I’ve had a lot of requests to print a talk I recently gave. Here it is. — Janet

Recently, I took part in a large, two-day community cancer seminar in Prescott, Arizona, presented by Prescott United Methodist Church.   Many people have asked for copies of my talk, so here it is.  Readers of this blog will find some of this material familiar, but I’ve collected it all into one place.  I would call it “Prostate Cancer in a Nutshell,” but that doesn’t sound very good… I’m sharing it with you now because I want you to know that there really is hope.

I’m not a doctor.  But I have been writing about the very latest in prostate cancer research and treatment for more than 25 years. What I hope to do today is give you kind of a “state of the union” talk on the latest advances. Some of these are not yet available, but they are coming. Everything I have to talk about is very hopeful.

I started writing about prostate cancer when my father-in-law died of it at age 53.  I was the editor of the Johns Hopkins medical magazine at the time, and so I arranged to interview Patrick Walsh, Director of the Brady Urological Institute at Hopkins.  I had no idea that he was the surgeon who invented the nerve-sparing radical prostatectomy, the operation to remove the prostate but preserve continence and potency. We wrote an article about prostate cancer in 1993, it got 3,000 requests for reprints, and when my daughter, Blair, was born, I left Hopkins and Pat Walsh and I wrote our first book.  We’re now on our sixth book.  At that time, PSA, prostate-specific antigen, was new, and although there was a PSA blood test, nobody knew what to do with the results.  I made my dad start getting the PSA test, and my mom and I made him start getting his prostate checked.  He did not appreciate it, especially the rectal exam.  But he did it, and in 1997 was diagnosed with prostate cancer, even though his PSA was very low – 1.2.  Patrick Walsh took out his prostate.  He had no complications from the operation, and his PSA remains undetectable today.  That was 21 years ago, and he just happens to be visiting today.  Dad, hold up your hand. (VJ readers, my dad got a big round of applause here!)


SCREENING

I’m starting with screening, because it just makes me mad.  Screening is the best thing you can do to avoid dying of prostate cancer.  But ever since 2012, millions of American men haven’t been screened for prostate cancer because their doctor said they didn’t need it, because that’s what the U.S. government told them.  And yet: About one out of seven American men – about 160,000 this year alone – will be diagnosed with prostate cancer at some point in his life.  Not all prostate cancer needs to be treated; many men with low-risk cancer can safely do Active Surveillance.  But many men do need treatment.

American men need a baseline PSA test and rectal exam to check for prostate cancer in their forties, and then they need follow-up screening at regular intervals.  Men who are at higher risk – men with a family history of prostate cancer and other cancer, and African American men – need to start screening earlier, ideally at age 40.

In 2012, the government – the Congressionally funded Band of Geniuses known as the U.S. Preventive Services Task Force, USPSTF for short –recommended against routine screening for “men of average risk” for prostate cancer.  There was not a single urologist on this panel, by the way. The USPSTF placed fear of overtreatment over the value of detecting curable disease.

Many urologists and oncologists believe the USPSTF made some bad assumptions. One is that many men are treated overzealously; that men who have slow-growing disease are subjected to surgery or radiation and suffer side effects from treatment they didn’t need. And it is absolutely true that, back in the 1990s when scientists were just beginning to figure out PSA, many men were treated who probably didn’t need it.

But that’s not the case today.

The other bad assumption was that all men are the same.  They’re not.  Some men are a lot more likely to develop the kind of prostate cancer that really needs to be treated.  These include men with a family history of prostate cancer and men of African descent.  Also, we now know that just having a history of cancer in your family – even if it’s not prostate cancer – raises your risk of getting prostate cancer.  Also, all men of average risk are not alike:  men who smoke cigarettes, for example, are at higher risk; so are men who are obese. We’ll get to that.

This summer, my boss at the PCF, medical oncologist and molecular biologist Jonathan Simons, sent me an article in the World Journal of Urology.  The senior author was Jim Hu, urologist and urologic oncologist at Weill Cornell Medicine.

The title: “Unintended Consequences of Decreased PSA-based Prostate Cancer Screening.” The article begins: “In May 2012, the USPSTF issued a grade D recommendation against PSA-based prostate cancer screening,” which is why so many family doctors stopped screening men for prostate cancer.

