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A staggering number of people are destined to experience a cardiovascular-related disorder sometime in their lives. Almost 1 million Americans die each year as a result of cardiovascular disease, whereas 556,000 die each year from cancer. Despite these facts, people are often more afraid of cancer than they are of vascular disease.


Americans have become complacent about the dangers of arterial disease. One reason is that the percentage of young people dying from acute heart attack has plummeted over the past 50 years. Explanations for these reductions include lifestyle changes, greater use of dietary supplements/preventive medications, and improved cardiac medical care.


The question is why are so many Americans continuing to die from heart attack and stroke? The fundamental answer is that people are living longer. What has happened is that much of the human population has succeeded in delaying the development of arterial disease. So instead of suddenly dying from a heart attack at age 50, the vascular symptoms do not manifest until the 60s or 80s are reached. At this point, systemic arteriosclerosis has damaged the major organ systems, and multiple degenerative diseases result in diminished quality and quantity of life.


Many of the underlying causes of arterial disease have been identified in the scientific literature. Regrettably, cardiologists have only addressed a limited number of these factors, such as prescribing cholesterol-lowering drugs, controlling hypertension, etc. By ignoring the other proven causes for the epidemic of vascular-related diseases, a significant number of Americans are experiencing needless suffering and are dying prematurely.


This overview presents some of the more important missing pieces of the puzzle about why cardiovascular disease remains the nation's leading crippler and killer. It provides solid information about what can be done to significantly reduce cardiovascular risk today.


For those who want to learn about every identified risk factor, the protocol that follows entitled Cardiovascular Disease: Comprehensive Analysis provides meticulous data that is especially important for anyone who already has a heart or vascular-related disorder.

Inflammation and Heart Disease

A growing consensus among scientists is that common disorders such as heart attack, stroke, and other vascular-related diseases are all caused in part by a chronic inflammatory syndrome. Numerous published articles demonstrate that the presence of blood indicators of inflammation are strong predictive factors for determining who will develop coronary artery disease and have cardiac-related death (Lindahl et al. 2000; Packard et al. 2000; Rader 2000).


The good news is lifestyle changes and certain dietary supplements can suppress these dangerous inflammatory components of blood.

One of the dangerous inflammatory markers that has been identified is a coagulation protein called fibrinogen. High fibrinogen levels can induce a heart attack via several mechanisms, including increased platelet aggregation, hypercoagulation, and excessive blood thickening.

The findings of published scientific studies show that persons with high levels of fibrinogen are more than twice as likely to die of a heart attack.

Another inflammatory marker is C-reactive protein. This marker indicates an increased risk for destabilized atherosclerotic plaque and abnormal arterial clotting. When arterial plaque becomes destabilized, it can burst open and block the flow of blood through a coronary artery, resulting in an acute heart attack.


Some studies show that people with high levels of C-reactive protein are almost three times as likely to die from a heart attack.

Why Cardiologists Are So Slow to React

In 1996 the Life Extension Foundation published an article showing that high levels of fibrinogen represented a significant risk factor for heart attack and ischemic stroke (Ridker et al. 2000). The article was based on studies dating back to the 1980s showing that people with elevated fibrinogen levels were more likely to die from a cardiovascular-related disease.

Despite numerous studies linking elevated fibrinogen to increased heart attack risk, few physicians bother to check their patient's blood levels of fibrinogen or other correctable risk factors such as homocysteine and C-reactive protein.

Many cardiologists are still demanding a higher standard of proof before they routinely test their patients' blood for what they consider to be "newly identified" cardiac risk factors. Even when a physician is aware of the importance of testing a patient's blood for the presence of inflammatory risk factors, a common problem is that managed care organizations (HMOs and PPOs) refuse to pay for them.

The sad fact is that the majority of practicing physicians are not yet aware of how to properly correct for elevated inflammatory risk factors (such as C-reactive protein and fibrinogen).

As a result of physician ignorance or insurance company stinginess, many Americans experience progressive debilitating congestive heart failure or cerebral circulatory impairment, when the underlying causes could have been corrected if the physician ordered and then properly interpreted these blood tests.

