THE CANCER PROJECT NUTRITION AND PROSTATE
HEALTH
BY NEAL D. BARNARD, M.D./PCRM
The
prostate is an organ that sits snuggled up under
the bladder. In spite of decades of research, we
still have no idea what it is doing there. We do
know that prostate secretions end up in semen. But
sperm are perfectly capable of fertilizing an egg
without the prostate’s contributions. When the prostate
is removed, men live without it quite happily. The
only health problems are caused by the surgery itself.1
One might wonder if the main purpose of the prostate
is to aggravate older men. As time goes on, many
men
have an enlargement of their prostates, causing annoying
an sometimes painful urinary problems. The prostate
is also the number one cancer spot in a man’s body.
These problems are not inevitable. They depend in
part on what men eat. Like so many other parts of
our biology, the mixture of nutrients we choose every
day can encourage prostate cells to grow into an
aggravating mass or can help them stay put.
The
bladder empties into a tube called the urethra, which
passes through the prostate gland, where it is joined
by another tube carrying sperm from the testes. Starting
at
about age 30, the prostate cells alongside the urethra
start to multiply. If this continues, they can pinch
off the urethra, causing a poor urinary stream, dribbling,
pressure, and, ultimately, infection and kidney damage.
Irritation of the urethra causes the urge to urinate and
repeated nighttime trips to the bathroom. It does not take
much prostate growth before the urinary symptoms begin.
The technical term for an enlarged prostate is “benign
prostatic hyperplasia.” It is not cancer because these
cells will not invade neighboring tissues or spread to
other organs.
By age 80,
some cell multiplication has occurred in most men.
Only about half of them actually have significant
enlargement of the gland, and only a quarter have any urinary
symptoms. In many men, the prostate actually shrinks as
they get older.2 Mild prostate symptoms sometimes improve
with no treatment at all. In one research study, men with
mild prostate enlargement were followed for five years,
by which time a quarter of them had improved without
treatment. About half stayed the same, and another quarter
had gotten worse.3 However, men with difficulty urinating
should not defer medical treatment because they can end
up with serious kidney problems, not to mention continued
discomfort. Doctors sometimes prescribe drugs to
relax the pressure in the prostate or to block the
hormones that lead to enlargement. Finasteride (Proscar)
is in the latter category. It shrinks the prostate
and is well tolerated.
In
more severe cases, urologists remove a bit of prostate
tissue, which, with modern techniques, can be done through
the penis. The operation is called a TURP, or transurethral
resection of the prostate, and is very commonly done.4
In some cases, a
simpler procedure works, making only small incisions
in the prostate (transurethral incision of the prostate,
or TUIP). A researcher named Burhenne developed a balloon
device for dilating the prostate (transurethral balloon
dilation of the prostate, TUDP) and actually tried it on
himself. Similarly, other researchers are trying out a
transurethral laser-induced prostatectomy (TULIP). Balloon
and laser procedures are
still experimental.5
Although
male readers have undoubtedly crossed their legs
by this point in the discussion, a TURP is actually
a fairly easy procedure, particularly compared to
treatments used in times past. The main downside
of the TURP is that, by eight years after the operation,
up to 16 percent have to be repeated.6
Your Prostate
Would Rather Be A Vegetarian
Changing
your eating habits can help prevent prostate problems.
The reason is not hard to imagine. The prostate is
under hormonal control. In the prostate cells,
testosterone is turned into a powerful hormone called
DHT (dihydrotestosterone), and DHT is what drives prostate
enlargement. This is the conversion that finasteride blocks.
Foods can strongly influence sex hormones, including
testosterone. Could it be that cutting out
meats and dairy products and
adding more vegetables to our plates could
turn down the hormonal stimulation of the prostate
and prevent prostate problems? That is, in fact, exactly
what researchers have found. Daily meat consumption
triples the risk of prostate enlargement. Regular milk
consumption doubles the risk and failing to consume vegetables
regularly nearly quadruples the risk.7 Prostate hyperplasia
is reportedly increasing in Asian countries, paralleling
the westernization of the diet that has occurred in recent
decades.8
The meat-based diet that has become routine in Western
countries and is now spreading to other parts of the world
encourages many hormone-related conditions, and prostate
enlargement is no exception. Even if you grew up as a meateater,
your prostate would rather be a vegetarian. By the way,
the enzyme that turns testosterone into DHT (5-alphareductase)
is also found in the scalp,9 where it works
mischief of a different sort. DHT plays a critical
role in baldness. Without it, men will not lose their
hair, no matter what their genetics may dictate. DHT activity
in the scalp may be subject to dietary manipulation.
