Heart failure is a common cause of death simply because heart failure is a disease of old age. When we grow old, our arteries become stiff.
The smooth muscle cells and the elastic fibers that surround our blood vessels when we are young are gradually replaced by more or less fibrous and rigid tissue. Apart from the fact that worrying about your health may provoke heart trouble, all this stress and anxiety are unnecessary. The cholesterol campaign is medical quackery of the first order. In fact, the eminent American physician and scientist George Mann called the diet–heart idea “the greatest scientific deception of this century, perhaps of any century.” The diet–heart idea is not scientifically sound, but it survives. The diet–heart idea is hopelessly incorrect, but it seems to have eternal life.
From the Second World War until 1963, the rate of mortality from
coronary heart disease rose steadily and alarmingly. Then it declined steeply throughout the 1970s
and into the early 1980s. By 1986, the
death rate was 42% lower than it had been at the 1963 peak. This decrease in mortality is due to advances
in emergency medicine. Meanwhile, the
advice offered by the medical establishment for the last 50 years to beat heart
disease has failed miserably.
The fear of dying is what has motivated millions of people into treatment for high cholesterol levels. The language of the cholesterol scare is simultaneously intimidating. “You are at high risk of dying of a heart attack” and “You have dangerously high cholesterol” are frightening words, indeed. However, research shows that from 1960 to 1980, there was virtually no change in the average serum cholesterol levels in the American population. Further, the issues play on our fears by labeling as “borderline-high” cholesterol levels which are actually average. As the widely publicized condemnation of “bad cholesterol”
would have us believe, one would suppose that it had been conclusively demonstrated that lowering blood cholesterol levels would save lives. No such evidence exists. Over twenty years, cholesterol levels declined very slightly, leaving the average just 3% lower in 1980 than it had been in 1960.Nowhere in medical literature is there a single case of cholesterol
having caused obstruction of the veins.
Venous blood moves far slower than arterial blood and thus would be more
inclined to have cholesterol deposits if the assumption of “bad cholesterol”
were accurate. Conventional medicine
has asked the wrong questions and has thus received the wrong answers. Research has been based on the assumption
that cholesterol is the bad type of fat that will clog our veins and by doing
so, it was supposed to be the main cause of heart attack. Proponents of the diet–heart hypothesis
routinely belittle, deny or explain away any scientific observations that
contradict their idea. Proponents of the
diet–heart idea often ask,”What is wrong?” but when they ask this, they mean
what is wrong with the conflicting evidence and not with their pet
hypothesis. Masses of valid scientific
evidence should have destroyed the diet–heart idea by now. Yet, like the ancient Greek Hydra, a
mythological monster that grew new heads whenever its old ones were chopped
off, the cholesterol Hydra continues its life as if nothing had happened. This perpetuation by the medical community,
and its capitalization by the pharmaceutical and food industries, has caused an
ongoing fraud against society. This is
probably the reason that the results of research done by scientists convinced
of the good which cholesterol does was hardly ever quoted in “scientific”
articles after 1970.
Are people who have high cholesterol at higher risk because they have more cholesterol in the blood, or are they at risk because they are obese, sedentary, smokers, eating their McDonald’s supersized meals in front of a TV?
Research over the past 50 years has
shown that blood cholesterol levels have very little to do with cholesterol and
fat in the diet. People whose blood
cholesterol is low develop just as many plaques in their blood vessels as
people whose cholesterol is high. If you
follow the so-called step-I diet of low cholesterol, low fat, high
carbohydrates, your cholesterol will most likely only decrease by between 0 – 4
% (British Medical Journal, 1991;303:953-957).
Additionally, you may find that your HDL (good cholesterol) will plummet
and your triglycerides will skyrocket, depending on the kinds of carbohydrates
you consume. Epidemiological studies
have repeatedly shown that having a high intake of animal products does not
result in having high cholesterol.
Moderate to severe dieting, even for years, does not produce a
measurable reduction in the risk of dying from a heart attack. The only effective way to lower cholesterol
is with drugs, but neither heart mortality nor total mortality have been
improved with drugs. On the contrary,
these drugs are dangerous to your health and may shorten your life.
