The China Study (19 page)

BROKEN HEARTS                             117
in Japan, who were more likely to smoke, still had less coronary heart
disease than the Japanese Americans. 19 The researchers pOinted to diet,
writing that blood cholesterol increased "with dietary intake of satu-
rated fat , animal protein and dietary cholesterol." On the flip side, blood
cholesterol "was negatively associated with complex carbohydrate in-
take .... "20 In simple terms, animal foods were linked to higher blood
cholesterol; plant foods were linked to lower blood cholesterol.
This research clearly implicated diet as one possible cause of heart
disease. Furthermore, the early results were painting a consistent pic-
ture: the more saturated fat and cholesterol (as indicators of animal food
consumption) people eat, the higher their risk for getting heart disease.
And as other cultures have come to eat more like us, they also have
seen their rates of heart disease skyrocket. In more recent times, several
countries have now come to have a higher death rate from heart disease
than America.
RESEARCH AHEAD OF ITS TIME
So now we know what heart disease is and what factors determine our
risk for it, but what do we do once the disease is upon us? When the
Framingham Heart Study was just beginning, there were already doc-
tors who were trying to figure out how to treat heart disease, rather
than just prevent it. In many ways, these investigators were ahead of
their time because their interventions, which were the most innovative,
successful treatment programs at the time, utilized the least advanced
technology available: the knife and fork.
These doctors noticed the ongoing research at the time and made
some common-sense connections. They realized that 2 l :
• excess fat and cholesterol consumption caused atherosclerosis (the
hardening of the arteries and the accumulation of plaque) in ex-
p e r i m e n t a l animals
• eating cholesterol in food caused a rise in cholesterol in the blood
• high blood cholesterol might predict andlor cause heart disease
• most of the world's population didn't have heart disease, and these
heart disease-free cultures had radically different dietary patterns,
consuming less fat and cholesterol
So they decided to try to alter heart disease in their patients by having
them eat less fat and cholesterol.
One of the most progressive doctors was Dr. Lester Morrison of Los

THE (HINA STUDY
118
Angeles. He started a study in 1946 (two years before the Framingham
Study) to "determine the relationship of dietary fat intake to the inci-
d e n c e of atherosclerosis."22 In his study he instructed fifty heart attack
survivors to maintain their normal diet and fifty different heart attack
survivors to consume an experimental diet.
In the experimental diet group he reduced the consumption of fat and
cholesterol. One of his published sample menus allowed the patient to
have only a small amount of meat two times a day: two ounces of "cold
roast lamb, lean, with mint jelly" for lunch, and another two ounces of
"lean meats" for dinner.22 Even if you loved cold roast lamb with mint
jelly, you weren't allowed to eat much of it. In fact, the list of prohibited
foods in the experimental diet was fairly long and included cream soups,
pork, fat meats, animal fats, whole milk, cream, butter, egg yolks and
breads and desserts made with butter, whole eggs and whole milk. 22
Did this progressive diet accomplish anything? After eight years,
only twelve of fifty people eating their normal American diet were alive
(24%). In the diet group, twenty-eight people were still alive (56%),
almost two and one-half times the amount of survivors in the control
group. After twelve years, every single patient in the control group was
dead. In the diet group, however, nineteen people were still alive, a
survival rate of 38%.22 While it was unfortunate that so many people in
the dietary group still died, it was clear that they were staving off their
disease by eating moderately less animal foods and moderately more
plant foods (see Chart 5.2).
CHART 5.2: SURVIVAL RATE OF DR. MORRISON'S PATIENTS
50
0'1
C
.s;:
40
.~
::;:J
Vl
.):a
c 30                                                          -+-Diet
(1)
.~
_Control
a..
20
'+-
0
~
..0
E 10
::;:J
z
0
12
0         3                  8
Time (years)

