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Greatest Threat to Longevity

January 2017

By William Faloon

William Faloon
William Faloon

Twenty years ago I was leaving a medical conference when one of our ardent supporters rushed up and handed me a huge textbook.1 She begged I take it home to read.

She was adamant that Life Extension® make a greater effort to enlighten its readers about the underlying cause of most disability and death in persons over age 50.1

The threat described in the textbook occurs when an abnormal blood clot forms inside an artery or vein. The medical term is thrombosis.

Two disorders involving arterial thrombosis are:

  • Heart Attack
  • Ischemic Stroke

Two disorders involving venous thrombosis are:

  • Deep Vein Thrombosis (DVT)
  • Pulmonary Embolism

Those stricken with cancer are particularly susceptible to venous thrombosis.2 Chemotherapy patients are up to 6-times more vulnerable.3

One reason we’ve recommended low-dose aspirin since 1983 is its ability to inhibit platelet aggregation, a major factor involved in arterial thrombosis, leading to a heart attack or ischemic stroke.4

Recent studies show that arterial thrombosis occurs more frequently than previously thought.5,6 Minor thrombotic events seldom display outward symptoms and, over time, predispose us to a host of degenerative illnesses including mind-robbing mini-strokes.6,7

Many of the nutrients you take have diverse antiplatelet effects. This is important in protecting against arterial thrombosis, but far less so for venous thrombosis.

The Surgeon General published a report showing that deep vein thrombosis (and subsequent pulmonary embolism) may cause 100,000-180,000 deaths each year in the US.8 To put this in perspective, pancreatic cancer is estimated to kill more than 41,000 Americans in 2016.9 Pancreatic cancer has a decidedly deadly reputation, yet the public is largely unaware that deep vein thrombosis (and subsequent pulmonary embolism) poses a greater overall health risk.

This is the 679-page textbook
given to me by an enthusiastic
Life Extension® supporter who
wanted the world to know that
thrombosis poses the greatest
threat to healthy longevity.

The Surgeon General was highly critical of mainstream medicine for not recognizing patients at risk for deep vein thrombosis and taking appropriate preventive measures.

Longtime readers of this magazine should be comforted with the knowledge that they are already taking steps to reduce their arterial thrombotic risk.

This issue describes startling new data about deep vein thrombosis, and what can be done to help prevent it.

People often take for granted that blood effortlessly flows through their arteries and veins like water moves through a hose.

The reality is that blood flow is highly dependent upon a complex interplay of different mechanisms, including coagulation factors that regulate the tendency of blood to form a clot.

For example, platelets play an important role in “plugging” holes in our circulatory system, helping to reduce bleeding in conjunction with other clotting factors.

Conversely, when platelets abnormally aggregate (clot) inside a blood vessel in response to arterial plaque and/or endothelial damage, the result is stoppage of blood flow to the affected part of the anatomy. An abnormal blood clot in a cerebral artery can lead to ischemic stroke, whereas a thrombus (clot) that forms in a coronary artery can result in a heart attack.

As humans age, mini-thrombotic events can occur to small arteries in the brain. This includes transient ischemic attacks (TIAs) in the brain that, over time, can cause damage to our cognitive abilities.

Preventing the development of these minor and major thrombotic episodes is critical for healthy longevity. The good news is that we know a lot about what causes pathologic blood clotting inside arteries and veins, and how to prevent it.

Role of Inflammation in Both Arterial and Venous Thrombosis

Inflammation sets in motion a sequence of events that can lead to arterial and venous thrombosis. Normal aging results in increasing levels of vascular inflammation, often without outward symptoms.

Readily obtainable blood markers that can reveal systemic inflammation are homocysteine,10-12 C-reactive protein,13,14and fibrinogen.15-17 Heightened levels of these inflammatory biomarkers are correlated with arterial thrombosis and subsequent risk of cardiovascular disease.18,19

Fish oil,20 vitamin D,21,22 curcumin,23,24 and other plant extracts inhibit many underlying inflammatory factors that increase C-reactive protein. The biologically active form of folic acid (5-MTHF)25,26 along with vitamins B1227 and B627 can slash elevated homocysteine through two distinct detoxification pathways.28

