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Risk Factors for
Prostate Cancer
Written for the American Council on Science and Health
by Kathleen Meister, M.A.
Based on an original paper by:
John W. Morgan, Dr.P.H.,
Thalia A. Beeles, M.P.H, and
Katherine Y. Le, M.P.H
Project Coordinator
Ruth Kava, Ph.D., R.D.
Nutrition Director, ACSH
Art Director
Yelena Ponirovskaya
President
Elizabeth M. Whelan, Sc.D., M.P.H.
February 2002
AMERICAN COUNCIL ON SCIENCE AND HEALTH
1995 Broadway, 2nd Floor, New York, NY 10023-5860
Tel. (212) 362-7044 • Fax (212) 362-4919
URL: http://www.acsh.org • E-mail: [email protected]
This report is based on an extensive review of the scientific literature
prepared for ACSH by John W. Morgan, Dr.P.H., Thalia A. Beeles, M.P.H.,
and Katherine Y. Le, M.P.H. That document was reviewed by the following individuals, whom we thank for their valuable input:
Joseph F. Borzelleca, Ph.D.
Gilbert L. Ross, M.D.
Virginia Commonwealth University
ACSH
Michael B. Bracken, Ph.D., M.P.H.
Kenneth J. Rothman, Dr.P.H.
Yale University School of Medicine
Newton Lower Falls, MA
Ralph Dittman, M.D., M.P.H.
Fredric M. Steinberg, M.D.
Houston, TX
Clothall, Baldock, England
Alan R. Kristal, Dr. P.H.
Elizabeth M. Whelan, Sc.D., M.P.H.
Fred Hutchinson Cancer Research
Center
ACSH
Elizabeth A. Platz, Sc.D., M.P.H.
John Muir Comprehensive Cancer
Center
Joel Elliot White, M,D., F.A.C.R.
Johns Hopkins School of Hygiene and
Public Health
ACSH accepts unrestricted grants on the condition that it is solely responsible for the
conduct of its research and the dissemination of its work to the public. The organization
does not perform proprietary research, nor does it accept support from individual corporations for specific research projects. All contributions to ACSH—a publicly funded
organization under Section 501(c)(3) of the Internal Revenue Code—are tax deductible.
Individual copies of this report are available at a cost of $5.00. Reduced prices for 10 or
more copies are available upon request.
Copyright © by American Council on Science and Health, Inc.
This book may not be reproduced in whole or in part, by mimeograph or any other
means, without permission.
About the cover: David (1623-1624), by Gian Lorenzo Bernini, Galleria Borghese, Rome
Table of Contents
Executive Summary
5
Introduction
6
Magnitude of the Problem
7
Symptoms and Treatment
8
Screening for Prostate Cancer
8
The Concept of Risk Factors
9
Risk Factors for Prostate Cancer
12
Established Risk Factors
12
Male Hormones: An Almost-Established Risk Factor
13
Lifestyle Factors: Equivocal Evidence at Best
14
Physical activity
14
Factors related to body size
14
Sexual history
15
Vasectomy
15
Dietary factors
16
Estrogens
17
Alcohol and tobacco
18
Rick Factors for Prostate Cancer:
Putting the Evidence into Perspective
18
For More Information
20
Tables
Table 1: Ranking of Possible Risk and Protective Factors for Prostate
Cancer Based on the Strength of Scientific Evidence
10
Executive Summary
Prostate cancer is the most frequently diagnosed cancer and the
second most frequent cause of cancer death among American men.
The number of reported cases of prostate cancer has increased in
the past twenty years, but this may be largely due to increases in
detection of the disease. Whether the actual number of prostate cancer cases changed during this time period is uncertain.
Conflicting recommendations have been made about prostate
cancer screening. Some authorities recommend annual tests for men
over age 50 and for high-risk men in younger age groups. Others,
however, oppose routine screening because it has not been shown
to save lives and because it may lead to unnecessary treatment.
Men should discuss prostate cancer screening with their physicians
and make individual decisions about whether to undergo this type
of testing.
The only fully established risk factors for prostate cancer are
increasing age, African-American ethnicity, and family history of
the disease. Research has almost conclusively established a role for
male hormones (androgens) in the causation of prostate cancer, but
the effects of these hormones are not fully understood. No lifestyle
factors (including diet and exercise) have been conclusively established as prostate cancer risk or protective factors. Among the
lifestyle factors, those with the most suggestive—but far from conclusive—supporting evidence are above-average intakes of energy
(calories), total fat, meat, and red meat. All of these risk factors
have “reasonable or promising” potential to be considered risk factors, but do not yet meet the classic criteria to be considered causal
factors. Other theoretical risk factors with “speculated, conflicting,
or limited” support include above-average body mass index, alcohol intake (either abstinence or heavy drinking), specific types of
dietary fat, and dietary intakes of poultry, fish, eggs, and milk.
Potential protective factors with “speculated, conflicting, or limited” support include vitamin A, carotenoids, lycopene, vitamin D,
vitamin E, and alcohol. Purported risk or protective factors with
very “weak” scientific support include physical activity, number of
sexual partners, history of sexually transmitted diseases, human
papilloma virus (HPV) infection, vasectomy, cheese or butter
intake, intake of phytoestrogens, and tobacco smoking. Purported
5
risk factors that are not supported by the scientific evidence include
vitamin E (as a risk factor), above-average body estrogen levels,
and in utero exposure to diethylstilbestrol (DES).
Introduction
“A Slice of Pizza Cuts Prostate Cancer Risk”
HealthSCOUT, December 20, 2001
“Obesity Linked to Aggressive Prostate Cancer”
Reuters, December 15, 2001
“Multiple Sex Partners May Increase Risk of Prostate Cancer”
Jet magazine, August 6, 2001
“Flaxseed May Limit Prostate Tumors”
Los Angeles Times, July 16, 2001
“Oily Fish May Cut Prostate Cancer Risk”
MSNBC, May 31, 2001
“Milk May Raise Prostate Cancer Risk”
USA Today, April 4, 2000
If you read enough news headlines, you may get the impression that practically every aspect of a man’s diet and lifestyle influences his chances of getting prostate cancer. But headlines can mislead you. News stories about factors that affect cancer risk are usually prompted by an announcement of the results of a new scientific study. No single study, however, should be considered definitive.
To truly understand the risk factors for prostate cancer, it is necessary to critically examine the findings of all of the hundreds of
studies that have been conducted on this subject. The conclusions
of this type of evaluation turn out to be very different from what a
quick look at the headlines might lead you to expect.
This report by the American Council on Science and Health
(ACSH) reviews the scientific evidence pertaining to a variety of
factors that may influence prostate cancer risk. It rates each of
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these factors on a scale ranging from “established” to “unsupported.” The report also includes brief summaries of prostate cancer
screening, symptoms, and treatment.
