Friday, July 25, 2008

Does prostatitis lead to prostate cancer?

The cause of prostate cancer is hard to pin down. Diet and genetics are huge factors. But increasingly, mainstream medical research is starting to uncover the link between prostatitis/BPH and prostate cancer....
....and the fact that former often leads to the latter.

If you leak, get up frequently in the night to pee, experience urinary burn, urgency, or even feel pain during ejaculation …. be aware these rather benign symptoms of prostatitis and BHP may get worse as you age ... and mainstream doctors may not be advising you on how to treat the cause for them.

Sure, they’ll monitor your prostate – probably enlarged – with annual digital exams and a PSA test. The latter is critical to guard against the worst-case scenario, cancer, and catching it early. They may prescribe drugs, like Avodart or Flomax, which claim to shrink the prostate and stop the symptoms over time.

But the question to ask your physician is whether any remedy they recommend will quell the chronic inflammation associated with prostatitis/BPH….because the inflammation, as it turns out, is a breeding ground for prostate cancer.

Eight years of inflammation

That’s what doctors did with me for eight years – they monitored my enlarged prostate and gave me round after round of antibiotics for my increasingly frequent bouts with acute bacterial prostatitis. (Which was misdiagnosed, by the way, as chronic bladder infections.)

It got so bad, I was rushed to the hospital with acute urinary retention -- the inability to pee -- because the inflammation squeezed shut the urethra. Talk about misery...predictably, they gave me more powerful antibiotics, which provided relief. But for how long?

I finally sought out an alternative healthcare practitioner to help me attack the “cause” rather than the “symptoms” of my problems. But it was too late. Soon after I headed down the road toward prostate health (colon cleanses, saw palmetto extracts, massage, etc.— more on all this later), I received the cancer diagnosis.

Mainstream Western medicine has been a true blessing with handling the big stuff, the cancer….but clearly lacking in everything that led up to it.

The road to PC is orderly

As I had learned too late, prostate disease tends to occur in an orderly fashion – prostatitis first, followed by BPH (benign prostate hypertasia), and finally the prostate cancer.

Even the doctors will tell you that prostatitis often starts in young men who can be in their teens, 20s, 30s ad 40s. BPH tends to occur in men over 50. And prostate cancer is most often diagnosed in men in their 60s and 70s.

It’s an orderly march, not inevitably ending with cancer – but the potential is there.

The truth is prostatitis is almost always found in conjunction with prostate cancer. In 1979, Drs. Kohnen and Drach found that 98 percent of surgically removed prostates showed signs of inflammation—the telltale sign of prostatitis. Urologist Timothy Moon, of the University of Wisconsin, and others report that 100 percent of the surgical and biopsied specimens they have examined, indicate the existence of prostatitis.

Not surprisingly, my biopsy revealed an inflamed prostate filled with prostatitis and some BPH….along with the clustered specs of cancer.

Looking for hard science?

Still, Western physicians – my urologist and internist included – are often dismissive of the idea that prostatitis is a cause of prostate cancer. Even if suspicious, many will tell you there’s just not enough hard science to link the two.

Until now….

Because Johns Hopkins researchers have now produced some hard science that supports the idea that inflammation of the prostate -- the very definition of prostatitis – is a likely precursor for prostate cancer.

An enlarged prostate due to chronic inflammation....a cause of cancer? Of course, this changes everything, in terms of what men should do if they experience the symptoms associated with prostatitis or BPH....or if diagnosed with an enlarged prostate.

If my doctors had told me – eight years ago – that my enlarged prostate and urinary tract problems were potentially stage one on the road to cancer, I would’ve aggressively begun a process of improving my overall prostate health. Then…not later.

I could’ve fought against the inflammation that sets in motion a series of cellular events that often leads to the cancer.

But I didn’t know.

Like most of the male population with prostatitis – THE MOST COMMON UROLOGICAL DISEASE IN AMERICA – we sit on our “benign” enlarged prostates, not thinking about how dangerous this condition is.

Yet…..whether our prostates are growing OUT (bigger in size) or growing IN (squeezing the urethra, causing urination problems) – the chronic inflammation in the prostate has become a potential breeding ground for malignant cells….

Okay, here’s the science

Straight from Johns Hopkins….

“Today scientists know that inflammatory cells produce free radicals—toxic molecules that can damage cells, especially cellular DNA. This type of DNA damage (also called oxidative damage) can cause genetic alterations (mutations) that lead to the uncontrolled cell division that characterizes cancer.

“Pathologists have found pockets of inflammation in the midst of cancerous prostate cells and abnormal (probably precancerous) cells known as prostatic intraepithelial neoplasia (PIN). Around the areas of inflammation, they discovered something new—groups of cells that look as if they are dying (atrophying) but are actually dividing (proliferating). The Hopkins researchers named these bizarre groups of cells proliferative inflammatory atrophy (PIA) and believe them to be either the very beginning of cancer formation or perhaps a breeding ground for prostate cancer.

“These areas containing PIA show high levels of an enzyme called glutathione S-transferase (GST), a critical substance that helps protect DNA from free radical damage. Ultimately, the gene that produces GST becomes inactivated in these areas of inflammation. GST production is halted, and the surrounding cells lose their DNA protection. Gene mutations may result, and the mutated genes may lead to prostate cancer.

“The theory is that inflammation—perhaps triggered by chronic infection, in conjunction with dietary or hereditary factors—leads to the DNA damage and the gene mutations that set prostate cancer in motion.”

Other evidence

Indirect evidence, gathered over many years, supports this inflammation-prostate cancer link. Some population-based studies, for example, have found a lower risk of prostate cancer among men who take inflammation-reducing medications or follow dietary patterns that are less likely to promote inflammation.

