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"All truth passes through three stages.
First, it is ridiculed.
Second, it is violently opposed.
Third, it is accepted as being self-evident."
Arthur Schopenhauer
(1788 - 1860)
What is the true cause of heart disease, and how can we truly reduce the risk of death?
Atherosclerosis, or Coronary Artery Disease (CAD), is the leading cause of death in both men and
women. In the U.S. alone, there are more than one million heart attacks every year, one third of
them resulting in death. The majority of men and women currently have, or are actively
developing, atherosclerosis. By age 20, most people already have a 15-25% narrowing of their
arteries due to plaque formation. By age 40, there is a 30-50% clogging of their arteries.
In the beginning of the Twentieth Century, congestive heart disease (CHD) was mostly a result of
rheumatic fever, which was a childhood disease. However by the year 1936 there was a dramatic
change in the main cause of heart disease. Cardiovascular disease caused by atherosclerosis, or
plaque buildup, took first place as the primary cause of heart disease, making congestive heart
failure a distant second.
During the 1950's, the autopsies conducted on men who died of heart disease that revealed
plaque-clogged arteries concluded that cholesterol was the cause of hardening of the arteries
(atherosclerosis) and coronary artery disease. Cholesterol, not calcium, was considered the
"cause" of heart disease, despite plaque consisting of 95% calcium and a relatively small
percentage of cholesterol. By 1956 there were 600,000 deaths annually from heart disease in the
U.S. Of those 600,000, 90% were caused by atherosclerosis, or clogged arteries. In fewer than 25
years, the number one cause of death in the U.S. had changed dramatically ...from congestive
heart disease to coronary artery disease.
Because cholesterol was dubbed the "cause" of atherosclerosis, the effort to lower cholesterol by
any means began in earnest. Both the food industry and the pharmaceutical industry seized upon
this opportunity to cash in on a cholesterol-lowering campaign by creating foods and drugs that
would supposedly save lives. Diets, such as the Prudent Diet, were established to lower the

2. amount of cholesterol intake from food. There was no doubt that both polyunsaturated oils and
drugs reduced cholesterol, but by 1966 it was also apparent that lowering cholesterol did not
translate into a reduced risk of death from heart disease.
As there was so much money to be made from pharmaceutical development, the campaign to
produce cholesterol-lowering drugs kicked into high gear, despite the lack of evidence showing
that the lowering cholesterol reduced the risk of untimely death from heart disease.
Heart disease kills 725,000 Americans annually, with women accounting for 2/3 or nearly 500,000
of those deaths. After thirty years of cholesterol-lowering medications' failure to significantly lower
the death rate from cardiovascular disease, in 1987 a new and more dangerous class of drugs
was unleashed upon the world: the "statin" drugs. Cholesterol-lowering statin drugs are now the
standard of care that physicians are indoctrinated into prescribing to reduce cardiovascular
disease. Are statin drugs the best way to prevent heart attacks and death?
Before 1936 the most common type of heart disease was congestive heart disease (CHD). It
rarely caused sudden death and could be treated with the drug digitalis. The incidence of CHD
remained stable until 1987, after which the incidence of the disease skyrocketed. Interestingly, the
timing of the increased incidence of congestive heart disease coincides with the introduction of
cholesterol-lowering statin drugs. Could cholesterol-lowering statin drugs have something to do
with the weakening of heart muscles and the increased incidence of congestive heart failure? We
will see that lowering the body's co-enzyme Q10 levels, a side effect of statin drugs, does indeed
increase the risk of muscle damage, including the muscles of the heart.
Atherosclerosis is a disease characterized primarily by inflammation of the arterial lining caused by
oxidative damage from homocysteine, a toxic amino acid intermediary found in everyone.
Homocsyteine, in combination with other free radicals and toxins, oxidizes arteries, LDL
cholesterol, and triglycerides, which in turn releases C Reactive Protein (CRP) from the liver-a
marker of an inflammatory response within the arteries. Inflammation (oxidation) is the beginning
of plaque buildup and ultimately, cardiovascular disease. Plaque, combined with the thickening of
arterial smooth muscles, arterial spasms, and clotting, puts a person at a high risk of suffering
heart attack or stroke.
