Prostate Cancer Prevention
The Avodart®-Proscar® Debate
Elevated levels of dihydrotestosterone (DHT) contribute to benign prostate enlargement (Andriole 2004).
Based on evidence that DHT is also involved in prostate cancer (NCI 2013c), two large studies were conducted in aging men to see if drugs that reduce DHT also lower prostate cancer risk (Thompson 2003; Andriole 2010; FDA 2013).
One study evaluated the drug Avodart® (dutasteride) and the other Proscar® (finasteride) (Thompson 2003; Andriole 2010). Both of these drugs inhibit the 5-alpha reductase enzyme, thus blocking the conversion of testosterone to much more powerful DHT (FDA 2013).
Findings from the two studies showed both drugs reduce prostate cancer risk by about 23-25% (Thompson 2003; Andriole 2010). These drugs also substantially reduce symptoms of benign prostatic hyperplasia (Andriole 2004; FDA 2013).
Some doctors, however, were concerned that in men who did develop prostate cancer, more in the group taking either of these drugs (Avodart® or Proscar®) developed high-grade prostate cancer (Thompson 2003; Andriole 2010). This is a justified concern. High-grade prostate cancer requires aggressive therapeutic intervention and is more challenging to cure (Tewari 2007).
This protocol will reveal overlooked findings showing that Avodart® or Proscar® do not increase high-grade prostate cancer risk and may reduce it.
When prostate cancer is suspected, the typical diagnostic procedure is a needle biopsy of the prostate gland (ACS 2013c). The biopsied specimen is sent to a pathologist to determine the “grade” of any suspicious structures observed from the biopsied specimen (ACS 2013c).
The “grade” is determined by the “Gleason” scoring system (ACS 2013c). It is based on microscopic tumor patterns assessed by a pathologist while interpreting the biopsied specimen. The Gleason “grade” is a fundamental determinate used today to estimate low-grade, intermediate-grade, or high-grade malignancy (ACS 2013c).
The Gleason score is one measure of a patient’s specific risk of dying due to prostate cancer (O’Dowd 2001). Once diagnosis of prostate cancer is made on biopsy, the Gleason score strongly influences decisions regarding options for therapy (O’Dowd 2001). Here is how Gleason numbers are correlated with tumor grade (ACS 2013c):
Gleason score under 7: Low-grade
Gleason score of 7: Intermediate-grade
Gleason score over 7: High-grade
The higher the Gleason score, the more aggressive the tumor is likely to act and the worse the patient’s prognosis (O’Dowd 2001).
Problems With Gleason Testing
Physicians and lay people often overestimate the degree of certainty when it comes to diagnostic testing. This is clearly seen with tests like Gleason scoring, which is open to the interpretation of the individual pathologist examining the biopsied specimen and other variables. Several studies show that significant percentages of Gleason scores are graded too high or too low (Shapiro 2012; Moreira 2009; Berglund 2008; Nayyar 2010).
One way that Gleason scores are found to be sometimes erroneous is to compare tissue obtained from surgical prostatectomy to what was removed during the fine needle biopsy on the same patient (Moreira 2009; Nayyar 2010). There is far more tissue volume to examine from surgically-removed prostate glands compared with the relatively minute amounts obtained from needle biopsies, thus enabling more accurate Gleason score-grading of surgically-removed samples.
As it relates to men taking drugs that dramatically collapse the size of the prostate gland (like Proscar® and Avodart®), pathologists have noted that a consequence may be to induce lower-grade cancer to resemble higher-grade cancer (Andriole 2004; Bostwick 2004; Nelson 2009). They have stated that in men taking drugs like Avodart® or Proscar®, there would be a “grading bias” in which Gleason scores would indicate a worse grade tumor than really exists.
Proscar® Study Subjects Had Lower Rates of High-Grade Tumors
In the study evaluating Proscar® over a 7-year period, there was a 25% reduction in the risk of prostate cancer, but with an apparent increase in the risk of high-grade disease (as measured by Gleason scores) (Redman 2008).
A further analysis of the data, however, revealed the contrary. When examining tissue taken from men who underwent radical prostatectomy (complete removal of prostate gland), there was a 27% reduction in high-grade disease in the Proscar® group as measured by Gleason scoring (Redman 2008).
It turned out that there was a biopsy-sensitivity issue in the Proscar® group that resulted in high-grade Gleason scores being assigned to some men that were really low-grade (Redman 2008).
