Prostate Cancer and Fatty Die t| A Comprehensive Review

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Prostate Cancer Linked to Western Diet
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National Institutes of Health -Prostate Health

What do burgers and fries have to do with prostate cancer? Plenty, according to a
new study by the Prostate Cancer Research Institute. Their research shows that
men who eat fatty Western diets face a higher risk of developing prostate cancer.

How much higher? Here's a comparison. The county of Qidong in China has the
lowest recorded incidence rate, 0.5 per 100,000 men. By comparison, Sweden has
a rate of 55.3 per 100,000 men and the U.S. has a rate of 102.1 per 100,000. Put
another way, if you are a man in the United States, you have a 200 times greater
risk of developing prostate cancer than a man in this province of China. And you
have almost double the risk of developing cancer than a man in Sweden.

Obesity promotes the development of cancer. As proof, the study observes that
Asian men who live in China and Japan suffer extremely low rates of prostate
cancer. But when these men move to the United States or other Western
countries, their diets change, and they "increase their risk of cancer within a single
generation".

Article Continues Below.

Several research studies have confirmed the link between fatty diets, obesity and
prostate cancer.

Fat emits hormones which have been implicated in the development of many forms
of cancer, including prostate cancer, pancreatic cancer, ovarian cancer, lung cance,
breast cancer, uterine cancer, kidney cancer and gallbladder cancer). All of these
are epithelial cell cancers. And interactions between epithelial and other
components (stromal components) inside cell tissues --as well as hormones that
the organs through the circulation of your blood -- stimulate the growth of
cancerous tumors.

Hormones may increase the growth of cancerous tumors in 4 different ways.

1. Obesity Boosts Levels of Natural Steroids in Your Body. When you are obese,
the fat increases teh production of steroids that stimulate growth of cells
throughout your body. These steroid hormones can bind to nuclear receptors in
tumor cells. Estrogen is one such hormone. Fat tissues produce excess amounts
of estrogen. It's one of the reasons that cancers occur in fatty tissues such as
breats. It's also one of the reasons that excess fat on a man's body increases hi
chances of developing prostate cancer.

2. Obesity Increases Free Floating Hormones. Obesity increases the amount of
free-floatng estrgen and testosterone in your blood stream. These free floating
hormones can create havoc by binding to tumors.

3. Obesity Triggers DNA Damage. Third, steroid hormone action can trigger
increased oxidant-stress-promoting cell proliferation and DNA damage. Androgens
have been demonstrated to increase oxidant stress in prostate cancer cells, and
oxidant defense mechanisms have been shown to be impaired early in the cancer
process.

4. Obesity Encourages Paracrine Factors. Obesity can increase the production of
paracrine factors and hormones which stimulate the production of steroid
hormones in cancer tissue through interactions between stromal and epithelial
compartments in tissues. Many of these paracrine factors are cytokines produced
by both fat cells and white blood cells.

Risks of Getting Prostate Cancer

Most cases of prostate cancer are detected with the PSA test. This test detects
prostate cancer before it becomes a lump that you can feel.

Over 180,000 American men were diagnosed with prostate cancer in 2000.
Prostate cancer develops as a result of both inherited and environmental factors.
It is associated with aging, and it occurs in a latent or clinically inactive form in
30% to 40% of men by age 30 to 50 years and in 75% of men by age 80.15,16
Because latent or clinically inactive cancers were not as effectively diagnosed prior
to the development of the PSA test, some uncertainty exists in predicting the
behavior of prostate cancer after diagnosis.

The cause of this disease is not fully understood, but a family history, the effects
of androgens (like testosterone) and other hormones, and environmental and
dietary factors may all be involved. The international variations in the rates of
prostate cancer are considerable. (See Figure 2.) The county of Qidong in China
has the lowest recorded incidence rate, 0.5 per 100,000 men. By comparison,
Sweden has a rate of 55.3 per 100,000 men and the U.S. has a rate of 102.1 per
100,000 men.17 Of course, diagnosing silent cancer by blood PSA increases the
statistical incidence of the disease because more clinically silent cancers are
diagnosed. Global differences in incidence are probably not due to inheritance. If
individuals with the same inherited genes are raised in two different environments,
the risk of prostate cancer is associated with the country in which they are
raised.18

