Iron and Sudden Death in the Insulin Resistance

Iron is essential for life, but excess iron can be toxic. As a potent free radical creator, iron generates hydroxyl radicals leading to significant oxidative stress. Iron overload, and plasma viscosity contributes to cardiovascular risk in the general population, particularly in men (Van der A, 2005; Junker, 1998). Iron influences glucose metabolism, even in the absence of significant iron overload, and its reduction may alleviate coronary heart disease and reduced or prevent their complications. In fact, high stored or free iron levels (measured by serum ferritin or catalytic iron concentrations) elevate risk for development of coronary atherosclerosis. Increased body iron stores may accelerate endothelial dysfunction in acute ischemic syndromes. Indeed , excess body iron originates oxidative injury that is associated with systemic and vascular inflammation, phrothrombotic conditions and insulin resistance (Williams, 2002). The greatest viscosity, the greatest vascular insulin resistance.

In the general population, body iron stores are positively associated with the development of glucose intolerance, type 2 diabetes and gestational diabetes. Furthermore, it has been demonstrated that blood donation significant drops in the incidence of cardiovascular events, as well as in procedures such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting (Holsworth, 2013): frequent blood donations decreased iron stores in healthy volunteers, improving insulin sensitivity and hemodynamic parameters. Iron and oxygen-derived free radicals are important in the pathogenesis of postischemic reperfusion injury and contributes substantially to endothelial dysfunction in acute coronary syndromes (Chekanov, 2002; Duffy, 2001).