Advanced age is associated with a dramatic increase in the rates of venous and arterial thrombotic events. Increases in fibrinogen, factors VIII and IX, and other coagulation proteins, without a proportional increase in anticoagulant factors, likely contribute to this risk. Recent studies have delineated a role for genomic elements in controlling age-related expression of some coagulation proteins. Enhanced platelet activity as well as molecular and anatomic changes in the vessel wall also contribute to the thrombotic propensity. Advanced age is associated with elevated interleukin-6 (IL-6) and C-reactive protein levels, indicating an inflammatory state that may be an important stimulus for thrombus formation in the elderly. Despite evidence of a prothrombotic state, many elderly people do not experience clinical thrombotic events. It is possible that the increase in coagulation proteins and activation markers conveys a survival advantage, such as inhibiting tumor angiogenesis. The recent epidemic in obesity may heighten thrombotic risks in the elderly because adipose tissue is an important source of inflammatory cytokines and plasminogen activator inhibitor-1 (PAI-1). As the population ages, further studies will be warranted to define the mechanisms for thrombosis in the elderly.