The startling finding that Proscar® (finasteride) may reduce high-grade prostate cancer was revealed in a study titled “Finasteride Does Not Increase the Risk of High-Grade Prostate Cancer: A Bias-Adjusted Modeling Report” (Redman 2008).
This study was published in the journal Cancer Prevention Research, but has been largely overlooked by the media, the FDA, and many physicians.
Shrinking Prostate Gland Makes High-Grade Cancer Easier To Detect
The impact of Avodart® or Proscar® on the size (volume) of the prostate gland is profound. Either drug reduces prostate gland volume by 17-25% over a relatively brief period of time (Andriole 2010; Nelson 2009).
Avodart® or Proscar® has been shown to reduce PSA more significantly in the presence of no cancer or low-grade prostate cancer (Kaplan 2002; Handel 2006; Nelson 2010). This effect can better enable physicians to identify cases of suspicious high-grade disease, since PSA levels don’t drop as low or stay as low in the presence of high-grade prostate cancer (Nelson 2010; Krejcarek 2007).
By reducing the size of the prostate gland, drugs like Avodart® or Proscar® can improve sensitivity of prostate biopsy and digital rectal exam (Redman 2008). To understand this concept, understand that there were a minimum of 6-core biopsies done in the Proscar® study and 10-core biopsies for the Avodart® trial (Andriole 2010; Redman 2008). These fine needle biopsies only remove a small percentage of tissue from a prostate gland. The larger the size of a prostate gland, the easier it is to miss malignant regions.
By reducing the bulk of the prostate gland, it was far easier to “hit” malignancies with a needle biopsy in men taking Avodart® or Proscar® compared to biopsies performed on the larger glands of those taking placebo (Andriole 2010; Redman 2008).
Needle biopsies of the prostate gland are only about 75% accurate to begin with (Taira 2010). So it may be easy to understand why needle biopsies uncovered more high-grade tumors in men taking Avodart® or Proscar® compared to the placebo arm.
Prostate gland marking a 6-core needle biopsy. Note how many areas of the gland may be missed when performing needle biopsies. The larger the gland, the more likely a needle biopsy may miss a tumor mass (Moreira 2009).
How Much Did Prostate Glands Shrink?
As noted, the median prostate volume in men taking finasteride was 25% lower compared to the placebo group, which represents a huge relative reduction in bulky prostate tissues (Cohen 2007).
A group of scientists calculated prostate gland volume differences along with other variables that were omitted when compiling the initial report on finasteride. When adjusting for all the variables, these scientists demonstrated a 45% lower risk of prostate cancer in the finasteride group (Cohen 2007). The scientists noted that, “Adjustment for gland volume and number of cores biopsied (i.e., sampling density) eliminated the differences in high-grade cancer between the two arms” (Cohen 2007).
Their published paper was titled: “Detection Bias Due to the Effect of Finasteride on Prostate Volume: A Modeling Approach for Analysis of the Prostate Cancer Prevention Trial.” According to these scientists, when all co-variables were added in there was a trend toward 12% fewer high-grade prostate cancers amongst men taking finasteride (Cohen 2007).
The conclusions from this analysis published in the Journal of the National Cancer Institute were:
“Although analyses using postrandomization data require cautious interpretation, these results suggest that sampling density bias alone could explain the excess of high-grade cancers among the finasteride-assigned participants in the PCPT” (Cohen 2007).
A review of several published reports attribute the higher Gleason scores observed in the groups taking the 5-alpha reductase inhibitors (Avodart® or Proscar®) to the fact that it was easier to find high-grade cancers in the shrunken glands of men taking these drugs compared to the much larger glands of men in the placebo group (Kulkarni 2006; Lucia 2007).
The fact that there are published reports defending the safety of Proscar® and Avodart® does not mean the matter is settled (Kulkarni 2006; Lucia 2007; Monga 2013). The debate may continue for years or decades. Aging men at risk for prostate cancer, however, do not have the luxury of waiting for uniform consensus.
Role of Estrogen
Estrogen is a cell growth promoter that has been implicated in the development of prostate cancer (Nelles 2011; Carruba 2007).
Life Extension customers have long been urged to keep estradiol (an estrogen) levels in the range of 18-30 pg/mL, yet many aging men present with estradiol levels around 40 pg/mL or higher, which markedly increase all-cause mortality (Jankowska 2009).
In a published analysis of the Proscar® study, scientists looked at levels of various sex hormones beyond just DHT. They found that men with the highest pre-treatment concentrations of testosterone were associated with a 36% reduced rate of prostate cancer when taking Proscar® (Kristal 2012). These same scientists also noted men with the highest level of estrone (an estrogen) had a 38% higher risk when taking Proscar® (Kristal 2012).
