Insulin Resistance and Thrombophilia
Insulin causes hypercoagulability
Insulin resistance and resulting hyperinsulinemia have been implicated in the development of hypercoagulability.
Insulin resistance causes thrombophilia and inflammation
A panel of novel (non-traditional) risk factors are ancillary features of the metabolic syndrome. They include biomarkers of chronic mild inflammation (e.g. C-reactive protein, CRP), increased oxidant stress (e.g. oxidized low density lipoprotein, LDL), thrombophilia (e.g. plasminogen activator inhibitor-1, PAI-1) and endothelial dysfunction (e.g. E-selectin).
Insulin Resistance and Miscarriage
Insulin resistance increases clotting factors and prevents clot breakdown
The metabolic syndrome is characterized by a combination of obesity, chronic inflammation and insulin resistance. This syndrome also has features of a hypercoagulable state, consisting of increased levels of clotting factors (tissue factor, factor VII and fibrinogen) as well as inhibition of the fibrinolytic pathway (fibrinolysis is the process of breaking down blood clots)(increased plasminogen activator inhibitor-1 and decreased tissue plasminogen activator activity).
Insulin resistance increases platelet reactivity and coagulation, and impairs clot breakdown
Diabetes and the metabolic syndrome (including insulin resistance) that underlies it are hyper-coagulable states. Increased platelet reactivity, augmented activity of the coagulation system, and impaired fibrinolysis (the process of breaking down blood clots) are characteristic and understood to a remarkable extent.