Correcting Inflammatory Risk Factors


Cardiovascular risk factors such as fibrinogen and C-reactive protein are produced in the liver by pro-inflammatory cytokines called interleukin-1B, interleukin-6, and tumor necrosis factor alpha (TNF-a) ( Ridker et al. 2000). Supplements such as highly concentrated DHA fish oil and DHEA suppress excess production of some of these dangerous cytokines.

Another study showed that interleukin-6 by itself increased the risk of heart attack, even after adjustment for the elevation in C-reactive protein induced by interleukin-6 (Rader 2000). Both vitamin K and DHEA suppress interleukin-6, which helps explain why these supplements have been shown to protect against such a wide range of age-related diseases (Reddi et al. 1995; Kipper-Galperin et al. 1999; Haden et al. 2000).


Concerning the suppression of the dangerous tumor necrosis factor alpha and interleukin-1B cytokines, nettle leaf extract appears to be the most effective dietary supplement (Obertreis et al. 1996; Teucher et al. 1996).


Protection Against Fibrinogen-Induced Heart Attacks

Agents that inhibit platelet aggregation reduce the risk that fibrinogen will cause an abnormal arterial blood clot. Platelet aggregation inhibitors include aspirin, green tea, ginkgo, garlic, and vitamin E (Bossavy et al. 1998; Kang et al. 1999; Logani et al. 2000; Rahman et al. 2000). For optimal protection against heart attack, it also makes sense to utilize therapies that directly lower elevated fibrinogen levels.


High serum vitamin A and beta-carotene levels have been associated with reduced fibrinogen levels in humans. Animals fed a vitamin A-deficient diet have an impaired ability to break down fibrinogen.

When animals are injected with vitamin A, they produce tissue plasminogen activator (tPA), which breaks down fibrinogen ( Lagente et al. 1993; Back et al. 1995; Ceriello et al. 1997).

Excessive homocysteine blocks the natural breakdown of fibrinogen by inhibiting the production of tissue plasminogen activator (tPA) ( Midorikawa et al. 2000). Folic acid, TMG, vitamin B12, and vitamin B6 reduce elevated homocysteine levels. High doses of fish or olive oil have also been shown to lower fibrinogen in humans with elevated fibrinogen levels (Flaten et al. 1990; Oosthuizen et al. 1994).

Vitamin C, in pharmacological doses, has been shown to break down excess fibrinogen. In one study, heart disease patients were given either 1000 or 2000 mg a day of vitamin C to measure the fibrinogen breakdown effect. At 1000 mg a day, there was no detectable change in fibrinolytic activity or cholesterol. At 2000 mg a day of vitamin C, there was a 27% decrease in the platelet aggregation index, a 12% reduction in total cholesterol, and a 45% increase in fibrinolysis (fibrinogen breakdown) activity (Bordia 1980).


A Lethal Misconception Among Vitamin Supplement Users

The medical establishment woke up to the dangers of homocysteine when The New England Journal of Medicine (Welch et al. 1998) and the Journal of the American Medical Association (Tucker et al. 1996) published articles suggesting that vitamin supplements be used to lower homocysteine levels.
(Many years earlier, this same message appeared in the November 1981 issue of a Life Extension Foundation publication entitled Anti-Aging News, pp. 85-86.)

Conventional medical journals have published hundreds of new studies in recent years that unequivocally link elevated homocysteine to greater risk of heart attack and stroke.

As a result of these findings, some cardiologists suggest that coronary artery disease patients take a multivitamin supplement to lower their homocysteine levels. Patients who follow this advice but fail to have their blood tested for homo-cysteine could be making a fatal mistake.


The Life Extension Foundation uncovered a flaw in the theory that a person can blindly take vitamin supplements to adequately reduce homocysteine levels. While folic acid, vitamin B12, vitamin B6, and tri-methylglycine (TMG) all lower homocysteine levels, it is impossible for any individual to know if they are taking the proper amount of nutrients unless they have a homocysteine blood test.


The clear message from new scientific findings is that there is no safe "normal range" for homocysteine. While commercial laboratories state that normal homocysteine can range from 5-15 micromoles per liter (umol/L) of blood, epidemiological data reported in the American Heart Association's journal Circulation reveal that blood levels of homocysteine levels above 6.3 cause a steep progressive risk of heart attack (Robinson et al. 1995).