Several population-based studies have suggested that men who take non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, have a lower risk of developing prostate cancer. In one large study of more than 90,000 men participating in the Kaiser Permanente Medical Care program, those who took six aspirin a day had a 24 percent risk reduction of developing prostate cancer.

Chronic inflammation of other organs is commonly associated with various cancers. One needs only to look at the connection between hepatitis and liver cancer.....inflammation of the lower esophagus and esophageal cancer … ulcerative colitis and colon cancer … to see this phenomenon in action.

Look at your diet first

Dietary habits also influence inflammation. The typical American diet— high in saturated fat, sugar, and red meat and low in fiber, fruits, and vegetables—encourages inflammation (not to mention obesity and heart disease).

Reducing your intake of saturated fat—found primarily in animal-based products such as meat, poultry, whole milk products, butter, and cheese—and increasing your intake of fruits and vegetables are important first steps to discouraging inflammation and thus reducing your risk of prostate cancer.

(This post served as the basis for expanding upon the prostate cancer-inflammation-diet connection in The Prostate Storm)

Friday, July 11, 2008

Prostate cancer heightened risk for DVT

...
A friendly warning to anyone suspected of prostate cancer, or any other form of cancer for that matter: Beware of the sudden blood clot, especially if you're an endurance athlete planning air travel.

Not to be an alarmist, but cancer can cause your blood platelets to become rather “sticky” and begin clotting. Should you, say, take those sticky platelets on a cramped airplane flight….you’re at risk, no matter your age or fitness level.

You’re at risk of your blood pooling and coagulating, in my case, in a deep vein in my calf. Hence the name, DVT, or Deep Vein Thrombosis. The risk is that if not treated, DVT can lead to pulmonary embolism in the lung, which can be fatal.

That’s what happened to the late NBC reporter David Bloom, in the beginning of the Iraq war. Cramped in tight quarters inside a tank for days on end, a clot formed in his leg, traveled to his lung, and sadly killed him.

DVT affects about 2 million Americans a year, and up to 300,000 of them die when a fragment breaks off, migrates to the lungs and blocks a pulmonary artery, according to the Coalition to Prevent DVT.

Alarmed doctors

I knew little about DVTs when first diagnosed. But I saw real alarm in the eyes of my doctors when the Clot was discovered in my left leg. More alarm than when I received the cancer diagnosis, only days earlier.

The prostate cancer, unattended to, might get me in two to eight years, which is bad enough; but the Clot....in the next 60 seconds.

For several weeks after a long, cramped plane ride home from a ski trip to Salt Lake City, I walked around -- unknowingly -- with the huge clot forming in my calf. It hurt at first, like a severe muscle cramp, for 10 days. But then it quieted down, and became more of an annoyance. The calf was swollen, the back of my knee looked bruised and fatty.

At the time, I was preoccupied with the cancer diagnosis, getting scans, the biopsy, doctors appointments – all the preliminary details for choosing and preparing for a cancer treatment.

So the pain and discomfort in my ugly, swollen leg – that could wait. A couple doctors saw the leg but misdiagnosed it. They thought it looked like a Baker’s Cyst, where fluids pool behind the knee, possibly from a torn meniscus.

Eventually I visited an orthopedic surgeon, who recommended an ultrasound on the leg. The ultrasound spotted the long clot – think eight inches of twined yarn – in a vein deep inside my left calf, mostly below my knee.

Immediately, my doctor "stablized" the clot with the drug heparin. Instead of hospitalizing me for 4-5 days, I gave myself daily injections in my stomach to help affix the clot to the vein wall.

All this while starting up the radiation for the cancer....

Flying marathoners at highest risk

To say the least, what I’ve learned since about DVTs is alarming, because I thought it was mainly a problem for older folks with serious blood circulation problems. Not so.

Airplane travel is a high risk factor. Among frequent business travelers, studies found 4.5 percent of them develop one or more clots per year – about 50 times as many clots as found in a non-flying population. Most of these clots dissolve naturally, but the few that don't are a huge public health problem.

About 85 percent of air travel thrombosis victims are athletic – mostly endurance athletes, like marathoners. People with slower resting blood flow are at greater risk of stagnant blood subject to clotting. Also athletes are more likely to have bruises and sore muscles that can trigger clotting.

Not surprisingly, clots often go misdiagnosed. Like mine, the clot often feels like a muscle cramp or a tight knot. So aggravating the injury and increasing the risk of permanent disability or death is higher among athletes than other groups.

A perfect storm

For me, the clot likely formed for several reasons – a perfect storm of circumstance: The cancer changing the coagulation properties in my blood. I’m an endurance athlete, albeit an aging one, with low heart rate (55-60 bpm), hence slow blood movement in my legs. And a long, cramped plane ride following a ski trip, where my legs were fairly beat up, possibly bruised.

Hydration level is also a factor in DVT. As dehydration occurs, the blood thickens. Thick blood moves slower through the veins.

Long treatment period

The trouble with the typical DVT is that after the serious threat has passed, it threatens to hang around forever. After three months of the standard heparin/warfarin treatment, my doctor is continuing the medication for another three months. The swelling is down, but it still has a way to go.

Dr. Richard Chang, a researcher at the National Health Institute, wrote to me that about 50 percent of patients have good clinical results, meaning no pain and no swelling, after 3-6 months of treatment. But the warfarin only thins the blood, it doesn’t dissolve the clot.

A natural tPA and plasinogen in the blood flows over the surface of the clot to dissolve it naturally. As long as the clot is only partially occluding the vein – as opposed to a full occlusion or blockage – blood will most likely slowly dissolve the clot in time.

“God or evolution – depending on your world view,” Dr. Chang wrote me, “arranged for clotting to be quick to prevent bleeding to death, and clot lysis (dissolving) to be relatively slow.”

His message: Be patient. Wear compression socks.