The Mystery of Heart Disease and the Need for More Research

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CHOLESTEROL AND HEART DISEASE
Cholesterol is a life sustaining substance needed to make
every cell in our body. It is not a source of calories like
sugar and fat. Eight hundred milligrams of this crucial
substance is made in our liver every day. Just one of those
milligrams is equivalent to the weight of 10 crystals of
table salt. The normal American diet contains only 400 mg
of cholesterol per day, half as much as supplied by our
own bodies.
After a meal, the fat and cholesterol in the intestinal
tract appear in the blood as tiny droplets called chylomicrons.
These are gradually cleared from the body by the
liver. Two fat carriers are formed in the liver from protein
that carry the cholesterol and fat in the blood. These are
the LDL and HDL lipoproteins.
A high LDL level indicates that you have eaten too
much fat; a low HDL level indicates that you have not
eaten enough protein, or enough food that contains the
8 essential amino acids to make the necessary apoprotein.
(These are listed in my book Cholesterol Won’t kill
you but Trans Fat Could.) The “bad” LDL (oxLDL) is an
oxidized form of LDL. What we do not know yet is why
more LDL is converted into oxLDL in patients with
heart disease.
Because sugar is soluble in blood and requires a minimum
of processing to become glycogen, or stored sugar,
it is used as the first source of energy. But after the sugar
in the blood decreases enough, LDL begins to provide
the energy. The reason that so many Americans are fat
around the waistline is that their diet contains so much
sugar and fat that they eat subsequent meals before they
have used up the initial energy sources. That fat is stored
around the waist.
DANGEROUS CHANGES IN THE CELLULAR
STRUCTURE
The cell membranes that encase each cell are largely composed
of cholesterol. They change in composition during a
person’s lifetime. This is a natural process that results in
hardening of the arteries (atherosclerosis) to some extent
in all of us as we age. One way to show this change is to
study the veins of artery by-pass patients.
By-pass procedures include finding veins in legs, or
perhaps arteries in arms, that can be harvested and then
used to by-pass the diseased arteries leading to the heart in
the same patient. Of particular interest is the chemical
composition of the veins that have been used as arteries to
the heart in second by-pass patients. These veins were
clear when they were first used in a by-pass. However, in
second-time by-pass patients, they too became clogged
and required replacement. By studying the chemical composition
of those veins, we found changes occur that cause
calcium deposits. They contained forty times more calcium
that they did when first inserted.
Oxysterols are what regulates the level of cholesterol in
the blood. They are formed from cholesterol in the liver.
Eight years ago, in our lab, we found that patients who
had undergone by-pass surgery contained a higher level of
these oxysterols in the blood than those patients who did
not need a by-pass.
We grew (cultured) human cells along with synthetic
oxysterols. Those cells cultured with an oxysterol resembled
the composition of the clogged cells in the vein of the
second by-pass surgery. This revealed that oxysterols are a
risk factor in heart disease.
These changes in cell structure allowed calcium to flow
into the cell and disrupted its normal functioning enough
to kill the cell. When the cell dies, enzymes remove the
protein and lipid portions of the cell, but allow the calcium
to remain embedded in the cell wall. It is this calcium
and lipid plaque that eventually lead to atherosclerosis in
the arteries. What we do not now know is why higher levels
of oxLDL and oxysterols are formed in the liver of
patients with heart disease.
We do know, however, that antioxidants in the blood
are necessary to keep the polyunsaturated fatty acid LDL
from forming oxidized, or “bad,” LDL. This is continually
being done in most people. However, in some people there
are just not enough antioxidants in the blood. We have
found one antioxident that keeps LDL from becoming
“bad” LDL. Once oxLDL is not found in the blood, the
possibility of atherosclerosis forming in the arteries is
diminished.
THE IMPORTANCE OF UNSATURATED FAT AND
FIBER
In 1957, Dr. Edward Ahrens reported the results of a
study entitled, “Dietary Fats and Human Serum Lipid
Levels.” He used an all-liquid diet consisting of salt-free
milk protein product and sugar, along with the vitamins
available in 1957. He found that saturated fats like butter
raised blood cholesterol levels while unsaturated
fats, like corn oil, lowered them. This diet contained no
magnesium, which was later found to be essential for
the metabolism of saturated
fat.
Dr. Ahrens also used this
diet in 1969 to measure the
absorption of cholesterol
from the intestinal tract.
Without any fiber in the
diet, 70% of the cholesterol
used in this test was
absorbed in the blood.
These 1957 and 1969 studies
indicated that saturated
fat and dietary sources of
cholesterol cause higher
blood cholesterol levels.
This is still believed to be
the case by many health
professionals today.
However, as far back at
1957, medical researcher
Dr. Warren Sperry found no
correlation between the
plasma cholesterol level
and atherosclerosis in
autopsied men who had died of heart disease. Subsequent
research has shown that the American diet contains
enough unsaturated fat to cancel out the effect of
saturated fat. When a source of fiber is present in the
diet, little cholesterol is absorbed from the intestinal
tract. Our own research has also shown no correlations
between the plasma cholesterol levels and heart disease
in 1,200 people who have been tested for heart disease.
THE NEED FOR MORE RESEARCH
The solving of the mystery of what causes atherosclerosis
will come from more basic research. The University of Illinois
has the staff to solve problems in metabolic diseases,
such as heart disease, but that requires more laboratory
space and more funds for research than are presently available
at the university. At the national level, Congress needs
to double the NIH budget and earmark at least $6 billion
for the construction and funding of research centers devoted
exclusively to solving the problems caused by metabolic
diseases.

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