Another study reported in The American Journal of Epidemiology found that each 3-unit increase in homocysteine equals a 35% increase in myocardial infarction (heart attack) risk (Verhoef et al. 1996).


People taking vitamin supplements think they are being protected from the lethal effects of homocysteine when, in reality, even supplement users can have homocysteine levels far above the safe level of 6.3.


The Life Extension Foundation has identified several cases of people with coronary artery disease who had lethal levels of homocysteine despite taking the recommended dose (and higher) of vitamin supplements.

One case involved a 60-year-old man who had previous bypass surgery, but was again experiencing angina pain with significant restenosis (reclogging of the coronary arteries) verified by angiography. This man knew about the dangers of homocysteine and had been taking more than 15,000 mcg daily of folic acid, along with other homocysteine-lowering vitamins. Because of the angina pain and re-stenosis, The Foundation recommended a homocysteine blood test.

The results showed this man had the shockingly high homocysteine reading of 18. (Homocysteine levels over 15 have been shown to be extremely dangerous.)

The Foundation immediately suggested that this man take 6 grams of TMG (trimethylglycine) daily. Within 1 month, his homocysteine level had dropped to 4. This case was a wake-up call that one or more homocysteine-lowering factors are not always the solution to keeping homocysteine levels in the safest range (below 7 micromoles per liter of blood).


How to Detoxify Homocysteine

Elevated homocysteine can be reduced (or detoxified) in two ways: via the remethylation process and via the trans-sulfuration pathway.


The most common way to reduce homocysteine is via the remethylation process in which "methyl groups" are donated to homocysteine to transform it into methionine and S-adenosylmethionine (SAMe).

TMG (tri-methyl-glycine) is a potent remethylation agent. The "tri" means there are three "methyl" groups on each "glycine" molecule that can be transferred to homocysteine to transform (remethylate) it into methionine and SAMe. The remethylation (or detoxification) of homocysteine requires adequate levels of folic acid and vitamin B12 in addition to TMG.


The other pathway by which elevated homocysteine is reduced is via its conversion to cysteine and eventually to glutathione via the "trans-sulfuration" pathway. This pathway is dependent on vitamin B6. The amount of vitamin B6 required to lower homocysteine has considerable individual variability. Methionine is the only amino acid that creates homocysteine.


People who eat foods that are high in methionine such as red meat and chicken may need more vitamin B6. Elevated homocysteine can occur when there are insufficient vitamin co-factors (such as folate and vitamin B6) to detoxify the amount of methionine being ingested in the diet.


Elevated homocysteine can also be caused by a genetic defect that blocks the trans-sulfuration pathway by inducing a deficiency of the B6-dependent enzyme cystathionine-B-synthase. In this case, high doses of vitamin B6 are required to suppress excessive homocysteine accumulation.

Since one would not want to take excessive doses of vitamin B6 (greater than 300-500 mg daily for a long time period), a homocysteine blood test can help determine whether you are taking enough B6 to keep homocysteine levels in a safe range. There are some people who lack an enzyme to convert vitamin B6 into its biologically active form pyridoxal-5-phosphate. In this case, if low-cost vitamin B6 supplements do not sufficiently lower homocysteine levels, then a high-cost pyridoxal-5-phosphate supplement may be required.


For many people, the daily intake of 500 mg of TMG, 800 mcg of folic acid, 1000 mcg of vitamin B12, 250 mg of choline, 250 mg of inositol, 30 mg of zinc, and 100 mg of vitamin B6 will keep homocysteine levels in a safe range. But the only way to really know is to have your blood tested to make certain your homocysteine levels are under 7.


If homocysteine levels are too high, then up to 6000 mg of TMG may be needed along with higher amounts of other remethylation cofactors. Some people with cystathione-B synthase deficiencies will require 500 mg daily or more of vitamin B6 to reduce homocysteine to a safe level. For the prevention of cardiovascular disease, you would also want your homocysteine blood level to be under 7 micromol per liter of blood.