For years, doctors have hyper-focused on cholesterol levels. First it was the total cholesterol; later
the focus became the ratio of "good" HDL cholesterol to "bad" LDL cholesterol. In other words,
how much of your cholesterol was good, and how much was bad? Of the two, the important
parameter is the level of HDL cholesterol, not LDL cholesterol. HDL, or high-density lipoprotein
cholesterol, is responsible for clearing out the LDL cholesterol that sticks to arterial walls.
Exercise, vitamins, minerals, and other antioxidants, particularly the bioflavonoid and olive
polyphenol antioxidants, increase HDL cholesterol levels and protect the LDL cholesterol from
oxidative damage, and therefore do more to reduce the risk of heart disease than any medication
ever could.
There is nothing inherently bad about LDL cholesterol. LDL cholesterol is critical to maintain life.
LDL cholesterol only becomes "bad" when it is damaged, or oxidized by free radicals. Only the
damaged, or oxidized form of LDL cholesterol sticks to the arterial walls to initiate the formation of
plaque.

3. Let us look towards cigarette smoking for a simple example demonstrating that we really need to
reduce oxidized LDL cholesterol to prevent atherosclerosis, as opposed to indiscriminately
lowering LDL cholesterol with statin drugs. Everyone knows that cigarette smoking increases the
risk of many chronic diseases, such as cancer, heart disease, and stroke. Smokers with normal
levels of LDL cholesterol are at an even greater risk of developing heart disease than a non-
smoker who has elevated levels of LDL cholesterol. Of course the reason why a smoker with
normal levels of LDL cholesterol is at greater risk of disease is because his LDL gets excessively
oxidized.
Cigarette smoke releases so many toxins and free radicals that the LDL cholesterol, the
triglycerides, and the arterial walls are extensively oxidized. Homocysteine levels are also
increased by cigarette smoking which further oxidizes LDL cholesterol and the arterial lining.
Oxidation is the initiating cause of atherosclerosis. Therefore, the more and longer one smokes,
the more oxidative damage he sustains and the greater his risk of developing heart disease. The
degree of oxidation directly corresponds to the risk of heart disease.
If you are not taking vitamins, minerals, and antioxidants then your LDL cholesterol is being
oxidized, it is sticking to your arterial walls, and you ARE developing heart disease EVEN IF
YOUR CHOLESTEROL LEVELS ARE NORMAL! LDL cholesterol starts sticking to arterial walls
before the age of 5.
Among the many free radicals that damage cholesterol, triglycerides and the arterial lining is
homocysteine, a toxic intermediate biochemical produced during the conversion of the amino acid
methionine into another important amino acid, cysteine. Both methionine and cysteine are non-
toxic, but homocysteine is very toxic to the lining of the arterial endothelium. Homocysteine
oxidizes LDL cholesterol, triglycerides and the arterial lining.
Homocysteine is an amino acid normally produced in small amounts from the amino acid
methionine. The normal role of homocysteine in the body is to control growth and support bone
and tissue formation. However a problem arises when homocysteine levels in the body are
elevated, causing excessive damage to LDL cholesterol, as well as to arteries. Furthermore,
homocysteine actually stimulates growth of arteriosclerotic plaque, which leads to heart disease.
Thyroid hormone controls the level of homocysteine, but numerous factors play a role in the
elevation of homocysteine. Normal aging, kidney failure, smoking, some medications, and
industrial toxins all elevate homocysteine levels. Interestingly, estrogen helps lower homocysteine.
