stroke Archives

Anticoagulant Natural Alternative

August 3, 2016 Philip Miller Comments 16 comments

Natural Anticoagulant Regimen

A natural anticoagulant routine. How could this benefit you? How can you implement this? Why is this a time-proven alternative to conventional approaches?

Hopefully, you have read part1, part2, and part 3 of this 4 part series. Primers on coagulation and thrombosis. I have carefully explained the process of coagulation resulting in heart attacks and strokes. We have talked about platelet aggregation. Which then leads to fibrin aggregation. Which leads to the final clot. All clots cause obstruction. Obstruction causes heart attacks and strokes. How can we prevent this?

I have alluded to the most powerful natural anticoagulants. These include the following:

Nattokinase — 100 mg twice daily
Ginkgo biloba — 120mg daily
High-dose fish oils — 1 tablespoon (10 grams) daily
Vitamin E — 800-1200 units daily
Adequate hydration — many glasses of pure water daily

Nattokinase

Let’s start with Nattokinase. Nattokinase is a derivative of the natto bean. This is a Japanese food source. Nattokinase is a serine protease produced by Bacillus subtilisduring during fermentation. Nattokinase is very bitter to the taste! Unpalatable. Therefore, the standardized extract is preferable and convenient.

Nattokinase is a fibrinolytic agent. You can refer back to all previous fibrin pathways. The goal is to prevent fibrinogen converting to fibrin.

Nattokinase has been studied extensively by the Japanese. Nattokinase biochemical activity is labeled in FU. That is fibrinolytic units. These activity units have a mg equivalent. A typical dose is 100 mg (2000 FU) twice daily. It is essential that you take this twice daily. Once daily is insufficient. This has been time proven through empirical observation.

I have treated thousands of cases with Nattokinase preventing recurrent thrombophlebitis, strokes and heart attacks. It is essential that you source NSK-SD.

There are alternatives to Nattokinase. Lumbrokinase is derived from the earthworm. It is commonly sold as Bolouke in Canada. By the manufacturer’s claims, it is even more potent. Higher biological activity. Serrapetase has similar but not identical properties. I use Serrapetase to treat arterial plaques.

Here is a great reference paper on the fibrinolytic and anticoagulant properties of Nattokinase.

Ginkgo Biloba

Ginkgo biloba has many actions. This is a time-honored and venerated Chinese herb. Ginkgo biloba has multiple constituents. These are flavonol and flavone glycosides, lactone derivatives (ginkgolides), bilobalide, and much more. We use a standardized 26% ginkgo extract. The Germans have studied this in detail. Reference the German E Commission. Here is a more readable guide.

The dose I recommend is 120 mg daily. Or 60 mg split twice daily. German studies have advocated as high as 240 mg. Through empirical observation, I find this dose to be way too aggressive. Ginkgo is so potent that 240 mg will probably cause adverse bleeding.

Ginkgo Biloba exerts its action primarily as an anti-platelet anticoagulant drug. It inhibits platelet aggregating factor. Ginkgo has many other uses. It is an antioxidant. Ginkgo may have vasodilatory effects. It is used for cognitive enhancement. I find it much more effective as a cardiac protective drug.

Be careful with your dosing ginkgo biloba. I advocate the use of 4Sight. This is a potent combination used to prevent eyesight deterioration. It includes 60 mg of ginkgo biloba. It is one example of adjusting the total dose of ginkgo biloba. And that is, again, 120 mg.

Because of its action, ginkgo biloba should not be combined with aspirin or NSAIDs. It will have synergistic effect.

High-dose fish oils

High-dose fish oils have a “rheological” effect. That is the prevent aggregation of red blood cells. It is the aggregation of platelets and/or red blood cells is the initiating process. High-dose fish oils act like Teflon to prevent this aggregating effect. The dose that I recommend is aggressive. 1 tablespoon daily. You will rarely achieve these doses with oral capsules. I highly recommend fish oils in liquid form.

Fish oils contain EPA (eicosapentanoic acid) and DHA (docsoahexanoic acid). I recommend 4000-5000 mg of EPA and 3000-4000 mg of DHA. That would total approximately 10 grams of fish oil. 1 tablespoon of high potency fish oil will yield this high dose of 5000 mg EPA and 4000 mg of DHA. I stress again, you will not achieve these doses with fish oil capsules.