Most research concludes that a lower level of cholesterol in the blood
hardly has any influence on the amount of heart attacks and none at all on the
life expectancy. One side note of
research has shown that old women with high cholesterol live longer than old
women with low cholesterol. A team of
physicians and researchers at Harvard University in 1987 concluded: “we
calculate a gain in life expectancy of 3 days to 3 months from a lifelong
program of cholesterol reduction.”
One of the most-quoted studies on cholesterol, the Multiple Risk Factor
Intervention Study (MR-FIT), studied the cholesterol levels of 300,000
middle-aged men, showed that after six years, 0.3% of the lowest cholesterol
group died of a heart attack while 1.3% of the highest cholesterol group died
of a heart attack. This is only a
difference of 1%. The MR-FIT Spin-Off
Report further showed:
Serum-Cholesterol Level Dead from Living Causes Dead from Coronary From all Heart Disease
Low (200 mg/dl or less)
97.8%
2.2%
0.5%
Average (203-244 mg/dl)
97.3%
2.7% 0.9%
High (245 mg/dl or more)
96.2%
3.8%
1.7%
The MR-FIT study has been called the “most exact database” ever produced. However, numerous reviews have been published
criticizing the accuracy of the study’s database.
What cholesterol does.
Two of the most important cholesterol compounds manufactured by the
human body are low-density lipoproteins (LDL, or “bad cholesterol”) and
high-density lipoproteins (HDL, or “good cholesterol”). In essence, HDL flows through to cleanse and
LDL is what picks up the impurities to take out of the body.
Cholesterol is a natural element from which many of our hormones are
made. It has been scientifically proven
that cholesterol:
Cholesterol is a natural element from which many of our hormones are
made.
It has been scientifically proven that cholesterol:
stabilizes and protects the cell membranes
protects the nerves
supplies us with the base material of bilious acids which you need for
digesting fat
supplies us with the base material for our stress hormones
helps to protect the skin
is an early stage of the material with which the skin produces vitamin D
supports our immune system
protects us from kidney disease in case of diabetes
provides the red blood corpuscles with the elasticity they need
is important for the growth and the repair of our brain cells.
If cholesterol is that important to maintain the human body, they why
did it get such a bad name? The “bad
cholesterol” myth has sustained its life even in spite of other research that
showed that the human body tries hard to maintain its level of cholesterol. The body is also capable of compensating the
effects of diet, either to lower or to raise the level. It appears that there are many reasons to
assume that everybody has his or her own level of cholesterol. The production of cholesterol increases when
you eat little cholesterol and decreases when you eat much. This explains why the “prudent” diet cannot
lower cholesterol more than on average a few percent.
Ramsey LE et al, Brit. Med. J.
1991/3003/page 1038:
Country
Testee Measure Period Results
England (UK Heart-DPP)
1278 diet 5-6 years –0.9%
Europe (WHO) 1898 diet 4 years –4.0%
USA (MRFIT) 6424
diet 6
years –2.0%
England (Diet & RT) 982 diet 2 years –3.5%
Finland ( Northern Karelia ) 2535 counseling 10 years –2.0%
USA (Stanford)
490 counseling 5.5 years –0.6%
England (UK Hear-DPP) 5373 diet +counseling 5–6 years +1.0%
Europe (WHO) 842 diet + counseling 4 years –2.1%
Sweden (Göteborg) 1473 diet + counseling 10 years –2.0%
Thus, it is hardly possible to speak in general terms about levels that
are “too high.” At the same time
scientists revealed that there seemed to be more reason to fear an insufficient
level! There seems to be a relation
between a too-low level of cholesterol and some forms of cancer.
The “other” cholesterol.
Oxy-cholesterol does cause change in our veins. Oxy-cholesterol gets in our bodies through
pre-prepared foods including meals, cookies and whatever we buy in packages to
eat or just to munch. Research was done
in Russia at the beginning of the century to demonstrate the devastating effect
of cholesterol on the body. Scientists
sprayed cholesterol (derived from egg yolk and brains) on the food given to
rabbits and found that these animals showed severe changes on the arteries
caused by a too high cholesterol level.