So, how is that working out for us?

To find out, Hu and colleagues looked at nearly 20,000 men at nine high-volume referral centers in the U.S. from 2008 to 2016.  They broke these men into two groups– from 2008-2012, and 2012-2016.  Before and after the Band of Geniuses.  From 2012-2016, they found fewer men were diagnosed with low-grade cancer, the kind that is easiest to kill.  Unfortunately, what this really shows is that these cancers were not caughtwhen they were low-grade.  They also found across the board that high-grade cancers increased by 24 percent.

Between 2008 and 2012, 6.2 percent of men had a biochemical recurrence, a return of PSA after treatment, which is not supposed to happen.  Between 2012-2016, that number had nearly tripled to 17.5 percent. All centers experienced consistent decreases of low-grade disease and absolute increases in intermediate and high-risk cancer.

The new guidelines give a grade of C, which is not exactly encouraging but is better than a D, to prostate cancer screening in men aged 55 to 69.  This is still not good enough.    

If you want to know the value of PSA screening, ask the 45-year-old guy diagnosed with metastatic prostate cancer who’s just starting ADT, androgen deprivation therapy, the suppression of male hormones including testosterone.  Oh, wait – 45-year-old men aren’t even mentioned in these guidelines.  Some men are diagnosed with prostate cancer in their early forties, and a few are diagnosed in their late thirties.  For many men, age 55 is too late to start screeningAnd 69 is too early to quit.  

Pat Walsh and other Hopkins scientists recently reported that even using age 75 as a blanket cutoff for PSA screening is missing some significant prostate cancer. Men diagnosed at 75 or older account for 48 percent of metastatic cancers and 53 percent of prostate cancer deaths.  So basically, if you’re in good health and are 75 and over and you don’t want to die of prostate cancer, you should keep getting screened.

Also: many men don’t know their family history.  You may be at higher risk and not know it.

Do you need screening for prostate cancer?  Well, Do you want to know, or not?  If you do, ask your doctor to start checking you for prostate cancer, with a PSA blood test and a physical exam.  If you don’t, then don’t.

But remember: If you are diagnosed with prostate cancer, that doesn’t necessarily mean that you need treatment.  You may be that guy who can safely live his life with a little bit of cancer that will never spread beyond his prostate.

If you are diagnosed with cancer that needs to be treated:  Prostate cancer that’s localized, confined to the prostate, can be cured with surgery or radiation; however, both treatments have a risk of side effects, including erectile dysfunction (ED) and, with surgery, the risk of incontinence. With an experienced surgeon at a high-volume center, the risk of complications is much lower.  These side effects are often temporary, and they can be treated.  With ED, where there’s a will, there’s a way:  in other words, if you want to have your sex life back, there are treatments that will restore it.  And don’t let anyone tell you that men who get radiation instead of surgery dodge the ED bullet.  They don’t. But again, there are good treatments, and I have specifics in the book and on my website.

Incontinence is usually temporary after surgery, and gets better as your muscles get stronger.  If it persists, there are treatments for this, as well.  

Maybe you’re thinking, “The treatment is not worth it. I don’t want the side effects. I’ll take my chances and just deal with cancer if I have to.”  If it turns out that you do have it, and that the cancer has spread outside the prostate, it may not only be very difficult to cure:  In this case, side effects aren’t just a “maybe.”  You will definitelyhave side effects from ADT– androgen deprivation therapy, the shutting down of male hormones including testosterone.  These can include impotence, breast swelling, weight gain, bone density changes, a higher risk of metabolic syndrome, diabetes, heart attack, stroke, or cognitive changes.   Note: These side effects can and should be fought with diet and exercise, and many men do very well on ADT for decades. But catching the disease early and treating it while it’s confined to the prostate, is better.

 

DIAGNOSIS 

Very briefly:  The whole point of getting regular PSA tests is to watch what the number does.  It should not be going up.  If it is, you should have a prostate biopsy.