The Silent Stroke Epidemic


Stroke is a common threat to aging humans. Most people believe a stroke can either kill suddenly or induce a state of paralysis requiring institutional care. However, newer studies reveal that most strokes cause no obvious symptoms, but over time these "silent" strokes lead to memory loss, neurologic disorders, and more strokes. According to one study, 11 million Americans have "silent" strokes annually, and by the time people reach their 70s, 1 in 3 experiences a silent stroke every year (Leary et al. 2000).

Health-conscious people should be comforted in knowing that following the proper lifestyle and consuming specific dietary supplements may dramatically reduce the risk of ever having a stroke. For example, a meta-analysis of 15 published studies showed that mild-to-moderate elevations in homocysteine were independently associated with an astounding 86% increase in the risk of stroke (Kelly et al. 2000). The use of extra vitamin B6, vitamin B12, and folic acid is one way of lowering homocysteine levels.


What Is a STROKE?



Stroke is the third leading cause of death in developed countries. About 25% die as a result of a stroke or its complications, and almost 50% have moderate-to-severe health impairments and long-term disabilities. Only 26% recover most or all normal health and function.
The majority of strokes occur when a blood clot blocks the flow of oxygenated blood to a portion of the brain. This type of stroke, caused by a blood clot blocking a blood vessel, is called "ischemic stroke." An ischemic stroke can result from a blood clot that forms inside the artery of the brain (thrombotic stroke) or by a clot formed somewhere else in the body that travels to the brain (embolic stroke).


In the case of ischemic stroke, abnormal blood clotting blocks large or small arteries in the brain, cutting off blood flow. Ischemic strokes account for 83% of all strokes and occur as either an embolic or thrombotic stroke. The other 17% of strokes are called "hemorrhagic stroke" and these occur when a blood vessel in the brain ruptures.


Thrombotic stroke represents 52% of all ischemic strokes. Thrombotic stroke is caused as the result of unhealthy blood vessels becoming clogged with a buildup of fatty deposits, calcium, or blood clotting factors such as fibrinogen, homocysteine, and LDL-cholesterol. We generally refer to this as atherosclerosis disease.

More recent information indicates that a chronic inflammatory process is also a cause of the arterial damage that leads to stroke. Elevated C-reactive protein is an indicator of underlying inflammatory disease ( Fichtlscherer et al. 2000; Ijem et al. 2000; Pasceri et al. 2000).


Elevated fibrinogen is also a significant risk factor for developing the most common form of stroke (Audebert et al. 2000; Bai et al. 2000; Chen et al. 2000; Trouillas et al. 2000). Some of the nutrients that can lower fibrinogen include at least 2000 mg a day of vitamin C, 2400 mg of flush-free niacin, 2800 mg of EPA/DHA from fish oil, and 2000 mg a day of bromelain.

To protect against fibrinogen inducing an arterial blood clot that can cause an ischemic stroke, we suggest low-dose aspirin, vitamin E, and garlic, along with ginkgo and green tea extracts.


One of the best-documented ways of determining who will have a stroke is to measure levels of C-reactive protein in the blood. One study showed that elevated C-reactive protein posed a two-to-three times greater risk of stroke (Kelly et al. 2000).

Another study showed that in those who have a major stroke, persons who had higher levels of C-reactive protein had a much greater likelihood of having another vascular event (such as a heart attack or stroke) or dying within the following year.


In this study, stroke patients with the highest C-reactive protein levels had nearly a 2.4 times greater chance of experiencing death or a vascular event within the next year compared to patients with the lowest levels (Di Napoli et al. 2001).


High levels of C-reactive protein also indicate a potentially destructive inflammatory autoimmune condition that could predispose a person to a host of degenerative diseases. C-reactive protein can be suppressed by ibuprofen, aspirin, or vitamin E (McMillan et al. 1995; Ikonomidis et al. 1999; Devaraj et al. 2000).


Some of the pro-inflammatory immune cyto-kines that cause elevated C-reactive protein include interleukin-6, interleukin 1(b), and TNF-a. Supplements such as DHEA, vitamin K, nettle leaf extract, and high levels of DHA fish oil can help suppress these dangerous inflammatory cytokines that can cause C-reactive protein elevation (Reddi et al. 1995; Teucher et al. 1996; Kipper-Galperin et al. 1999).


