High cholesterol does NOT cause heart attacks. Cholesterol medications have no basis in medical research for preventing death from heart disease. The statin drugs they prescribe actually cause more damage than they prevent, like Lipitor damages the liver and cuts off a vital nutrient called CoQ10 which the heart really depends on. This is why your medical doctor runs blood tests on your liver every few months when you are taking these dangerous medications.
Having cholesterol above 200 is FINE! Many studies from Europe showed that cholesterol levels above 300 were actually good for longevity and overall well being.
So why does my doctor prescribe cholesterol medications if it’s not a problem and the medications are dangerous? They don’t have the time to do the research on their own to find out. I don’t know I guess they just listen to the drug company sales reps that knock on their doors every day and take them out to lunch and pay for exotic trips. Who knows? But you can ask your MD to read a few good books on the subject and see what they do.
Here is a wonderfully researched article by Dr. Mercola, DO.
What? No time read it then use our handy Cholesterol Guide Graphic, click here.
Could
it be possible that nearly everything your doctor and the media is telling you
about high cholesterol and how it relates to heart disease and strokes is
wrong?
Absolutely!
The media and health experts have been giving out massive misinformation about cholesterol. In a thought-provoking two-part series, Dr. Ernest N. Curtis, a doctor of internal medicine and cardiology, puts to rest several decades-old studies that supposedly “proved” the cholesterol-heart disease link.
Debunking
the Cholesterol “Science” and Unveiling the Truth
If high
cholesterol and high-fat diets are really NOT the cause of heart disease, then
how did this massive misinformation campaign start? It actually started more
than 100 years ago when the Lipid Hypothesis or the Cholesterol Theory was
developed by a German pathologist named Rudolph Virchow. After studying
arterial plaques from corpses, he theorized that cholesterol in your blood led
to the development of plaques in your arteries.
Meanwhile,
in 1913 in St. Petersburg, Russia, Nikolaj Nikolajewitsch Anitschkow
fed rabbits cholesterol and determined that it led to atherosclerotic changes
(apparently no one questioned the fact that rabbits are herbivores and do not
naturally consume cholesterol!). This started the notion that eating
cholesterol leads to plaque deposits in your arteries, and at that time it was
believed that all cholesterol in your blood was due to dietary sources.
This, of
course, is not true, as it’s now known that your liver makes about 75 percent
of your body’s cholesterol. That’s right! Even if you didn’t eat any
cholesterol, you would still have cholesterol in your body, which is a good
thing considering it’s needed by every one of your cells to produce cell
membranes.
Your diet
is actually an afterthought when it comes to what your cholesterol levels will
be, but this simple truth is largely ignored or unrealized even by many
physicians.
In the
early 1900s, the Cholesterol Theory was already taking root, but it received
even more completely flawed support in the 1950s and subsequent years
thereafter. The string of research that effectively solidified the cholesterol
myth we know all too well today.
The Seven
Countries’ Study Incorrectly Links Dietary Fat to Heart Disease
Several
decades ago, Dr. Ancel Keys published a seminal paper that serves as the basis
for nearly all of the initial scientific support for the Cholesterol Theory.
The study is known as the Seven Countries
Study, that linked the consumption of dietary fat to coronary
heart disease. What you may not know is that when Keys published his analysis
that claimed to prove the link between dietary fats and coronary heart disease
(CHD), he selectively analyzed information from only seven countries to prove
his correlation, rather than comparing all the data available at the time —
from 22 countries.
As you
might suspect, the studies he excluded were those that did not fit with his
hypothesis, namely those that showed a low percentage fat in their diet and a
high incidence of death from CHD as well as those with a high-fat diet and low
incidence of CHD. If all 22 countries had been analyzed, there would have been
no correlation found whatsoever; it should have been called the 22 Countries
Study!
The
nutrition community of that time completely accepted the hypothesis, and
encouraged the public to cut out butter, red meat, animal fats, eggs, dairy and
other “artery clogging” fats from their diets — a radical change at
that time that is still very much in force today.
Most of
the experts I know believe that Dr. Keys’ research was pivotal for perpetuating
the low-fat approach to health. This is a major part of the solid science you
will need to know if anyone seeks to disagree with you when you share this
information; this study is really the foundation that triggered the massive
emphasis on low-fat diets and the flawed belief that cholesterol is so
pernicious.
