The Heart Attack Culprit: Cholesterol
Isn't to Blame
Heart disease is the number-one killer of American men
and women today – and this is odd, considering that heart
disease was an uncommon cause of death at the beginning of the
twentieth century. While it’s true that more people died
of infectious diseases in those days and often didn’t live
long enough to die of heart disease, they also consumed much greater
amounts of long-chain omega-3 fatty acids. As subsequent generations
began eating less fish and more beef, the rates of heart disease
for those generations shot up.
Hippocrates said, “Whatever is good for the heart is probably
good for the mind.” Let’s reverse his insight a little
and say, “Whatever is good for the mind is probably good
for the heart.” As you now know, my dietary program provides
excellent benefits for your brain. You can also assume that it’s
going to provide extraordinary benefits for your heart. In fact,
that’s the reason I started my research twenty years ago.
I wanted to see if I could change the expression of my own genes,
which were programmed for an early death from heart disease –
something that occurred in my father, his brothers, and my grandfather.
This led me to the concept of the Zone and to my continuing research
to evolve and refine that concept.
One of the best ways to live a longer and better life is to reduce
your likelihood of developing heart disease. If we could eliminate
heart disease tomorrow, the average life expectancy of every American
would increase by an estimated ten years. Advances in medical
care have cut the death rate from heart disease, but they haven’t
touched the incidence rates. We are getting heart disease more
than ever, and as our population ages, more of us will die from
this condition. We are simply not doing a good enough job of addressing
the underlying cause of heart disease – a decrease in blood
flow to the heart and an increase in inflammation in the arteries.
These both result from an increased production of “bad”
eicosanoids. Rather than putting your faith in the hope that some
major surgery or new drug treatment will save your life after
you get heart disease, why not just avoid getting it in the first
Protecting yourself against heart disease requires far more than
just simply lowering your cholesterol levels. In fact, 50 percent
of the people who are hospitalized with heart attacks have normal
cholesterol levels, and 25 percent of people who develop premature
heart disease have no traditional risk factors at all. Maybe elevated
cholesterol isn’t the real cause of heart disease in the
The best predictors of a future heart attack come from prospective
studies that follow healthy people for a number of years to determine
which ones go on to develop heart disease, and then to figure
out why. Because these are expensive trials, very few of them
are done. But those that exist have indicated that cholesterol
levels are, in fact, a very poor predictor of future heart attacks.
In fact, the likelihood of future heart attacks has everything
to do with excess levels of “bad” eicosanoids –
exactly the hormones that can be modified by my dietary recommendations.
A heart attack is simply the death of muscle cells in the heart
from a lack of oxygen. This occurs when blood flow can’t
reach the heart because of a blockage or clot in the arteries
caused by a clumping of blood platelets, or because of inflammation
that causes an unstable plaque to break off and block the blood
flow in the artery. Sometimes a spasm in the artery blocks the
flow to the heart, or the heart goes into electrical chaos and
simply stops its synchronized beating on its own.
Causes of Heart Attacks
1. Clot formation
2. Plaque instability
4. Electrical chaos (sudden death)
None of these four causes of heart attacks has much to do with
increased cholesterol levels, but all of them have everything
to do with “bad” eicosanoids.
When I first wrote The Zone, I was strongly criticized
for asserting that elevated insulin levels were a major factor
in heart disease. (This is despite the fact that diabetics are
known to be at highly increased risk of heart disease.) People
still wanted to believe that the vast majority of heart problems
were caused mainly by dietary fat and high cholesterol levels.
Now the tide of medical opinion is beginning to turn. During the
past several years, more and more research, especially from prospective
studies, has shown that elevated insulin puts you at a greatly
increased risk of heart disease. The reason why elevated insulin
levels increase your risk of heart disease is that excess insulin
causes your body to overproduce “bad” eicosanoids.
This is why you need to combine insulin control with high-dose
fish oil if your goal is treating heart disease. Only this one-two
dietary punch can maximally reduce the AA/EPA ratio and thus restrict
the formation of “bad” eicosanoids.