An American Cancer Society survey of 750,000 individuals demonstrated that
being obese increased the risk of prostate cancer.19 Among the various nutritional
factors examined, per capita total fat consumption correlates with increased
prostate cancer incidence in cross-national studies. In a population-based
case-control study of prostate cancer among blacks, whites and Asian-Americans
in Los Angeles, San Francisco, Hawaii, Vancouver and Toronto, a positive
statistically significant association of prostate cancer risk and total fat intake was
found for all ethnic groups combined. This association was attributable to energy
intake from saturated fats.20 In Japan, an increase in prostate cancer risk has
been noted as the per capita intake of dietary fat has increased.21 In Hawaii, a
correlation was found between saturated fat intake and prostate cancer incidence.
A representative sample of over 4,000 adults at least 45 years of age from the five
main ethnic groups in Hawaii were interviewed regarding their diet, and multiple
regression analysis was used to assess the statistical relationship between
ethnic-sex-specific dietary intakes and corresponding population-based cancer
incidence rates. Significant positive associations were found for prostate cancer
with fat intake from saturated and animal sources, and for animal protein
intake.22 In the U.S., counties with higher prostate cancer incidence have higher
per capita fat intake.5

Using questionnaires that ask how often a particular food is normally eaten,
scientists have found clues to the association of dietary fat with cancer. In a
retrospective study by West et al23 and a prospective study by Giovannucci et
al,24 the more aggressive prostate cancers in patients were significantly correlated
with high fat intake. In the Giovannucci study, those individuals eating the highest
amount of meat had a risk of developing prostate cancer 2.64 times that of those
eating the least. The course of prostate cancer may also be affected by fat intake.
Kolonel et al25 found a significant relationship between dietary fat and prostate
cancer mortality in Hawaiian men 70 years and older. In addition, several studies
have demonstrated a positive association between saturated fat intake from meat
and dairy products and prostate cancer.26-31 Other factors in the diet may
enhance or diminish the risk for prostate cancer. Several retrospective and
prospective studies have found an association between prostate cancer and
dietary fat; however, none has shown a negative correlation.

Latent vs. Clinically Active Prostate Cancer
Approximately 60% of all men have latent or clinically silent prostate cancer, and
the incidence of this latent form is the same in the United States and Japan.32
These estimates are based on autopsies of men who die for reasons other than
prostate cancer. At the same time, clinically significant prostate cancer is much
more common in the United States than in Japan. When Japanese men migrate to
the United States, their incidence of clinically detected prostate cancer rises within
one generation. These facts suggest that nutrition and lifestyle practices in
lower-risk countries suppress the growth of prostate cancer so that it remains
small and confined and is rarely diagnosed clinically.

The Effects of Aging
Prostate cancer is a disease associated with aging and obesity. It has been said
that if you live long enough you will have prostate cancer, and over 90 percent of
men over the age of 90 have detectable carcinomas in prostatic tissue. Men who
have premature accidental deaths are found to have precancerous lesions such as
prostatic intraepithelial neoplasia (PIN) in their prostate glands if they are
between 40 and 60 years of age. Above 60 years of age, foci of prostatic cancer
are found in addition to PIN lesions. Also commonly associated with increasing age
is a shift in the pro-oxidant-anti-oxidant balance of many tissues toward a more
oxidative state. Recently, foci of proliferative inflammatory atrophy (PIA) have
been found in prostatic cancer biopsy specimens. While the DNA in PIN and
cancerous lesions have multiple abnormalities, the DNA in the PIA lesions is normal.

Given the common occurrence of prostatitis, both clinical and sub-clinical, it has
been hypothesized that the prostate gland with aging undergoes repeated
inflammation leading to DNA damage, mutation, and ultimately the formation of
precancerous and cancerous lesions. African-American men have a significantly
higher incidence of prostatic cancer compared to Caucasian men and have higher
levels of IGF-1 and androgens at puberty. It has been proposed that androgen
exposure, which has long been associated with the development of prostate
cancer, may be a means by which the pro-oxidant-anti-oxidant balance of prostate
cells is altered.

In rats, prostatic cancer can be induced by prolonged administration of
testosterone. The ablation of androgens has formed the basis for first-line therapy
of metastatic prostate cancer. It has also been proposed that hormones play a role
in the progression of prostate cancer from silent to clinically significant forms.
Since diet can influence circulating sex steroid hormones, diet and androgens may
alter prostate cancer biology via common pathways. Urinary levels of androgens
and estrogens were decreased in a group of Caucasian and African American men
fed a diet in which fat content was reduced from 40% to 30% of total calories.33
A very low-fat, high-fiber diet has been shown to reduce sex steroid levels in a
group of normal men34 Therefore, changes in sex hormones may mediate in part
the effects of diet on prostate cancer growth.