More Flawed
“Proof”: The Framingham Study
The next major support for the cholesterol theory came from a
study you have likely heard of called the Framingham Heart Study, which is
often cited as proof of the lipid hypothesis. This study began in 1948 and
involved some 6,000 people from the town of Framingham, Massachusetts who
filled out detailed questionnaires about their lifestyle habits and diets. The
study is credited with identifying heart disease risk factors, such as smoking,
high blood pressure, lack of exercise and, yes, high cholesterol.
The cholesterol link was weak, as researchers noted those who
weighed more and had abnormally high blood cholesterol levels were slightly
more at risk for future heart disease, but widely publicized. What you don’t
hear about is the fact that the more cholesterol and saturated fat
people ate, the lower
their cholesterol levels.
In a 1992 editorial
published in the Archives
of Internal Medicine, Dr. William Castelli, a former
director of the Framingham Heart study, stated:
“In
Framingham, Mass., the more saturated fat one ate, the more cholesterol one
ate, the more calories one ate, the lower the person’s serum cholesterol. The
opposite of what… Keys et al would predict…We found that the people who ate the
most cholesterol, ate the most saturated fat, ate the most calories, weighed
the least and were the most physically active.”
The
“MrFit” Study: Hypothesis Proven by Omission
The U.S.
Multiple Risk Factor Intervention Trial (MRFIT), sponsored by
the National Heart, Lung and Blood Institute, is another study that is highly
misleading. It compared mortality rates and eating habits of over 12,000 men,
and the finding that was widely publicized was that people who ate a
low-saturated fat and low-cholesterol diet had a marginal reduction in coronary
heart disease.
What did they leave out?
Their mortality from all causes was higher! As Mary Enig and Sally
Fallon stated in The Truth About
Saturated Fat:
“The
few studies that indicate a correlation between fat reduction and a decrease in
coronary heart disease mortality also document a concurrent increase in deaths
from cancer, brain hemorrhage, suicide and violent death. After 10 years of
lowering fat intake and not smoking, they found no significant difference in
death from heart disease or total death compared to the control group of
smokers, poor diet etc.”
Statistical
Lies: The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT)
Around the same time as the MRFIT study was the Lipid Research Clinics Coronary Primary Prevention
Trial (LRC-CPPT), which cost $150 million and is often cited to
justify a low-fat diet, even though dietary factors were not tested in the
study at all. Instead, the study tested the effects of cholestyramine, a
cholesterol-lowering drug.
As Enig and Fallon
wrote:
”
Their statistical analysis of the results implied a 24% reduction in the rate
of coronary heart disease in the group taking the drug compared with the
placebo group; however, non-heart disease deaths in the drug group increased —
deaths from cancer, stroke, violence and suicide. Even the conclusion that
lowering cholesterol reduces heart disease is suspect.
Independent
researchers who tabulated the results of this study found no significant
statistical difference in coronary heart disease death rates between the two
groups. However, both the popular press and medical journals touted the
LRC-CPPT as the long-sought proof that animal fats are the cause of heart
disease …”
What really happened, and how LRC-CPPT came to lend further
support to the lipid hypothesis was nothing more than another masterful case of statistical manipulation.
As Dr. Curtis stated:
“After
10 years the number dying from coronary heart disease (CHD) plus those
suffering a non-fatal myocardial infarction (NFMI) were totaled for both
groups. The total incidence in the cholestyramine group was 7.0% and the
control group 8.6%.
This small
difference of 1.6% was reported as a 19% reduction in death and heart attack by
using relative risk reduction (the difference of 1.6% is roughly 19% of 8.6) in
place of the less misleading absolute risk reduction (1.6%). Furthermore, this
tiny difference was given the designation of “statistically significant”
by changing the criteria originally given for determination of significance
after the data was in.”
It is often the case that leaders who want to use the cholesterol
agenda use statistics to “prove” their point.
Cholesterol
Drug Benefits Perpetuated by Statistical Myths
The LRC-CPPT study was only able to show a meaningful benefit
because it focused on relative risk reduction rather than absolute
risk reduction. What’s the difference? You can find a very simple explanation
of relative risk vs. absolute risk at the Annie Appleseed Project web site, but
let me sum it up here.
- Relative risk reduction is calculated by dividing the absolute
risk reduction by the control event rate
- Absolute risk reduction is the decrease in risk of a treatment in
relation to a control treatment
In plain English, here’s what that means: let’s say you have a
study of 200 women, half of whom take a drug and half take a placebo, to
examine the effect on breast cancer risk. After five years, two women in the
drug group develop breast cancer, compared to four who took the placebo. This
data could lead to either of the following headlines, and both would be correct:
“New Miracle Drug Cuts Breast Cancer Risk by 50%!”