Magnitude of the Problem
Prostate cancer is the most frequently diagnosed cancer among
American men. During 2001, approximately 198,000 new cases
were diagnosed, and approximately 31,500 men died of the disease.
Prostate cancer is the second most frequent cause of cancer death
among American men (lung cancer is number one). However, most
cases of prostate cancer are not fatal.
It is unclear whether prostate cancer has become more or less
common in recent years. The number of reported cases of prostate
cancer has definitely increased since the 1980s, but this may reflect
improved detection of the disease rather than a true increase in the
number of men who develop it.
Many prostate cancers grow slowly. They start relatively late in
a man’s life and may never progress to the point at which they
would cause obvious symptoms. Until the 1980s, elderly men with
slow-growing prostate cancers usually died of other diseases without ever knowing that they also had prostate cancer. Doctors use a
surgical method to treat men with noncancerous prostate problems;
during these operations, they sometimes discovered that the patient
had a previously unsuspected prostate cancer. Then, in the early
1990s, a blood test to screen for prostate cancer (the prostate-specific antigen or PSA blood test) became available. The widespread
use of this test led to further increases in the number of cancers that
were diagnosed. As a result of the use of the PSA test, the number
of reported cases of prostate cancer increased substantially.
Subsequently, the rate leveled off. However, it is uncertain whether
the actual number of cancers has changed.
Changes in prostate cancer death rates have been less dramatic
than changes in the reported number of cases. The reported number
of deaths inceased during the late 1980s and early 1990s and
declined during the late 1990s.
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Symptoms and Treatment
Early-stage prostate cancer sometimes has no symptoms at all.
In other instances, a man may notice some urinary tract symptoms,
such as having difficulty starting to urinate, needing to urinate frequently during the night, or feeling as though his bladder hasn’t
emptied completely after urination. Having these kinds of symptoms does not necessarily mean that a man has prostate cancer,
however. The same kinds of symptoms are most often produced by
a noncancerous disorder called benign prostatic hypertrophy/hyperplasia (often referred to as BPH or prostate enlargement) that is
very common among older men.
Treatment methods for prostate cancer vary, depending on the
extent to which the cancer has spread at the time of diagnosis, the
man’s age, and other factors. Most prostate cancers are limited to
the prostate gland at the time of diagnosis. A variety of treatment
options are available for these early-stage cancers, including surgical removal of the prostate gland, several types of radiation therapy, and “watchful waiting” (careful follow-up without immediate
treatment). Watchful waiting is appropriate primarily for elderly
men with slow-growing cancers, who may not live long enough to
ever need active treatment for prostate cancer.
If cancer has spread beyond the prostate gland, hormonal treatment and/or chemotherapy may be used to slow the growth of the
cancer. It is unlikely, however, that such advanced cancers can be
cured.
Screening for Prostate Cancer
Sometimes the most unlikely things can turn out to be controversial.
In 1999, the U.S. Postal Service issued a postage stamp urging
“Prostate Cancer Awareness.” You might think that everyone
involved in prostate cancer research would have welcomed this
stamp because it helped to focus public attention on the disease.
But in actuality, some scientists and health professionals were critical. Their problem: the stamp featured the words “Annual
Checkups and Tests,” even though there is no consensus that test-
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ing healthy men for prostate cancer actually has the effect of prolonging life.
Some health organizations and experts, such as the American
Cancer Society and the American Urological Association, encourage annual screening for prostate cancer, using the prostate-specific
antigen (PSA) blood test and a rectal exam, for all men age 50 and
over and for younger men in high-risk groups. These experts argue
that screening can identify latent prostate cancer cases, leading to
earlier diagnosis and treatment – and hopefully, fewer deaths.
Other equally knowledgeable authorities, however, including
the U.S. Preventive Services Task Force and the National Cancer
Institute, do not favor routine screening for prostate cancer. These
experts argue that there is no proof that screening is directly linked
to a reduction in death rates. They also point out that screening may
lead to an increase in the number of men who suffer side effects
from prostate cancer treatment. These effects may include incontinence and impotence from surgical treatment or bowel problems
due to radiation therapy.
This conflict in views is not likely to be resolved until future
research shows whether the overall impact of prostate cancer
screening is beneficial or harmful. Until new information becomes
available, it is prudent for all men to discuss prostate cancer screening with a trusted family physician and make individual decisions
about whether to undergo this type of testing.
It’s important for men to realize that the controversy over the
use of the PSA blood test applies only to the use of this test as a
screening tool for seeking latent disease among apparently well
men. The disagreement in expert recommendations does not apply
to the use of the PSA test as an aid to diagnosis in men who have
symptoms of prostate disease or to its use for follow-up of men
already diagnosed with prostate cancer.
The Concept of Risk Factors
Unlike some other diseases, such as infections, most cancers do
not have a single cause. Instead, they result from the interaction of
multiple factors that range from genetic characteristics to personal
lifestyle. Researchers who study the causes of cancer use the term
9
Table 1. Ranking of Possible Risk and Protective Factors*
for Prostate Cancer Based on the Strength of
Scientific Evidence
Risk or Protective Factor
Score
Age > 50 years
3
African-American
3
Family history of prostate cancer
3
Above-average levels of male hormones (androgens)
2+
Genetic predisposition
2
Total dietary fat
2
Total dietary energy (calories)
2
Meat
2
Red meat
2
Above-average body mass index (BMI)
2-
Dietary animal fat
2-
Saturated fat
2-
Monounsaturated fat
2-
Polyunsaturated fat
2-
Poultry and fish
2-
Eggs
2-
Milk
2-
Vitamin A (protective)
2-
Carotenoids (protective)
2-
Lycopene (protective)
2-
Vitamin D (protective)
2-
Vitamin E (protective)
2-
Alcohol (protective)
2-
Alcohol (risk)
2-
Above-average physical activity (protective)
1+
Above-average physical activity (risk)
1+
Above-average lean body mass
1+
Above-average height
1+
Above-average number of sexual partners
1+
History of sexually transmitted disease (gonorrhea or syphilis) 1+
Human Papilloma Virus (HPV) infection
10
1+
Vasectomy
1+
Cheese/butter
1+
Phytoestrogens (protective)
1+
Tobacco smoking
1+
Vitamin E (risk)
1
Above-average endogenous (natural) estrogen level
(protective)
1
In utero exposure to diethylstilbestrol (DES)
1
* All characteristics listed are risk factors unless they are explicitly identified as protective factors.
Key:
3 — Established (supported by the scientific evidence)
2+ — Nearly established, but not fully accepted or fully understood
2 — Reasonable scientific hypothesis, but lacking solid scientific support
2- — Speculated, conflicting, or limited scientific support
1+ — Weak scientific support
1 — Not supported by the scientific evidence
risk factor to refer to anything that is associated with an increased
chance of developing a particular type of cancer. Factors that are
associated with a decreased chance of developing a particular cancer are called protective factors.
