Social Isolation, Loneliness and Subclinical Atherosclerosis

Purpose of Review 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. Recent Findings 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. Summary 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 studies and intervention trials are needed to determine whether improving social connectedness can slow atherosclerosis progression and reduce cardiovascular risk.