“New Drug Results in 2% Drop in Breast Cancer Risk!”
How can this be?
The Annie Appleseed Project explains:
“The
headlines represent two different ways to express the same data. The first
headline expresses the relative risk reduction — the two women who took the
drug (subjects) and developed breast cancer equal half the number (50%) of the
four women who took the placebo (controls) and developed breast cancer.
The second
headline expresses the absolute risk reduction — 2% of the subjects (2 out of
100) who took the drug developed breast cancer and 4% of the controls (4 out of
100) who took the placebo developed breast cancer — an absolute difference of
2% (4% minus 2%).”
You can now see why clinical trials, especially those funded by
drug companies, will cite relative risk reductions rather than absolute risk
reductions, and as a patient you need to be aware that statistics can be easily
manipulated.
As STATS at George
Mason University explains:
“An
important feature of relative risk is that it tells you nothing about the
actual risk.”
How Statins Really Work Explains Why They Don’t Really Work
A new look at statin cholesterol-lowering drugs from the Massachusetts
Institute of Technology claims that no study has ever proven that statins
improve all-cause mortality — in other words, they don’t prolong your life any
longer than if you’d not taken them at all. And rather than improving your
life, they actually contribute to a deterioration in the quality of your life,
destroying muscles and endangering liver, kidney and heart function.
According to Stephanie
Seneff, author of this stunning revelation:
“Statin
drugs inhibit the action of an enzyme, HMG coenzyme A reductase, that catalyses
an early step in the 25-step process that produces cholesterol. This step is
also an early step in the synthesis of a number of other powerful biological
substances that are involved in cellular regulation processes and antioxidant
effects.
One of
these is coenzyme Q10, present in the greatest concentration in the heart,
which plays an important role in mitochondrial energy production and acts as a
potent antioxidant …
Statins
also interfere with cell-signaling mechanisms mediated by so-called G-proteins,
which orchestrate complex metabolic responses to stressed conditions. Another
crucial substance whose synthesis is blocked is dolichol, which plays a crucial
role in the endoplasmic reticulum. We can’t begin to imagine what diverse
effects all of this disruption, due to interference with HMG coenzyme A
reductase, might have on the cell’s ability to function …
There can
be no doubt that statins will make your remaining days on earth a lot less
pleasant than they would otherwise be … “
It’s widely known that statins lower your CoQ10 levels by blocking
the pathway involved in cholesterol production — the same pathway by which Q10
is produced. Statins also reduce the blood cholesterol that transports CoQ10
and other fat-soluble antioxidants.
The loss of CoQ10
leads to loss of cell energy and increased free radicals which, in turn, can
further damage your mitochondrial DNA, effectively setting into motion an evil
circle of increasing free radicals and mitochondrial damage.
There are no official warnings in the U.S. regarding CoQ10
depletion from taking statin drugs, and many physicians fail to inform you
about this problem as well. Labeling in Canada, however, clearly warns of CoQ10
depletion and even notes that this nutrient deficiency “could lead to
impaired cardiac function in patients with borderline congestive heart failure.”
As your body gets more and more depleted of CoQ10, you may suffer from fatigue, muscle weakness and soreness, and eventually heart failure, so it is imperative if you take statin drugs that you take CoQ10 or, if you are over the age of 40, the reduced version called ubiquinol.
Statins May Even
Cause Diabetes!
Statins carry other side effects as well, including diabetes. A meta-analysis, published in JAMA in June,
concluded that those taking higher doses of statins were at increased risk of
diabetes compared to those taking moderate doses. What this means is that the
higher your dose, the higher your risk of developing diabetes.
The “number needed to harm” for intensive-dose statin
therapy was 498 for new-onset diabetes—that’s the number of people who need to
take the drug in order for one person to develop diabetes. In even simpler
terms, one out of every 498 people who are on a high-dose statin regimen will
develop diabetes. (The lower the “number needed to harm,” the greater
the risk factor is.)
(As a side note, the “number needed to treat” per year
for intensive-dose statins was 155 for cardiovascular events. This means that
155 people have to take the drug in order to prevent one person from having a
cardiovascular event.)
Aside from what I’ve already covered above, statin drugs are associated with a rather extensive list of harmful side effects, including:
Weakness, polyneuropathy, sexual dysfunction, cataracts, pancreatic disease, Rhabdomyolysis, a serious degenerative muscle tissue, muscle pain and aches, Suppressed immune function, Increased cancer risk, anemia and acidosis!