One of the strengths of C-reactive protein testing is its ability to detect at-risk patients with normal cholesterol levels. The Physician's Health Study found that apparently healthy men with the highest C-reactive protein levels had twice the risk of future stroke, three times the risk of future heart attack, and four times the risk of future peripheral vascular disease (Ridker et al. 1997).

The Women's Health Study reported that C-reactive protein was the single strongest predictor of future vascular risk (Ridker et al. 1998).


Taking Steps to Reduce Your Stroke Risk Profile

For the last 50 years, physicians have concentrated on controlling blood pressure as the primary method of preventing stroke. While guarding against even borderline hypertension is critical in reducing stroke risk, there are factors that can be tested in the blood to further determine stroke risk.

Everyone over age 40 should have their blood tested to be certain their homocysteine, fibrinogen, C-reactive protein, LDL-cholesterol, etc. levels are in the safe range.


If any of these risk factors for stroke are elevated, they can be safely lowered with therapies that are proven to work. Since these same risk factors also predispose one to heart attack and other diseases, anyone concerned with living a long and healthy life should keep them in the optimal ranges.


Blood Test



"Standard Reference Range" Allows The "Optimal" Level: Where YOU Want to Be

Fibrinogen Up to 460 mg/dL Under 300 mg/dL

C-reactive protein Up to 4.9 mg/L Under 2 mg/L [Some studies indicate C-reactive protein levels should be below 1.3 mg/L (Kaneko et al. 1999; Sandrick 2000) ]

Homocysteine Up to 15 micromol/L Under 7 micromol/L

Glucose Up to 109 mg/dL Under 100 mg/dLIron Up to 180 mg/dL Under 100 mcg/dL

Cholesterol Up to 199 mg/dL Between 180-220 mg/dL

LDL cholesterol Up to 129 mg/dL Under 100 mg/dL

HDL cholesterol No lower than 35 mg/dL Over 50 mg/dL

Triglycerides Up to 199 mg/dLUnder 100 mg/dL

DHEA Males: no lower than 80 mcg/dL

Females: no lower than 35 mcg/dL Between 400-560 mcg/dL
Between 350-430 mcg/dL

Fasting Insulin 6-27 uIU/mL 0-5 uIU/mL

If your physician will not prescribe these blood tests, or if your insurance company will not pay for them because the cost is too expensive, call (800) 208-3444 to inquire about obtaining these tests via mail order.

All of this new research points to the fact that the common forms of mental impairment, disability, and death in the aging population (vascular dementia, stroke, and heart attack) are potentially avoidable. While conventional physicians focus solely on blood pressure control, they are failing to recommend important blood tests, drugs, and supplements to reduce the stroke epidemic that continues to plague the aging human population.

HMOs and insurance companies often refuse to pay for these important blood tests even though overall medical costs could be significantly reduced if common diseases like stroke were prevented.


Testing Your Blood to Avoid Cardiovascular Disease


Do not let complacent physicians put you at risk for heart disease and stroke. The following table provides the most common blood tests that can help reveal underlying cardiovascular disease risk factors.


As can be seen from the table, blood test results that conventional physicians accept as being "normal" can be lethal for you. In other words, what the "Standard Reference Range" allows is not always a practical indicator for where your "optimal" level should be.


In many cases, a "standard reference range" reflects what is expected in the average population. Since cardiovascular disease remains the number one killer of Americans, you do not want to ever be part of the "average" range when it comes to cardiovascular disease risk factors.


By keeping your blood levels in the "Optimal Range," rather than the average "Standard Reference Range," you take advantage of the increasing volume of evidence showing that most heart attacks and strokes are preventable.
In the table, you can also see that the "Standard Reference Range" differs (often dangerously) from what the published research indicates is protective against cardiovascular disease.



How Excess Insulin Causes Heart Attacks


According to the Centers for Disease Control (CDC), results of the National Health and Nutrition Examination Survey (NHANES) indicate that 35% of U.S. adults aged 20-74 were overweight and almost 20% of adults in the same population were obese (CDC 2002a,b).