Nutritional treatments for prostate enlargement are being
explored by an increasing number of practitioners. The
first step is a low-fat, vegetarian diet. Physician and
medical author David Perlmutter, M.D., has reported success
in reducing prostate symptoms using the following regimen
(all listed supplements can be found at health food stores)
in addition to a vigorous program of dietary changes. Note,
these are for prostate enlargement, not cancer:
- 1.
Saw palmetto (Serenoa repens), a natural plant
extract, taken in a dose of 160 milligrams twice
a day.
- 2. Cold-pressed
flaxseed oil, two tablespoons per day. If this
causes loosening of the stool, the problem usually
abates after a week or so.
- 3. Vitamin
E, 400 IU per day with food. Reduce to 100 IU per day
if you have high blood pressure.
- 4. Vitamin
B6 , 100 milligrams per day.
- 5. Avoid
caffeine and keep alcohol consumption to
a minimum.
Saw
palmetto is extracted from a type of palm tree
and has been shown to prevent the conversion
of testosterone to
DHT and to reduce prostate symptoms in clinical
tests.10
The flax oil provides essential fatty
acids and vitamin E
is used to protect the flax oil against oxidation.
Prostate Cancer
Prostate
cancer differs from prostate enlargement in that
cancer cells can invade neighboring tissues and spread
to other parts of the body. If cancer cells would
simply stay put, the disease would be little more
than an inconvenience.
Researchers have examined the prostates of men who have
died from accidents or other causes and have found something
you might not have expected. Among
30- to
40-year-old American men, 30 percent have cancer
cells in their prostates.11 By age 50, this figure
rises to about 40 percent.12 This is a shockingly high
percentage. But in most cases, these are latent cancer
cells. While they are clearly abnormal, they are not yet
at the stage where they rapidlymultiply and spread. In
many cases, they never will be. Again,foods can make the
difference.
A
comparison of different countries is revealing. In
Asia and Latin America, latent cancers are much rarer
than they are in the United States or Western Europe.
Moreover, the risk of these cells growing into invasive
or spreading tumors varies in precisely the same
way. A man in Hong Kong has a 16 percent likelihood
of having latent cancer cells in his prostate after
age 45, while a Swede’s risk is double that figure,
at 32 percent. And compared to a man in Hong Kong,
the Swede is eight times more likely to die of the
disease.13
Cancers are like weeds whose seeds blow from place
to place. On moist, fertile soil, they take root
and grow uncontrollably. But if the soil is not watered
or fertilized, they
lie dormant or even wither away. The Swedish diet
makes the male body fertile soil for cancer. Asian
diets do not provide such welcoming ground for cancer growth.
No country has a perfect diet, but the trend is clear.
Countries with fatty, meaty
diets have much higher cancer rates than countries
that use rice, other grains, beans, or vegetables
as their staples.
Testosterone
and related hormones stimulate prostate cancer cells
like fertilizer on weeds. The high-fat, meat-based
diet boosts testosterone’s effects and has been linked
in many studies to high rates of prostate cancer.14
Vegetarians and populations whose culinary traditions
are based on rice, soy products, or vegetables not
only
have
lower cancer rates; they also have a far lower
risk of progression should cancer cells gain a
foothold.15 The possibility that survival for cancer patients
may be improved to the extent that they adopt a plant-based
diet is bolstered further by the findings that vegetables
and fruits strengthen the immune cells that seek out and
destroy cancer cells and inhibit their spread.
More
research is needed to know just how extensive the
effects of dietary change might be, but one
high-profile case suggests the potential. Anthony J. Sattilaro,
M.D., was president of Methodist Hospital in Philadelphia
and became perhaps the most famous advocate of
the use of diet against cancer. In his best-selling
book Recalled by Life,16 he raised the question as
to whether diet can turn the tide on cancer, and
the fact that there was simply not enough information
yet available to speak with assurance.
Dr. Sattilaro was a young man when he was found
to have prostate cancer. By the time it was diagnosed,
it had spread throughout his body. Surgical removal
was impossible;
there was nothing for him to do but to get his
affairs in order. By chance, he happened to meet
some young people who were advocates of macrobiotics, which
is essentially a
traditional Asian diet including generous amounts
of rice and vegetables. There is a wealth of literature
drawn from Asian traditional medicine on using
diet in dealing with
cancer and many other health problems. Although
Dr. Sattilaro was skeptical and initially taken
aback
by the idea of such a radical change in his diet,
he felt he had nothing to lose. He
began a macrobiotic program with the same rigidity that
he had applied to his medical career. And as his book described,
his symptoms began to fade. Before long, all trace of the
cancer, including that on his X-rays, disappeared. There
were no double-blind studies, no control patients, or anything
else that would suggest that what happened to Dr. Sattilaro
will happen for anyone else, although there is a
large cadre of people who report similar results.