Risk factors are a matter of probability. They influence an individual’s odds of developing a disease. That’s not the same thing as
actually causing the disease to occur. On the other hand, some risk
factors, such as cigarette smoking and lung cancer, are so strongly
linked that “causation” is an appropriate synonym for “risk factor.”
Some people with one or more risk factors for a particular type of
cancer never develop it, while other people who have no known
risk factors do develop the disease.
Different cancers have different risk factors. For example,
smoking is the most important risk factor (indeed, cause) for lung
cancer, but it is not a risk factor for skin cancer.* Conversely, exposure to ultraviolet light from the sun is a risk factor for skin cancer
but not for lung cancer.
Some risk factors, such as smoking or dietary habits, are modifiable. Individuals may be able to reduce their risk of becoming ill
by changing these aspects of their lifestyle. For example, having a
first child after the age of 35 is a risk factor for breast cancer, but is
*
For more information on the health effects of cigarette smoking, see the ACSH book,
“Cigarettes: What the warning label doesn’t tell you.”
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a “lifestyle factor” that is not always under control of the individual. Other risk factors, such as age, gender, ethnic background, or
family history of a disease, obviously cannot be modified.
Risk Factors for Prostate Cancer
Scientists have investigated a wide variety of factors in an
effort to determine whether they might increase or decrease the risk
of prostate cancer. The evidence pertaining to most of these factors
is not conclusive. Table 1 lists some of the factors currently under
investigation, with rankings of the strength of the scientific evidence for each. Factors with a ranking of “3” have been solidly
established as risk factors for prostate cancer. The one factor
ranked “2+” has nearly achieved the status of fully established, but
it is not completely understood. Factors ranked “2,” “2-“, or “1+”
have some degree of scientific support, but the evidence in their
favor is tentative or conflicting. Factors ranked “1” are not supported by the current scientific evidence.
Established Risk Factors
Only a few factors have been conclusively established as risk
factors for prostate cancer, and none of them are readily modifiable
aspects of a man’s lifestyle.
The most obvious risk established risk factor for prostate cancer is male gender. Since women do not have any prostate tissue in
their bodies, they cannot develop prostate cancer.
Increasing age is one of the most solidly established risk factors for prostate cancer. The risk of prostate cancer begins to
increase when a man reaches his late forties, and it continues to
increase as he grows older. More than 70% of all prostate cancers
are diagnosed in men over the age of 65.
Being an African-American man is also a clearly established
risk factor for prostate cancer. For reasons that are not completely
understood, prostate cancer rates vary greatly in different parts of
the world and among men of different ethnic backgrounds. AfricanAmerican men have one of the highest prostate cancer rates in the
world. They are 69% more likely than white American men to be
12
diagnosed with prostate cancer, and they are more than twice as
likely to die from it.
Having a family history of prostate cancer in close male relatives is also an established risk factor. This risk factor may reflect a
combination of inherited characteristics and common lifestyles
shared by family members. It is believed that approximately 9% of
all prostate cancer cases result from genetic mutations and that as
many as half of all prostate cancer cases in younger men may result
from inherited conditions. The evidence specifically linking genetic
predisposition to prostate cancer risk is not as strong as the evidence for family history, however.
Male Hormones (Androgens): An Almost-Established Risk
Factor
The prostate gland is part of the male reproductive system, and
its normal growth and function are regulated by male sex hormones
(androgens). Thus, it’s logical to suspect that androgens (testosterone and related substances) might have some effect on the risk of
prostate cancer.
Scientists have been investigating the possible role of androgens in prostate cancer since the 1970s, and the results of their
studies have been reasonably consistent. It now seems certain that
androgens do play some role in the causation of prostate cancer,
and that having higher than average levels of androgens in the body
probably increases risk. However, many questions remain about the
roles of specific androgens, the mechanisms by which the hormones might exert an effect, and the timing of the relationship. (Is
it androgen levels early in life that matter? Or in later life? Or
both?)
Differences in androgen levels may explain at least part of the
variation in prostate cancer rates among ethnic groups. For example, several studies have shown that androgen levels in AfricanAmerican men tend to be higher than those in men of other ethnic
groups. This may partially explain the high susceptibility of
African-American men to prostate cancer. Effects on androgens
might also be a mechanism by which some lifestyle factors could
influence prostate cancer risk. For example, changes in dietary
habits may lead to changes in androgen levels and thus perhaps to
changes in prostate cancer risk.
13
Although there’s nothing a man can do (at least right now)
about his androgen levels, the almost certain link between androgens and prostate cancer is of great interest to scientists because it
may enable them to develop chemoprevention methods. The term
chemoprevention refers to the use of drugs to reduce the risk of a
disease. Drugs with anti-androgenic effects may be of value in
prostate cancer chemoprevention. One such drug, finasteride, is
currently being evaluated. However, since the testing has not been
completed, no one knows whether this drug will actually help to
reduce prostate cancer risk.
Lifestyle Factors: Equivocal Evidence at Best
Many lifestyle factors have been investigated in relation to
prostate cancer, but none of these factors has been conclusively
established as a risk or protective factor. The current state of the
evidence on some of the most frequently discussed risk factors is
summarized in the next few sections.
Physical Activity. It has been proposed that physical activity
may influence androgen levels in men, indirectly affecting their
risk of prostate cancer. In several studies, scientists have looked for
associations between high physical activity levels and prostate cancer risk in an effort to see whether activity might increase or
decrease risk. One study associated high activity levels with
increased risk and another with decreased risk, while still other
studies found no evidence of any effect. Thus, there is currently little support for the concept that physical activity either increases or
decreases prostate cancer risk.
Factors Related to Body Size. It has been speculated that larger
men—those who are heavier, taller, or both—may be at increased
risk of prostate cancer. Most studies of body size have focused on
body mass index (BMI), a measure that incorporates both weight
and height. High BMI is indicative of obesity. It is often associated
with high calorie intake and low physical activity, both of which
are also being investigated as possible prostate cancer risk factors.
Some studies have found higher prostate cancer rates among men
with high BMI, but a larger number have found no such relationship. Other studies have investigated the relationship of lean body
14
mass (LBM) and/or height to prostate cancer risk; most failed to
detect any relationship, but a few indicated that taller or larger men
might be at higher risk. Overall, the evidence for a relationship
between factors related to body size and prostate cancer risk is
weak.
Sexual History. Several studies have attempted to relate various
aspects of a man’s sexual history, such as above-average number of
sex partners or history of sexually transmitted diseases, to prostate
cancer risk. Some of these studies have found that these factors predict an increased risk of prostate cancer, but the findings are questionable because of problems with study design. In many of the
studies, the data were collected by asking elderly men with and
without prostate cancer about sexual events that occurred decades
in the past. Men who have been diagnosed with a disease that can
affect their sexual functioning, such as prostate cancer, may recall
past sexual events differently than healthy men do. These differences in recall could distort the results of a study. In addition, some
studies found differences in the relationship between sexually transmitted diseases and prostate cancer risk among men in different
ethnic groups; such differences are hard to explain.