Homocysteine becomes elevated in the blood with a deficiency of the B vitamins-B6, B12 and folic
acid. Genetics also play a role. About 12% of the population has an undetected defect requiring
higher levels of folic acid than the rest of population to help maintain homocysteine levels in a safe
range (below 6.5). Therefore if you have high homocysteine levels (> 7.0) even though you are
taking supplemental B complex vitamins, then you may be among the 12% who need more than
1000 mcg of folic acid per day. In addition, betaine, also known as trimethylglycine (TMG) lowers
homocysteine.
Homocysteine is second only to cigarette smoking in its oxidative destruction. It causes small
nicks or tears in the arterial lining, while also oxidizing and damaging LDL cholesterol. The
damaged, or oxidized LDL cholesterol sticks to the homocysteine-damaged areas of the arterial

4. lining. The combination of oxidized LDL cholesterol and a damaged arterial lining is what causes
LDL cholesterol to stick to the arteries, whether or not the LDL cholesterol level is normal.
Cholesterol-lowering statin drugs are the standard for treating high cholesterol. This is dogma, and
anyone who states otherwise is committing medical heresy. Many people find it hard to believe
that pharmaceutical companies could ever succeed in paying medical researchers, medical
associations, and doctors to recommend something detrimental to our health.
Most people do not know that pharmaceutical companies fund medical institutions, medical
education, medical conferences, and still reward doctors and research institutions for providing
favorable results on their drugs. Likewise, pharmaceutical companies often suppress negative
results from studies done on their drugs. Money has the power to sweep negative results and
serious side effects under the rug. Money has the power to influence the FDA to decide which
drugs make it to market and which drugs become the "standard" of treatment.
Former editor of the New England Journal of Medicine (NEJM), Dr. Marcia Angell, warned of the
problem of commercializing scientific research in her outgoing editorial titled "Is Academic
Medicine for Sale?" Angell called for stronger restrictions on pharmaceutical stock ownership and
other financial incentives for researchers. She said that growing conflicts of interest were tainting
science, warning "When the boundaries between industry and academic medicine become as
blurred as they are now, the business goals of industry influence the mission of medical schools in
multiple ways." She did not discount the benefits of research but said, "a Faustian bargain" now
existed between medical schools and the pharmaceutical industry. Angell left the NEJM in June
2000 and has written a book, "The Truth About the Drug Companies: How They Deceive Us and
What to Do About It."
Two years later, in June 2002, the NEJM announced that it was going to begin accepting articles
that were written by biased researchers, as there weren't enough unbiased researchers left to
write articles. In other words, most research institutions were now funded by one or more of the
numerous pharmaceutical companies.
An ABC report noted that a survey of clinical trials revealed that when a drug company did not
fund a study, favorable results regarding a drug were found only 50% of the time. In studies
funded by drug companies favorable results about the drugs were reported an amazing 90% of the
time. Money can and does buy the desired results. This is how most medical research and drugs
are now developed and brought to market.
In 1977, the internationally-renowned heart surgeon, Dr. Michael DeBakey pointed out that only
30-40% of people with blocked arteries and heart disease have elevated blood cholesterol levels,
and posed the logical question, "How do you explain the other 60-70%?"
Because lowering cholesterol did not reduce the risk of death from heart disease, the Cholesterol
Consensus Conference in 1984 developed new guidelines to lower the "acceptable level" of
cholesterol. High cholesterol would now be the diagnosis for any man or woman with a cholesterol
level over 200. Doctors had to convince their patients that they had the disease and needed to
take one or more expensive drugs for the rest of their lives.
However, when lowering total cholesterol levels below 200 did not translate into saving lives from

5. heart attacks, the focus then turned to LDL cholesterol levels. The "disease" of high cholesterol
was refined to the disease of high LDL cholesterol. The unfortunate patient who had an LDL
cholesterol level above 130 was now condemned to a lifetime of expensive drugs. Though
completely illogical, even when a person with normal LDL cholesterol levels suffered a heart
attack, he would still be prescribed a cholesterol-lowering drug.