Biopsies are not infallible.  Even with 12 or 14 cores of tissue (it used to be 6), cancer can still be missed.  Why?  Prostate cancer is multifocal– that means, there’s not one obvious tumor that sticks up like a marbleand screams, “Here I am, I’m cancer!”  The average prostate that has cancer in it has seven individual spots of cancer– and if you think of the prostate as a strawberry, these spots of cancer are like the little black seeds on it.  Just little dots.  They’re easy to miss.  African American menhave an even tougher situation; their prostate cancer tends to develop in an out-of-the-way place at the apex of the prostate – the attic, instead of the basement, where the needle comes in, so it’s harder to reach.

Several new forms of MRI can help target a biopsy and detect cancer.  I recently wrote about a man named Rob who was a human pincushion; he had endured five prostate biopsies, some saturation biopsies – all inconclusive.  But his PSA kept rising.  In fact, he had developed scar tissuein his prostate that masked the presence of cancer.  But a fusion biopsy, guided by MRI and ultrasound, found cancer.  Robhad his prostate out, the cancer turned out to be intermediate grade; it was confined within the prostate, and he’s fine now.  Rob is just 49 years old.

MRI is even more effective when combined with PHI – the Prostate Health Index.  This is a “second-line” blood test that combines three molecular forms of PSA into a single score.  There are other “second-line” biomarker tests, and more on the horizon, including tests for circulating tumor cells in the blood, urine tests, and molecular and genetic tests of biopsy sample tissue. One of these, developed by Hopkins pathologist Angelo De Marzo, is called the PTEN IHC test.  IHC is immunohistochemistry, and it involves using antibodies to stain cells.  PTEN is a “tumor suppressor” gene; it puts the brakes on cancer.  But cancer doesn’t like brakes, so in about half of all lethal prostate tumors, PTEN is knocked out. The loss of PTEN is a powerful predictor of aggressive cancer.  This test is not widely available yet.

Second opinion on pathology:

Another thing you can do is get a second opinion on your biopsy slides.  You can send your biopsy tissue to an experienced tertiary-level hospital to have a urologic pathologist take a look at it.  At Hopkins, world-class pathologist Jon Epstein and colleagues do second opinions on 15,000 cases a year, sent from all over the world.  They can also do IHC and other tests.

 WHAT CAUSES PROSTATE CANCER? 

Chronic Inflammation.  One cause of chronic inflammation is charred meat.

When meat is cooked at a high temperature – when a steak, burger, hot dog, or even a piece of cooked fish gets those grill marks that most of us really like to see – it produces a bad ingredient called PhIP.   PhIP is a “pro-carcinogen,” a chemical that turns into something that can attack and mutate your DNA.  PhIP is known to cause prostate and other cancers in rats.  However, when scientists feed rats tomatoes and broccoli along with PhIP, the rats live longer and have fewer prostate and other cancers than the rats that ate the PhIP alone.  Vegetables help counteract PhIP.  In the entire world, those least likely to get prostate cancer are men in rural Asia, who eat the traditional anti-inflammatory diet – low in meat, high in fruits and vegetables, with hardly any processed carbs.  No soda, lots of green tea.  No fries, lots of rice.  No burgers, lots of vegetables.  However,when those same men with their low risk come to America, over time, their risk goes up to the level of an American man’s. You are what you eat.

Good news: Men of any age can benefit from eating anti-inflammatory foods.

The opposite is also true: Obesity and one of its consequences, diabetes, make these flames of inflammation burn even higher.   This may be one reason why ruralAsian men are less likely to get prostate cancer: they have a lower body mass index, BMI, which means less stress on their cells.  If you are overweight or borderline diabetic, you turn on more insulin to try to control your blood sugar.  Insulin secretes molecules called cytokines, which can encourage inflammation.  This can put added stress on the body and perhaps tip the balance toward cancer.

The prostate is particularly vulnerable to inflammation because it’s just chock full of inflammatory cells called prostaglandins. So the prostate is already a tinderbox.

Bad genes:  We’ll cover this more in a minute, but the good news even with bad genes is that they are not automatically your destiny: we know this from studies of identical twins.  There are many cases where one twin gets cancer, and one does not.  Their genes are the same, so it must be something in their diet or lifestyle, too.

