The Real Cause of Prostate Cancer — And How to Stop It!

Dr. Frank Shallenberger, MD

May 20, 2019



If you really want to cure a disease, you have to find the cause of it and fix the cause. Sometimes, finding the cause of cancer is very difficult. But I’d like to tell you about a preliminary report that unravels the mysterious cause and development of prostate disease.

What’s more, there is a way to prevent, treat, and possibly even cure the disease.

The report comes from Israel, where researchers discovered the role testosterone plays in prostate cancer. As you may know, there’s been a debate raging in medicine about testosterone. Some believe testosterone is a fountain of youth. While others think it’s a time bomb waiting to explode. The truth, as you’re about to find out, is that it can be both. For those who have the symptoms of low testosterone, treatment with bio-identical testosterone can invigorate their body.

But this new study shows that the testosterone your body produces — not the testosterone most doctors use to treat low levels — can cause prostate cancer.

Too Much Testosterone Is Bad for Your Prostate

Until now, researchers felt testosterone played little, if any, role in causing prostate cancer. That’s because studies have shown no relation between testosterone levels in the blood and prostate cancer.

In this study, the Israeli team discovered a new route for testosterone to reach your prostate. They found that a certain condition in men can cause testosterone to back flow through the veins. And this floods your prostate with a massive overdose of testosterone.

Ordinarily, your testicular production of testosterone moves into your general circulation through the spermatic vein, where it reaches the inferior vena cava near the kidneys. Once in the general circulation, the blood greatly dilutes the huge concentration of testosterone. And most of it gets bound to sex hormone binding globulin (SHBG). That leaves only a tiny fraction of free testosterone to exert its powerful hormonal effects. Normally, testosterone reaches your prostate after the blood dilutes it nearly 100-fold, and with 98% of it bound to SHBG.

Now remember that your testicles secrete testosterone into veins. Your testicles are a long way from where their veins dump into your vena cava. The blood has to move up to the level of your kidneys. That’s about 35 cm on the right and 40 cm on the left. This height gives rise to extreme levels of pressure. These veins have a series of one-way valves, which assist in upward movement of blood against gravity.

The problem is, as we age, these valves age as well. Just like everything else that ages in your body, they just don’t work as efficiently. That allows for gravity to push the blood back down. This blood has to go somewhere though. There are collateral veins that can carry the blood through alternative routes. Unfortunately, one of those routes is back through the circulation of your prostate. A dilated, enlarged network of these veins is called a varicocele.

Why Taller Men Are More at Risk

The prevalence of varicocele increases rapidly in older men. Nearly 75% of men have this by age 70. Taller men are more affected, as the blood has farther to travel, creating greater downward pressure. And, taller men are at greater risk of prostate cancer. Interestingly, human-type prostate disease doesn’t normally occur in four-legged animals. Their testicular drainage is horizontal, not vertical! They don’t have (nor need) valves in their spermatic veins.

Now remember, the blood coming from your testicles carries 130 times the concentration of testosterone in your general circulation. What’s worse, virtually all of it is “free,” unbound, fully active testosterone. As this testosterone-rich blood backflows into the prostate, it sets up a very dangerous scene for hormone sensitive prostate cells. There, the free testosterone metabolizes to dihydrotestosterone (DHT), which can cause disease in prostate cells. And these diseased cells can turn into cancer.

This testosterone-rich blood is not detectable in your general circulation. But locally, your prostate cells are still bathing in a sea of testosterone. When your doctor checks the blood levels of testosterone, he may find a deficiency. This explains why studies have found that men with prostate cancer often times have LOW testosterone in their general blood circulation.

The Israeli team actually measured hydrostatic pressure, prostate volume, and PSA scores on 72 men with prostate cancer. Their findings are startling. All 72 men had incompetent veins (higher pressure). Their PSA levels averaged 8.89 ng/ml. Their prostate volumes averaged 65.3 ml.

The team reasoned that cutting out the collateral circulation might help the situation. They performed highly technical sclerosing (closing veins with scarring substances) therapy to the veins in the scrotal cavity eliminating back flow to the men’s prostate glands. The results confirmed their theory. Six months after treatment, PSA levels declined to an average of 5.95 ng/ml and prostate volume shrank to an average of 36 ml. That’s an extraordinarily effective treatment!

