The Cholesterol Conspiracy

The Cholesterol Conspiracy - The Truth About Statins And Nutritional Supplementation

By
Ladd McNamara, M.D.




"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 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.
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 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 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 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 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, 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.
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.
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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