In contrast to the association between risk of arterial thrombosis and C-reactive protein elevation, C-reactive protein is not very useful in predicting future venous thrombosis or pulmonary embolism. Recent evidence does point to the role of proinflammatory cytokines like IL-8 and tumor necrosis factor-alpha in venous thrombosis risk.29

Nattokinase is an enzyme extracted from a Japanese food (natto) prepared from fermented soybeans.30 Venous inflammation tends to raise fibrinogen levels, and fibrinogen is an important factor involved in inflammation as well as venous thrombosis formation.31 Nattokinase has been shown to decrease levels of fibrinogen along with clotting factors VII and VIII, which are involved in the formation of venous thrombosis.32

Conventional Arterial Thrombotic Risk Factors

LDL cholesterol is a common factor involved in development of atherosclerotic plaque in arteries.33

Elevated LDL contributes to deposits of plaque that cause arterial pathways to gradually narrow until normal blood flow is disrupted. When this happens, there is a greater propensity for arterial clot formation (arterial thrombosis).33

Hypertension increases the velocity at which blood is thrust through the arterial system. As blood pressure elevates, platelets become more likely to aggregate and create a thrombotic event.34

Conventional cardiovascular and arterial thrombosis risk factors are diabetes, smoking, abdominal obesity, and hyperlipidemia (elevated LDL and triglycerides).35-38 Some of these same factors are also associated with increased risk of deadly venous thrombotic events.

The encouraging news is that proven methods exist to control underlying causes of thrombosis and the vascular diseases that can develop acutely or chronically.

Epidemic of Deep Vein Thrombosis

Deep venous thrombosis and pulmonary embolism are major causes of disability and death.39

Each year, as many as 900,000 Americans may be affected by venous thromboembolism. Of those diagnosed, up to 30% will die within one month, and the first symptom will be sudden death in about 25% of those who have a pulmonary embolism.40

Venous thrombosis is the formation of a blood clot inside a vein that can obstruct flow in the localized affected part of the venous circulatory system. When a venous blood clot dislodges from its primary location and travels to block circulation in another body part, this is referred to as a venous thromboembolism. When a deep vein thrombosis dislodges and travels to the lungs, this worrisome and potentially life-threatening condition is called a pulmonary embolism.

A variety of factors are implicated in the formation of venous thrombosis. Two major, related risks for the development of deep vein thrombosis are:

  • Hemostasis (reduction/stagnation of blood flow)
  • Hypercoagulability (propensity of blood to clot inside veins due to lifestyle, cancer or genetics)

The good news is that steps can be taken to reduce the risk of deep vein thrombosis, as well as thrombotic risks throughout the circulatory system. This means that strategies to protect against deep vein thrombosis may also confer protection against stroke and heart attack.

Symptoms of Deep Vein Thrombosis

A blood clot in one of the deep veins can include the following symptoms:83

  • Mild to severe pain in the affected arm or leg
  • Swelling of an arm or leg
  • Redness or color change
  • Warmth of the skin

A venous blood clot that has traveled to the lung (called a pulmonary embolism) has symptoms that include:83

  • Chest pain
  • Shortness of breath
  • Fast heartbeat

What Causes Blood Vessel Clots in Arteries?


To sustain life, blood must remain in a fluid state so that it can freely circulate, while simultaneously being able to properly clot at the site of a vascular injury.

Any event that activates platelets can cause them to aggregate to form an occlusive thrombus.

As it relates to aspirin, fish oil and certain plant polyphenols, you’ll often read about their “antiplatelet” properties. What this describes is their ability to interfere with platelet activity, adhesion, and aggregation, thereby reducing arterial thrombotic risk.

Antiplatelet therapies, however, can be sabotaged by dysfunction of our endothelium (inner arterial lining). A healthy endothelium produces substances that stabilize platelets and impede their unwanted adhesion.

When the endothelial lining is lost, platelets are exposed to parts of the arterial wall that cause them to aggregate. Protecting against endothelial dysfunction is thus essential to maintain vascular health as we age. This is where pomegranate and other plant polyphenols play a critical role.

Antiplatelet strategies employed today, utilizing certain medications and nutrients, can greatly mitigate these arterial thrombotic factors.

Nutrients that Help Protect Against Arterial Thrombosis

How Arterial and Venous Clots Differ


There are distinctions between the processes that cause arterial and venous thrombosis.