As sedentary men age, they often experience an increase in fat mass, a decrease in
lean body mass, and a change in hormone levels. These factors have been shown
to increase the risk of prostate cancer. In a study of Seventh-Day Adventists,
obesity was shown to significantly increase the risk of fatal prostate cancer
compared with ideal weight.35 This association was also noted in the American
Cancer Society's study of 750,000 individuals.5 With aging, the prevalence of
benign prostatic hyperplasia (BPH) increases; this is an androgen-dependent
chronic disorder.36

Dihydrotestosterone (DHT) formed from testosterone in the prostate and in the
testes appears to promote hyperplasia in humans, dogs and rats. Horton et al37
found increased levels of circulating DHT in elderly men compared with young men
(89 ng/dl vs. 49 ng/dl); in this study, nearly all the elderly men had BPH. Since
the prostate can convert testosterone to DHT, some have hypothesized that
increased metabolic conversion of testosterone to DHT may account for the
increased DHT levels in elderly men. Therefore, the effects of a high-fat diet on
prostate cancer are partially explained by the changes in hormones resulting from
that diet and by a decreasing lean body mass.38

In prostate cancer cell lines exposed to physiological levels of 5-alpha-reductase
(5AR) dihydrotestosterone (DHT) and to the synthetic androgen R1881,
proliferative responses and changes in oxidative stress were correlated.10
Physiologic levels of androgens are capable of increasing oxidative stress in
androgen-responsive LNCaP prostate carcinoma cells. The evidence suggests that
this result is due in part to increased mitochondrial activity. Androgens also alter
intracellular glutathione levels and the activity of certain detoxification enzymes,
such as gamma-glutamyl transpeptidase, that are important for maintenance of the
cellular pro-oxidant-anti-oxidant balance.

Conclusion
Although there is no clinical trial data available to define the benefits of weight
reduction, there is a clear association of obesity with cancer risk, incidence, or
progression for a number of common forms of cancer. Evidence is much stronger
for certain forms of cancer than others, but clearly, the endocrine and immune
systems may play an important role in mediating the effects of increased adiposity
on cancer risk based on the hormones and adipocytokines produced by fat cells.
Many of the changes observed in these systems among obese patients are related
but secondary phenomena of unknown significance, but others may be important
in cancer development, promotion, or progression. Abnormalities in adipocytokine
production and action are central to many of the observed metabolic changes in
the obese patient, and may play a role in the cause and maintenance of the obese
state as well as in associated forms of cancer.

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References
1. Heber D, Blackburn GL, Go VLW (eds). Nutritional Oncology. Academic Press,
San Diego CA, 1999.

2. Jaax S, Scott LW, Wolf JE, Thornby JI, and Black HS. General guidelines for a
low fat diet effective in the management of nonmelanoma skin cancer. Nutr.
Cancer 1997; 27:150-156.

3. 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: 617-631.

4. Shimizu H, et al. Cancers of the prostate and breast among Japanese and white
immigrants to Los Angeles County. Br. J. Cancer 1991; 63: 963-966.

5. Garfinkel L. Overweight and Cancer. Ann of Int Med. 1985; 103:1034-36.

6. Newman SC, Miller AB, and Howe GR A study of the effect of weight and dietary
fat on breast cancer survival time. Am J Epidemiol 1986; 123: 767.

7. Heber D. The role of nutrition in cancer prevention and control. Oncology
1992;6: 9-14.

8. Nimrod A, Ryan KH: Aromatization of androgens by human abdominal and
breast fat tissue. J Clin Endo Metab 1975;40:367.

9. Kissebah AH, Evans DJ, Peiris A, et al. Endocrine characteristics in regional
obesities: Role of sex steroids. In Vague J, Bjorntorp P, Guy-Grand B et al (eds). :
Metabolic Complications of Human Obesities. Amsterdam, Excerpta Medica,1985, p.
115.

Sources:

Prostate Cancer Research Institute

Source: Prostate Cancer Research Institute

The Linkage Between Obesity and Prostate Cancer
David Heber, MD, PhD, FACP, FACN
Professor of Medicine and Director, UCLA Center for Human Nutrition
Reprinted from PCRI Insights May 2004 vol. 7, no. 2

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Men Who Eat Western Fatty
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Quick Fact: The county of
Qidong in China has the lowest
recorded prostate cancer
incidence rate, 0.5 per 100,000
men. By comparison, Sweden
has a rate of 55.3 per 100,000
men and the U.S. has a rate of
102.1 per 100,000

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