As we shall see, statin drugs reduce the risk of death by repeat heart attacks by as much as 30%,
but interestingly enough, the mechanism of action in reducing the risk of death after a heart attack
is not via statin drugs' ability to lower cholesterol! It has been discovered that statin drugs have a
modest anti-inflammatory and antioxidant effect. Yet, there are many natural antioxidants that
reduce inflammation and oxidation of LDL cholesterol and the lining of the arteries, which may
soon be discovered to be more effective in reducing the risk of death than "antioxidant drugs,"
without toxic side effects.
The myth that high LDL cholesterol is the primary cause of heart disease, and that we must be on
drugs to protect ourselves is dispelled by the evidence. If the premise were true that people with
high levels of LDL cholesterol get heart disease, then we could assume that people with normal
levels of LDL should not get heart disease, or at least very few should get it. However, as Dr.
DeBakey observed, approximately 60% of those who die from heart disease have normal LDL
cholesterol levels!
Furthermore, after over 45 years of doctors prescribing cholesterol-lowering drugs, heart disease
and stroke still remain the number one cause of death in both women and men. This says that
regardless of whether you have a high or a normal level of cholesterol, you have a 50% chance of
dying from heart disease. If this is so, and it is, then why take a dangerous drug to attempt to lower
your cholesterol in the first place?
In 2001, the target level of LDL cholesterol was lowered from 130 to 100, and overnight the
number of people considered to be candidates for cholesterol statin drugs doubled. Many people
such as myself bristled at the news, because we knew the effectiveness of vitamins, minerals, and
antioxidants in preventing and reversing heart disease. Many of us could see the conspiracy for
what it was.
The level at which LDL cholesterol is considered normal has continually been influenced by
pharmaceutical companies, who pull the financial strings of research grants that keep medical
schools and medical organizations in business. The lower they can establish the level at which
LDL cholesterol is considered to be normal, the more people automatically become victims of the
dreaded disease of "high cholesterol." Therefore, more people will be persuaded that they need to
be taking a statin drug, and voilà, more profit for the manufacturers. When you consider
the size of the profits already received, let alone the potential profit from statin drugs over the next
several years, the cholesterol conspiracy is one of the largest money making schemes ever
perpetrated on the world.
In July 2004, the level of LDL cholesterol considered normal underwent another change. The new
norm plunged from 100 to 70, virtually doubling again the number of people who are "infected"
with the plague of high cholesterol. Why, it's the epidemic of our time! Many enlightened people
howled at this news, wondering if the masses would ever wake up and see who is behind this, and
why. Why is the medical establishment ignoring the thousands of published medical studies that

6. show the beneficial effects of nutritional supplements against heart disease? Why is the medical
establishment down-playing the dangerous and deadly side effects of statin drugs?
The "updated" LDL cholesterol recommendations were published in the July 2004 issue of the
American Heart Association's publication, Circulation. A panel from the National Heart, Lung and
Blood Institute, a division of the National Institutes of Health, which is endorsed by the American
College of Cardiology, and the American Heart Association, were the ones who actually
pronounced the new cholesterol level at which drugs should be prescribed. Sounds pretty official
and reliable if these powerful medical institutions are backing up these recommendations, right?
The fact is eight of the nine panel members making the new LDL cholesterol recommendations
were being paid by the statin-producing pharmaceutical companies. The panelists did not disclose
their financial conflict of interest. This information was uncovered by Newsday, a Long Island, New
York
newspaper (D. Ricks and R. Robins, Newsday, July 15, 2004). Seven of the nine panelists have
financial connections to Pfizer, the makers of Lipitor®. Five of the nine served as "consultants"
to Pfizer. So, what did the other two panelists do to deserve their money? Seven of the nine
panelists also received money from Merck, the producers of Zocor®, with four of them serving
as "consultants" to the company. Eight of the panelists who made the recommendations that
would increase the prescribing of statin drugs have received either research grants or honoraria
from Pfizer, Merck, AstraZeneca, Novartis, Glaxo Smith Kline, Johnson & Johnson, Bayer,
and many other drug companies that produce statin drugs.