Arterial thrombosis largely involves platelet aggregation forming around clogged/jagged points in the arterial system, or in response to irregular heart beat (atrial fibrillation) or an artificial heart valve.

Deep vein thrombosis typically occurs due to hemostasis (reduction in venous blood flow) and hypercoagulability (tendency of the blood in veins to clot due to genetic, cancer or lifestyle factors).

One major cause of reduction in venous blood flow is chronic venous insufficiency. This frequently occurs from obesity, lack of physical activity/sitting with the legs in a dependent position, and previous deep vein thrombosis, which injures or destroys one or more of the valves that are located in the deep veins of the leg.

In order to efficiently return blood to the heart when a person is sitting or standing, veins contain tiny valves that open and close. Properly functioning valves prevent blood from flowing backward while muscles surrounding the veins compress them, helping pump venous blood back to the heart.8

Veins contain valves while arteries do not. When veins are damaged by prior venous clot, or physical inactivity leads to pooling of blood in the deep veins of the legs, venous blood flow decreases, setting the stage for venous thrombosis.

In contrast with the venous system, platelets in the arterial system are adversely activated as they bump into buildups of plaque along the arterial walls and interact with a dysfunctional endothelium. In this scenario, platelets begin to clump together, causing a cascade that can lead to blood flow being cut off to vital tissue (such as a portion of the heart muscle).

In the venous system, normal blood flow can slow, and if left to stagnate too long, the blood within these veins begins to coagulate (clot). The problem of deep vein thrombosis, however, extends beyond mere stagnating pools of blood in the lower legs.

Formation of Deep Venous Thrombosis
Formation of Deep Venous Thrombosis

Fibrinogen converts to fibrin that creates a fibrin mesh inside a vein. Platelets and red blood cells adhere to fibrin mesh to cause deep vein thrombosis.

Nattokinase reduces fibrinogen and has fibrinolytic effects, which means it can enzymatically break down the fibrin mesh component of blood clots.

Beyond “Antiplatelet” Strategies

Inflammation and some other factors that contribute to arterial thrombosis (such as excess homocysteine) also are linked with an increased risk of deep vein thrombosis.84,85 Several of these dynamics, however, play a larger role in the venous system than in arteries.

What happens with deep vein thrombosis is that fibrinogen, also a proinflammatory regulator, excessively converts to a fibrin mesh that traps red blood cells. In deep vein thrombosis, formation of fibrin is also linked with excess inflammation in veins.86 This helps explain the limited efficacy of antiplatelet drugs (aspirin and Plavix®) in venous thrombosis, i.e., they don’t stop the initiating phase of proinflammatory fibrinogen converting to red blood cell-trapping fibrin.

There are multiple underlying coagulation factors that can initiate a deep venous thrombosis. Some require preventive treatment using anticoagulant drugs (warfarin, Pradaxa®, Eliquis®, Xarelto®). There is a common venous thrombotic mechanism, however, that can be impeded with a low-cost nutrient.

Nattokinase has been shown to decrease fibrinogen levels and help dissolve fibrin clots that obstruct blood flow.32,87

The flow chart on this page shows a simplified version of the complex process of coagulation involved in thrombosis formation. The fibrinogen/fibrin-dissolving effects of nattokinase can help stop this coagulation cascade at several checkpoints.

Cancer-Related Thromboembolism

Cancer is associated with a 4.1-fold increased risk of venous thromboembolism.88

Poor mobility, venous obstruction, and ongoing chemotherapy further increase risk of recurrence.89,90 Venous thromboembolism is associated with advanced and more aggressive cancers.91,92

Cancer patients with venous thromboembolism have worse survival than cancer patients free of this complication.91 For example, after a diagnosis of venous thromboembolism, the mortality rate at 6 months for cancer patients on anticoagulant therapy is 40%.92

Cancer patients today are dying prematurely from venous thromboembolism. This is why Life Extension® long ago recommended aspirin and low-molecular weight heparin as adjuvant cancer therapies. Not only do overly-active platelets contribute to thrombosis, but they facilitate metastasis.93-95

What might surprise you is that venous thromboembolisms can be the first clinical manifestation of cancer somewhere in one’s body. About 10% of patients with unprovoked venous thromboembolism are diagnosed with cancer. Of these, more than 75% are diagnosed within the first year after their thrombotic episode.2

Impressive Human Data!

