Possible mechanism of chronic systemic inflammation, most cardiovascular diseases and cancer

This article presents a speculative pathophysiological hypothesis proposing a common mechanism underlying chronic systemic inflammation (CSI), cardiovascular diseases, metabolic syndrome, cancer, and several age related disorders. The author suggests that prolonged psychological and physical stress may induce episodic opening of large arteriovenous anastomoses, leading to abnormal arterial-to-venous blood shunting. According to the hypothesis, these recurrent blood leaks may disrupt systemic and pulmonary circulation, promote oxidative stress, impair tissue oxygenation, and contribute to chronic inflammatory activation. The proposed mechanism is further linked to endothelial dysfunction, atherosclerotic plaque formation, venous congestion, metabolic disturbances, and progressive multiorgan damage. The article also discusses the possible relationship between chronic systemic inflammation and carcinogenesis, emphasizing disease comorbidity as evidence of a shared underlying process. Existing international research on chronic inflammation and aging is reviewed to support the conceptual framework. Preventive strategies focused on stress reduction, circulation regulation, physical activity, and monitoring of vascular shunts are proposed. The article is intended to stimulate scientific discussion and future experimental investigation rather than provide established clinical conclusions.