You would think that with all the advertising and recommendations from medical experts on the
benefits of statin drugs, the medical community would possess overwhelming evidence that the
drugs reduce the risk of death from cardiovascular disease. A hint of some of the smoke and
mirrors in the pharmaceutical companies' advertising can be seen in their TV commercials. Read
carefully the small print on some of Crestor's® commercial advertising. Their commercial
states how much it lowers LDL cholesterol. However, in the same ad you can read,
"...Crestor® has not been shown to reduce the risk of heart disease or heart attack." If so, then
why take it? Isn't the bottom line to prevent death?
The system for reporting adverse effects from medications is tremendously flawed, so much so
that many people are seriously harmed or killed by some medications before they are finally
removed from the market. Most doctors do not know what symptoms or effects are due to the
drug, what should be reported, or even to whom to report adverse effects. They assume that the
research that went into developing the drug has already identified all the effects and that a drug
brought to market is "safe." However, only one in twenty side effects is ever reported to either
hospital administrators or the FDA.
Statin drugs block cholesterol production in the body by inhibiting the enzyme called HMG-CoA
reductase in the early steps of its synthesis in the mevalonate pathway. Cholesterol is one of three
end products in the mevalonate chain. This same biosynthetic pathway is also used to create co-
enzyme Q10, or co-Q10, as well as dilochol. Therefore, one unfortunate consequence of statin
drugs is the unintentional inhibition of both Co-Q10 and dilochol synthesis.
The drug information insert of a statin drug states that it lowers co-enzyme Q10 levels. Most
doctors have forgotten their biochemistry class in medical school, and forgotten about the

7. importance of Co-Q10. Therefore they apparently are not concerned about such a statement on
the drug labeling information sheet. They may even reassure their patients that lowering Co-Q10
is nothing to worry about, but at the same time warn them that the drug may cause liver damage
and to have their liver enzymes checked every three to six months to make sure the drug isn't
killing them. They do not realize that it is the depletion of Co-Q10 that leads to liver damage and
death.
Ubiquinone, or co-enzyme Q10, is a critical cellular nutrient created in the cell's mitochondria, the
"engines" that produce energy for the cell. Mitochondria use sugar, oxygen, and water to produce
energy molecules known as ATP. Without ATP cells could do nothing. Damaged tissues could not
be repaired. Cells could not divide or produce or utilize proteins, enzymes, or hormones. Death of
cells, and indeed of the human body would occur if ATP could no longer be produced and utilized.
Co-Q10 functions within the mitochondria as an electron carrier to cytochrome oxidase, our main
respitory enzyme, which helps turn oxygen and sugar into energy. The heart requires high levels
of oxygen, sugar, and Co-Q10 since it utilizes a lot of energy. A form of Co-Q10 called ubiquinone
is found in all cell membranes, where it plays a role in maintaining membrane integrity, so critical
to nerve conduction and muscle contraction. Co-Q10 is also vital for the formation of elastin and
collagen, which make up the connective tissues of the skin, musculature, and the cardiovascular
system.
The most common side effect of statin drugs is muscle pain and weakness. In fact, many patients
who start on the statin drugs almost immediately notice generalized fatigue and muscle weakness.
This is due to the depletion of Co-Q10 needed to support muscle function. Dr. Beatrice Golomb of
San Diego, California, is currently conducting a series of studies on statin side effects. The
pharmaceutical industry insists that only 2-3% of patients get muscle aches and cramps, when in
fact in one study, Golomb found that 98% of patients taking Lipitor®, and one-third of the
patients taking Mevacor® (a lower dose statin), suffered noticeable to significant muscle
problems.
Some people on statin drugs lose coordination of their muscles. Some develop pain in their
muscles, some are not able to write due to loss of fine motor skills. Many lose the strength to
exercise. Others are falling more frequently as their muscles give out, still others have trouble
sleeping due to muscle cramping and twitching. Even worse, many people are experiencing most
of these side effects. The problems are so numerous, it is difficult to list all the symptoms people
might experience. These problems do not come from the "disease" of high cholesterol, but the
disease of ignorance in prescribing these drugs.