High blood sugar: Men who have diabetes are not more likely to getprostate cancer, but they are three times more likely to die of it if they do get it. Nondiabetic men who have high blood sugar have almost a five-times greater risk of dying from prostate cancer.  If you are pre-diabetic or diabetic, you can lower your risk of lethal prostate cancer by getting your blood sugar under control, improving your diet, and exercising.

Smoking:  Men who smoke, even if they don’t have a diagnosis of prostate cancer, are more likely to die of prostate cancer in the future.  Men who have been treated for prostate cancer who keep smokingare more than twice as likely to die of it, too, because cancer is more likely to recur.  The good news: Recent smoking matters more than if you smoked 30 years ago.  Your risk of dying of prostate cancer starts going down the day you stop smoking!  In 10 years, it’s the same as if you had never smoked!  Quitting now can make a big difference.  If you smoke, you should quit, and if you have prostate cancer, you should definitelyquit. There is no point in the spectrum of prostate cancer where quitting smoking is not helpful.

No drug protects against prostate cancer as much as having a healthy weight and being physically active. 

Lose that gut. Like smoking, obesity is linked to more aggressive disease and death from prostate cancer.  For men who have prostate cancer, being obese and continuing to gain weight is associated with higher disease recurrence and death. Among 2,500 men with localized prostate cancer in the Physicians’ Health Study, a one-unit increase in body mass before cancer diagnosis was associated with a 10-percent increase in a man’s risk of dying of prostate cancer.  A five unit increase raised the risk of dying of prostate cancer by 20 percent.

If you’re a young man, losing weight might stop prostate cancer from developing.  If a tumor is already there, but very small and not detectable, losing weight may delay the growth of cancer.  If you have a diagnosis of cancer, losing weight can slow cancer or help prevent it from spreading.  “It’s never too late to lose weight.”

Drink coffee.  Coffee is good!  Regular or decaf!  Let’s look at this study from Italy, published in the International Journal of Cancer:  In the Moli-sani Project, investigators looked at coffee consumption in nearly 7,000 men, age 50 and up in rural Italy.  They followed them, on average, at least four years, and during this time 100 of these men were diagnosed with prostate cancer.  It turns out that the more coffee the men drank every day, the less likely they were to develop prostate cancer.  Men who drank more than three cups a day had the lowest risk of getting prostate cancer.

Note:  these men took their coffee black, or maybe with a bit of milk.  In other words, they didn’t have five shots of whipped cream, etc. Also, their coffee was unfiltered– not brewed or instant.

A Harvard study published in the Journal of the National Cancer Institutefound that coffee was associated with a lower risk of gettingprostate cancer, andof developing aggressive, potentially lethalcancer.  Men who drank one to three cups a day, regular or decaf, had a 29-percent lower risk, and the risk went down as the coffee drinking went up.  Men who drank at least six cups a day had a 60-percent lower risk.  Amazingly, the heavy coffee drinkers also tended to be smokers – so coffee seems to have helped counteract cigarettes.

In other studies, coffee has been linked to a lower risk of developing Type 2 diabetes; liver cancer, endometrial cancer, postmenopausal cancer and colorectal cancer.

Coffee has powerful antioxidant effects.  Coffee is the number one source of antioxidants in the diet of the American man. This is sad.

Coffee is also anti-inflammatory.  Many studies have shown that heavy coffee drinkers have lower levels of circulating inflammatory markers in their blood.

Coffee has helpful effects on insulin and glucose metabolism.

Coffee cuts lipids, the body’s fatty acids.  It reduces fasting cholesterol and triglycerides.

Coffee helps the gut’s microbiome.  It increases diversity in the microbiome, the eight pounds of bacteria living happily in your gut.  Bad gut flora may promote inflammation, and vice versa.

