The China Study (25 page)

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cancer in American women is not due to family history or genes. But
genetic fatalism continues to define the nation's mindset.
Among the genes that influence breast cancer risk, BRCA-1 and
BRCA-2 have received the most attention since their discovery in
1994. 26-29 These genes, when mutated, confer a higher risk both for
breast and ovarian cancers. 30, 3) These mutated genes may be passed on
from generation to generation; that is, they are inherited genes.
In the excitement over these discoveries, however, other information
has been ignored. First, only 0,2% of individuals in the general popu-
l a t i o n (1 in 500) carry the mutated forms of these genes. 25 Because of
the rarity of these genetic aberrations, only a few percent of the breast
cancer cases in the general population can be attributed to mutated
BRCA-l or BRCA-2 genes. 32 , 33 Second, these genes are not the only
genes that participate in the development of this disease32 ; many more
will surely be discovered. Third, the mere presence ofBRCA-l, BRCA-2
or any other breast cancer gene does not guarantee disease occurrence,
Environmental and dietary factors play a central role in determining
whether these genes are expressed.
A recent paper3) reviewed twenty-two studies that assessed the risk
of breast (and ovarian) cancer among women who carried mutated
BRCA-l and BRCA-2 genes. Overall, disease risk was 65% for breast
cancer and 39% for ovarian cancer by age seventy for BRCA-l women,
and 45% and 11%, respectively, for BRCA-2 women, Women with these
genes certainly face high risks for breast cancer. But even among these
high-risk women, there is still good reason to believe that more atten-
t i o n to diet is likely to pay handsome rewards. About half of the women
who cany these rare, potent genes do not get breast cancer.
In short, although the discovery of BRCA-l and BRCA-2 added an
important dimension to the breast cancer story, the excessive emphasis
given to these particular genes and genetic causation in general is not
warranted.
I do not mean to diminish the importance of knowing all there is to
know about these genes for the small minority of women who carry
them. But we need to remind ourselves that these genes need to be
"expressed" in order for them to participate in disease formation, and
nutrition can affect this. We've already seen in chapter three how a diet
high in animal-based protein has the potential to control genetic expres-
sion.

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Screening and Non-Nutritional Prevention
With all of this new information regarding genetic risk and family his-
tory, women are often encouraged to get screened for breast cancer.
Screening is a reasonable step, especially for women who may have
tested positive for the BRCA genes. But it's important to remember that
doing a mammography or getting a genetic test to see if you harbor
BRCA genes does not constitute prevention of breast cancer.
Screening is merely an observation to see whether the disease has
progressed to an observable state. Some studies 34- 36 have found that
groups of women who undergo frequent mammography have slightly
lower mortality rates than groups of women who do not undergo fre-
q u e n t mammography. This implies that our cancer treatments are more
likely to be successful if the cancer is found at an earlier stage. This is
likely to be true, but there is some concern over the way statistics are
used in this debate.
One of the statistics used to support early detection and the ensuing
treatments is that once diagnosed with breast cancer, the likelihood of
surviving for at least five years is higher than ever before.37 What this
really means is that with the aggressive campaign for regular screening,
many women are discovering their breast cancer at an earlier stage of
disease. When disease is discovered at an earlier stage it is less likely to
lead to death within five years, regardless of treatment. As a consequence,
we may have an improved five-year survival rate simply because women
find out that they have breast cancer earlier in the disease progression, not
because our treatments have improved over time.38
Beyond the current screening methods, there are other non-nutri-
tional options for prevention that have been promoted. They are espe-
cially of interest to women who have a high risk of breast cancer due to
family history and/or to the presence of the BRCA genes. These options
include taking a drug such as tamoxifen and/or mastectomy.
Tamoxifen is one of the most popular drugs taken to prevent breast
cancer,39, 40 but the long-term benefits of this option are not clear. One
major U.S. study showed that tamoxifen administered over a period of
four years to women at increased risk of breast cancer reduced the num-
ber of cases by an impressive 49%.41 This benefit, however, may be limited
to women whose estrogen levels are very high. It was this result that led
the U.S. Food and Drug Administration to approve use of tamoxifen by
women who met certain criteria. 42 Other studies suggest that the enthusi-