This study supports the theory that when prostate cancer cells are deprived of a primary growth factor like DHT, they may readily adapt to utilizing estrogen to fuel propagation (Kristal 2012). The doctors who conducted this study concluded:
Further research is needed to evaluate whether “low post-treatment serum estrogens may identify men more likely to benefit from the use of finasteride to prevent prostate cancer” (Kristal 2012).
Life Extension’s long-standing position has been for aging men to have their estrogen blood level tested and if it is elevated, initiate aromatase-inhibiting therapy to suppress estrogen to safe ranges. This may be of particular importance for men seeking to impede or reverse the course of prostate cancer. It also helps explain why some men taking Proscar® developed prostate cancer despite suppressing their DHT level.
The Proscar® (Finasteride) Studies
The Prostate Cancer Prevention Trial (PCPT) was a large-scale, long-term randomized, placebo-controlled study designed to evaluate if Proscar® (finasteride) could reduce risk of prostate cancer (Nelson 2009).
Participants in this PCPT study were all aged 55 years or older and had baseline PSA levels less than or equal to 3 ng/mL. One group received 5 mg/day of finasteride and the other a placebo (Thompson 2003).
This study was initiated based on multiple lines of evidence available in the early 1990s that suggested that treatment with finasteride (Proscar®) would reduce a man’s risk of developing prostate cancer. Finasteride functions to inhibit the 5-alpha reductase enzyme, which then lowers dihydrotestosterone (DHT) levels (Kulkarni 2006).
The plan was to evaluate the prevalence of prostate cancer in each group (finasteride and placebo) during the 7-year trial. About 15 months before the trial was scheduled to end, however, it was terminated because it had already met its primary objective (Nelson 2009).
The PCPT study demonstrated a 24.8% reduction in the prevalence of prostate cancer with finasteride treatment. An unanticipated finding, however, was that cancers with a high-grade Gleason score of 7-10 were more common in men treated with finasteride (6.4%) than in men treated with placebo (5.1%) (Cohen 2007).
To put these percentages of high-grade Gleason scores into perspective, they suggest that if all 18,882 men who entered the trial were given the placebo, 963 of them would have been diagnosed with high-grade disease. If all 18,882 men had taken finasteride, 1,208 men would have been diagnosed with high-grade disease. The difference is 245 more men being diagnosed with high-grade disease based on this assumption.
Of these 18,882 men, however, 4,323 would have contracted any grade of prostate cancer if all were given placebo based upon the results of the study, whereas only 3,134 would have contracted any grade of prostate cancer if all were given finasteride (Cohen 2007). That’s a difference of 1,189 men who would have avoided prostate cancer altogether during the study trial period if they all took finasteride.
We at Life Extension are well aware that high-grade prostate cancer grows faster and is more likely to spread beyond the prostate gland (Tewari 2007). Depending on your long-term longevity objectives, however, the data showing 1,189 fewer men developing any form of prostate cancer compared to 245 more men being diagnosed with high-grade disease might favor the finasteride group. And as you’ve read already, it was much easier to detect prostate cancer in men taking finasteride, meaning that the drug itself should not be blamed for the higher rate of diagnosis (Cohen 2007).
As we’ve shown, there appears to be no increase in high-grade disease in men taking finasteride, just higher rates of biopsy detection based on smaller size prostate volume, along with misinterpreted pathologies of biopsies that later showed 27% fewer high-grade cases in men taking finasteride based on examination of surgically-removed prostate glands (Nelson 2009).
More recent data provided further insight into the benefits of finasteride for prostate cancer prevention. At the 2018 American Urological Association Annual Meeting, Dr. Ian Thompson, a urologist from the University of Texas Health Science Center at San Antonio, and principal investigator of the PCPT, reported that the daily use of finasteride does not increase the long-term risk of prostate cancer. As he reported during an interview, this finding opens the possibility to use this inexpensive and effective drug to prevent prostate cancer (Mulcahy 2018).