A Harris Poll of a smaller population of 1011 people indicated that an even higher level (79%) were overweight, based on their body mass index (CNN 2002). Despite aggressive use of existing weight-loss therapies, far more Americans have excess body fat today than at any prior time.



Weight gain has most often been associated with cardiovascular disease and diabetes, but new studies reveal that other age-related disorders such as cancer (endometrial, breast, prostate, and colon) occur at sharply higher rates in overweight individuals (CDC 2002c).



The government is now encouraging people to lose weight to protect their health. In 2002, U.S. Surgeon General David Satcher stated that obesity may soon become a greater health hazard than cigarette smoking and issued a Call to Action urging the nation to find solutions to the problem of obesity and overweight (Surgeon General 2002).


As people age, they accumulate unwanted body fat even though they may be consuming fewer calories than when they were young. The overlooked culprit responsible for unwanted body fat and bulging waistlines is the hormone insulin.


We are not talking about normal insulin secretion. Instead, it is the overproduction of insulin that causes so many people to uncontrollably gain weight. Because insulin is required to sustain life, the public mistakenly "sees" this hormone in a favorable light.


As you will learn, too much insulin not only causes weight gain, but it is also a prime factor contributing to a multitude of diseases associated with obesity.


There are serious misconceptions about why people accumulate so much body fat as they age. One overlooked factor is that overweight people have startlingly high levels of insulin in their blood. When the blood is saturated with insulin, the body will not release significant fat stores, even when a person restricts calorie intake and exercises.


Additionally, persons who are overweight face a significant risk for developing Type II diabetes (Jallut et al. 1990; Kadowaki et al. 1994; McCance et al. 1994). The treatment of obesity and Type II diabetes is interrelated. By effectively treating either one of these diseases, one can mitigate or control the other.


Having diabetes also sharply increases the risk of heart attack and stroke. It is critical that persons concerned about preventing cardiovascular disease reverse the diabetic process. Losing excess body fat is a mandate for most persons seeking to control a Type II diabetic condition.


Hyperinsulinemia is the medical term used to describe a condition in which too much insulin is produced. One way that excess insulin makes people gain weight is that it causes them to be chronically hungry.


This happens because high insulin levels rapidly deplete glucose from the blood. This causes a state known as "reactive hypoglycemia," meaning the blood becomes deficient in glucose because there is too much insulin in the blood.


The May 8, 2002, issue of the Journal of the American Medical Association (JAMA) featured an article that described the effects of consuming high-glycemic index foods and the subsequent hyperinsulinemia, hunger, and weight gain that occurred (Ludwig 2002). The author of this JAMA article summarized his position by stating: "It is possible that the hunger incident to hyperinsulinemia may be a cause of overeating and therefore the obesity that so often precedes diabetes."


A surprising number of studies show that excess serum insulin (hyperinsulinemia) is a major health problem (Despres et al. 1996; Chu et al. 2001; Thakur et al. 2001). For people trying to reduce body fat, excess insulin suppresses the release of growth hormone in addition to preventing fat from being released from cells.


High serum insulin is associated with the development of abdominal obesity and the number of health problems this induces, including atherosclerosis and impotence (Aversa et al. 1998; Jeremy et al. 1998; Despres et al. 2000).
Perhaps the simplest method of evaluating the toxic effects of excess insulin is to look at its effects on human mortality.

One study showed that over a 10-year period, the risk of dying was almost twice as great for those with the highest levels of insulin, compared to those with the lowest.

The scientists who authored this study stated that hyperinsulinemia is associated with increased all-cause and cardiovascular mortality independent of other risk factors (Pyorala et al. 2000).


Another study showed that the risk of developing coronary artery disease increased by 60% for each single-digit increase in fasting insulin level among men aged 45-76 years (after other risk factors were controlled) (Despres et al. 1996). In optimal health, fasting insulin levels should be in the range of 0-5 (uIU/mL).

As people age, their fasting insulin levels normally increase by several single digits. Fasting insulin levels in the obese often exceed 20.
Having too much insulin in the blood has become so commonplace that laboratory reference ranges now indicate that fasting insulin levels of 6-27 are "normal."


While it is normal for aging individuals to have high fasting insulin, it is by no means desirable. Unfortunately, aging people experience a wide range of vascular diseases, such as kidney failure, heart attack, stroke, etc., that are directly attributable to elevated insulin.