The Importance of Your TG/HDL Ratio
When I first started doing cardiovascular research in the early
1970s, two prevailing theories of heart disease fought for supremacy.
One theory held that high cholesterol levels predominantly caused
heart disease, and therefore that simply lowering total cholesterol
could cure heart disease. The other theory was more complicated
and had to do with looking at heart disease as a complex inflammatory
Scientists used to think we had to worry only about our total
cholesterol level, but then researchers found this wasn’t
a very strong predictor of heart disease. Next came the realization
that there was both “good” and “bad” cholesterol.
The “good” cholesterol was found in high-density lipoprotein
(HDL) particles, and the “bad” cholesterol in low-density
lipoprotein (LDL) particles. This launched a war against “bad”
cholesterol, which is predominantly elevated by saturated fat.
In more recent years, scientists discovered two types of LDL
cholesterol. One type consists of large, fluffy LDL particles
that appear to have no potential to cause atherosclerosis or the
development of plaques on the large or medium-sized arteries.
The other type consists of small, dense LDL particles that are
strongly associated with arterial plaques and this can increase
the risk of heart disease. So now you have good “bad”
cholesterol (large, fluffy LD particles) and bad “bad”
cholesterol (small, dense LDL). Getting confused? Well, so is
everyone else who is fighting the cholesterol wars, because we
now know that the more bad “bad” cholesterol
you have, the more likely you are to have a heart attack, whereas
having a high level of the good “bad” cholesterol
isn’t likely to have any adverse health effects.
How can you tell which type of LDL you have? All you have to
do is determine your ratio of triglycerides to HDL cholesterol,
which would be found as part of the results of your last cholesterol
screening. If you ratio is less than 2, you have predominantly
large, fluffy LDL particles that are not going to do you much
harm. If your ratio is greater than 4, you have a lot of small,
dense LDL particles that can accelerate the development of atherosclerotic
plaques – regardless of your total cholesterol levels.
The importance of this TG/HDL ratio was confirmed by studies
from the Harvard Medical School. This research found that the
higher your TG/HDL ratio, the more likely you would be to have
a heart attack. How much more likely? In one study, those with
the highest ratio had sixteen times the risk of those with the
lowest ratio. That’s a huge increase in risk of for the
most common cause of death!
In contrast to our national wars on smoking and high cholesterol,
you hear nothing of our battle plan for reducing elevated TG/HDL
levels. Since a high TG/HDL ratio is a surrogate marker for elevated
insulin, you can see why I was making my plea to launch a national
war on elevated insulin many years ago.
How You Can Improve Your TG/HDL Ratio
You can improve your TG/HDL ratio in two ways. First, decrease
your insulin levels. Excess insulin has been shown to increase
triglyceride levels; lowering insulin will lower these levels.
Another way to decrease the TG/HDL ratio is to supplement your
diet with high-dose, ultra refined-grade fish oils.* Of course,
the fastest and most effective way is to do both simultaneously.
The speed at which simple changes in the diet can improve your
TG/HDL ratio was demonstrated in a study, conducted by Gerald
Reaven at Stanford, in which patients were put on diets consisting
of the same number of calories but differing in their protein-to-carbohydrate
ratio. When these patients consumed a high-carbohydrate diet,
they had a much higher TG/HDL ratio than when they switched to
a lower-carbohydrate diet. These changes occurred within four
weeks of each dietary change.
Likewise, Bruce Holub at the University of Guelph in Canada has
shown that postmenopausal women can rapidly reduce their diets
with 3.5 grams of ultra refined-grade fish oil per day.
Now let’s say we combine these approaches. This could only
result in an enhanced improvement in the ratio. This combined
approach is my dietary program.