The 2003 PCPT study, which first reported that finasteride decreases the risk of prostate cancer, found an effect that was so dramatic that the placebo-controlled arm of the trial was stopped, and the results were published. However, at the same time, the results also revealed an increase in the risk of high-grade prostate cancers as compared to placebo (Thompson 2003). This small, but statistically significant increase in the risk of high-grade prostate cancer made people subsequently avoid finasteride for prostate cancer prevention. However, several pieces of evidence revealed that this is not the case. A more recent, 2018 analysis that used Medicare claims to examine the long-term prostate cancer risks of finasteride, with a median follow-up of 16 years, reported that finasteride provided a substantial decrease in prostate cancer risk. The benefits were most pronounced in the first 7.5 years (Unger 2018). This finding is also supported by the new analysis that was presented at the 2018 American Urological Association meeting, where participants were followed for a median of 18.4 years. The study was conducted to examine whether daily finasteride for seven years would prevent prostate cancer in men over 55 years old. Investigators found that finasteride led to fewer prostate cancer deaths than placebo. An analysis of the risk of high-grade prostate cancer found that most high-grade disease was diagnosed in the first year after randomization, but there were no differences later on, supporting the idea that finasteride does not cause high-grade cancers (Mulcahy 2018).
The Avodart® (Dutasteride) Study
A study involving over 8,000 men was initiated to ascertain if Avodart® (dutasteride) could reduce prostate cancer risk over a 4-year period (Andriole 2010). The criteria to participate in this trial were:
- Age between 50 and 75 years
- PSA level of 2.5 to 10 ng/mL
- A single pre-study negative needle biopsy of the prostate
- A prostate volume ≤ 80 mL
Patients were randomized to receive 0.5 mg of Avodart® daily or placebo. All patients received 10-core prostate biopsies at baseline and 10-core prostate biopsies at 2 years and at 4 years after study enrollment (Androle 2010).
Here are summary results of the trial (Andriole 2010):
- The mean age of the men enrolled was 63 years in each arm.
- The mean PSA level of the patients in each arm at baseline was 5.9 ng/mL.
- Avodart® reduced the risk of prostate cancer by 22.8% compared to placebo over the 4 years of the study.
- Avodart® reduced the rate of acute urinary retention by 77.3% compared with placebo.
- The Avodart® group showed a 33% increase in high-grade (8-10) Gleason scores 0.9% for Avodart® compared to 0.6% for placebo.
The higher number of high-grade Gleason scores in the Avodart® group can be attributed to the same factors identified in the finasteride (PCPT) study, such as higher rates of biopsy detection based on smaller prostate gland size in men taking Avodart®, along with biopsy bias based on collapsing prostate glands that may have made some tumors appear higher-grade than they really were (Andriole 2010).
The FDA’s response, however, was to issue a label change for Avodart® and Proscar® to warn of the increased risk of being diagnosed with a higher-grade prostate cancer while taking these drugs (FDA 2012). This warning provides little benefit to aging men who are routinely prescribed these drugs to treat benign prostatic hyperplasia. It creates confusion as patients query their doctor as to why a drug that the FDA says is potentially dangerous is being prescribed to them.
In 2012, the results of another study (Lancet) were released showing that Avodart® was effective in slowing the progression of low-grade prostate tumors in 38% of men undergoing active surveillance (watchful waiting) (Fleshner 2012). This study of 302 men diagnosed with low-grade prostate cancer used 12-core biopsies obtained at 1.5 and 3 years. This Lancet study showed there to be slightly fewer (14%) higher-grade tumors in the Avodart® group compared to placebo (16%) (Fleshner 2012).
A study published in May 2013 evaluated 82 men with very low-risk prostate cancer who underwent active surveillance (watchful waiting) and were treated with a 5-alpha reductase inhibitor drug over a 3-year period. The results demonstrated the safety of the drugs and noted that at the first re-staging biopsy, 54% of the subjects no longer had prostate cancer (Shelton 2013). This small study helps substantiate the value of Avodart® or Proscar® for low-risk prostate cancer patients, but is not relevant to those with high-grade tumors that often require aggressive treatment.
We Must Avoid A “Tomato Effect”
“The Tomato Effect” was first described in the Journal of the American Medical Association in 1984 (Goodwin 1984). It analogized how doctors historically have ignored or rejected efficacious treatments that did not fit with accepted theories of disease prevention/treatment at the time.
“The Tomato Effect” is named for a period from the 1600s to early 1800s in America where tomatoes were considered poisonous and therefore unsafe to eat. This fear persisted despite the fact that Americans knew Europeans were regularly eating tomatoes with no ill effects.
The perception of the tomato changed in 1820 when a man ate a tomato on the steps of a New Jersey courthouse to prove they are safe (Goodwin 1984). Within a decade, Americans were regularly eating tomatoes that for over 200 years were considered poisonous.