If having multiple sexual partners does turn out to be associated with increased risk of prostate cancer, the human papilloma
virus (HPV) might be responsible for the relationship. HPV, which
is a known cause of cervical cancer in women, is transmitted sexually, and people with multiple sexual partners are more likely than
those with fewer partners to be infected with this virus. However,
the evidence for a role of HPV in the causation of prostate cancer is
equivocal.
Vasectomy. A scientific study completed in the late 1980s indicated that men who had undergone vasectomies had an increased
risk of prostate cancer. Later studies, however, did not confirm this
finding. They showed only weak associations, if any, between
vasectomy and prostate cancer risk.
Men who have vasectomies may be more likely to be diagnosed with prostate cancer simply because they have to go to a
doctor in order to have the surgery. Both during the initial visit and
during the follow-up period after the operation, the physician is
likely to conduct careful urologic examinations, which might lead
15
to the detection of prostate cancer. Thus, any small increase in the
number of diagnosed prostate cancers among men who have had
vasectomies, as opposed to those who have not, may reflect an
increase in diagnosis rather than an increase in the true number of
cancers. The idea that there is an association between vasectomy
and any true increase in prostate cancer risk has only weak scientific support (1+).
Dietary Factors. Many scientific studies have evaluated the
relationship between dietary fat and/or energy (calorie) intake and
prostate cancer risk. Although the results of this body of research
are not entirely consistent, there is suggestive evidence (a score of
2) that both high fat intake and high calorie intake may be associated with increased risk.
Studies that have attempted to relate specific components or
types of fat (such as saturated vs. unsaturated fatty acids) to
prostate cancer risk have had less consistent results. There is only
limited scientific evidence supporting any specific type of fat as a
prostate cancer risk factor.
There is consistent suggestive evidence (rated 2) that aboveaverage intake of total meat or red meat may be associated with
increased risk of prostate cancer. The findings for other foods of
animal origin—such as poultry, fish, eggs, and various dairy products, are less consistent, with none ranking higher than 2-.
Despite interest-group campaigns and news reports to the contrary, the drinking of milk is not an established—or even reasonably suggestive—risk factor for prostate cancer. In fact, the evidence for a role of milk is merely speculative. The results of various studies have been about evenly divided, with about half suggesting that milk might be associated with increased risk, and the
others showing no evidence of an effect.
It has been suggested that several vitamins and related substances, including vitamins A, D, and E, the carotenoids as a group,
and the specific carotenoid lycopene (which is found in tomatoes
and their products) may protect against prostate cancer. However,
the evidence for a protective role for any of these substances is
limited. Although some studies have associated above-average
intakes of these substances with reduced risk of prostate cancer,
other studies have not found any evidence of an association.
The possible role of lycopene has attracted particular attention
16
in the mass media, perhaps because people are intrigued by the idea
that a well-liked food such as tomato sauce could help prevent cancer. There is good reason to speculate that lycopene might be protective: this carotenoid is found in higher levels in the prostate than
in most other body organs, and it has several biological actions
which might be cancer-protective. However, only some of the studies that attempted to relate men’s lycopene intakes to their risk of
prostate cancer found a relationship. Thus, the role of lycopene as a
prostate cancer protective factor is still considered merely speculative.
Estrogens. Although people tend to think of androgens as
exclusively male hormones and estrogens as exclusively female
hormones, people of both sexes actually have both types of hormones in their bodies. It has been suggested that men who have relatively high levels of natural estrogens in their bodies might be at
lower risk of prostate cancer, but scientific studies have not supported this idea. Some studies have found higher blood estrogen
levels among men with prostate cancer as compared to healthy
men, while other studies showed the opposite relationship or no
relationship.
The scientific evidence also does not support the idea that
exposure before birth to the estrogen diethylstilbestrol (DES) has
any influence on prostate cancer risk. (Several decades ago, DES
was used as a drug for the prevention of miscarriage. Girls who
were exposed to this drug because their mothers used it during
pregnancy were later found to have an increased risk of certain cancers of the female reproductive tract. The effects of DES on boys
are less clear.)
Another way in which men may be exposed to estrogens is
through consuming substances in food which have weak estrogenic
activity. These substances, called phytoestrogens, are found in soybeans and certain other plant-derived foods. Investigation of the
relationship of phytoestrogens to prostate cancer has been prompted
largely by the observation that Japanese men, who frequently eat
foods rich in phytoestrogens, have much lower prostate cancer rates
than American men, most of whom eat these foods infrequently.
Only a small number of human studies have assessed the relationship between phytoestrogens and prostate cancer, and the results of
these studies have not been impressive. The idea that phytoestro-
17
gens might protect against prostate cancer has only weak scientific
support (1+).
Alcohol and Tobacco. In the 1960s, it was suggested that heavy
consumption of alcohol might reduce the risk of prostate cancer,
perhaps by lowering male hormone (androgen) levels in the body.
More recently, it has been suggested that heavy intake of alcohol
might increase prostate cancer risk by interfering with nutrition or
by reducing the ability of the liver to detoxify cancer-causing
agents. However, there is little evidence to support either of these
ideas. Investigations of the relationship of alcohol intake to
prostate cancer risk are continuing.
Because tobacco smoking is an established risk factor for a
wide variety of cancers, researchers have considered the possibility
that it may be linked with prostate cancer as well. However, the
evidence for such an association is weak at best. Most studies have
found no important difference in prostate cancer rates between
smokers and nonsmokers or have shown only a small excess of
prostate cancers among smokers. Any small excess could easily be
attributable to increased diagnosis of latent prostate cancers among
smokers. Because smokers tend to have more health problems than
nonsmokers do, they go to the doctor more often and therefore may
be more likely to be tested for prostate cancer.
Risk Factors for Prostate Cancer: Putting the
Evidence into Perspective
In summary, the only fully established risk factors for prostate
cancer are increasing age, African-American ethnicity, and family
history of prostate cancer. Male hormones are almost fully established as a risk factor but their role is incompletely understood.
There is suggestive, but far from conclusive, support for the idea
that above-average intakes of dietary energy (calories), total fat,
meat, and red meat are associated with increased risk of prostate
cancer. The evidence for all other purported risk or protective factors is even more conflicting or limited.
Because prostate cancer is such a common disease, both scientists and the general public are eager to find ways for men to
18
reduce their risk. It is important, however, not to exaggerate the
strength of the scientific evidence. The risk factors for prostate cancer are not as well understood as those for some other types of cancer, such as lung cancer and skin cancer. Much more research will
have to be done before health authorities can issue definitive recommendations about how a man should modify his lifestyle to minimize his prostate cancer risk. For now, men must accept the frustrating situation that there are very few things that they can do
specifically for the purpose of preventing prostate cancer.