Then the relation between food that contains cholesterol and health
problems was a fact. It took a long time
until someone realized that the food given to laboratory animals was enriched
with cholesterol by spraying it with the help of a solvent over the food, after
which the solvent evaporated. It was
only then that cholesterol levels were raised.
However, in the process, the original pure cholesterol oxidized and
while pure cholesterol does not bring about characteristic changes in the
veins, oxidized cholesterol (in short “oxy-cholesterol”) will. Oxy-cholesterol originates when some food
elements are dried with air – for instance, in the drying process of grated
cheese and egg powder. Since these
products are frequently used in processing food in the industrial way, it will
be found in most prefab food.
The research.
If a scientific hypothesis is sound, it must agree with all
observations. A hypothesis is not like a
sports event, where the team with the greatest number of points wins the
game. Even one observation that does not
support a hypothesis is enough to disprove it.
The proponents of a scientific idea have the burden of proof on their
shoulders. The opponent does not have to
present an alternative idea; his task is only to find the weakness in the hypothesis.
! The Framingham
Study. In 1948, researchers set up shop
in the community ofFramingham , Massachusetts , population 28,000. What emerged over the following 24 years was
a series of risk factors for coronary heart disease which public service
advertisements, newspaper articles, books, and television talk shows have made
familiar to most Americans. The two
biggest risk factors could not be changed.
Men were much more likely to develop heart disease than women,
especially before age 55. Premenopausal women were practically immune. Half of all deaths from coronary heart
disease in the United States occur in the 5% of the population who are over 75
years old. But other important risk
factors were determined in the study.
High blood pressure could be reduced directly with medication, and the
presence of smoking, obesity and a sedentary lifestyle greatly influenced the
occurrence of heart disease. The study
showed a modest relationship between cholesterol levels and heart disease. (Could the high cholesterol be a symptom of a
disease rather than acause?) The association was strongest in young and
middle-aged men. It was found that high
blood cholesterol levels generally do not increase the risk of coronary heart
disease among women. “For women there
was no relationship except in the middle decade of life (ages 40–50).” (Thomas Dawber, the study’s first
director). The link between high
blood-cholesterol levels and increased risk of coronary heart disease in both
men and women weakened ab about age 50 and then disappeared entirely. Among the elderly, the group in whom most
deaths from coronary heart disease occur, high cholesterol levels did not
appear to be a risk factor. The study
compared the cholesterol in the subjects’ diets with the cholesterol levels in
their blood. To their surprise, there
was no relationship. Next, the
researchers studied the intake of saturated facts and overall calories. None had an effect.
! In the late 1960s,
another group of research was investigating ways to lower blood cholesterol
levels with diet. But even crude
experiments involving feeding quantities of egg yolks to volunteers
demonstrated that it took huge changes in the consumption of dietary cholesterol
to affect the cholesterol level in the bloodstream. The body manufactures, circulates, and uses
such great quantities of cholesterol compounds that small additions or
subtractions from dietary sources appeared to be insignificant. By the mid-1960s, many researchers had
dismissed dietary cholesterol.
! When the evidence is
weak, argue more loudly. Diet studies
quoted to this day as authoritative had as few as 5 subjects. If any enduring truth has emerged about human
beings and diet, it is that everyone is remarkably different, and studies that
don’t involve dozens of not hundreds of participants are of extremely limited
value. While these studies were still in
process, some health promoters – notably the American Heart Association – were
already urging the public to cut down on dietary cholesterol and eat more
polyunsaturated fat. Cautious voices in
the medical community replied to these announcements, stating that if it was so
clear that proper diet would reduce the risk of coronary heart disease, why not
prove it in an objective scientific experiment?
Since the health advice they proposed to test was already being given
and followed on a wide scale, this was a curious reversal of the horse and
cart.