In today’s world, we have an opposite problem that nonetheless can create a lethal “tomato effect” when it comes to rejecting lifesaving therapies. Physicians and patients are overloaded with information and lack the time to analyze data to accurately determine safety and efficacy.
Humans have a strong propensity to remember negative details. This human failing has caused many physicians and patients to reject 5-alpha reductase inhibitors because they recall something about more high-grade prostate tumors in men taking Proscar® or Avodart®. Never mind hard facts showing the opposite. People today want a succinct summary, a curbside explanation, and not too many distracting details.
As we have repeatedly shown in this protocol, what appeared to be more high-grade tumors in two studies of Proscar® and Avodart® were apparently based on a mistaken interpretation of the data.
In the haste of today’s busy medical practices, we are concerned that huge numbers of men who could benefit enormously from 5-alpha reductase inhibitors will not be prescribed them. We hope Life Extension customers appreciate the effort we have made to analyze the data so that they can make rational choices when confronted with real or potential low-grade prostate cancer.
Worst Case Scenario: Assume We Are Wrong?
We have provided solid evidence that Avodart® (dutasteride) or Proscar® (finasteride) do not increase high-grade prostate cancer risk. But what if we are wrong?
Here is what would happen under such circumstance using the Prostate Cancer Prevention Trial (PCPT) study for reference:
- More than 238,000 men will be diagnosed with prostate cancer in 2013 (PCF 2013a).
- If all these men had taken Proscar®, about 57,120 of them (24%) would avoid it.
- Based upon the results of the PCPT study, if none of these men took Proscar®, 52,598 would have high-grade (Gleason score ≥ 7) disease as opposed to 65,840 who would be diagnosed with high-grade disease (assuming Proscar® somehow causes high-grade disease) (Shepherd 2008).
- So each year, 57,120 men would avoid prostate cancer altogether, but 8,720 more men would be diagnosed with high-grade disease (assuming Proscar® [or Avodart®] really cause it).
- Under this worst case scenario, one could argue there would be greater numbers of beneficial outcomes (as opposed to adverse ones) if all men took Proscar® (or Avodart®).
We at Life Extension® don’t recommend these drugs for all men. They appear effective for reducing risk of low-grade prostate cancer and helping to better diagnose high-grade prostate cancer by shrinking prostate gland volume and better enabling the PSA marker to identify high-grade malignancy.
Our opposition might state that most men over age 69 with low-grade prostate cancer don’t have to be concerned because they are likely to die of something else before their prostate cancer spreads to other parts of the body.
While this may be the case for typical men over age 69, it’s a far cry from the longevity objectives of Life Extension customers. And low-grade prostate cancers do kill some men and are the most prevalent form of prostate cancer diagnosed.
With all due respect to Patrick Walsh, MD, who is advocating that urologists change the medical classification of low-grade prostate malignancy to remove the word “cancer” so as not to create psychological stress in aging men, and to avoid overly aggressive medical procedures, pretending low-grade malignancies are something else will not make them go away.
The documentation presented in this protocol that low-grade prostate cancers may be reversible in some men using a variety of inexpensive drugs, nutrients and dietary changes mandates that aging men have annual PSA blood tests and other diagnostics needed to assess the health of their prostate gland. If high-grade disease is detected, it is curable in its early stages, whereas the more prevalent low-grade prostate cancers are often controllable or reversible without requiring side effect-prone treatments.
New 18-Year Study Confirms Benefits of Finasteride
As we were finalizing the Life Extension magazine article titled The Avodart®-Proscar® Debate, a new study was published in the New England Journal of Medicine that further verified the safety and efficacy of finasteride in the prevention of prostate cancer (Thompson 2013).
This study meticulously followed all the men in the original Prostate Cancer Prevention Trial for up to 18 years (Thompson 2013).
The findings showed that long-term prostate cancer risk was reduced by about 33% in men who had received finasteride compared to the placebo group (Thompson 2013). This approximate 33% reduction in prostate cancer incidence was greater than the original study findings that looked at these same men over a shorter (7-year) time period (Thompson 2003; Thompson 2013).
Of men who did develop prostate cancer, those in the finasteride group had a 17% greater chance of high-grade disease, yet long-term mortality data was virtually identical in both groups (Thompson 2003). This adds a tremendous weight of evidence as to the safety of finasteride since if it really caused an increase in high-grade disease, more men in the finasteride group would be expected to have died sooner.