Why Blocking Testosterone Production Is a Bad Idea

Compare that to cancer doctors who seek to remedy the driving force of testosterone by giving you drugs that block your production of increase testosterone, causing a near chemical castration. Free testosterone drops in your blood to about 4% of normal, knocking you into an immediate uncomfortable andropause. (You get hot flashes, man boobs, wasting muscles, tiredness, and more.)

However, with varicocele the small amount of testosterone your body still produces in spite of these hormone blockers manages to arrive at your prostate at a concentration of five times the normal serum level. Your prostate cancer cells still see testosterone. And this testosterone, though in far smaller amounts, continues to fuel the cancer.

Over time, mutations allow your prostate cells to survive without the extremely high levels of testosterone, regardless of the chemical castration. Free of their need for high testosterone, they become incredibly aggressive. They can now survive in distant tissues (like bone). So the cancer spreads throughout the body.

The researchers reason that this process explains why prostate cancer is so slow to spread. Cells escaping early from the prostate, are fed far less testosterone than they had within the gland. They are unlikely to survive. Only when the cells (perhaps aided by chemical castration) learn to become independent of testosterone can they spread like most other cancers.

For this reason, according to the authors, chemical castration (androgen deprivation) may actually shorten the time to progressive disease. Androgen deprivation may also increase genetic pressure on the cancer cells to survive.

They can develop additional mutations, which may permit the cells to produce their own free testosterone. This isn’t a stretch, as most cancers are able to produce their own insulin. The latter enables them to gobble up sugar (their food source).

The Real Cause and the Best Treatment for Prostate Cancer

The researchers have proposed a new paradigm of prostate cancer development and treatment. They believe the first step should be correction of the back flow of testicular blood to the prostate. That eliminates the “back door” entry of massive amounts of free testosterone into the vulnerable gland. Indeed, correction of the venous problem reduces the free testosterone in the afflicted glands by 99.25%. Compare that to the only 80% reduction with chemical castration.

Does this explain why conventional prostate cancer regimens often fail? I suspect so. Radiation implants do nothing to correct the carcinogenesis of the massive prostatic levels of testosterone. Hormone blockade has the limitations presented above. Prostate resection might be successful if done in time — before any testosterone-independent cells escape.

The researchers suggest that there is a window of opportunity to eradicate the disease without chemical castration, and without the potential serious problems prostate resection might inflict. Simply correcting the venous pressure might deprive the testosterone-dependent cancerous cells of so much hormone that they will all simply and quickly die. The surgery also may alleviate the need for testosterone replacement therapy, as it could restore the testosterone levels in your blood to normal.

The first thing you need to know is whether you have a varicocele or not. A doctor can often (but not always) find them with a physical examination. I suggest a urologist, since a physical exam can miss it and you might need studies like ultrasound.

I’m not a fan of surgery. But, on this one, I’m not against surgically precise injections into target veins to close them up (sclerosis, like for varicose leg veins). Of course, prevention is best. Stay slim. Eat a healthy diet to keep your veins younger longer. Exercise. Rebounders are great here to move blood and fluids out of your pelvis. This research is a most exciting breakthrough in prostate disease, both benign and malignant. It also explains, in part, why obese men have far more prostate disease. Their abdominal fat increases hydrostatic pressure on their spermatic veins. This leads to more rapid development of valvular incompetency.

By the way, if you’re on bio-identical testosterone replacement therapy, you have little to fear as long as you take safe doses. This is true even if you have this venous condition. The small amount of testosterone you’re taking will have a negligible effect on the extremely high concentrations of testosterone in your prostate. Remember, the increase in testosterone in your prostate comes from your testicles and enters through the “back door.” So the testosterone you apply to your skin doesn’t go through the same pathway. But, there might be a correctable cause (venous drainage) to your low testicular production of hormone.

If fixed, you might not need the additional testosterone at all!


Andrologia, 41, 2009, 305-315. The U.S. government itself tracked this study, completed in 2008, at; Journal of Andrology, vol. 29, no. 2, March/April 2008.

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