I
became interested in Dr. Sattilaro’s story, so I
went in search of him. He had resigned his job as
head
of Methodist Hospital and had moved to Florida.
I met him in 1986. He was not only alive ten years after
his anticipated death, but youthful and vigorous.
He had adhered to the macrobiotic diet and adopted
a specific exercise program. He went swimming every
day. His cancer seemed to be gone, and he kept X-ray
films
in a file for when he needed to remind himself of
his remission. Dr. Sattilaro had been deluged with
letters from other cancer patients, but always answered
that he did not know if what had happened to him
could also happen for them. He was not even sure
that his dietary program should get the credit.
Eventually, he began to deviate from the diet,
adding fish and chicken, as if to test whether
he was cured or simply in remission. If it was a test,
he failed. In July 1989, I called Dr. Sattilaro and found
him to be gravely ill. His cancer had recurred—“viciously,”
he said. He was in good spirits, but harbored no illusions
about the grim situation he was in. He knew that the end
was very near. He had resumed the use of painkillers, which
at times made him quite groggy. Can
the regimen he followed be given credit for his decade-long
reprieve from cancer? Did his deviation from the diet compromise
his defenses against cancer? These are questions that,
while intriguing, are not answerable.
For
the patient contemplating surgery, doctors are often
less aggressive than for other cancers. This is
partly because prostate surgery can cause a lot
of problems, at least in the short term. Incontinence
can last for weeks and is permanent in a small percentage
of cases.17 Damage to nerves and arteries during
surgery often causes impotence, although in some
cases the nerves and arteries can be spared.18 Doctors
realize that prostate cancer often advances very
slowly. Most patients live many years whether they
have surgery or not, and some researchers believe that
surgery does not always change the long-term odds very
much.19 It is essential to tailor your treatment to your
specific condition, taking advantage of a second
opinion if necessary.
Doctors may recommend observation alone, particularly
for older men whose tumors are small and less aggressive,
as determined by biopsy results.20 If surgery is
deferred, the physician can periodically monitor levels
of PSA, prostate-specific antigen, which indicates changes
in the tumor.
Prostate-Specific
Antigen (PSA)
PSA, a protein made within the prostate and secreted
into semen, shows what the prostate is doing.
If the gland is disrupted for any reason—surgery,
biopsy,
trauma, or
cancer—PSA leaks into the bloodstream and easily
shows up on a simple blood test. A low level
of PSA is present in the blood of any man with a functioning
prostate; higher levels alert physicians that a change
of some type has occurred in the prostate.
PSA levels vary greatly from one person to the
next. For cancer patients, doctors are less
interested in the exact PSA level than in changes over
time. If
the prostate is surgically removed and there has been
no spread
of the tumor elsewhere in the body, the PSA will become
undetectable within three weeks after the operation.
Radiation treatments cause a slower drop.21 A PSA increase
may be
a sign that further
treatment is needed. Increased PSA levels do not necessarily
mean cancer. They can also be caused by benign prostate
enlargement, infection, or surgical manipulation.
If your diet is right, you may never know you even
have a prostate except when your doctor asks
to check it. The very same low-fat, vegetarian diet
that is
so good for you in many other ways is by far the best
diet for preventing prostate problems.
References
1. Isaacs
JT. Etiology of benign prostatic hyperplasia. Eur Urology
1994;25(suppl 1):6-9.
2. Ibid.
3. Ball AJ, Feneley RC, Abrams PH. The natural
history of untreated “prostatism.” Brit J Urology
1981;53:613-6.
4. Jonler M, Riehmann M, Bruskewitz RC. Benign
prostatic hyperplasia: current pharmacological
treatment. Drugs 1994;47:66-81.
5. Wasserman NF, Reddy PK. Therapeutic alternatives
to surgery for benign prostatic hyperplasia.
Invest Radiology 1994;29:224-37.
6. Ibid.; Hald T. Review of current treatment
of benign prostatic hyperplasia. Eur Urology
1994;25(suppl 1):15-9.
7. Araki H, Watanabe H, Mishina T, Nakao M. High-risk
group for benign prostatic hypertrophy. Prostate
1983;4:253-64.
8. Ibid.
9. Jonler M, Riehmann M, Bruskewitz RC. Benign
prostatic hyperplasia: current pharmacological
treatment. Drugs 1994;47:66-81.