Exercise:  Your prostate doesn’t care about six-pack abs and “gun show” biceps.  But your cardiovascular health matters a lot.  Cardiovascular exercise can lower your risk of getting lethal prostate cancer, or of having cancer come back if it’s already been treated.   UCSF scientistJune Chan and colleagues found that vigorous exercise (jogging or bicycling) after diagnosis was associated with a lower risk of prostate cancer death in men with localized cancer. “Three or more hours a week of vigorous activity was associated with a 60 percent reduction in the risk of dying of prostate cancer.” Now they are looking to see if moderate exercise, the kind anybody can do, can lower the risk of dying of prostate cancer.  “Biochemically, exercise could help deter metastasis, spread of cancer, by changing the environment for the cancer.”  This is like spraying fire retardant on the tumor. Not necessarily extinguishing the flame altogether, but making it burn slower, and helping the body set up fire breaks to keep the cancer from spreading.

Here’s an odd thought:  Exercise seems to make prostate cancer fat and happy.  “Prostate cancer may be the most common cancer where exercise, used like a drug, can confer an increase in survival,” says Jonathan Simons. “There is no form of treatment that has this effect.”  It may be that just as it improves blood flow in the arteries, exercise gives cancer a better blood supply that keeps it happy where it is, “so the tumor has no motivation to leave.” So basically, exercise makes cancer feel like it’s at a nice hotel, with free cable TV and a pool.  It’s content to stay there indefinitely. “When tumors are stressed” – when they’re in a bad neighborhood, in effect – “they have genes that are programmed to help them survive by getting them to crawl away to someplace that better serves their needs.”  One of those genes, Simons discovered, not only pipes in more blood to supply the tumor; it gets rid of waste products – the cancer cells’ sewage.  “When tumors build a supply line of blood vessels, to bring in more nutrients, they also build their own plumbing system.  Once they have this infrastructure, they launch a genetic program that lets them grow and spread.  But giving the cancer a better blood flow might sabotage the cancer’s need to boost its own blood supply. It just may be that exercise makes cancer, rather than head for the door, sit back in the recliner and reach for the remote. A contrary notion, isn’t it – that in order to turn your prostate cancer into a couch potato, your best chance is not to be one yourself?

This doesn’t mean that men who exercise are immune to prostate cancer. “There are very fit athletes who have had forms of prostate cancer that are so aggressive, so genetically mutated, that they have proved fatal. However, those men are at one end of the spectrum of prostate cancer. There are many thousands of men at the other end or in the middle, for whom exercise may make a real difference.

Here are some other things that can lower your risk, which I cut out of this talk to save time.

Oligometastasis:  Is the Window of Curability Wider Than We Thought?  Now: What if you have cancer that is confined to the prostate, with just a little tiny bit somewhere else? Are you doomed? It used to be that doctors thought, “Oh, man, he’s a goner, the cancer’s spread.” But scientists are learning that just because a spot of cancer has popped out of the prostate, this doesn’t necessarily mean that it can’t still be cured.

Here’s the old-school thinking:  You’re lying on a chair at the dentist’s office, and the dentist says, “You’ve got a cavity, decay is inevitable. We’ll just wait and pull all your teeth in a few years.” Like the poor guy in “Monty Python” who is mistakenly left for dead:” “I don’t want to go on the cart!”

Until very recently, the dividing line between prostate cancer that was considered curable and cancer that might not be was the prostate itself. That’s not the case anymore, says Johns Hopkins radiation oncologist Phu Tran, also a contributor to our book.

New evidence suggests that in men with oligometastasis – just a few spots of cancer outside the prostate – by treating “not only the primary disease in the prostate or the pelvis, but alsothe few metastatic spots, perhaps men can actually live a long time without disease progression and even be cured.” It’s the difference between being reactive – waiting for the next shoe to drop, the rise in PSA or development of symptoms – and being proactive. In other words: not just suspecting cancer is there, but knowing its precise location and going after it.

Now, how do they know where these little bits of cancer are?  There is a new form of technology called PSMA PET scanning,which can showbits of cancer as small as a BB.  There is also highly focused radiation, called:  SBRT (stereotactic body radiation therapy) or SABR (stereotactic ablative radiation).  Tran says it’s like spot welding—focused on a small area, very intense, and theoretically ablative, meaning it kills all the cancer in that spot.” Tran is testing this in clinical trials at Hopkins.