Standard laboratory reference ranges can sometimes be misleading. For instance, it was once considered normal to have a cholesterol reading of up to 300 (mg/dL). While it is true that a cholesterol count of 300 was normal at that time in history, so was an epidemic of heart attacks. Once the danger of high cholesterol became known, laboratories reduced the high normal reference range to 200.


As more research substantiates the dangers of excess insulin, we believe that laboratory reference ranges will show that fasting insulin levels of 0-3 are desirable and that levels in excess of 5 put an individual at increased risk for developing a host of age-related ailments.



However, suppressing excess serum insulin is not as easy as lowering cholesterol or homocysteine. To access an in-depth protocol dealing with proven methods to lower excess insulin, refer to the Obesity protocol in this book.


Testosterone and the Heart


Normal aging results in gradual weakening of the heart, even in the absence of significant coronary artery disease. If nothing else kills an elderly male, his heart will just stop beating at some point.
Testosterone is a muscle-building hormone, and there are many testosterone-receptor sites in the heart (Bricout et al. 1994). Weakening of the heart muscle can sometimes be attributed to testosterone deficiency (Sewdarsen et al. 1990; Phillips et al. 1994).


Tes-tosterone is not only responsible for maintaining heart muscle protein synthesis, but it is also a promoter of coronary artery dilation (Rosano et al. 1999; Webb et al. 1999) and helps to maintain healthy cholesterol levels (Zgliczynski et al. 1996; Gelfand et al. 1997).


There is an ever-increasing number of studies indicating an association between high testosterone and low cardiovascular disease rates in men (Gelfand et al. 1997). In the majority of patients, symptoms and EKG measurements improve when low testosterone levels are corrected.


One study showed that blood flow to the heart improved 68.8% in elderly male coronary heart disease patients who received testosterone therapy (Wu et al. 1993b). In China, physicians successfully treat angina with testosterone therapy (Wu et al. 1993a, b, c).


The effects of low testosterone on cardiovascular disease are given in the following list:
Cholesterol, fibrinogen, triglycerides, and insulin levels increase (Glueck et al. 1993; Winkler 1996; De Pergola et al. 1997).
Coronary artery elasticity diminishes.


Blood pressure rises.

Human growth hormone (HGH) declines (weakening heart muscle).
Abdominal fat increases (increasing the risk of heart attack).
Persons with cardiovascular disease should have their blood tested for free testosterone and estrogen.

Some men (who have the full cooperation of their physicians) may be able to stop taking expensive drugs to stimulate cardiac output, to lower cholesterol, and to keep blood pressure under control if a testosterone deficit or a testosterone-estrogen imbalance is corrected.


A compelling study of 1100 men showed that men with serum DHEA-S in the lowest quarter (<1.6 mcg/mL) were significantly more likely to incur symptoms of heart disease (Feldman et al. 2001). In a review of several studies, other authors have confirmed this association (Porsova-Dutoit et al. 2000). Note: DHEA is produced by the adrenal gland and is a precursor hormone for the manufacturing of testosterone.


Despite numerous studies substantiating the beneficial effects of testosterone therapy in treating heart disease, conventional cardiologists continue to overlook the important role this hormone plays in keeping their cardiac patients alive (Tripathi et al. 1998; Webb et al. 1999; Rosano et al. 1999).


Testosterone replacement therapy is normally indicated in aging men who do not have prostate cancer. It should be done in cooperation with a knowledgeable physician. To learn the facts about safely restoring testosterone levels, refer to the Male Hormone Modulation protocol in this book.


Summary

This cardiovascular disease overview has addressed the following five significant cardiovascular risk factors that conventional physicians often overlook to the detriment of their patients:

Elevated C-reactive protein
Elevated fibrinogen
Elevated homocysteine
Excess insulin
Too little free testosterone (men)

Persons concerned about arterial system health should have their blood tested for all of the potential indicators of a pending cardiovascular event. A table has been provided in this protocol so that the reader will know what blood tests to ask for and what the optimal ranges should be.

