fair fit by taking modification indices into account. The highest order had a g-factor called the GSI. On a second level the latent variables stress, HADS and CTQ were directly loading on the GSI. A third level with the six CTQ subscales was implemented. On the lowest hierarchical level all manifest variables and the DRRI-2/PDS sum scores were located. The presented GSI serves as a valuable and individual stress profile for soldiers and could potentially complement classical cardiovascular risk factors.

Psychosocial stress increases cardiovascular risk, which coincides with enhanced oxidative DNA damage. Increased sympathetic tone-related catecholamine release causes oxidative stress, which contributes to catecholamine-related cardiotoxicity. Therefore, we tested the hypothesis whether acute psychosocial stress induces oxidative DNA damage, its degree being related to the cardiovascular risk profile and depending on the sympathetic stress response. After assessment of the prospective cardiovascular Münster score (PROCAM) to determine the risk of acute myocardial infarction, 83 male and 12 female healthy volunteers underwent the Trier social stress test for groups (TSST-G). Heart rate variability was quantified by measuring the standard deviation (SDNN) and root mean square of successive differences (RMSSD) between normal-to-normal inter-beat intervals. Salivary α-amylase (sAA) activity was assessed as a surrogate for noradrenaline plasma concentrations. Oxidative DNA damage was determined using whole-blood single-cell gel electrophoresis (“tail moment” in the “comet assay”). A total of 33 subjects presented with a prospective risk of myocardial infarction (risk+) vs. 59 subjects without risk (risk-). The TSST-G stress significantly increased blood pressure, heart rate, and sAA in both groups, while oxidative DNA damage was only increased in the risk+ group. Immediately after the TSST-G, the “tail moment” showed significant inverse linear relations with both SDNN and RMSSD. Acute psychosocial stress may cause oxidative DNA damage, the degree of which is directly related to the individual cardiovascular risk profile and depends on the stress-induced increase in the sympathetic tone.

Background: Alterations in the central and peripheral energy metabolism are increasingly recognized as key pathophysiological processes in psychiatric disorders. We investigated mitochondrial respiration and density linked to cellular energy metabolism and oxidative DNA damage in borderline personality disorder (BPD). Methods: This cross-sectional case–control study compared three groups matched for age and body mass index: women with acute BPD, remitted BPD, and female healthy controls ( n = 32, 15, 29). Peripheral blood mononuclear cells were investigated for differences in mitochondrial respiration, density, and markers of oxidative DNA damage. Results: Participants with acute BPD showed significantly reduced and less efficient mitochondrial ATP production compared to both remitted individuals and controls. Mitochondrial coupling and respiration were inversely associated with oxidative DNA damage, although DNA damage levels did not differ significantly across diagnostic groups. Sensitivity analyses indicated that comorbid major depressive episodes and antidepressant use did not account for the results. Conclusions: These findings indicate mitochondrial alterations accompany acute symptom severity in BPD and may improve with remission. Unraveling causes and consequences of mitochondrial downregulation and its interplay with DNA maintenance in the context of stress and psychopathology could contribute to novel models and treatment strategies in BPD and related severe psychiatric disorders.

Alterations in the central and peripheral energy metabolism are increasingly recognized as key pathophysiological processes in various psychiatric disorders. This case-control study investigates mitochondrial energy production and oxidative DNA damage in Borderline Personality Disorder (BPD). We compared mitochondrial respiration, density, and DNA damage in peripheral blood mononuclear cells between women with acute BPD, remitted BPD, and healthy controls ( n = 32, 15, 29), matched for age and BMI. Acute BPD was characterized by reduced and less efficient mitochondrial ATP production compared to both remitted BPD and controls (e.g., coupling efficiency: r _x = −0.36 and −0.35, p _adj ’s < .037). Decreased mitochondrial activity was closely associated with greater DNA damage (e.g., coupling efficiency: r _S = −0.57, p < .001), although DNA damage did not differ between diagnostic groups. Our findings suggest mitochondrial energy production processes as promising and sensitive biomarkers for acute disorder severity and clinical remission in BPD.