The importance of the TG/HDL ratio can be seen from the recently
published results of the ongoing Copenhagen Male Study, which
studied the effect this ratio has on the long-term development
of heart disease. The researchers tracked healthy patients who
had either a low TG/HDL ratio (less than 1.7) or a high TG/HDL
ratio (greater than 6). They were amazed to find that the patients
with the low TG/HDL ratio who smoked, didn’t exercise, had
hypertension, and had elevated levels of LDL cholesterol had a
much lower risk of developing heart disease than those who had
a far better lifestyle but a higher TG/HDL ratio. This indicated
that lowering your TG/HDL ratio may have a far greater impact
on whether you develop heart disease than adopting a better lifestyle.
Does this mean you should smoke, stay sedentary, and not worry
about your blood pressure or cholesterol levels? Not at all, but
it does indicate that you need to significantly focus your efforts
to lower your TG/HDL ratio if your goal is to reduce heart disease.
If cholesterol levels are not the best way to predict heart disease,
what is? The other theory about the molecular cause of heart attacks,
put forward in the 1970s, primarily by Russell Ross of the University
of Washington, was that atherosclerosis was an inflammatory disease
(like Alzheimer’s disease). Since inflammation is a very
complex process and very difficult to measure in the bloodstream,
this theory of heart disease had far fewer advocates.
Cholesterol was still blamed for most cases of heart disease
up until the mid-1990s. Through the 1970s and 1980s, drug companies
kept rolling more and more cholesterol-lowering drugs into the
marketplace, even though these drugs caused only modest reductions
in the rate of heart attacks. In 1995, though, a new class of
cholesterol-lowering drugs, called statins, came onto the scene.
These drugs were found to be far more effective at preventing
heart attacks than other cholesterol-lowering drugs. Cardiovascular
researchers were certain that those wonder drugs worked their
magic by lowering “bad” cholesterol levels. (The fact
that lowering insulin did the same was never considered.)
As it turns out, statins were like the great and powerful Oz
– just a man behind the curtain. They didn’t work
their magic by lowering cholesterol levels. They actually had
a much broader spectrum of action than anyone ever anticipated:
they were also powerful anti-inflammatory agents. At the same
time as this discovery was made, researchers at the Harvard Medical
School found that certain pro-inflammatory proteins, called C-reactive
proteins, were highly predictive markers for an increased risk
of heart disease. With this new clinical tool, they and other
researchers found that statin drugs lowered the levels of these
C-reactive proteins. In fact, it was in the patients with the
highest levels of C-reactive protein that the statins had their
greatest impact. Thus, statins worked just like aspirin to reduce
inflammation and thus reduce heart attacks – only statins
cost a lot more and are less effective. (The statins also involve
one other small problem: they potentially decrease cholesterol-production
in the brain. This would lead to decreased production of new synaptic
connections and loss of memory, which is one of the known side
effects of these drugs.)
Heart Disease Rx: Reduce Inflammation
If reducing inflammation is so powerful in reducing our death
rate from heart attacks, the solution should be simple: add more
fish oil to the diet. This idea was first posed in the 1970s by
researchers who found through epidemiological studies that Eskimos
in Greenland had virtually no heart disease even though they consumed
a high-fat diet. Over the years, additional studies suggested
that the more fish you consume, the lower your risk of dying from
One of these studies was the DART study, which found that eating
one serving of fish per week decreased heart attacks by 29 percent
in patients who had had a previous heart attack. The researchers
couldn’t definitely prove, however, that it was the fish
oil in the fish that conferred these protective benefits, or whether
there was confounding factor, such as that people who eat fish
have healthier lifestyles in general.
More definitive proof of the benefits of fish oil was found in
the results of the GISSI trial, in which patients with heart disease
who took about 1 gram per day of ultra refined-grade long-chain
omega-3 fatty acids had a 45 percent reduction in their risk of
having a sudden fatal heart attack, a 30 percent reduction in
their total risk of cardiovascular mortality, and a 20 percent
reduction in overall mortality. Surprisingly, vitamin E (given
by itself or in combination with fish oil) had no benefits.
The most powerful statement on the role of diet in preventing
heart disease, however, comes from the Lyon Diet Heart Study.
