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Prostate Cancer : What We Know

No cancer strikes men in the US more frequently than prostate cancer. More than 40,000 die each year from the disease.

Black men are at special risk, native American men the lowest. Rates have increased steadily since careful record keeping began in the United States.

The surge in cases diagnosed beginning in the early '90s seen in the figure above is an artifact of better detection methods. Cases were discovered earlier than they would have been. The leveling off after the surge is also an artifact, for the same reason. Men who under old methods would have been diagnosed post-surge where detected earlier, decreasing the number of new cases discovered 1994-1999.

Prostate cancer has been increasing steadily in the US for the last several decades, as evident in the graph above. These data from the National Cancer Institute's Surveillance, Epidemiology and Results program (SEER) are adjusted to take into account the fact that the US population is gradually growing older. Hence this long term trend is definitely not due to the ageing of the population.

There are many proposed causes for prostate cancer. Inherited genetic factors are involved, at least in some cases, perhaps as many as 5-10%.

But inherited factors alone cannot explain the rapid rise in prostate cancer during the second half of the 20th century. Something involving environment and/or life-style is also changing.

Much of the research on prostate cancer risk factors and causes has focused on conditions during adulthood.

After all, the risk of prostate cancer becomes more prevalent with age, rising rapidly after age 50.

This research has identified a series of risk factors in addition to age, including race (note the racial differences in the figure above), diet and geography. A diet high in animal fat, but not fat from fish or vegetables, promotes prostate cancer risk.

Countries vary markedly in the rates of prostate cancer. But when men migrate from a low-rate country to a higher-rate country, their risk increases.

Men in certain occupations appear more likely to develop prostate cancer. Many studies find an increased incidence of prostate cancer among farmers and pesticide applicators.

New research, however, is suggesting that the conditions for prostate cancer, even the initiation of the cancer itself, may begin much earlier in life. The evidence comes from several sources. Autopsies of men dying from other causes have revealed microscopic evidence of prostate cancer in a significant percentage of men as young as 30-39 years of age. Signs of abnormal prostate growth are evident even earlier, as a condition called prostatic intraepithelial neoplasia (PIN) were found in 9% of 20-29 yr olds. And animal experiments show that adult prostate characteristics can be altered dramatically by conditions experienced by the fetus in the womb, including shape, size and sensitivity to hormonal stimulation. 

These changes in animals can be caused at extremely low levels of exposure by very common contaminants, levels to which virtually all Americans are exposed. No one yet knows how relevant these animal experiments are to prostate health in people. It is an area of active research.

This new way of looking at prostate cancer suggests that research focused upon conditions around the time of cancer diagnosis may be of limited value.

It also suggests the following plausible but unproven framework, one that may be helpful in understanding why prostate cancer has increased so much over the past 50 years, and why some men develop it while others don't:

  Inherited genes induce some prostate cancers, and also cause differences in susceptibility to other factors, such as the ability to detoxify contaminants. Developmental disruption, caused by contaminants or by other variables affecting the hormonal experience of the fetus, induces changes in the prostate which may initiate very early stages of prostate cancer (similar to what happens with testicular cancer) or alter the hormonal responsivity of the prostate to conditions the man encounters later in life, for example, occupational exposures or dietary. As a man ages, something he encounters either triggers the formation of a tumor in a prostate sensitized by earlier experience, or encourages the growth of microscopic tumors (or pre-tumors) that were laying dormant.  

The available data from human studies are too uncertain to provide firm guidance for ways to reduce prostate cancer risk. The best-established risk factors—age and ethnicity—can't be changed. Certain occupations, especially farming, appear to have higher risks; at the very least, farmers with a family history of prostate cancer should be screened regularly. For individuals wishing to take a more precautionary approach, reducing exposures to compounds that have been found in animals to alter adult prostate characteristics is an option.

One of these compounds, bisphenol A, has also been found to cause biochemical changes in prostate tumor cells (in the laboratory) that would make treatment for prostate cancer less effective. Hence precautionary measures to reduce bisphenol A exposure could be considered.

 

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