As we age, Co-Q10 levels decline naturally. From the age of 20 to 80, Co-Q10 levels fall by nearly
50%. Along with the natural decline of Co-Q10, comes a natural decrease in energy and an
increase in the risk of heart disease, stroke, and cancer. If the natural decline of Co-Q10 levels
increases the risk of fatigue, cancer, heart disease, and stroke, would it not make sense that
accelerating the decline of Co-Q10 levels with statin drugs would have the same effect? They do
indeed!
Demonstrating the importance of Co-Q10 to cardiovascular health, in a randomized, double blind,
placebo-controlled study of people either taking or not taking statin drugs, supplementation with
Co-Q10 reduced the risk of heart attacks and death in those with heart disease and prior heart
attacks by 50%, regardless of whether they were on a statin drug or not. (Singh R, Neki N,

8. Kartikey K, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent
myocardial infarction. Mol Cell Biochem. 2003 Apr; 246(1-2):75-82.)
Additionally, Co-Q10 was shown to increase blood levels of vitamin E and significantly increase
the levels of protective HDL. As low HDL is a major risk factor for heart disease, increasing it is a
definite benefit. Statin drugs were shown not to provide any benefit beyond that of supplementing
with Co-Q10. Let me make this clear - in this study only the co-enzyme Q10 provided any benefit,
not the drugs!
Cardiologist Dr. Peter Langsjoen of East Texas University reported the effects of Lipitor®
among 20 patients who started with completely normal hearts. After six months on a low dose of
20 mg of Lipitor® per day, two thirds of the patients started to show signs of heart failure, as
seen by abnormalities in the heart's filling phase. According to Dr. Langsjoen, this malfunction is
due to Co-Q10 depletion. Nine controlled trials using statin drugs in humans have been conducted
thus far. Eight of these showed significant statin-induced Co-Q10 depletion leading to a decline in
left ventricular function and other biochemical imbalances.
In the United States, the incidence of heart attacks over the past ten to fifteen years has declined
slightly. But congestive heart failure and cardiomyopathy have risen alarmingly. Is it a coincidence
that statin drugs were first marketed in 1987, and then from 1989 to 1997, deaths from congestive
heart failure more than doubled? 38 It scares me that virtually all patients with heart failure are put
on statin drugs, even if their cholesterol is already low. In my opinion, the worst thing to do for a
failing heart is take a statin drug. The best thing is to take is a full range of quality nutritional
supplements, ...vitamins, minerals, fish oil, and other antioxidants, including Co-Q10.
Various antioxidants work synergistically, each contributing to the fight against free radicals in
different areas and in different ways. In the blood stream, water-soluble antioxidants, such as
vitamin C, and grape seed extract come in contact with and neutralize free radicals before they
damage LDL-cholesterol. Other antioxidants saturate arterial walls and other tissues, and protect
collagen and elastic fibers from free radical damage, reducing inflammation and plaque formation.
The fat-soluble antioxidants, vitamin E, beta carotene, and co-enzyme Q10 ride along in the blood
fat (triglycerides) and LDL cholesterol, protecting them and the endothelium from oxidation.
Vitamin E sits on the surface of LDL cholesterol, protecting it from free radical damage. Beta
carotene, grape seed extract and olive extract penetrate deeper inside the LDL cholesterol and
arterial walls, adding more protection from oxidation. Quercetin and alpha lipoic acid work through
nitrous oxide pathways to reduce high blood pressure, a major risk factor for heart disease.
A report published in the Archives of Internal Medicine in 2005 looked at 97 double-blind controlled
studies comparing the efficacy of cholesterol-lowering statin drugs to fish oil. They found that
cholesterol-lowering statin drugs reduced the risk of death from heart disease by only 13%, and
interesting enough it was NOT due to the effect of lowering cholesterol. The benefits, although
small, were derived from the fact that statin drugs have a slight antioxidant effect.