In this study, survivors of heart attacks were split into two
groups. One group was put on a diet that followed the American
Heart Association recommendations (basically the USDA Food Pyramid),
and the second group was put on a Mediterranean-type diet (rich
in fruits, vegetables, and fish; supplemented with short-chain
omega-3 fatty acids; and very low in omega-6). At the end of four
years, the two groups had the same cholesterol levels. There was,
however, a more than 70 percent reduction in both fatal and nonfatal
heart attacks in the group on the Mediterranean diet compared
with the control group, who were allowed to eat hefty amounts
of omega-6 fatty acids. This study was very damaging for the cholesterol
theory of heart disease.
More important, during the four years the group on the Mediterranean
diet experienced no sudden deaths (a term used to describe electrical
chaos in the heart, which makes it stop beating in rhythm and
is the primary cause of cardiovascular mortality), the primary
difference between the two groups was the ratio of the arachidonic
acid to eicosapentaenoic acid in the blood. The AA/EPA ratio of
the individuals in the active group was 6.1, compared with 9.0
in the group following the American Heart Association diet. Thus,
a 30 percent reduction in the AA/EPA ratio resulted in a greater
than 70 percent reduction in fatal and nonfatal heart attacks,
despite the fact that the TG/HDL ratio didn’t change for
either group. This is why I believe that the AA/EPA ratio is by
far the most powerful predictor of future heart disease.
As dramatic as the results of the Lyon Diet Heart Study were,
I believe they could have been even better if the patients had
followed my dietary recommendations. The group on the Mediterranean
diet never reached an AA/EPA ratio of 1.5, which is similar to
that found in the Japanese, who have the lowest rates of heart
disease in the world. This is the ideal that I define in my dietary
program. Also, the TG/HDL ratio was still elevated in both groups
in the study, and this indicates that insulin levels hadn’t
been lowered and that both groups were still eating diets too
rich in carbohydrates.
My dietary program represents a considerable improvement over
the intervention diets used in both the GISSI study and the Lyon
Diet Heart. Where the GISSI study provided a little less than
1 gram of pharmaceutical-grade fish oil, I recommend five times
as much. (You need at least 3 to 4 grams of ultra refined long-chain
omega-3 fatty acids per day to lower triglycerides and thus lower
the TG/HDL ratio.) While the Lyon Diet Heart Study recommended
eating more fruits, I recommend 10 to 15 servings of fruits and
vegetables per day.
Compared with the Lyon Diet Heart Study, my dietary program would
have lowered the TG/HDL ratio through improved insulin control
(which reduces the production of “bad” eicosanoids)
and would have provided greater eicosanoid control with the increased
intake of ultra refined-grade fish oil. These differences would
have been reflected in the blood by the reduction of the TG/HDL
and AA/EPA ratios. On the basis of all the available evidence
we have from prospective studies, achieving the clinical goals
that define the Omega Rx Zone would bring your risk of heart disease
down to almost zero.
Excerpted from The Omega RX Zone: The Miracle of the New
High-Dose Fish Oil by Dr. Barry Sears. Copyright ©
by Dr. Barry Sears.
*These statements have not been evaluated by the Food and
Drug Administration. This product is not intended to diagnose,
treat, cure, or prevent any disease. As with any natural product,
individual results will vary.
For more information about Dr. Barry Sears, his incredible fish
oil supplements, or the popular Zone Diet, please visit www.zoneliving.com.
If you purchase any Zone Labs, Inc. products, part of the
proceeds support CBN ministries.
Dr. Barry Sears is a leader in the field of
dietary control of hormonal response. A former research scientist
at the Boston University School of Medicine and the Massachusetts
Institute of Technology, Dr. Sears has dedicated his efforts over
the past 25 years to the study of lipids and their inflammatory
role in the development of chronic disease. He holds 13 U.S. patents
in the areas of intravenous drug delivery systems and hormonal
regulation for the treatment of cardiovascular disease.
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