10. Walker, M. Feb.-Mar. 1991. Serenoa repens
extract (Saw palmetto) relief for benign prostatic
hypertrophy (BPH). Townsend Letter for Doctors: 1991;2-3:107-10;
Perlmutter D. LifeGuide. Naples, FL, LifeGuide Press, 1994.
11. Sakr WA, Haas GP, Cassin BF, Pontes JE, Crissman
JD. The frequency of carcinoma and intracpithelial
neoplasia of the prostate in young males. J Urology 1993;150:379
85.
12. Thompson IA. Observation alone in the management
of localized prostate cancer: the natural history
of untreated disease. Urology 1994;43(suppl):41-6.
13. Breslow N, Chan CW, Dhom G, et al. Latent
carcinoma of prostate at autopsy in seven areas.
Int J Cancer 1977;20:680-8.
14. Armstrong B, Doll R. Environmental factors
and cancer incidence and mortality in different
countries, with special reference to dietary practices.
Int J Cancer 1975;15:617-31; Howell MA. Factor analysis
of international cancer mortality data and per capita food
consumption. Brit J Cancer 1974;29:328-36; Rotkin ID. Studies
in the epidemiology of prostatic cancer: expanded
sampling. Cancer Treatment Report 1977;61:173-80;
Blair A, Fraumeni JF. Geographic patterns of prostate cancer
in the United States. J Nat Cancer Inst 1978;61:1379-84;
Kolonel LN, Hankin JH, Lee J, Chu SY, Nomura AMY, Hinds
MW. Nutrient intakes in relation to cancer incidence in
Hawaii. Brit J Cancer 1981;44:332-9; Schuman LM, Mandel
JS, Radke A, Seal U, Halberg F. Some selected features
of the epidemiology of prostatic
cancer:
Minneapolis-St. Paul, Minnesota case control
study, 1976-1979. In Magnus K., ed. Trends in Cancer Incidence:
Causes and Practical Implications. Washington, DC, Hemisphere
Publishing Corp., 1982; Graham S, Haughey B, Marshall J,
et al. Diet in the epidemiology of carcinoma of the prostate
gland. J Nat Cancer Inst 1983;70:687- 92; Ross RK, Shimizu
H, Paganini-Hill A, Honda G, Henderson BE. Case-control
studies of prostate cancer in blacks and whites
in Southern California. J Nat Cancer Inst 1987;78:869-74;
Oishi K, Okada K, Yoshida O, et al. A case-control
study of prostatic cancer with reference to dietary habits.
Prostate 1988;12:179-90; Severson RK, Nomura AM, Grove
JS, Stemmermann GN. A prospective
study of demographics, diet, and prostate cancer
among men of Japanese ancestry in Hawaii. Cancer
Res 1989;49:1857-60; Mettlin C, Selenskas S, Natarajan
N, Huben R. Beta-carotene and animal fats and their relationship
to prostate cancer risk: a case-control study. Cancer 1989;64:605-12.
15. Breslow et al., Latent carcinoma of prostate;
Howell, Factor analysis of international cancer
mortality data; Severson et al., Prospective study of demographics,
diet, and prostate cancer; Hirayama T. Changing patterns
of cancer in Japan with special
reference to the decrease in stomach cancer mortality.
In Hiatt HH, Watson JD, Winstein JA, eds. Origins
of Human Cancer. Book A, Incidence of Cancer in Humans.
Cold Spring Harbor, NY, Cold Spring Harbor Laboratory,
1977; Hirayama T. Epidemiology of prostate cancer with
special reference to the role of diet. Nat Cancer Inst
Monographs 1979;53:149-54; Phillips RL. Role of life-style
and dietary habits in risk of cancer among Seventh-Day
Adventists. Cancer Res 1975;35:3513-22; Mills P, Beeson
WL, Phillips RL, Fraser GE. Cohort study of diet,
lifestyle, and prostate cancer in Adventist men.
Cancer 1989;64:598-604.
16. Sattilaro AJ, Monte T. Recalled by Life.
Boston, Houghton Mifflin, 1982.
17. Hautmann RE, Sauter TW, Wenderoth UK. Radical
retropubic prostatectomy: morbidity and urinary
continence in 418 consecutive cases. Urology 1994;43(suppl):47-51.
18. Hauri D, Knonagel H, Konstantinidis K. Radical
prostatectomy in cases of prostatic carcinoma:
the problem concerning erectile impotence. Urologia Internationalis
1989;44:272-8.
19. Thompson, Observation in management of localized
prostate cancer.
20. Ibid.
21. Ploch NR, Brawer MK. How to use prostate-specific
antigen. Urology 1994;43(suppl):27-35.