Even more interesting, the salmon oil was shown to reduce the risk of death from heart disease by
23%, nearly double the benefit of statin drugs. Salmon oil is an omega-3 fatty acid that gets
incorporated into cholesterol and triglycerides and prevents the oxidation of LDL cholesterol. Since
LDL cholesterol is protected from excessive oxidation there is less plaque buildup and less risk of
heart disease.

9. Inflammation is a well-known component in the formation of atherosclerosis. To keep it simple,
think of inflammation and oxidation as the same process. The immune system's response to
inflammation is to
release peroxides that act like acid to break down damaged tissues, so that cells from the immune
system, macrophages, can consume the molecules and clean up the site. But peroxides escalate
the oxidation/inflammation process, thus damaging more tissue. The arterial walls become more
inflamed, escalating the formation of plaque and scarring. The downward cycle continues until
atherosclerosis is so advanced that the occurrence of a heart attack or stroke becomes imminent.
The liver's response to inflammation is to release C reactive protein (CRP) into the blood. Other
inflammatory causes can cause elevated CRP levels, including cigarette smoking, obesity, insulin
insensitivity, diabetes, rheumatoid arthritis, infections, dementia, colorectal cancer, high blood
pressure, and aging. Accordingly, elevated CRP levels are a direct indication of inflammation in
the body and that atherosclerosis, including heart disease, is actively developing.
Homocysteine and high sensitivity CRP levels can and should be tested. Dr. Jialal, of the
Universtity of Texas Southwestern Medical School at Dallas, is well known for his research
correlating oxidized LDL cholesterol as the true cause of atherosclerosis, has also identified high
sensitivity C reactive protein as a predictive risk factor for inflammation of arterial walls and plaque
formation. Your doctor may not test for these routinely, but you should insist on getting these tests
done. Both of these predictive values can be kept at "safe" levels. Vitamins, minerals, antioxidants,
and omega-3 fatty acids can lower the levels of homocysteine and CRP. The B vitamins, along
with betaine, or tri-methyl-glycine (TMG), change homocysteine into safer amino acids and reduce
inflammation of the LDL cholesterol and the arterial lining.
When you receive the results of your homocysteine test, do not accept the answer, "Your test was
normal." Ask for the actual number. The doctor and nurse usually know what is normal by what the
lab slip states as the "normal range." Most lab results report a normal homocysteine level as being
below 10.4, when in fact, since the early 1990's, researchers have known that a homocysteine
count above 6.5 signals a rapid linear rise in the risk for heart disease.
Furthermore, with every 3 point elevation of homocysteine above 6.5, e.g., when homocysteine
levels are 9.5, the risk of coronary artery disease (CAD) rises by an additional 35%! Yet you may
be told that 9.5 is "normal and not to worry." With a homocysteine level of 12.5, the increase in the
risk for heart disease exceeds 70%. The greater the homocysteine level, the greater the oxidation
of both LDL cholesterol and the arterial lining. The greater the inflammation, the higher the CRP. Is
it any wonder that homocysteine and CRP levels are more predictive for risk of heart disease than
cholesterol levels and ratios?
I need to emphasize that anyone whether they have a medical problem or not, should discuss this
information with their physician before acting upon anything written here. The information provided
is not meant to diagnose or treat any disease. It is for informational purposes only; and no one
should make decisions about their medications without consulting with their physician. No one
should come off a cholesterol-lowering statin drug in lieu of nutritional supplements without a
thorough discussion with their physician who is keenly aware of all the pros and cons of both
treatment modalities.

10. In summary, I recommend a full spectrum of quality nutritional supplements, along with a healthy
diet and exercise, to help obtain and maintain optimal heart and arterial health. I believe all would
agree that lifestyle changes are the most important factor for optimal health, ...and many believe
that quality nutritional supplements are key in protecting against the process that leads to, and
accelerates the development of almost all chronic degenerative diseases, that of oxidation. To
combat oxidation we need a full range of quality antioxidants.
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