BROKEN HEARTS                               119
In 1946, when this study began, most scientists believed that heart
disease was an inevitable part of aging, and nothing much could be done
about it. While Morrison didn't cure heart disease, he proved that some-
t h i n g as simple as diet could significantly alter its course, even when the
disease is so advanced that it has already caused a heart attack.
Another research group proved much the same thing at about that
time. A group of doctors in Northern California took a larger group of
patients with advanced heart disease and put them on a low-fat, low-
cholesterol diet. These doctors found that the patients who ate the low-
fat, low-cholesterol diet died at a rate four times lower than patients who
didn't follow the diet. 23
It was now clear that there was hope. Heart disease wasn't the inevi-
table result of old age, and even when a person had advanced disease, a
low-fat, low-cholesterol diet could significantly prolong his or her life.
This was a remarkable advance in our understanding of the number one
killer in America. Furthermore, this new understanding made diet and
other environmental factors the centerpieces of heart disease. Any dis-
cussion of diet, however, was narrowly focused on fat and cholesterol.
These two isolated food components became the bad guys.
We now know that the attention paid to fat and cholesterol was mis-
guided. The possibility that no one wanted to consider was that fat and
cholesterol were merely indicators of animal food intake. For example,
look at the relationship between animal protein consumption and heart
disease death in men aged fifty-five to fifty-nine across twenty different
countries in Chart 5.3.16
This study suggests that the more animal protein you eat, the more
heart disease you have. In addition, dozens of experimental studies
show that feeding rats, rabbits and pigs animal protein (e.g., casein)
dramatically raises cholesterol levels, whereas plant protein (e.g., soy
protein) dramatically lowers cholesterol levels. 24 Studies in humans not
only mirror these findings, but show that eating plant protein has even
greater power to lower cholesterol levels than reducing fat or choles-
terol intake. 25
While some of these studies implicating animal protein were con-
d u c t e d in the past thirty years, others were published well over fifty
years ago when the health world was first beginning to discuss diet and
heart disease. Yet somehow animal protein has remained in the shadows
while saturated fat and cholesterol have taken the brunt of the criticism.
These three nutrients (fat, animal protein and cholesterol) characterize

120                            THE CHINA STUDY
CHART 5.3: HEART DISEASE DEATH RATES FOR MEN
AGED 55 TO 59 YEARS AND ANIMAL PROTEIN CONSUMPTION
ACROSS 20 COUNTRIESI6
2
o    800
o
•
6
o
•• •
600               R = .64
400
200
8
4                   6
5                                       9
3                                       7
Percent of total calories coming from animal protein
animal-based food in general. So isn't it perfectly reasonable to wonder
whether animal-based food , and not just these isolated nutrients, causes
heart disease?
Of course, no one pointed a finger at animal-based foods in general.
It would have led immediately to professional isolation and ridicule
(for reasons discussed in Part IV). These were contentious times in
the nutritional world. A conceptual revolution was taking place, and
a lot of people didn't like it. Even talking about diet was too much for
many scientists. Preventing heart disease by diet was a threatening idea
because it implied that something about the good old meaty American
diet was so bad for us that it was destroying our hearts. The status quo
boys didn't like it.
One status quo scientist had a good time making fun of people who
appeared to have a low risk of heart disease. In 1960, he wrote the fol-
lowing piece of "humor" to mock the then-recent findings 26 :
Thumbnail Sketch of the Man Least Likely
to Have Coronary Heart Disease:
An effeminate municipal worker or embalmer, completely lacking
in physical and mental alertness and without drive, ambition or
competitive spirit who has never attempted to meet a deadline of
any kind. A man with poor appetite, subsisting on fruit and veg-
etables laced with corn and whale oils, detesting tobacco, spurning

BROKEN HEARTS                             121
ownership of radio, TV or motor car, with full head of hair and
scrawny and un-athletic in appearance, yet constantly straining
his puny muscles by exercise; low in income, B.P (blood pressure),
blood sugar, uric acid and cholesterol, who has been taking nico-
tinic acid, pyridoxine and long term anticoagulant therapy ever
since his prophylactic castration.
The author of this passage might just as well have said, "Only REAL
men have heart disease." Also notice how a diet of fruits and vegetables
is described as "poor" even though the author suggests that this diet
is eaten by those people who are least likely to have heart disease. The
unfortunate association of meat with physical ability, general manliness,
sexual identity and economic wealth all cloud how the status quo scien-
tists viewed food, regardless of the health evidence. This view had been
passed down from the early protein pioneers described in chapter two.
Perhaps this author should have met a friend of mine, Chris Camp-
bell (no relation). Chris is a two-time NCAA Division 1 wrestling cham-
pion, three-time U.s. Senior wrestling champion, two-time Olympic
wrestler and Cornell Law School graduate. At the age of thirty-seven
he became the oldest American ever to win an OlympiC medal in wres-
tling, weighing in at 198 pounds. Chris Campbell is a vegetarian. As a
man not likely to have heart disease, I think he might disagree with the
characterization above.
The battle between the status quo and the dietary prevention camp
was intense. I remember attending a lecture at Cornell University dur-
ing the late 1950s when a famous researcher, Ancel Keys, came to talk
about preventing heart disease by diet. Some scientists in the audience
just shook their heads in disbelief, saying diet can't pOSSibly affect heart
disease. In those first decades of heart disease research, a heated, per-
sonal battle flared , and open-mindedness was the first casualty.
RECENT HISTORY
Today, this epic battle between defenders of the status quo and advo-
cates of diet is as strong as ever. But there have been significant changes
in the landscape of heart disease. How far have we come, and how have
we proceeded to fight this disease? Mostly, the status quo has been pro-
tected. Despite the potential of diet and disease prevention, most of the
attention given to heart disease has been on mechanical and chemical
intervention for those people who have advanced disease. Diet has been