164                          THE CHINA STUDY
asm for this drug is not warranted. Two less substantial European trials 43 .
44 have failed to show any statistically significant tamoxifen benefit, rais-
ing some doubt about how dramatic the benefit really is. Moreover, there
is the additional concern that tamoxifen raises the risks for stroke, uter-
ine cancer, cataracts, deep vein thrombosis and pulmonary embolism,
although the overall benefits of breast cancer prevention are still believed
to outweigh the risks.42 Other chemicals have also been investigated as
alternatives to tamoxifen, but these drugs are encumbered by limited ef-
fectiveness and/or some of the same troublesome side effects. 45.46
Drugs such as tamoxifen and its newer analogues are considered anti-
estrogen drugs. In effect, they work by reducing the activity of estrogen,
which is known to be associated with elevated breast cancer risk.4.5 My
question is quite simple: why don't we ask why estrogen is so high in
the first place, and once we recognize its nutritional origin, why don't
we then correct that cause? We now have enough information to show
that a diet low in animal-based protein, low in fat and high in whole
plant foods will reduce estrogen levels. Instead of suggesting dietary
change as a solution, we spend hundreds of millions of dollars develop-
ing and publicizing a drug that mayor may not work and that almost
certainly will have unintended side effects.
The ability of dietary factors to control female hormone levels has
long been known in the research community, but a recent study was
particularly impressive. 47 Several female hormones, which increase
with the onset of puberty, were lowered by 20-30% (even 50% lower
levels for progesterone!) simply by having girls eight to ten years of
age consume a modestly low-fat, low animal-based food diet for seven
yearsY These results are extraordinary because they were obtained with
a modest dietary change and were produced during a critical time of a
young girl's life, when the first seeds of breast cancer were being sowed.
These girls consumed a diet of no more than 28% fat and less than 150
mg cholesterol/day: a moderate plant-based diet. I believe that had they
consumed a diet devoid of animal-based foods and had they started this
diet earlier in life, they would have seen even greater benefits, including
a delay in puberty and an even lower risk of breast cancer later in life.
Women at high risk for breast cancer are given three options: watch
and wait, take tamoxifen medication for the remainder of their lives or
undergo mastectomy. There should be a fourth option: consuming a
diet free of animal-based foods and low in refined carbohydrates, aided
by regular monitoring for those at high risk. I stand by the usefulness

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of this fourth option even for women who have already had a first mas-
tectomy. Using diet as an effective treatment of already-diagnosed dis-
ease has been well documented in human studies with advanced heart
disease,48,49 clinically documented Type 2 diabetes (see chapter seven) ,
advanced melanoma5o (a deadly skin cancer) and, in experimental ani-
mal studies,sl liver cancer.
Environmental Chemicals
There is another breast cancer conversation that has been taking place
for some years now. It concerns environmental chemicals. These widely
distributed chemicals have been shown to disrupt hormones, although
it is not clear which hormones in humans are being disrupted. These
chemicals may also cause reproductive abnormalities, birth defects and
Type 2 diabetes.
There are many different types of offending chemicals, most of which
are commonly associated with industrial pollution. One group, includ-
ing dioxins and PCBs, persist in the environment because they are not
metabolized when consumed. Thus they are not excreted from the body.
Because of this lack of metabolism, these chemicals accumulate in body
fat and breast milk of lactating mothers. Some of these chemicals are
known to promote the growth of cancer cells, although humans may
not be at significant risk unless one consumes excessive quantities of
meat, milk and fish. Indeed, 90-95% of our exposure to these chemicals
comes from consuming animal products-yet another reason why con-
s u m i n g animal-based foods can be risky.
There is a second group of these environmental chemicals that are also
commonly perceived to be significant causes of breast5 2 and other can-
cers . They are called PAHs (Polycyclic Aromatic Hydrocarbons) and are
found in auto exhaust, factory smoke stacks, petroleum tar products and
tobacco smoke, among other processes common to an industrial society.
Unlike the PCBs and dioxins, when we consume PAHs (in food and wa-
ter), we can metabolize and excrete them. But there is a snag: when the
PAHs are metabolized within the body, they produce intermediate prod-
ucts that react with DNA to form tightly bound complexes, or adducts
(see chapter three). This is the first step in causing cancer. In fact, these
chemicals have recently been shown to adversely affect the BRCA-l and
BRCA-2 genes of breast cancer cells grown in the laboratory.53
In chapter three, I described studies in my laboratory showing that
when a very potent carcinogen is put into the body, the rate at which