PSMA-PET:  

Hopkins scientist Marty Pomper, who was one of my husband’s interns when he was Chief Resident at Hopkins, figured out how to engineer a small molecule that binds to PSMA, prostate-specific membrane antigen, which sits on the surface of prostate cells. He then used innovative biochemistry to glue F18, the radioactive fluorine that glows in a PET scan, to that small molecule.  What he achieved is a way to see cancer that no one could see before.

This is very exciting for two reasons: PSMA-targeting molecules can find prostate cancer.  But if you switch out the radioactive tracer for a radionuclide – a little grenade of radiation that is targeted precisely to PSMA – then this technology can also be used to kill prostate cancer.  This is in clinical trials in the U.S., but it has been used for several years in Europe and Australia. Germany got the leap on everyone, because they don’t have to go through all the rigorous testing that we do.  Some doctors in the U.S. are sending patients with widely metastatic disease out of the country for these treatments, and some of these men have gone into long-term remission.  There are still some bugs to be worked out.  There are different radionuclides, and we need to know which is better. Also, it turns out that PSMA didn’t know that its name was prostate-specific… it is also in the salivary glands, and so there has been a problem with men getting their cancer into remission but having no salivary glands, so this is not ready for prime time yet.  But it is extremely hopeful.

IF YOU HAVE ADVANCED PROSTATE CANCER

If you need to start ADT, androgen-deprivation therapy, thanks to several recent studies, you also need to start taking an androgen receptor blocker.  There are three:  abiraterone (which you also take with prednisone), enzalutamide, and apalutamide.

The LATITUDE study, released last summer at the ASCO meeting, showed that giving abiraterone (Zytiga) and prednisone along with Lupron to men who are just starting ADT increased survival by an average of 18 monthslonger than ADT alone. But the study found that 25 percent of men showed an increased survival of four years, and a small percentage of those men appear to be “exceptional responders” who have had no progression of cancer for at least six years

In real estate, it’s location, location, location. With cancer drugs, scientists are learning, the key to success may be timing, timing, timing.  Starting abiraterone earlier, while the cancer is more vulnerable – before it has had a chance to mutate, to develop resistance and strengthen its armor – makes a huge difference.

Who should be interested in these findings?  Between 50,000-60,000 American men just this year alone.  Men who are on ADT, whose PSA is rising rapidly and doubling every 10 months or less.  And men who are just starting ADT.

Apalutamide (Erleada) is the newest FDA-approved drug for advanced prostate cancer.  Enzalutamide (Xtandi) is the third.  These are game-changers, and the game they are changing is a terrible one, the agony of wait-and-see, played out with each PSA test by men whose cancer looks like it’s going to metastasize.  This game sucks.  Until now, men who did not yet have metastatic cancer did not have access to the next level of treatment.

The idea is that now, not only do you nothave to wait for metastasis, you may very well change the course of the cancer, delaying the time to metastasis by more than two years longer than ADT alone.  Again, for some men, doctors aren’t even sure how longmetastasis can be delayed, because their cancer stillhasn’t progressed.  The SPARTAN study, of apalutamide, was published February 2018 in the NEJM.  Its senior author, Eric Small of UCSF, told me that the idea behind this study was actually to see if we could somehow put advancing cancer in a holding pattern.  Maybe metastasis is not a done deal.  In fact, he says, “this was really the first metastasis prevention study.”

For the men in the apalutamide group, the average metastasis-free survival was 40.5months – and some of these men stillhaven’t developed metastasis.

“We are talking about a 72-percent reduction in the risk of metastasis,” Small says.    What nobody knows yet is whether earlier treatment will lengthen overall survival. “We believe it will,” says Small, “but it’s way too early.”  For now, though, “We’re having a dramatic impact on delaying metastasis.”   At nearly four years, “50 percent of men in the apalutamide group still have not developed PSA progression.  They are doing well, they don’t have metastatic cancer, and haven’t been ravaged by extensive disease.  That’s remarkable.”