! The Heart-Diet Pilot,
a nationwide study involving thousands of individuals, began in 1971 and
lasting 15 years, led by Ivan Frantz of the University of Minnesota and funded
by the heart institute. The task force
concluded that the cholesterol reductions were so small that a trial with as many
as 100,000 participants, costing up to $1 billion, would be required to produce
a reduction in coronary heart disease large enough to measure. The task force was not convinced that dietary
intake could be monitored accurately enough.
! Multiple Risk Factor Intervention Study (MR-FIT) (see opening paragraphs, above). The study involved 300,000 middle-aged men.
Half of the men were allowed to
continue their lifestyle with no changes.
The other half were placed in a special intervention group whose
cholesterol intake was cut by 42%, their saturated fat consumption by 28% and
their total calories by 21%. To
conclude, the enormous lifestyle change over the 6-year period had little
effect on the level of cholesterol in their blood. No significant difference in the overall
number of deaths could be found between the two groups. In fact, slightly more deaths occurred among
the special-intervention group. That
small difference was not statistically significant – it was probably the result
of chance. During the 6 years, those in
the special intervention group who were diagnosed with high blood pressure were
given medication. The medication not
only lowered blood pressure but also raised blood cholesterol by 7%. Theoretically, the hypertension medicine
might also have contributed to the deaths of some.
Enter... the pharmaceutical companies.
{The Emperor’s clothes cost a lot of money}
In January 1984, the Journal of the American Medical Association devoted
its issue to cholesterol and the studies done to date. The pharmaceutical companies used this
opportunity to begin publishing advertisements in medical journals promoting
cholesterol-lowering drugs, and salesmen were knocking on the doors of
physicians’ offices from coast to coast.
Thus began a public relations campaign.
The National Cholesterol Education Program slowly began surfacing from
the bureaucratic swamps of the National Heart, Lung and Blood Institute. As a result of this campaign, at least a
quarter of all adults would be referred to their physicians for treatment “to
lower their cholesterol levels.” A
majority of the nation’s physicians disagreed.
The public had been easier to convince of the dangers of cholesterol
than were the doctors who dealt with heart disease every day. Therefore, the physicians became the National
Cholesterol Education Program’s first target.
Thomas N. James, then the president of the American Heart Association,
had dissented on diet. “I wish to
express some personal reservations about our non-exceptional advice, which is
taken by the public as meaning everyone should be deeply concerned about their
dietary cholesterol.” Eliot Corday, a
prominent Los Angeles cardiologist and the council member who led the dissent,
stated in 1986, “Physicians just aren’t convinced about cholesterol.” The opponents of the cholesterol campaign
nonetheless seemed to lose ground. They
conducted research and wrote analyses, and that was the end of it. They had no money to sponsor national
conferences. Their articles weren’t
mailed, along with press releases, to medical writers in the popular
press. The heart institute’s eager
partners in promoting cholesterol consciousness are the drug companies, which
are understandably excited that the government had created their largest new
market in decades. The heart institute,
in turn, is tied closely to the drug industry.
Not only does it frequently test promising new drugs at no charge to the
companies, but it readily endorses products it deems useful. The saga continues: the drug companies are
the largest contributors to medical research efforts. The world was learning how much money could
be made scaring people about cholesterol.
The National Cholesterol Education Program costs society $10 billion to
$20 billion a year.
The drugs.
For a drug to qualify, it had to be able to lower blood cholesterol
levels significantly for long enough to measure the benefits. Second, the cholesterol reductions, once
achieved, have to be shown to reduce the incidence of coronary heart disease. Third, the treatment used to lower blood
cholesterol levels could not harm more people than it helped. In the 1970s, a drug called cholestyramine
(Questran) reduced blood cholesterol by interfering with normal digestion. Because cholestyramine is indigestible, bile
acid is excreted from the body, prompting the liver to manufacture more, thus
taxing the liver. The side effects might
not have been so important had it not been for one unfortunate result. The investigators did not even come close to
achieving the desired reduction in blood cholesterol. They could not lower blood cholesterol levels
by more than a marginal amount, even under the most carefully planned clinical
conditions.