In addition, the 17% greater chance of high-grade disease seen in this long-term follow up was far lower than the 25.5% seen in the early phase of the Prostate Cancer Prevention Trial (Thompson 2003; Thompson 2013). The authors of this new study emphasized that the reason that more men in the finasteride group were found with high grade disease was “detection bias.” As we stated earlier, 5-alpha reductase inhibitor drugs like finasteride (Proscar®) and dutasteride (Avodart®), markedly shrink prostate gland volume, thus making detection of tumors much more efficient (Nelson 2009). Proscar® or Avodart® do not appear to cause high-grade tumors, they just make finding them much easier, which is of significant importance in obtaining curative treatment before these aggressive cancer cells escape from the confines of the prostate gland.
An editorial accompanying this New England Journal of Medicine study stated:
“For men who choose regular prostate cancer screening, the use of finasteride meaningfully reduces the risk of prostate cancer and thus the morbidity associated with treatment of the disease” (LeFevre 2013).
In maintaining the conventional party line that recommends against PSA screening, the editorial also stated:
“Men who are aware of and understand the benefits, risks, and uncertainties associated with the use of finasteride for prevention may make a rational decision to take the drug to reduce the potential harms of PSA screening. Of course, another way to reduce the harm of screening is to choose not to be screened” (LeFevre 2013).
Said differently, the author of this editorial is stubbornly sticking to irrational conventional dogma that advises men to avoid prostate cancer screening because of side effects that may occur during needle biopsy or treatment. The data the author is reporting, however, clearly shows that by taking just finasteride alone for a relatively short time period, an aging man can reduce the risk he will ever contract prostate cancer (and thus the need for “harmful” diagnostics and treatment) by 33% (Thompson 2013)!
There is evidence to suggest that prostate cancer risk reduction would have been greater had these men continued taking finasteride. As Life Extension reveals in this protocol, there are many other steps men can take to slash low- and high-grade prostate cancer risk, and at the same time, reduce overall incidence of degenerative disease.
Medical Technology Is Regressing!
We are witnessing a lethal regression in the use of technologies that could spare tens of thousands of aging men from prostate cancer deaths each year. Instead of seeking to incorporate proven methods to reduce side effects associated with conventional treatment, doctors are telling patients today to avoid screening. While this will save Medicare and Medicaid big dollars in the short-term, the epidemic of metastatic prostate cancer that will manifest in 5-10 years will extract a horrific toll of human suffering, premature death, and catastrophic costs to government healthcare systems.
Treating metastatic prostate cancer is a prolonged and extremely expensive process. Death can be postponed, but the side effects of treating advanced disease are often harsh.
A Real World Example of What This Nation Faces
When taking on the federal government and medical establishment like Life Extension routinely does, we seek to be meticulously accurate in everything we publish. Our credibility is at stake in every one of these scientific debates.
A friend of mine used to have his blood tested annually using Life Extension’s comprehensive Male Panel that includes PSA. He retired 7 years ago at the age of 60 and received “free” healthcare from his union (and later Medicare). So he stopped using Life Extension’s testing and instead let his doctor prescribe annual blood tests.
Each year he would have his blood tested, and each year his doctor said his results were fine. What my friend did not know is that the doctor stopped testing for PSA. When my friend started developing health problems his wife contacted me and said his doctors could not figure out what was wrong. I suggested he have his blood tested using our comprehensive Male Panel.
His PSA came back at 31. He appears to have metastatic disease and is undergoing aggressive treatment. He wrote me that he was shocked his doctor had not tested for PSA.
What happened to my friend is occurring throughout the United States right now. Doctors are following federal government guidelines and are intentionally omitting PSA screening. This devolution in health care must be reversed.
Startling Statistic Reported by New England Journal of Medicine
In reporting on the long-term data showing that finasteride slashed prostate cancer risk, the authors of the New England Journal of Medicine editorial opened by stating:
“With the advent of prostate-specific antigen (PSA) testing in the 1980s, the rate of diagnosis of prostate cancer rose dramatically… The timing and magnitude of the 44% reduction in prostate cancer mortality after the widespread adoption of PSA testing suggests that both screening and treatment improvements have contributed to this decline” (Thompson 2013).
The authors then go on to list all the side effects of treatment that prompted the federal government to suggest men should avoid PSA screening. Recommending against PSA screening will go down as one of the great travesties in medical history.
Prostate cancer is one of the most prevalent malignancies striking aging men. Technology developed four decades ago has resulted in a steep drop in prostate cancer-related deaths. Yet our federal government proclaimed in 2012 that this technology (PSA screening) should be abandoned.
Don’t be victimized by this nonsense.