Fish oils, in addition to their anticoagulant effect, may have multiple benefits:

enhance brain function – cognitive enhancement
prevent cardiovascular events
antidepressant
improve skin turgor
lower blood pressure
treat gastric reflux

Vitamin E

Vitamin E also has rheological properties. It prevents red blood cell aggregation. Vitamin E exists as a family of tocopherols.

I highly recommend mixed tocopherols. This is a isomeric mix of natural tocopherols including the alpha, beta, gamma and delta forms of vitamin E. There is a difference between “natural” vitamin E and “synthetic” natural vitamin E. Synthetic vitamin E is a tocopheryl not tocopherol.

I routinely recommend a 400-800 units of mixed tocopherols (vitamin E) daily. In many instances I will recommend 800-1200 units of vitamin E. Studies have shown that Gamma tocopherol is much more potent than alpha tocopherol. Most studies only investigate the alpha form of Vitamin E.

Water – Hydration

And last but not least, hydration. Keep well hydrated. Hydration will also prevent red blood cell and platelet aggregation. It will improve skin turgor. I highly recommend water in glass bottles, not plastic bottles. You should avoid all plasticizers. PVCs, phthalates and BPA. The softer the plastic bottle the higher the plasticizer content. Never tap drink water. Most likely, all your municipal water sources are contaminated or polluted. Chlorine, chloramine, flouride, and heavy metals. Flint Michigan is just the tip of the iceberg.

Potency and efficacy

So this routine when fully implemented will prevent platelet and red blood cell aggregation. It prevents the conversion of fibrinogen to fibrin. This treats all pathways of coagulation. It is a much more comprehensive approach to anticoagulant therapy than conventional drugs. Less expensive. With fewer complications. Is it effective?

Virtually every surgeon now has been taught to ask, “what other vitamins and herbs are you taking?” Every surgeon knows that each and all of these agents clearly have anticoagulant effects. Surgeons see the effects of drugs. Internists only infer the effects of drugs. Surgeons know that prior to surgery anticoagulants can significantly increase complications. However, just following surgery the opposite effect is noted. The body may react with a vigorous coagulation response.

So empirically and rationally you can see this routine has the ability to effectively prevent heart attacks, strokes and recurrent thrombophlebitis.

Medical Supervision is Essential

A major caveat! I never advocate abruptly stopping conventional anticoagulant routines. You need medical supervision to start and monitor your progress. This anticoagulant routine requires special knowledge of potency, dosing and the value of these natural sources. I have been treating thousands of cases over the past 20 years. This is time-tested. It is effective. But this regimen is not “validated” through conventional guidelines or task force committees. It is not the “standard of care.” For this reason, your internist, cardiologist or family practitioner will have little understanding of the rationale or efficacy of this routine.

This is not a DIY — do it yourself advocacy.

So where do we go from here? Let me give you some suggestions. Call us or write for further information.

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AntiPlatelet AntiCoagulant Drugs

August 1, 2016 Philip Miller Comments 2 comments

Coagulation and Anticoagulatant Therapy

Read part I and part II of this series for background. So you will have a basic understanding of coagulation pathways. Yes, it is complex.

Remember, coagulation or clotting starts with platelet aggregation. That initiates the complex coagulation cascade. This causes the mature thrombus or blood clot. Aggregated platelets with a thick fibrin mesh causes the thrombus. The thrombus causes heart attacks, strokes or thrombophlebitis. Here is the final complete picture:

injury activates platelets causing thrombus formation — fig 1- click for full size

So let’s discuss anticoagulant therapy medications.

Antiplatelet Agents – Aspirin and Plavix are first line of defense

Figure 2 shows how we prevent platelet aggregation and activation at various stages. Look at figure 1. Aspirin has been the mainstay of antiplatelet therapy. There has been a succession of drugs over the last three decades. Newer antiplatelet drugs supersede older ones. Are these true advances or simply marketing campaigns?

antiplatelet drugs classified by site of action. Aspirin and Plavix are the most common platelet inhibitors — fig 2 – click for full size

Aspirin has been well studied in the literature. A full 325 mg dose will prevent platelet aggregation. Over time, aspirin has significant adverse reactions. These are direct and indirect reactions. It can cause tinnitus (ringing or buzzing noises in the ear). It can cause major gastrointestinal bleeding. This is a significant problem.