In July 2018, the FDA approved enzalutamide (Xtandi) for men with non-metastatic CRPC.  Same thing: this used to be second-line hormonal therapy, recommended only in men who developed metastatic cancer afterbeing on ADT.  This decision is based on the PROSPER clinical trial, led by oncologist Maha Hussein, M.D., of Northwestern.  In this study, 1,400 men with non-metastatic CRPC whose PSA levels were doubling every 10 months or sooner were randomly given either ADT with a placebo, or ADT plus enzalutamide.

Men who received enzalutamide had a delay in time to metastasis or death by an average of 21.9 months longerthan men in the placebo group, and some men haven’t had metastasis at all.

And now we get to Bad Genes and Immunotherapy

In 2016, a breakthrough study came out.  It was led by Fred Hutchinson Cancer Research Center medical oncologist Pete Nelson, and published in the New England Journal of Medicine. The study found that:

Prostate cancer is a lot more of an inherited disease than anybody thought;

There are 16 bad genes that we now know to look for; and

If you have a mutation in one of these genes, your sons and daughters and their children should get tested, so they can be considered high-risk for certain types of cancer, screened vigilantly, treated aggressively, and live to a ripe old age and not die of cancer.

These particular genes, called DNA-repair genes, are tiny quality control specialists; they’re the spell checkers.

Nelson’s study looked at 20 DNA-repair genes, in 692 men with metastatic prostate cancer in the U.S. and United Kingdom.  They found mutations in 16 of them, including some unexpected ones, like BRCA1 and BRCA2.

“Now wait,” you may be thinking, “aren’t they the breast cancer genes?”  Yes, and for years, nobody linked these genes to prostate cancer.  Now we know that the very same mutation that can cause breast and ovarian cancer in women can cause lethal prostate cancer in men.

Other bad DNA-repair genes include one that sounds like it should be at a bank, called ATM; and one that sounds like a roadie making sure the microphones work at a concert, called CHEK2; there’s also one that sounds friendly but isn’t at all, PALB2, which is strongly involved in pancreatic cancer.

Nelson and colleagues estimate that one in nine – 12 percent – of men with metastatic cancer have one of these bad genes.

In another study led by William Isaacs of Johns Hopkins, investigators did a genetic analysis of 96 men who died of prostate cancer at an early age – younger than 65.  Billy Isaacs says: “Surprisingly, we found that more than 20 percent of these patients carry inherited mutations in genes responsible for repairing damaged DNA.

  Why Genes Matter:  There are entirely new kinds of cancer-fighting drugs that target specific genes.  One class of drugs is known as PARP inhibitors like Olaparib, which is being used to treat women with BRCA mutations in ovarian cancer. It has now been approved as a treatment for advanced prostate cancer in some men.  Men with BRCA mutations also respond well to carboplatin, nota standard drug in prostate cancer.

What should you do?  If you have high-risk or metastatic prostate cancer, or if you have a strong family history of prostate or other cancers, ask your doctor about genetic testing. One of them is made by Color Genomics, and it costs $250.  You just spit into a test tube.

Checkpoint Inhibitors

In July 2016, a small but very exciting study led by investigators at the Oregon Health & Science University and Johns Hopkins, was published in the journal, Oncotarget.  It involves checkpoint inhibitors.

Basically, your immune system can do great and powerful things: like cause an autoimmune disease to devastate your body.  Ideally, it should only attack bad things, like cancer. But cancer has a lot of devious tricks.

T cells are some of the body’s most powerful warriors. They kill enemy cells.  But prostate cancer basically makes a nice cup of chamomile tea for these T cells, and puts them to sleep.  If you look at a sample of prostate cancer tissue, you can see the T cells right there next to cancer cells, and the T cells are asleep.  They have checkpoints on them; these are like a straitjacket.  Here, the cancer is hijacking a normal process that happens in every pregnant woman, so she doesn’t make an immune reaction to her unborn child.

Checkpoint inhibitors are a class of drugs, invented by Jim Allison with funding from the Prostate Cancer Foundation; in fact, he just shared the Nobel Prize for this work this month!  Checkpoint inhibitors take off the straitjacket and unleash the T cells.

But not every checkpoint inhibitor works for every cancer.  Also, compared to other kinds of cancer, prostate cancer looks pretty normal.  It doesn’t have many mutations.  Some forms of cancer have so many mutations – think of any villain in Batman – that the immune system says, ‘Hey, that guy looks weird. Let’s kill him.”  But prostate cancer can blend in, so this is one problem: getting the immune system to recognize prostate cancer as the enemy.

