Written for and published by the Turmeric User Group, copyright Liz Wallis 2017
We get so many questions about turmeric’s function as an anticoagulant that I thought it might be helpful to explain how clotting works and how it’s affected by turmeric.
Antiplatelet or anticoagulant?
Though it’s common to do so, anticoagulation and antiplatelet adhesion should not really be seen as separate functions. Coagulation is a complex multistage cascade of events during which interdependent mechanisms operate in parallel. Anything which affects one of them will have an effect on all of them downstream from that point. But it’s true that some substances affect only one portion of those pathways.
The physiological steps that lead to clotting are normally kept within tight bounds by at least one cellular mechanism, and sometimes several. Clotting involves both the formation of thrombin and the structural changes that lead to platelet adhesion. Some pharmaceutical preparations affect only half of that equation. Warfarin and heparin affect thrombin formation, for example, while clopidogrel (Plavix) and several others of that class inhibit platelet adhesion. Turmeric does both.
Clotting begins when trauma to a blood vessel exposes platelets to collagen. Our blood vessels are lined with endothelial cells that contain large amounts of collagen. Inside this lining of endothelial cells is a lining of platelet cells. When the endothelial cell layer is damaged because of trauma to the blood vessel, the platelets are exposed to the collagen in the endothelial cells. Through several different receptor sites on the surface of the platelet cells, they bind to the collagen. The platelets then undergo a dramatic change in shape and surface area. Their normal flattened sphere configuration deforms into a rough surface covered with spiky-looking protrusions. They release several substances into their environment, including one called thromboxane X2 (or TxA2). TxA2 is secreted via a pathway called the arachadonic-acid (AA) cascade.
More platelets are attracted to the site of the injury by the presence of these chemicals in the environment. At the same time, via a different cascade of events, thrombin is being formed from prothrombin. There are two parallel pathways for the activation of thrombin from prothrombin. At the point where those pathways converge, an enzyme called activated factor X (or factor Xa) causes the release of large amounts of thrombin. This is the point at which several of the other prescription anticoagulants act (Eliquis and Xarelto, for example).
On the surface of the platelets, the presence of TxA2 and two other substances (ADP and factor IIa) prompt available thrombin to bind to the platelets. The thrombin then converts fibrinogen molecules to strands of fibrin, which provide platelet aggregation by connecting each platelet to multiple others, forming a physical plug at the site of the trauma.
So how does turmeric fit into this picture?
Turmeric inhibits the synthesis of factor Xa through its interference with the arachadonic acid cascade. It thus inhibits the release of thrombin. With less thrombin available, less fibrinogen is converted to fibrin, and therefore platelet aggregation is slowed. The prescription pharmaceuticals Xarelto, Pradaxa and Eliquis are also Factor Xa inhibitors.
Turmeric also directly inhibits platelet aggregation by interfering with the production of several of the chemicals that participate in its formation. Platelet-activating factor (PAF), normally present at low levels throughout the body, is synthesized in large amounts by platelets when blood vessel trauma takes place. Turmeric inhibits that synthesis. Arachadonic-acid (AA), another chemical that participates in platelet aggregation, is also inhibited by turmeric, as mentioned above. Both of these take place at low percentages of curcumin typical of whole turmeric. Higher concentrations of curcumin will inhibit other platelet-aggregating agonists as well.
Turmeric’s anticoagulant mechanism is well-documented and well-understood. Unlike some prescription anticoagulants and some foods, its effect lasts only as long as it’s being consumed. Garlic and gingko biloba, for example, are irreversible platelet inhibitors whose effect last for the full lifetime of a platelet (7 to 9 days). The same is true for the prescription anticoagulants clopidogrel and ticlid, and several others. New platelets are always being formed, of course, so the actual effective period of platelet inhibition is usually only about 5 days. But like aspirin, turmeric’s effect on platelet adhesion stops when turmeric is metabolized and excreted. That’s why it’s safe to continue using it up to within 24 to 48 hours of a surgical procedure.
One last thing. Anticoagulants are often referred to as ‘blood thinners.’ As you can see, they do not bring about any change in blood viscosity. They simply slow down the body’s clotting mechanisms in one or more ways.