About the same time another drug called clofibrate was tested. Clofibrate lowered blood cholesterol levels
by only 9%, about half the treatment effect expected. While there was no difference in the number
of fatal heart attacks in the group taking clofibrate, significantly fewer
nonfatal attacks occurred. However,
scientists reported excess deaths in the treatment group. In the group taking clofibrate, 162 deaths
had occurred, compared with 127 in a similar control group with equally high
initial cholesterol levels. Over 2
years, the mortality of those taking clofibrate was due to a variety of
ailments, especially cancer, which affected the liver and the digestive system.
In the early 1980s, the heart institute also experimented with estrogen
on men on the theory that it might account for the dramatically lower
heart-attack rates among premenopausal women.
Barely a year into the trial, the researchers stopped giving large doses
of estrogen when the early results showed convincingly that this treatment
caused heart attacks rather than prevented them. Three years later, they discontinued giving
moderate doses of estrogen after no evidence had emerged as to its efficacy.
The cholesterol-lowering drugs seem to have killed more than they
saved. The benefits of treatment, if
any, were small. Seven years of
treatment had reduced the chances of experiencing a heart attack from 8% to 7%.
The statin drugs. In 1987, the Food and Drug Administration
approved the statin drugs (Lovastatin, Lipitor) without having completed any
trials to measure their effect on coronary heart disease and systematically
monitor potential side effects. The drug which was intended to be used over a
lifetime was approved after a clinical trial of only 12 weeks and a long-term
experiment on 200 people over 2 years.
The statin drugs deserve careful scrutiny. The liver is the biggest consumer and
manufacturer of cholesterol compounds in the human body. The statin drugs inhibit the liver’s capacity
to synthesize cholesterol. Therefore,
the liver must obtain the cholesterol it needs by absorbing greater quantities
from the bloodstream, and blood cholesterol levels plunge as a result. Hailed as miracle substances that
“significantly reduce cholesterol and incidence of heart attacks”, the statin
drugs are probable carcinogens (women on the drugs had a much higher incidence
of breast cancer) and the overall statistical reduction of heart disease in the
drug trials is negligible. The potential
long- and short-term hazards of the statin drugs include heart attacks, cancer,
stroke, liver damage, cataracts, and severe muscle pain and damage. It has been found that when patients are taken
off statin, they feel better, are stronger and their tissue samples begin
looking normal again. “Because the
latent period between exposure to carcinogen and the incidence of clinical
cancer in humans may be 20 years or more, the absence of any controlled trials
of this duration means that we do not know whether statin treatment will lead
to . . . cancer in coming decades. Thus,
millions of people are being treated with medications the ultimate effects of
which are not yet known.” (Uffe
Ravnskov, MD, PhD, “The Cholesterol Myths”)
The dangers of low cholesterol.
In 1974, a group of leading epidemiological researchers believed that
cholesterol was going to be found guilty of another crime: an association with high
rates of colon cancer. A study of men in
6 big epidemiological studies showed that the men with cancer had cholesterol
levels which were lower than average.
The same relationship between low cholesterol levels and cancer was
found again in 1978 in the World Health Organization’s trial of
clofibrate. By 1980, French researchers
had found the same relationship in a study of 7603 males, where the incidence
of cancer began to climb steadily as cholesterol levels fell below 200 mg/dl,
into the range that the heart institute today calls “desirable.” “In some cancer cases... the
serum-cholesterol level was lower than that expected at as much as 16–18 years
before cancer diagnosis.”
Studies from Japan raise the question of whether low cholesterol levels
increase the risk of stroke. The effect
of the Japanese diet in keeping blood-cholesterol levels and heart-disease
deaths far below those found in the United States has resulted in
Japanexperiencing far higher rates of strokes and stomach cancer than the United
States .
Despite decades of clinical trials using a multitude of strategies, the
sad fact remains that none of them reduced cholesterol enough to provide an
opportunity to understand either the risks or the benefits of low cholesterol
levels. The most aggressive dieting
lowered cholesterol levels by only 5–7%, drugs by only 8–10%.
