In our current medical paradigm, screening for cancer is considered a preventive measure by virtue of providing an earlier diagnosis. Getting an early jump on a disease process like cancer makes treatment exponentially easier and outcomes generally better. Under the current guidelines, that early jump on prostate cancer starts at age 55 for men at low to moderate risk and 40-45 for men at high risk. It takes years for cancer to grow to a detectable point after the tumor's initial induction from a normal cell to a cancerous one. There's been a lot of research done to determine what those inducers are and how they work. Three of these inducers are simple to test for and completely modifiable with treatment and/or avoidance:
- Bisphenol A
- Catechol estrogens
Bisphenol A (BPA)
It may come as a surprise to know that BPA, a chemical found in plastics and linings of food containers has hormonal activity and could be correlated with your risk of prostate cancer down the road. A study that looked at urinary BPA levels in men with and without prostate cancer found more than a 2 fold increase in BPA in the urine of the men withprostate cancer. Here at ZRT, we also routinely see elevated urinary BPA levels in testers with prostate cancer, a result consistent with what the research is bearing out to date.
BPA Affects Prostate Specific Antigen (PSA) Testing
Individuals with a high body burden of BPA were likely to have false negative results for PSA
Even though it's infamous for leading younger men to needless biopsies and missing some cancers when levels are within normal range, we nonetheless use the less-than-perfect PSA test to screen patients for prostate problems including cancer and also to monitor prostate cancer treatment to the end point of lowering PSA as much as possible. To add insult to injury, the same study mentioned above found that high BPA levels may cause PSA levels to look low when they shouldn't be. In other words, individuals with a high body burden of BPA were likely to have false negative results for PSA. Particularly, they found high urinary BPA levels associated with low PSA levels in prostate cancer patients, a population where we expect to see much higher PSA levels with increasing statistical significance in men under the age of 65. "Under the age of 65" here is important because this is the group of men in which most of our prostate cancer diagnoses are made (and missed). So, not only could BPA be responsible for increasing prostate cancer risk, it also decreases the chances of an early diagnosis. It may make sense then that an individual with an elevated BPA and an allegedly normal PSA should be counseled on proper avoidance of BPA and have their PSA retested in 4-6 weeks.
In hefty amounts arsenic is poisonous, having killed scores of literary characters and famous historical figures. Most people think of arsenic this way, probably. But in small amounts, arsenic finds its way naturally into our air, soil, food and water. It's used in industrial processes and more than occasionally concentrates in areas around those industries that use it. I was amazed to see this first hand here in environmentally-conscious Portland, OR when elevated arsenic levels were discovered around a neighborhood glass blowing business – one tiny example of a possibly much larger issue across the nation and certainly the world.
Without a doubt, chronic arsenic exposure is associated with increased risk of many cancers including prostate. A most compelling research article I came across on the matter of hazardous effects of arsenic studied a community of people who lived on the southwestern coast of Taiwan. The residents lived on and consumed water from a well contaminated with arsenic for 50+ years. This group of people had a very high prostate cancer incidence and mortality that only began to decrease once the source of that arsenic exposure was removed with treatment of the water supply.
Urinary arsenic levels should be taken into consideration when assessing a patient for prostate cancer risk
The Strong Heart Study published in 2013 followed nearly 4,000 Native American men for almost 20 years and concluded that higher urinary arsenic levels were associated with prostate cancer mortality. Studies performed in vitro show that under arsenic exposure, prostate cancer cell lines are transformed from normal to malignant and can progress a tumor from androgen-sensitive to androgen-independent.
In case you're still not worried, a recent study that was just published assessed arsenic levels in drinking water in areas of Illinois along with prostate cancer rates in those counties and found that counties with higher arsenic levels had a higher incidence of prostate cancer.
Certainly, individual urinary arsenic levels should be taken into consideration when assessing a patient for prostate cancer risk. Avoiding arsenic means breathing clean air and drinking and using clean water, steering clear of second-hand smoke or quitting smoking, educating yourself on hing arsenic foods, and managing any workplace exposure.
Men's bodies make estrogens from androgens like testosterone and androstenedione. Estrogen has both protective and proliferative effects in the body so estrogen balance is crucial. This means estrogen biosynthesis should be in balance with metabolism and excretion from the body. In order to leave the body, estrogens are further modified through a 2-part "detoxification" pathway. The first part yields the catechol estrogens – they're more water soluble and closer to being ready for excretion but they can be dangerous because by virtue of their new structure, they're more susceptible to oxidation (or quinone formation). In the proper cell environment in the absence of oxidative stress, those catechol estrogens are methylated by the COMT enzyme complex to form the inert final products that enter the urine and stool for elimination.
What if oxidative stress transforms catechol estrogens to quinones?
Catechol estrogens that have been oxidized instead of methylated can bind to areas of DNA and create sites of altered genes that in some cases can become mutations that initiate cancer. High urinary catechol estrogens (in particular high levels of 2-hydroxyestrone, 4-hydroxyestradiol and 16-hydroxyestrone), have been tied to increased prostate cancer risk. The way estrogens are metabolized can be influenced by the health of the rest of the endocrine system, body composition, smoking status, diet, and an individual’s genetics.
Catechol estrogen activity in the body can be attenuated by treating endocrine imbalances (like hypothyroidism, for instance), promoting and supporting proper methylation pathways, improving nutrition, decreasing inflammation and most of all reducing oxidation.
When should prostate cancer prevention start?
It's always a great time to avoid chemicals and poisons and to adopt a healthful lifestyle. It's worth a conversation between doctor and patient – identify those areas of susceptibility and take it from there.
Original of this article was published on ZRT Laboratory Blog.