The current evidence justifies the following recommendations:
•
Men who are at increased risk because of their age, ethnic
background, or family history should talk to their physicians
and see if any screening tests for prostate cancer are warranted.
•
All men should eat a sensible diet that includes only moderate
amounts of fat and meat and should keep an eye on their calorie intake. Weight control and a prudent diet play important
roles in the prevention of heart disease, diabetes, and other serious health problems, and they may help to reduce the risk of
prostate cancer as well, although this is not absolutely certain.
Other things that a man does to stay healthy—such as exercising regularly, abstaining from the use of tobacco, and eating
plenty of vitamin-rich fruits and vegetables—are of benefit in
other forms of cancer prevention, but have not yet been confirmed as beneficial for prostate cancer.
•
Men should be extremely wary of making unusual changes in
their lifestyles in the hope of reducing their prostate cancer
risk. For example, it would not make sense for a man to take
high doses of vitamin supplements in an effort to reduce his
risk of prostate cancer. High doses of some vitamins can have
serious adverse effects, and the evidence that any vitamin protects against prostate cancer is merely speculative. Similarly, it
doesn’t make sense for a man to stop drinking milk in an effort
to prevent prostate cancer. Milk contributes important nutrients
to the diet, and the evidence that drinking milk has any effect
on prostate cancer risk is conflicting. Similarly, there is no reason for men to exclude moderate amounts of meat and other
animal products from their diets for the purpose of reducing
19
prostate cancer risk.
Extensive research on prostate cancer is currently underway at
universities and medical centers in the U.S. and throughout the
world. The results of studies that are now in progress may allow
more definitive recommendations for prostate cancer prevention to
be made in the future. At the present time, however, there is no
conclusive evidence that modification of any aspect of a man’s
lifestyle can reduce his risk of prostate cancer.
For More Information
Good sources of information about prostate cancer include:
The American Cancer Society
1-800-ACS-2345
www.cancer.org
The National Cancer Institute
1-800-4CANCER
www.nci.nih.gov
20
The arguments for and against prostate cancer screening are
presented in the following documents:
Smith RA, von Eschenbach AC, Wender R, Levin B et al.
American Cancer Society guidelines for the early detection of cancer: update of early detection guidelines for prostate, colorectal,
and endometrial cancers. CA: A Cancer Journal for Clinicians
51(1): 38-75, 2001.
Guide to Clinical Preventive Services: Report of the U.S.
Preventive Services Task Force. 1996. 2nd ed. Williams & Wilkins,
Baltimore.
21
AC SH
E XEC UT IVE
S TA F F
Elizabeth M. Whelan, Sc.D., M.P.H.
President
A CSH
BOA RD
O F
DI REC TORS
Fredric M. Steinberg, M.D.
Thomas R. DeGregori, Ph.D.
Stephen S. Sternberg, M.D.
Chairman of the Board, ACSH
Hertfordshire, England
University of Houston
Memorial Sloan-Kettering Cancer Center
Terry L. Anderson, Ph.D., M.S.
Henry I. Miller, M.D.
Mark C. Taylor, M.D.
Hoover Institution
Physicians for a Smoke-Free Canada
A. Alan Moghissi, Ph.D.
Lorraine Thelian
Political Economy Research Center
Elissa P. Benedek, M.D.
University of Michigan
Norman E. Borlaug, Ph.D.
Institute for Regulatory Science
Ketchum Public Relations
John H. Moore, Ph.D., M.B.A.
Kimberly M. Thompson, Sc.D.
Grove City College
Harvard School of Public Health
Texas A&M University
Michael B. Bracken, Ph.D., M.P.H.
Yale University School of Medicine
Albert G. Nickel
Elizabeth M. Whelan, Sc.D., M.P.H.
Lyons lavey Nickel swift, inc.
American Council on Science and Health
Kenneth M. Prager, M.D.
Robert J. White, M.D., Ph.D.
Columbia College of Physicians and
Surgeons
Case Western Reserve University
University of California
Taiwo K. Danmola, C.P.A.
Fredrick J. Stare, Ph.D., M.D.
Christine M. Bruhn, Ph.D.
Arthur Andersen llp
Harvard School of Public Health
A CS H
Ernest L. Abel, Ph.D.
BO ARD
OF
S CIE NTI FIC
AN D
P OLI CY
ADVISORS
C.S. Mott Center
Edward E. Burns, Ph.D.
Texas A&M University
Charles R. Curtis, Ph.D.
Alwynelle S. Ahl, Ph.D., D.V.M.
Francis F. Busta, Ph.D.
Ilene R. Danse, M.D.
University of California, Los
Angeles
Julie A. Albrecht, Ph.D.
Elwood F. Caldwell, Ph.D.,
M.B.A.
Ernst M. Davis, Ph.D.
Stephen K. Epstein, M.D.,
M.P.P., FACEP
Tuskegee University, AL
University of Nebraska, Lincoln
James E. Alcock, Ph.D.
Glendon College, York University
Thomas S. Allems, M.D.,
M.P.H.
San Francisco, CA
Richard G. Allison, Ph.D.
American Society for Nutritional
Sciences (FASEB)
John B. Allred, Ph.D.
Ohio State University
Philip R. Alper, M.D.
University of California, San
Francisco
Karl E. Anderson, M.D.
University of Texas, Medical
Branch
Dennis T. Avery
Hudson Institute
Robert S. Baratz, D.D.S.,
Ph.D., M.D.
International Medical
Consultation Services
University of Minnesota
Ohio State University
Novato, CA
University of Texas, Houston
Zerle L. Carpenter, Ph.D.
Harry G. Day, Sc.D.
Indiana University
Beth Israel Deaconess Medical
Center
Texas A&M University System
Robert M. Devlin, Ph.D.
Harvard School of Public Health
Champaign
University of Oxford
National Eye Institute
Dale J. Chodos, M.D.
John Doull, M.D., Ph.D.
David N. Ferro, Ph.D.
University of Minnesota
University of Massachusetts
Kalamazoo, MI
University of Kansas
University of Massachusetts
Martha A. Churchill, Esq.
Theron W. Downes, Ph.D.
Madelon L. Finkel, Ph.D.
Nigel M. Bark, M.D.
Milan, MI
Allentown, PA
Manhattan Eye, Ear & Throat
Hospital
University of Washington
Thomas G. Baumgartner,
Pharm.D., M.Ed.
Dean O. Cliver, Ph.D.
U.S. Army Institute of Surgical
Research
University of Florida
Barry L. Beyerstein, Ph.D.
Simon Fraser University
Blaine L. Blad, Ph.D.
University of Nebraska, Lincoln
Hinrich L. Bohn, Ph.D.
