Reduction of carotid plate with nattokinase and stabilization with picnogenol

Carrotidea atherosclerosis is one of the main pathological conditions associated with the risk of ischemic stroke and major cardiovascular events. The formation of atheromasic plaque is not a simple passive accumulation of cholesterol but a dynamic and complex process involving chronic inflammation, lipid oxidation, endothelial dysfunction and fibrine deposition. In this context the growing interest in nattokinase, a phybrinolitic enzyme extracted from the nose, traditional Japanese food obtained from soy fermentation, which in recent years has been the subject of clinical studies for its possible role in regression of atherosclerotic plaques.

Nattokinase mainly acts through a powerful direct fibrinolytic effect, favoring the degradation of the fibrin which is an important structural component of the plaque. This adds the ability to stimulate the endogenous fibrinolytic system by increasing the activity of plasmine and improving the fluidity of blood. This dual mechanism allows not only to reduce blood viscosity but also to intervene directly on the structure of the plate, making it less compact and favoring a progressive reduction.

One of the most significant studies in this area is that conducted by Ren and collaborators in 2017 and indexed on PubMed, which involved 82 patients with carotid atherosclerosis and hyperlipidemia. Participants were divided into two groups, one treated with nattokinase at the dose of 6,000 FU per day (2+2+2 cps away from meals) and the other with Simvastatina 20 mg, for a total duration of 26 weeks. The results showed a reduction of the carotid plate of 36.6 percent in the group treated with nattokinase, with a passage from 0.25 to 0.16 cm2, while in the group treated with statin the reduction stopped at 11.5 percent. Also the carotid intimate-media thickness has decreased in both groups but to a greater extent in patients taking nattokinase. Although both treatments have improved the lipid profile with reduction of total cholesterol, LDL and triglycerides and increase of HDL, the effect on the plate observed with nattokinase seems partly independent of the reduction of cholesterol, suggesting a direct action on the fibrin component and structural stability of the lesion.

To achieve a real systemic effect, it is essential to consider how nattokinase is taken. As a protein enzyme, it can be inactivated by digestive enzymes when taken together with meals. For this reason the intake must take place away from food, preferably on an empty stomach, so as to promote intestinal absorption and allow the enzyme to enter the circle in an active form. The daily dose of 6,000 FU in three administrations distributed over the course of the day allows to maintain a constant and more effective phybrinolithic activity on the clinical level.

However, reducing plaque is not the only therapeutic goal. A crucial aspect, often underestimated, is the stabilization of the plaque itself. The atherosclerotic plaques are not all the same. Some are relatively stable and tend to grow slowly without causing acute events, while others are unstable, rich in oxidized lipids, inflammatory cells and with a thin fibrous cap that can easily break. It is precisely the rupture of the plaque to represent the most dangerous moment, since it exposes the trombogenic material to the circulating blood and can determine the rapid formation of a trombo capable of obstructing the artery or migrating to the brain causing a stroke.

In this scenario it becomes essential to combine the reduction of the plate with a stabilization action. The picnogenol, extracted from the bark of the French maritime pine, represents one of the most studied natural compounds for this purpose. Its activity is based on powerful antioxidant and anti-inflammatory properties that help protect vascular endothelium and reduce oxidative stress, one of the main factors that make plaque unstable. Picnogenol also promotes the strengthening of the fibrous plate cap, making it more resistant to breakage, and improves endothelial function by increasing the production of nitric oxide, resulting in improved vasodilation and tissue perfusion.

The association between nattokinase and picnogenol is therefore a synergistic approach. On the one hand, nattokinase contributes to progressively reduce the mass of plaque by intervening on the fibrin component and improving the fluidity of the blood, on the other, the picnogenol acts by stabilizing the structure of the plaque and reducing the risk of sudden breakage. This double action is particularly relevant from the clinical point of view because it does not merely intervene on a single factor but acts simultaneously on the regression and safety of atherosclerotic injury.

In light of the available evidence, the use of nattokinase at the dose of 6,000 FU per day, divided into three assumptions away from meals (2+2+2 cps), associated with a stabilizing agent such as picnogenol, is an interesting and rational strategy in the management of carotid atherosclerosis, especially in subjects with moderate cardiovascular risk or in those who do not tolerate traditional pharmaceutical therapies. However, a personalised medical framework is essential, considering the possible increase in hemorrhagic risk in subjects taking anticoagulant or anti-aggregant drugs.

This integrated approach does not replace conventional medicine but opens up new perspectives in the prevention and treatment of vascular diseases, placing attention not only on the reduction of cholesterol but also on the quality and stability of atherosclerotic plaque, determining elements for the prevention of acute events.

The link to the nattokicasi study (to read it frame the Qr-code)

Link to the study on picnogenol