What Is Nattokinase?

According to legend, about a thousand years ago, the warrior Minamoto no Yoshiie found and tasted boiled soybeans that had been left on straw and had fermented. That was the discovery of Nattō. It is believed that by the end of the Edo period (1603-1867), Nattō had become a regular part of Japanese cuisine in some areas. It is no secret that the Japanese live longer, have less cardiovascular disease and are not affected by heart attack and stroke as frequently as people in the Western world. Many now believe that Nattō has been the secret to their well-being.

How is Nattō made? In the past, bundles made from rice straw were filled with steamed beans and then stored in a warm, humid environment. This resulted in fermentation by Bacillus Nattō, a bacterium that lives in rice straw. During fermentation, proteins and glucide contained in the soybeans decompose, generating the distinctive Nattō strings, which can stretch up to 20 feet.

Nowadays, Nattō is mass-produced in automated factories, where steamed soybeans are sprayed with the ideal amount of Bacillus Nattō. The beans are then transferred to small containers by machine. A conveyor moves them to storage, where preset temperature and humidity levels allow the beans to ferment and mature.

In 1980 Japanese researcher Hiroyuki Sumi accidentally discovered that Nattō had the ability to dissolve blood clots. He then set out to isolate the enzyme within Nattō primarily responsible for this clot busting ability. He purified and isolated the enzyme, which he called nattokinase, literally Nattō enzyme ( Interview with Doctor of Medicine Hiroyuki Sumi, Japan Bio Science Laboratory Co., Ltd., 1998).

When we suffer a cut or wound, our blood has the ability to seal off these breaks to prevent us from bleeding to death. In response to the emergency, the blood-vessel walls or the clotting factors in the blood release a chemical into the bloodstream. This causes fibrinogen, an inert protein found in blood plasma, to be converted into fibrin. The fibrin molecule is unique in its ability to link together, forming long threads that wrap around the platelet plug. The threads act much like a spider-web, catching more platelets, red blood cells, and other substances to form a clot. The newly formed, jellylike clot is about 99 percent water. So two proteins are released by the platelets, causing the clot to contract and squeeze out the fluid. A solid clot has now formed. On the skin surface, where the clot has been exposed to air, it is commonly called a scab.

Once begun, the process must be stopped so that the clot does not become so big that it blocks the vessel and cuts off blood circulation. How is it stopped? After the mending work is done, blood flow rapidly returns to normal and disperses the clotting factors. There are also several anticoagulants in the blood that prevent excessive clotting and keep platelets from collecting together when there is no emergency.

However, unnecessary blood clotting can also occur in the absence of a wound. Why does this occur? Our body produces only one enzyme that has the ability to break up clots by dissolving fibrin – plasmin. As we age, the body produces less plasmin. On the other hand, fibrinogen levels increase as we age. The older we get, then, the more clotting and the less clot busting ability we have. Thus, millions of Americans each year suffer heart attacks or strokes resulting from unnecessary blood clots – leading to death or permanent disability (Montalescot, G. et al. “Fibrinogen as a risk factor for coronary heart disease.” Eur Heart J 1998, 19 Suppl H:H11-17).