Emil William Chynn, M.D.
University of California, Davis
F. M. Clydesdale, Ph.D.
University of Massachusetts
Donald G. Cochran, Ph.D.
Virginia Polytechnic Institute and
State University
W. Ronnie Coffman, Ph.D.
University of Arizona
Cornell University
Ben Bolch, Ph.D.
Bernard L. Cohen, D.Sc.
Rhodes College
University of Pittsburgh
Joseph F. Borzelleca, Ph.D.
John J. Cohrssen, Esq.
Medical College of Virginia
Michael K. Botts, Esq.
Ames, IA
George A. Bray, M.D.
Pennington Biomedical Research
Center
Ronald W. Brecher, Ph.D.,
C.Chem., DABT
GlobalTox International
Consultants, Inc.
Robert L. Brent, M.D., Ph.D.
Alfred I. duPont Hospital for Children
Allan Brett, M.D.
University of South Carolina
Gale A. Buchanan, Ph.D.
Public Health Policy Advisory
Board
Michigan State University
Adam Drewnowski, Ph.D.
Michael A. Dubick, Ph.D.
Fort Valley State University
James R. Dunn, Ph.D.
Averill Park, NY
Robert L. DuPont, M.D.
Institute for Behavior and
Health, Inc.
Henry A. Dymsza, Ph.D.
Cornell University
Buffalo
Michael D. Corbett, Ph.D.
J. Gordon Edwards, Ph.D.
Omaha, NE
Morton Corn, Ph.D.
John Hopkins University
Nancy Cotugna, Dr.Ph.,
R.D., C.D.N.
University of Delaware
San José State University
George M. Burditt, J.D.
H. Russell Cross, Ph.D.
Future Beef Operations, L.L.C.
University of California, San
Diego
Charles O. Gallina, Ph.D.
Professional Nuclear Associates
Raymond Gambino, M.D.
Quest Diagnostics Incorporated
Rapid City Regional Hospital
University of Miami School of
Medicine
University of Florida
Frederick K. Goodwin, M.D.
The George Washington
University Medical Center
Timothy N. Gorski, M.D.,
F.A.C.O.G.
Arlington, TX
Ronald E. Gots, M.D., Ph.D.
International Center for
Toxicology and Medicine
Michael Gough, Ph.D.
Bethedsa, MD
Henry G. Grabowski, Ph.D.
Duke University
James Ian Gray, Ph.D.
Michigan State University
Ralph W. Fogleman, D.V.M. William W. Greaves, M.D.,
M.S.P.H.
Medical College of Wisconsin
Christopher H. Foreman,
Jr., Ph.D.
Kenneth Green, D.Env.
Upper Black Eddy, PA
University of Maryland
Reason Public Policy Institute
E. M. Foster, Ph.D.
Laura C. Green, Ph.D.,
D.A.B.T.
University of Wisconsin, Madison
F. J. Francis, Ph.D.
Cambridge Environmental, Inc.
Glenn W. Froning, Ph.D.
Zol Consultants
University of Massachusetts
University of Nebraska, Lincoln
Vincent A. Fulginiti, M.D.
University of Colorado
George E. Ehrlich, M.D.,
Arthur Furst, Ph.D., Sc.D.
F.A.C.P., M.A.C.R., FRCP (Edin) University of San Francisco
Philadelphia, PA
Robert S. Gable, Ed.D.,
Michael P. Elston, M.D., M.S. Ph.D., J.D.
Roger A. Coulombe, Jr., Ph.D. William N. Elwood, Ph.D.
Utah State University
Cornell University Medical
College
Jack C. Fisher, M.D.
Kenneth D. Fisher, Ph.D.
Greg Dubord, M.D., M.P.H. Washington, DC
Leonard T. Flynn, Ph.D., M.B.A.
RAM Institute
Edward R. Duffie, Jr., M.D. Morganville, NJ
William H. Foege, M.D.,
Savannah, GA
M.P.H.
David F. Duncan, Dr.Ph.
Emory University
Neville Colman, M.D., Ph.D. University of Rhode Island
St. Luke’s Roosevelt Hospital
Michael W. Easley, D.D.S.,
Center
M.P.H.
Gerald F. Combs, Jr., Ph.D. State University of New York,
University of Georgia
Bell, Boyd & Lloyd LLC
William G. Gaines, Jr.,
M.D., M.P.H.
Scott & White Clinic
Randy R. Gaugler, Ph.D.
Myron E. Essex, D.V.M., Ph.D. Rutgers University
LaNelle E. Geddes, Ph.D., R.N.
Terry D. Etherton, Ph.D.
Columbia, MD
Purdue University
Seymour Diamond, M.D.
Pennsylvania State University
Diamond Headache Clinic
Robert G. Cassens, Ph.D.
J. Bernard L. Gee, M.D.
University of Wisconsin, Madison Donald C. Dickson, M.S.E.E. William Evans, Ph.D.
Yale University School of Medicine
Georgia State University
Gilbert, AZ
Ercole L. Cavalieri, D.Sc.
K. H. Ginzel, M.D.
Daniel F. Farkas, Ph.D.,
University of Nebraska Medical
University of Arkansas for
John Diebold
M.S., P.E.
Center
Medical Sciences
The Diebold Institute for Public
Oregon State University
Policy
Studies
Russell N. A. Cecil, M.D., Ph.D.
William Paul Glezen, M.D.
Richard S. Fawcett, Ph.D.
Albany Medical College
Baylor College of Medicine
Ralph Dittman, M.D., M.P.H. Huxley,
IA
Houston, TX
James J. Cerda, M.D.
Jay A. Gold, M.D., J.D.,
John B. Fenger, M.D.
University of Florida
M.P.H.
John E. Dodes, D.D.S.
Phoenix, AZ
Medical College of Wisconsin
National Council Against Health
Morris E. Chafetz, M.D.
Fraud
Owen R. Fennema, Ph.D.
Health Education Foundation
Roger E. Gold, Ph.D.
University
of
Wisconsin,
Madison
Texas
A&M University
Sir Richard Doll, M.D.,
Bruce M. Chassy, Ph.D.
Frederick L. Ferris, III, M.D. Reneé M. Goodrich, Ph.D.
University of Illinois, UrbanaD.Sc., D.M.
C. Jelleff Carr, Ph.D.
Stephen Barrett, M.D.
Albert Einstein College of Medicine
James E. Enstrom, Ph.D.,
M.P.H.
Claremont Graduate University
Shayne C. Gad, Ph.D.,
D.A.B.T., A.T.S.
Gad Consulting Services
Saul Green, Ph.D.
Richard A. Greenberg, Ph.D.
Hinsdale, IL
Sander Greenland, Dr.P.H.,
M.A.
UCLA School of Public Health
Gordon W. Gribble, Ph.D.
Dartmouth College
William Grierson, Ph.D.