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it causes problems is mostly controlled by nutrition. Thus the rate at
which PAHs are metabolized into products that bind to DNA is very
much controlled by what we eat. Very simply, consuming a Western-
type diet will increase the rate at which chemical carcinogens like PAHs
bind to DNA to form products that cause cancer.
So when a recent study found slightly increased levels of PAH-DNA
adducts in women with breast cancer in Long Island, New York,54 it
may well have been that these women were consuming a more meaty
diet, which increased the binding of the PAHs to DNA. It is entirely pos-
sible that the quantity of PAHs being consumed had nothing to do with
increasing breast cancer risk. In fact, in this study, the number of PAH-
DNA adducts in these women seem to be unrelated to PAH exposure. 54
How is this possible? Perhaps all of the women in this Long Island study
consumed a relatively uniform, low level of PAHs, and the only ones
who subsequently got breast cancer were the ones who ate a diet high
in fat and animal protein, thus causing more of the ingested PAHs to
bind to their DNA.
In this same Long Island study, breast cancer was not associated
with PCBs and dioxins , the chemicals that can't be metabolized. 55 As
a result of the Long Island study, the hype associating environmental
chemicals with breast cancer has been somewhat muted. This and
other findings suggest that environmental chemicals seem to play a
far less significant role for breast cancer than the kind of foods we
choose to eat.
Hormone Replacement Therapy
I must briefly mention one final breast cancer issue: whether to use hor-
m o n e replacement therapy (HRT), which increases breast cancer risk.
HRT is taken by many women in order to alleviate unpleasant effects of
menopause, protect bone health and prevent coronary heart disease. 56
However, it is now becoming widely acknowledged that HRT is not as
beneficial as once thought, and it may have certain severe side effects.
So what are the facts?
I am writing this commentary at an opportune time because the
results of some large trials of HRT use have been released in the last
year.5 Of special interest are two large randomized intervention trials:
6
the Women's Health Initiative (WHI)57 and the Heart and Estrogen!
Progestin Replacement Study (HERS) .58 Among women who take HRT,
after 5.2 years the WHI trial is shOwing a 26% increase in breast cancer

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cases while the HERS study is seeing an even greater 30% increase. 59
These studies are consistent. It appears that increased exposure to fe-
male hormones, via HRT, does indeed lead to more breast cancer.
It has been thought that HRT is associated with lower rates of coro-
n a r y heart disease. 56 However, this is not necessarily true. In the large
WHI trial, for every lO,OOO healthy postmenopausal women who took
HRT, there were seven more women with heart disease, eight more with
strokes and eight more with pulmonary embolism 57- t h e opposite of
what had been expected. HRT may increase cardiovascular disease risk
after all. On the other hand, HRT did have a beneficial effect on colorec-
tal cancer and bone fracture rate. Among every lO,OOO women, there
were six fewer colorectal cancers and five fewer bone fractures. 57
So how do you make a decision with such information? Just by add-
i n g and subtracting the numbers we can see that HRT may well be the
cause of more harm than good. We can tell each individual woman to
make her own decision depending on which disease and which un-
pleasantry she fears the most, as many physicians are likely to do. But
this can be a tough decision for women who are having a difficult time
with menopause. These women must choose between living unaided
through the emotional and physical symptoms of menopause in order
to preserve a low risk of breast cancer, or taking HRT to manage their
menopause discomforts while increasing their risk of breast cancer and,
possibly, cardiovascular disease. To say that this scenario troubles me
would be an understatement. We have spent well over a billion dollars
on the research and development of these HRT medical preparations,
and all we get is some apparent pluses and probably even more minuses.
Calling this troubling doesn't begin to describe it.
Instead of relying on HRT, I suggest that there is a better way, using
food. The argument goes like this:
• During the reproductive years, hormone levels are elevated, al-
t h o u g h the levels among women who eat plant-based diets are not
as elevated.
• When women reach the end of their reproductive years, it is en-
tirely natural for reproductive hormones of all women to drop to a
low "base" level.
• As reproductive years come to an end, the lower hormone levels
among plant eaters don't crash as hard as they do among animal
eaters. Using hypothetical numbers to illustrate the concept, the