A recent study highlighted the risk of deep vein thrombosis in response to conditions that predispose to stagnation of venous blood in the lower extremities (legs)—specifically, air travel.96

Many people are not aware that air travel, and associated pooling of venous blood in the legs due to inactivity during flight, is a major risk factor for deep vein thrombosis and potentially life-threatening pulmonary embolism.97,98

Using ultrasound imaging, the presence of venous thrombosis was detected in a startling 5%-7% of passengers of flights lasting 7-8 hours.96 These passengers were asymptomatic, meaning they did not know they had developed a venous blood clot!

When a nondrug approach for prevention of deep vein thrombosis was studied in this group of passengers, no lower leg venous clots were detected and lower leg edema (swelling) was drastically reduced.

Whenever you are faced with long-haul air travel, you should stand up every few hours and take a walk through the plane cabin. Consider obtaining high quality compression stockings to wear whenever you fly to reduce stagnation of blood in lower leg veins.99

As you will read in this month’s issue, ingestion of two nutrients taken two hours before the plane departs and again six hours into the flight drastically reduced detection of venous blood clots and lower leg edema at the end of the flight. These nutrients have a dual effect of inhibiting platelet aggregation and helping to thwart fibrin-induced clots.

The fact that short-term dosing of these two nutrients demonstrated such a profound effect in protecting against deep vein thrombosis implies significant systemic benefits for those who supplement daily.

An intriguing article in this month’s issue describes the robust benefits of these nutrients for reducing deep vein thrombosis risk.

The first article unveils a novel way of enhancing the efficacy of your probiotic by selectively killing off harmful intestinal bacteria.

Surgeon General’s Call to Action

In a report published 8 years ago, the Surgeon General stated:

“DVT [deep vein thrombosis] and PE [pulmonary embolism] are major public health problems in the United States. Much is known about how to reduce their burden, yet this knowledge is not being applied systematically today. Without a concerted effort to stem this public health crisis, the incidence and burden of these diseases will only grow larger as the population ages.”8

Sadly, this medical neglect continues as hurried physicians are not doing enough to prevent thrombotic events that not only cause DVT/pulmonary embolism, but many strokes and heart attacks.

Obtain Nutrient Formulas at Year’s Lowest Prices

This is the time of year when we discount prices on every one of our advanced nutritional formulas.

Longtime supporters take advantage of the once-a-year Super Sale to stock up on their favorite nutrient formulas.

Those who have engaged in healthy lifestyle choices should find comfort knowing that nutrients they may have been using for decades confer considerable protection against thrombosis, which remains the most prevalent underlying cause of disability and death in persons over age 50.

When Anticoagulant Drugs Are Needed

People with artificial heart valves or atrial fibrillation are at high risk for developing a thrombus that breaks loose and travels up a carotid artery, where it can cause an acute ischemia stroke.100,101

There are also inherited conditions in which blood clotting proteins improperly react, either causing blood to overcoagulate or preventing expression of normal clot dissolving factors. Some of these coagulation disorders that result in too much clotting include:

  • Factor V Leiden
  • Antithrombin III (ATIII) deficiency
  • Protein C or protein S deficiency
  • Prothrombin (PT) gene mutation
  • Antiphospholipid antibody syndrome

Those in a hypercoagulable state are usually prescribed one of the four following anticoagulant drugs:

  • Pradaxa®
  • Eliquis®
  • Xarelto®
  • Coumadin® (warfarin)

The major side effect risk of these drugs is unwanted bleeding. These drugs also don’t always prevent a thrombotic event. Those who choose the oldest of these drugs (warfarin) are subjected to severe vitamin K deficiency that rapidly calcifies tissues. This can lead to future degenerative illnesses (such as accelerated atherosclerosis and aortic valve stenosis).

Despite these side effect risks, those at high thrombotic risk should work closely with their physician to use the anticoagulant drug that best meets their individual needs. To review our detailed report on the pros and cons of each of these drugs, log on to:

Our Commitment

No organization is working harder to accelerate human age reversal research than Life Extension.

Your support enables scientists to engage in biomedical research that would have been inconceivable just a few years ago.

To order nutrients you need today at Super Sale prices, call 1-800-544-4440.

For longer life,

For Longer Life

William Faloon


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