122                          THE CHINA STUDY
pushed aside. Surgery, drugs, electronic devices and new diagnostic
tools have stolen the spotlight.
We now have coronary bypass surgery, where a healthy artery is
"pasted" over a diseased artery, thereby bypassing the most dangerous
plaque on the artery. The ultimate surgery, of course, is the heart trans-
plant, which even utilizes an artificial heart on occasion. We also have
a procedure that doesn't require cracking the chest plate open, called
coronary angioplasty, where a small balloon is inflated in a narrowed,
diseased artery, squishing the plaque back against the wall, opening up
the passage for increased blood flow. We have defibrillators to revive
hearts, pacemakers and precise imaging techniques so that we can ob-
serve individual arteries without having to expose the heart.
The past fifty years have truly been a celebration of chemicals and
technology (as opposed to diet and prevention). In summarizing the
initial widespread research on heart disease, one doctor recently high-
lighted the mechanical:
It was hoped that the strength of science and engineering devel-
o p e d after World War II could be applied to this battle [against
heart disease] ... . The enormous advances in mechanical engineer-
i n g and electronics that had been stimulated by the war seemed to
lend themselves particularly well to the study of the cardiovascu-
lar system .... 4
Some great advances have been made, to be sure, which may account
for the fact that our death rate from heart disease is a full 58% lower
than what it was in 1950. 2 A 58% reduction in the death rate seems a
great victory for chemicals and technology. One of the greatest strides
has come from better emergency room treatment of heart attack vic-
tims . In 1970, if you were older than Sixty-five years, had a heart attack
and were lucky enough to make it to the hospital alive, you had a 38%
chance of dying. Today, if you make it to the hospital alive, you only
have a 15% chance of dying. The hospital's emergency response is much
better, and consequently huge numbers of lives are being spared. 2
In addition, the number of people smoking has steadily been decreas-
ing ,2 7,28 which in turn lowers our death rate from heart disease. Between
hospital advances, mechanical devices, drug discoveries, lower smoking
rates and more surgical options, there clearly seems to be much to cheer
about. We've made progress, so it seems.
Or have we?

BROKEN HEARTS                              123
After all, heart disease is still our number one cause of death. Every
twenty-four hours, almost 2,000 Americans will die from this disease.2
For all the advances, there are a huge number of people still succumb-
ing to broken hearts.
In fact, the incidence rate (not death rate) for heart disease 29 is about
the same as it was in the early 1970s. 2 In other words, while we don't
die as much from heart disease, we still get it as often as we used to. In
seems that we simply have gotten slightly better at postponing death
from heart disease, but we have done nothing to stop the rate at which our
hearts become diseased.
SURGERY: THE PHANTOM SAVIOR
The mechanical interventions that we use in this country are much less
effective than most people realize. Bypass surgery has become particu-
larly popular. As many as 380,000 bypass operations were performed
in 1990,3° meaning that about lout of 750 Americans underwent this
extreme surgery. During the operation, the patient's chest is split open,
blood flow is rerouted by a series of clamps, pumps and machines, and
a leg vein or chest artery is cut out and sewn over a diseased part of the
heart, thereby allowing blood to bypass the most clogged arteries.
The costs are enormous. More than one of every fifty elective patients
will die because of complications3 1 during the $46,000 procedure. 32
Other side effects include heart attack, respiratory complications, bleed-
ing complications, infection, high blood pressure and stroke. When the
vessels around the heart are clamped shut during the operation, plaque
breaks off of the inner walls. Blood then carries this debris to the brain,
where it causes numerous "mini" strokes. Researchers have compared
the intellectual capabilities of patients before and after the operation,
and found that a stunning 79% of patients "showed impairment in some
aspect of cognitive function" seven days after the operation. 33
Why do we put ourselves through this? The most pronounced ben-
efit of this procedure is relief of angina, or chest pain. About 70-80% of
patients who undergo bypass surgery remain free of this crippling chest
pain for one year.34 But this benefit doesn't last. Within three years of the
operation, up to one-third of patients will suffer from chest pain again. 35
Within ten years half of the bypass patients will have died, had a heart
attack or had their chest pain return. 36 Long-term studies indicate that
only certain subsets of heart disease patients live longer because of their
bypass operationY Furthermore, these studies demonstrate that those