Dauerstress und Zellalterung: Was die Forschung zeigt und was Sie tun können

Chronic psychological stress refers to repeated or prolonged exposure to adverse social or emotional threats that exceed an individual's adaptive capacity. It is recognized as a risk factor for aging-associated diseases. A growing body of research has shown that there is a link between chronic psychological stress and accelerated aging. Here, we highlight recent findings on the interconnected relationship between chronic psychological stress and major aging hallmarks, including mitochondrial dysfunction, telomere attrition, cellular senescence, epigenetic alterations, inflammation, and genomic instability. We discuss the mechanisms by which chronic psychological stress may drive this effect and explore intervention strategies that could mitigate its adverse effects and promote healthy aging. Moreover, we address current research gaps and propose future research directions to improve our understanding of the intricate relationship between psychological stress and aging.

<h4>Background</h4>Oxidative stress and inflammation contribute to telomere length (TL) attrition, a hallmark of cellular senescence. Systemic lupus erythematosus (SLE) is associated with premature cellular aging; however, the clinical relevance of TL shortening remains unclear. This study aimed to compare the relative TL of SLE patients and healthy controls and explore its association with clinical features and disease burden.<h4>Methods</h4>We conducted a cross-sectional study including adult SLE patients and age- and sex-matched healthy controls (18-60 years). Demographic and clinical data were collected, and TL was measured using quantitative polymerase chain reaction (qPCR). Among SLE patients, disease activity, cumulative damage, fatigue, depression, anxiety, stress, and physical activity were also assessed. Statistical analyses included descriptive statistics, Student's t-test or Mann-Whitney test for group comparisons, Spearman's correlation, and multiple linear regression models selected based on the lowest Akaike information criterion (AIC).<h4>Results</h4>Sixty SLE patients (37 years ± 11.5) and 55 controls (38 years ± 10.5) were enrolled. SLE patients exhibited significantly shorter TL [median (IQR): 0.80 (0.29-2.94)] compared to controls [1.07 (0.38-2.32); p = 0.005]. In multivariate analysis, moderate anxiety was associated with shorter TL compared to none/low anxiety [β= -0.353 (95%CI: -0.645; -0.061); p = 0.019]. An alternative model indicated that moderate st

Socio-economic and environmental factors significantly influence health by driving epigenetic changes that alter genetic expression and impact disease prevention. Lifestyle elements such as diet, exercise, mindfulness, and environmental exposure play crucial roles in modulating these mechanisms. A systematic review of studies from the past 13 years, conducted under PRISMA guidelines, examined interventions, epigenetic outcomes, and health impacts. Mindfulness practices, particularly meditation, were found to regulate DNA methylation, reducing stress and inflammation. Dietary interventions, such as the Mediterranean and DASH diets, enhanced health biomarkers and slowed epigenetic aging through favorable DNA methylation. Physical activities, such as high-intensity interval training and hybrid training, induced epigenetic modifications, improving metabolic function, mitochondrial biogenesis, and insulin sensitivity. These findings emphasize the importance of adopting modern lifestyle choices to promote health and prevent chronic diseases by influencing gene expression. Combining mindfulness, balanced diets, and regular physical activity offers substantial benefits for metabolic, cardiovascular, and mental health. However, more research is needed to understand the long-term effects of lifestyle factors on epigenetics and to develop personalized strategies that optimize disease prevention and overall wellbeing.