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Coagulation Heart Attack and Stroke – Part 2

July 18, 2016 Philip Miller Comments 0 Comment

It is necessary to understand the interaction of fibrin coagulation pathways and platelet aggregation. Once we understand these interactions we can then discuss current treatment modalities. My goal is to show you a more creative and natural approach to anti-coagulation.

Initial Platelet Aggregation

In part one I emphasized the importance of platelet aggregation as the initial step. There is an initial injury to an arterial or venous wall. As a response, activated platelets cause a clumping reaction to repair the injury. Somewhat like Hans Brinker’s “finger in the dike.”

This injury could be a laceration. It could be a rupture of a atheromatous plaque. It could simply be a tear in an arterial wall. Or simply from low-flow stasis. Atrial fibrillation is an example.

You can see from fig 2 above that the platelets initiate an array of reactions. I will elaborate even more detail in the next post. This is ever-increasing overview.

Aspirin is the most common drug to prevent platelet aggregation. We will look at an array of drugs that have been used over the years. But there is a more creative approach.

Once the initial platelet plug has formed the long-term fibrin coagulation pathway is initiated.

Fibrinogen pathways

fibrin to fibrinogen cascade from intrinsic and extrinsic pathways — fig 3

The classic fibrin clotting pathway is divided into the intrinsic and extrinsic systems. The intrinsic system starts with Factor XII. There is a cascading series of reactions to the final common pathway. This is prothrombin activating thrombin. Thrombin then catalyzes the reaction of fibrinogen to fibrin. Finally, fibrin is polymerized to an insoluble mesh. The extrinsic arm interacts with the intrinsic arm.

As discussed previously, the production of fibrin can be blocked at various stages. The conversion of fibrinogen to fibrin can be reversed through a process called fibrinolysis. An important concept.

So now we have a complete picture. The following diagram summarizes the evolution of this thrombus from platelet aggregation to fibrin clot.

Decision-making – Blocking Which Pathway?

Now we have rapidly covered the two aspects of thrombosis (clot) production. This is where the subject becomes indeterminate. Some “guidelines” emphasize the prevention of platelet aggregation. While other guidelines emphasize the long-term use of anti-fibrin drugs. What is the best strategy? Depends on the guidelines. These evolving guidelines are determined by age, associated risk factors, and preceding condition.

These guidelines were originally developed to make decision-making simple. And uniform. And coherent. The community standard of care. But guidelines eventually become bloated and incoherent. Much like IRS tax code. I anticipate this decision-making process will soon be totally computerized. Remove the human discretionary input. I do not agree. Look here to see just how complex this decision tree for anticoagulant therapies can be.

The entire purpose of this series of posts is to present a novel combination of anti-fibrin anti-platelet modalities.

Now you have an overview of the basic flow. In part 3 we will examine current and past drug interventions.

Coagulation Stroke Heart Attack Part 1

July 15, 2016 Philip Miller Comments 0 Comment

Heart Attack and Stroke Coagulation Basics

Let’s talk about heart attack and stroke causes and the complexity of the underlying coagulation (clotting) pathways. What a heady subject. You need a PhD in medical hematology, just to fully understand the complexities of coagulation. So let’s work through this step by step. This will be a multi part series. I will help you achieve a clearer understanding. None of us wants to suffer a heart attack or stroke!

What causes these these catastrophic vascular events? What are the risks? What medications are commonly used? Why are they not necessarily the best or even the healthiest choice? Can we assess risk benefit ratios? And what are the natural herbal-based alternatives? Ones that can be just as effective with fewer side effects and less costly. This is what you will not hear from your personal internist, cardiologist or even family physician.

Blood Clot is a Thrombus or Embolus

A thrombus totally blocks (occludes) blood flow from activated coagulation factors — fig 1

A blood clot usually starts with an injury to a vascular wall. This could be one of your arteries or veins. An intricate series of reparative or reactive events is set in motion. Your body tries to rapidly repair injury to the vascular wall. Atrial fibrillation is an alternative source of thrombus formation. In this instance, stasis and not injury, initiates the reaction.

Fig 1 above shows you a representation of the well formed blood clot. It has the potential for blocking blood flow (vascular occlusion) which deprives tissues distal to the block of vital cell oxygenation. The medical term is myocardial infarction or cerebral infarction. Cells die from lack of oxygen.

The initial early phase begins with activation and aggregation of platelets.

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Dr. Philip Lee Miller

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Category: stroke