University of Florida
Lester Grinspoon, M.D.
Harvard Medical School
AC SH
F. Peter Guengerich, Ph.D.
Vanderbilt University School of
Medicine
B OAR D
David M. Klurfeld, Ph.D.
O F
SCI ENT IFI C
AND
POL ICY
John J. McKetta, Ph.D.
ADVISORS
John J. Powers, Ph.D.
Wayne State University
University of Texas at Austin
Donald J. McNamara, Ph.D. William D. Powrie, Ph.D.
Egg Nutrition Center
Hillsborough, CA
Kathryn M. Kolasa, Ph.D.,
R.D.
East Carolina University
Philip S. Guzelian, M.D.
Alan R. Kristal, Dr.P.H.
University of Virginia
U.S. Trust Co.
Thomas H. Milby, M.D.,
M.P.H.
Cornell University
Caryl J. Guth, M.D.
University of Colorado
Alfred E. Harper, Ph.D.
Fred Hutchinson Cancer
Research Center
Patrick J. Michaels, Ph.D.
University of Georgia
University of British Columbia
University of Nebraska, Lincoln
Marvin P. Pritts, Ph.D.
Barry University
Walnut Creek, CA
University of Illinois at UrbanaChampaign
Mitzi R. Krockover, M.D.
Joseph M. Miller, M.D.,
M.P.H.
Robert D. Havener, M.P.A.
Manfred Kroger, Ph.D.
Pennsylvania State University
University of Georgia
William J. Miller, Ph.D.
Virgil W. Hays, Ph.D.
University of Kentucky
Laurence J. Kulp, Ph.D.
University of Washington
Dade W. Moeller, Ph.D.
Cheryl G. Healton, Dr.PH.
Leonard T. Kurland, M.D.,
Dr.P.H.
Grace P. Monaco, J.D.
William O. Robertson, M.D.
Brian E. Mondell, M.D.
University of Washington School
of Medicine
Sandford F. Kuvin, M.D.
Baltimore Headache Institute
Carolyn J. Lackey, Ph.D.,
R.D.
Yale University School of Medicine
Clare M. Hasler, Ph.D.
Sacramento, CA
Columbia University, School of
Public Health
Clark W. Heath, Jr., M.D.
American Cancer Society
Dwight B. Heath, Ph.D.
Brown University
Robert Heimer, Ph.D.
Yale School of Public Health
The Wistar Institute
Humana, Inc.
Mayo Clinic
University of Miami
North Carolina State University
J. Clayburn LaForce, Ph.D.
Rutgers University, Cook College
University of California, Los
Angeles
Donald A. Henderson,
M.D., M.P.H.
James C. Lamb, IV, Ph.D.,
J.D.
Zane R. Helsel, Ph.D.
Johns Hopkins University
Blasland, Bouck & Lee
James D. Herbert, Ph.D.
Lawrence E. Lamb, M.D.
MCP Hahnemann University
San Antonio, TX
Victor Herbert, M.D., J.D.,
M.A.C.P.
Lyda Associates, Inc.
Lillian Langseth, Dr.P.H.
Bronx Veterans Affairs Medical
Center
University of Arizona
Gene M. Heyman, Ph.D.
Larry Laudan, Ph.D.
McLean Hospital/Harvard
Medical School
Richard M. Hoar, Ph.D.
Williamstown, MA
Robert M. Hollingworth,
Ph.D.
Michigan State University
Edward S. Horton, M.D.
Joslin Diabetes Center
Brian A. Larkins, Ph.D.
National Autonomous University
of Mexico
Tom B. Leamon, Ph.D.
Liberty Mutual Insurance Company
Jay H. Lehr, Ph.D.
Environmental Education
Enterprises, Inc.
Brian C. Lentle, M.D.,
FRCPC, DMRD
Joseph H. Hotchkiss, Ph.D.
University of British Columbia
Steve E. Hrudey, Ph.D.
University of Texas, Austin
Susanne L. Huttner, Ph.D.
UMDNJ-Robert Wood Johnson
Medical School
Cornell University
University of Alberta
University of California, Berkeley
Robert H. Imrie, D.V.M.
Seattle, WA
Lucien R. Jacobs, M.D.
University of New Hampshire
Harvard University
Medical Care Management Corp.
Daniel J. Raiten, Ph.D.
National Institute of Health
David W. Ramey, D.V.M.
Ramey Equine Group
University of Texas, San Antonio
J. D. Robinson, M.D.
Eric W. Mood, LL.D., M.P.H. Georgetown University School of
Medicine
University of Utah
Michigan State University
Kevin B. Murphy
Kenneth J. Rothman, Dr.P.H. University of Nebraska, Lincoln
Dimitrios Trichopoulos, M.D.
Harvard School of Public Health
Stanley Rothman, Ph.D.
Smith College
Murray M. Tuckerman, Ph.D.
Edward C. A. Runge, Ph.D. Winchendon, MA
Texas A&M University
Robert P. Upchurch, Ph.D.
University of Arizona
Stephen H. Safe, D.Phil.
Texas A&M University
Mark J. Utell, M.D.
University of Rochester Medical
Wallace I. Sampson, M.D.
Cantox Health Sciences International
Merrill Lynch, Pierce, Fenner &
Smith
Harris M. Nagler, M.D.
Beth Israel Medical Center
Daniel J. Ncayiyana, M.D.
University of Cape Town
Philip E. Nelson, Ph.D.
Purdue University
Northwestern University Medical
School
Malden C. Nesheim, Ph.D.
Stanford University School of
Medicine
Joyce A. Nettleton, D.Sc.,
R.D.
Harold H. Sandstead, M.D.
Elmhurst, IL
University of Texas Medical
Branch
John S. Neuberger, Dr.P.H.
Herbert P. Sarett, Ph.D.
Cornell University
Lawrence J. Schneiderman,
M.D.
Yale University School of
Medicine
James L. Oblinger, Ph.D.
North Carolina State University
Lowell D. Satterlee, Ph.D.
Marvin J. Schissel, D.D.S.
University of California, San
Diego
Edgar J. Schoen, M.D.
John Patrick O’Grady, M.D. Kaiser Permanente Medical
Tufts University School of Medicine Center
Oregon State University
James E. Oldfield, Ph.D.
David Schottenfeld, M.D.,
M.Sc.
George D. Lundberg, M.D.
William T. Jarvis, Ph.D.
Medscape
Stanley T. Omaye, Ph.D.,
F.-A.T.S., F.ACN, C.N.S.
Joel M. Schwartz, M.S.
University of Nevada, Reno
Daland R. Juberg, Ph.D.
Howard D. Maccabee,
Ph.D., M.D.
ican, Inc.
Michael Kamrin, Ph.D.
Janet E. Macheledt, M.D.,
M.S., M.P.H.
