Einsamkeit als Dauerstress: Was sie mit Gefäßen, Herz und Gedächtnis macht

Lack of social connection is a major risk factor for Alzheimer's disease and related dementias, on a par with other common risk factors like physical inactivity and smoking. Yet we still know surprisingly little about how social connection affects cognitive health. Our review provides updated guidance for researchers interested in testing new mechanistic models of social connection and cognitive health over the life course. First, we conceptualize social connection and its various components. Second, we provide readers with a supplemental compendium of social connection measures and discuss how to tailor different types of measures to specific research goals. Third, we advance a conceptual model linking social connection to cognitive health across different social, spatial, and temporal contexts, while also considering potential sources of confounding and reciprocal causation. Finally, we outline five priority areas for future research into social connection and cognitive health across the life course.

Loneliness, the subjective perception of inadequate social connection, is increasingly recognized as a significant and modifiable determinant of health with implications extending beyond psychosocial well-being to cardiovascular and cognitive outcomes. A growing body of evidence links loneliness to increased risk of cardiovascular disease, cognitive decline, and dementia; however, these domains have often been studied in parallel. This review advances a brain-heart axis framework to integrate these literature, conceptualizing loneliness as a chronic psychosocial stressor that contributes to cognitive aging through interconnected neuroendocrine, autonomic, inflammatory, and vascular pathways. Loneliness is associated with sustained activation of stress-responsive systems, including the hypothalamic-pituitary-adrenal axis and sympathetic nervous system, leading to cumulative physiological burden, or allostatic load. These processes contribute to endothelial dysfunction, vascular injury, and increased risk of cardiovascular conditions, which in turn impair cerebral perfusion and promote neurodegeneration. In parallel, loneliness is associated with neurobiological effects, including hippocampal atrophy, neuroinflammation, and reduced cognitive reserve. Behavioral and psychological pathways further amplify these effects. This paper synthesizes epidemiologic, mechanistic, and clinical evidence to propose a multi-pathway model linking loneliness to cognitive aging through neurobiolo

<h4>Purpose of review</h4>Social isolation and loneliness have emerged as important cardiovascular risk factors, yet the biological mechanisms linking adverse social experiences to cardiovascular disease remain incompletely understood. This review examines current evidence relating social isolation and loneliness to subclinical atherosclerosis and explores the underlying neuroendocrine, autonomic, inflammatory, and vascular mechanisms.<h4>Recent findings</h4>Recent epidemiological studies have associated social isolation and loneliness with endothelial dysfunction, arterial stiffness, carotid plaque, carotid intima-media thickness, and coronary artery calcium. Advances in transcriptomic and proteomic research have identified molecular signatures characterized by increased inflammatory signaling and altered immune regulation in socially isolated individuals. Experimental animal studies further support a causal relationship between adverse social environments and accelerated atherosclerosis. Accumulating evidence suggests that social isolation and loneliness contribute to subclinical vascular disease through interconnected pathways involving hypothalamic-pituitary-adrenal axis activation, autonomic dysregulation, chronic inflammation, oxidative stress, and endothelial dysfunction. Although available studies are limited and predominantly cross-sectional, findings support a biologically plausible link between social disconnection and early atherogenesis. Future longitudinal studi

BACKGROUND: Loneliness and social isolation are established risk factors for adverse cardiovascular, cerebrovascular and cognitive outcomes in later life, yet the pathways underlying these associations remain underexplored. This study tests the structure of a published framework linking social isolation and loneliness to health outcomes through psychological, behavioural and physiological pathways. METHODS: We analysed cross-sectional data from 1,685 Singaporean adults over the age of 60 from the Wellbeing of the Singapore Elderly study. Path analysis was used to examine the psychological (subsyndromal and syndromal anxiety and depression), behavioural (smoking, alcohol use, poor diet and sedentary lifestyle), and physiological (hypertension, obesity, diabetes and sleep disruption) pathways from social isolation and loneliness to health outcomes (cardiovascular, cerebrovascular and cognitive health). RESULTS: The final model fit the data well (χ²(60) = 67.62, p = .233; CFI = 0.986; TLI = 0.993; RMSEA = 0.009). Loneliness was positively associated with psychological burden (b = 0.20, p < .001), unhealthy behaviours (b = 0.06, p = .001), and physiological burden (b = 0.06, p = .005). Social isolation was positively associated with psychological burden (b = 0.07, p = .005) and unhealthy behaviours (b = 0.14, p < .001). Physiological burden was positively associated with cardiovascular disease (b = 0.22, p < .001) and cerebrovascular conditions (b = 0.34, p < .001), while unhealt