If any of the indicators are out of the optimal range, appropriate corrective actions should be taken. A number of suggested methods to restore blood indicators to optimal ranges have also been discussed. A review of the approaches that may be considered to specifically correct the five cardiovascular disease risk factors outlined in this protocol will now be provided:


1. Elevated C-Reactive Protein


To reduce C-reactive protein to below 1.3 mg/L of blood, first try the following natural supplements that reduce pro-inflammatory cytokine production and oxidative stress:

Vitamin E (alpha tocopherol), 1200 IU daily along with 400 mg of gamma tocopherol.

DHEA, 15-75 mg a day. (Refer to DHEA Replacement protocol for precautions.)
Essential fatty acids, a supplement that provides at least 1000 mg of DHA and 400 mg of EPA from fish oil along with 900 mg of gamma-linolenic acid (GLA) from borage oil.

Vitamin K, 10 mg a day.

Nettle leaf extract, 1000 mg a day.
If the natural supplements do not work, consider trying:

Ibuprofen, 200-800 mg a day, or aspirin, 81-325 mg a day.
A statin drug such as Pravacol, 40 mg a day (as long as total cholesterol levels do not drop substantially below 180 mg/dL).
Persons taking ibuprofen or doses of aspirin in excess of 81 mg a day should take 900-1800 mg a day of polyenylphosphatidylcholine (PPC) to protect against damage to the stomach lining. (Statin drugs are available only by prescription.)


2. Elevated Fibrinogen

To reduce fibrinogen to below 300 mg/dL of blood, try:
Flush-free niacin (inositol hexanicotinate), 2400-3000 mg a day.
Vitamin C, 4000 mg a day.
Bromelain, 2000 mg a day.
Fish oil, a supplement that supplies 2400 mg of EPA and 1800 mg of DHA a day.

Vitamin A 25,000 IU a day.
Note: When taking high doses of niacin or flush-free niacin, have a blood liver enzyme test done within 60 days, at which time the blood should also be tested to ascertain if adequate fibrinogen reduction has occurred.
If the natural fibrinogen-lowering supplements do not work, consider trying:
Pentoxiphylline (Trental), 400 mg two times a day. (Trental is a prescription drug.)

3. Elevated Homocysteine

If homocysteine levels are above 6.3 micromol/L of blood, try:
Folic acid, 800-2400 mg a day.
Vitamin B12, 300-1000 mcg a day.
Vitamin B6, 100-250 mg a day.
Trimethylglycine (TMG), 500-2000 mg a day.


If the homocysteine-lowering supplements do not work, consider:
Reducing dietary sources of methionine (the precusor to homocysteine). This means cutting back on red meat, chicken, and dairy proteins.
Increasing vitamin B6 to 500-750 mg a day. Note that long-term use of vitamin B6 in excess of 250 mg has been associated with peripheral neuropathy that normally goes away upon cessation of the high B6 intake. Taking other B-complex vitamins and magnesium has been reported to reduce neu-ropathy risk.Increasing TMG to 3000-9000 mg a day.


4. Excess Insulin


Attempt to reduce fasting insulin levels to below 5 uIU/mL of blood:
Consume a low-glycemic diet.
Take 200 mg of d-mannoheptulose (avocado sugar extract) 1 hour after the evening meal.

If these natural approaches to reducing fasting insulin do not work, consider taking:
A standardized avocado extract after dinner and possibly before bedtime.
500-1000 mg a day of Metformin (a prescription drug).


5. Low Testosterone (Men Only)

If blood tests reveal free testosterone in lower ranges of normal, consider asking your physician for a prescription for a testosterone patch, gel, or cream, usually in a dose of 5 mg a day. If estrogen levels are significantly above 30 pg/mL, ask your physician for a prescription for an aromatase-inhibiting drug such as Arimidex (0.5 mg twice a week).

Super MiraForte, a dietary supplement, inhibits the aromatase enzyme, which boosts free testosterone and lowers estrogen in some men. Testerone replacement therapy cannot be used by men with prostate cancer.

Because cardiovascular disease remains the number one killer in Western societies, there is more published scientific information about prevention and treatment than exists for other diseases. Based on the sheer volume of information available, we only discussed five commonly overlooked factors in this chapter.

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