International Center for
Toxicology and Medicine
Radiation Oncology Center
Osterholm, Michael T.,
Ph.D., M.P.H.
M. Alice Ottoboni, Ph.D.
Michigan State University
Houston, TX
Sparks, NV
John B. Kaneene,Ph.D.,
M.P.H., D.V.M.
Roger P. Maickel, Ph.D.
Michael W. Pariza, Ph.D.
Purdue University
University of Wisconsin, Madison
Michigan State University
Henry G. Manne, J.S.D.
Stuart Patton, Ph.D.
University of Michigan
University of Nebraska, Lincoln
Michael B. Shermer, Ph.D.
Skeptic Magazine
Sidney Shindell, M.D., LL.B.
Kathryn E. Kelly, Dr.P.H.
Earl G. Siegel, Pharm.D.
Judith A. Marlett, Ph.D., R.D. Mary Frances Picciano, Ph.D. University of Cincinnati Medical
George R. Kerr, M.D.
University of Texas, Houston
James R. Marshall, Ph.D.
Arizona Cancer Center
George A. Keyworth II, Ph.D. Margaret N. Maxey, Ph.D.
Progress and Freedom Foundation
University of Texas at Austin
Michael Kirsch, M.D.
Mary H. McGrath, M.D.,
M.P.H.
Highland Heights, OH
John C. Kirschman, Ph.D.
Loyola University Medical Center
Ronald E. Kleinman, M.D.
University of Saskatchewan
Emmaus, PA
Massachusetts General Hospital
University of Illinois, UrbanaChampaign
Thomas T. Poleman, Ph.D.
Cornell University
Charles Polk, Ph.D.
University of Rhode Island
Alan G. McHughen, D.Phil.
Charles Poole, M.P.H., Sc.D
James D. McKean, D.V.M.,
J.D.
Gary P. Posner, M.D.
Iowa State University
University of North Carolina
School of Public Health
Tampa, FL
Steven D. Wexner, M.D.
Cleveland Clinic Florida
Joel Elliot White, M.D.,
F.A.C.R.
John Muir Comprehensive
Cancer Center
Carol Whitlock, Ph.D., R.D.
Burke, VA
Mark L. Willenbring, M.D.
Veterans Affairs Medical Center
Lloyd D. Witter, Ph.D.
Timothy Dukes Phillips, Ph.D.
David R. Pike, Ph.D.
University of California at SanFrancisco
Sarah Short, Ph.D., Ed.D.,
R.D.
Karl Maramorosch, Ph.D.
University of Wisconsin, Madison
Janet S. Weiss, M.D.
Carl K. Winter, Ph.D.
John G. Keller, Ph.D.
Delta Toxicology
Miles Weinberger, M.D.
Medical College of Wisconsin
University of Illinois, UrbanaChampaign
Texas A&M University
George Washington University
University of Iowa Hospitals and
Clinics
Christopher F. Wilkinson,
Ph.D.
University of California, San
Diego
Pennsylvania State University
Donald M. Watkin, M.D.,
M.P.H., F.A.C.P.
Rochester Institute of Technology
George Mason University Law
School
Rutgers University, Cook College
Willard J. Visek, M.D., Ph.D.
University of Illinois College of
Medicine
Reason Public Policy Institute
Pennsylvania State University
Olney, MD
Center
Shashi B. Verma, Ph.D.
University of Nebraska, Lincoln
Patrick J. Shea, Ph.D.
Syracuse University
Philip G. Keeney, Ph.D.
Sita R. Tatini, Ph.D.
University of Minnesota
Steve L. Taylor, Ph.D.
Editor, Epidemiology
Environmental Medicine, Inc.
Loma Linda University
Gaithersburg, MD
Topeka, KS
Steven T. Rosen, M.D.
Steven P. Novella, M.D.
Oregon State University
Michael M. Sveda, Ph.D.
Glenn Swogger, Jr., M.D.
Health Education Enterprises, Inc.
Woodhaven, NY
Daryl Lund, Ph.D.
Potomac, MD
Colorado State University
Ian C. Munro, F.A.T.S.,
Ph.D., FRCPath
University of Wisconsin
University of Toronto, Canada
Rudolph J. Jaeger, Ph.D.
C. Joseph Stetler, Esq.
David B. Roll, Ph.D.
Stephen J. Moss, D.D.S., M.S. Dale R. Romsos, Ph.D.
Palo Alto, CA
William M. Lunch, Ph.D.
University of California, Davis
California Cancer Registry
University of Western Ontario
Paul J. Lioy, Ph.D.
Alejandro R. Jadad, M.D.,
D.Phil., F.R.C.P.C.
Pennsylvania State University
Judith S. Stern, Sc.D., R.D.
W. K. C. Morgan, M.D.
Sarasota, FL
Miami, FL
University of Texas, Houston
Robert D. Steele, Ph.D.
Dartmouth Medical School
Oklahoma State University
Frank C. Lu, M.D., BCFE
Ronald T. Stanko, M.D.
University of Pittsburgh Medical
Center
Bill D. Roebuck, Ph.D., D.A.B.T. Martha Barnes Stone, Ph.D.
Gordon W. Newell, Ph.D.,
M.S.,F.-A.T.S.
University of California, Los
Angeles
Robert A. Squire, D.V.M.,
Ph.D.
Baltimore, MD
John W. Morgan, Dr.P.H.
University of Kansas School of
Medicine
William M. London, Ed.D.,
M.P.H.
Leonard T. Sperry, M.D., Ph.D.
R.T. Ravenholt, M.D., M.P.H. James H. Steele, D.V.M.,
Population Health Imperatives
M.P.H.
Russel J. Reiter, Ph.D.
Floy Lilley, J.D.
Fort Lee, NJ
Rutgers State University of New
Jersey
Roy F. Spalding, Ph.D.
Kary D. Presten
David Kritchevsky, Ph.D.
University of Wisconsin, Madison
Myron Solberg, Ph.D.
A. J. Siedler, Ph.D.
Center
University of California, Davis
University of Illinois, UrbanaChampaign
James J. Worman, Ph.D.
Rochester Institute of Technology
Russell S. Worrall, O.D.
University of California, Berkeley
Lee M. Silver, Ph.D.
Panayiotis M. Zavos, Ph.D.,
Ed.S.
Michael S. Simon, M.D.,
M.P.H.
Steven H. Zeisel, M.D., Ph.D.
S. Fred Singer, Ph.D.
University of Iowa
Princeton University
Wayne State University
Science & Environmental Policy
Project
Robert B. Sklaroff, M.D.
Elkins Park, PA
Gary C. Smith, Ph.D.
Colorado State University
The opinions expressed in ACSH publications do not necessarily represent the views of all ACSH Directors and Advisors.
ACSH Directors and Advisors serve without compensation.
University of Kentucky
The University of North Carolina
Ekhard E. Ziegler, M.D.