There’s a lot of work that needs to happen. However: some people have had spectacular success with checkpoint inhibitors. Tumors that should have killed people with metastases in their lungs, liver, and brain, have melted awayinstead.

In this study, led by Julie Graff of Oregon, they used a checkpoint inhibitor called a PD-1 inhibitor.  The results were so dramatic, and so unexpected, that they published the results early.  Julie Graff was working with immunologist Chuck Drake, of Columbia University.  Previously, she had seen two men with advanced prostate cancer who responded exceptionally well to a PD-1 inhibitor:  their PSA went away, and their cancer appeared to be undetectable.   Chuck Drake suggested that maybe enzalutamide, which targets the androgen receptor, might stimulate the immune system to make the PD-1 inhibitor work better.

So they did this study, of men who were taking enzalutamide but whose cancer was still progressing.  The men continued to take enzalutamide as they receive four doses of a PD-1 inhibitor called pembrolizumab. The first 10 patients were enrolled from March 2015 to January 2016.  Their ages ranged from 61 to 80, and their PSA ranged from a little over 4 to nearly 2,503.

In three men, the disease did not change; it did not get noticeably better, but it didn’t get noticeably worse, either.  Four men did not have any evidence of a benefit, and one of these men died of his cancer.  So that’s seven men; what about the other three?  Their response blew the investigators away:  Their PSA – including the man with the PSA of nearly 2,503 – dropped to the undetectable rangeof less than 0.1.  Two of these men had been on narcotics for pain, and stopped taking them.  One man’s liver metastases went away.  “These three men had a complete response,” says Graff.  “Their tumors shrank radiographically” – meaning that they couldn’t be seen in imaging – “in the lab” – their PSA falling to nearly nothing – “and clinically,” with the need for pain medication going away.  “None has had a recurrence.”

Another very promising form of immunotherapy, on the horizon, is Tumor-targeting CAR T cell immunotherapy.  This is custom-tailored for each patient:  they take a patient’s T cells, and engineer a gene that enables the T cell to pick a cancer cell out and kill it.

Now here’s a question you are probably wondering:  How is cancer affected by my gut bacteria? It may be that being able to increase “good” bacteria will help the immune system do a better job of fighting off disease – may soon help people with some types of cancer respond better to immunotherapy.  Recently, scientists studying colon cancer found that certain bacteria are found in half of all colon tumors and when the cancer spreads, the bacteria spread right along with them. In another study, scientists found that two different forms of bacteria work together, like fertilizer, to help colon cancers grow.  Scientists studying melanoma found that the presence of certain gut bacteria can change how cancer patients respond to immunotherapy.  Karen Sfanos of Johns Hopkins is working on this in prostate cancer.   It may be that special probioticsor even a fecal transplantmay help immunotherapy work better.

Gene-Targeted Therapy

Already, at major academic medical centers, getting treatment for advanced prostate cancer involves a talk with a genetic counselor.  Heather Cheng, a medical oncologist at the University of Washington and Fred Hutchinson, was the first one.  She started the world’s first prostate cancer genetics clinic.  Here is a story about one of her patients, an amazing guy I interviewed named Mark Meerschaert.

In a matter of weeks, Mark went from being an athlete to someone who could barely walk; metastatic prostate cancer had come from nowhere and spread like wildfire throughout his body. Mark is a university math professor – the kind who fills up the blackboard in his classroom with calculations to answer questions of probability, and statistics.  So when he got sick, he did what he does best: looked at the numbers. Men with widespread prostate cancer that is not responding very well to standard treatment don’t live very long.

So then Mark did what I hope everyone with a challenging diagnosis will do: He became his own advocate. He did some research and found Heather Cheng.

It turns out that Mark has a mutated BRCA2 genethat runs in his family.  Cheng immediately focused on this gene and suggested a very different type of treatment – off-label use of olaparib, approved by the FDA to treat ovarian cancer. Olaparib is a PARP inhibitor; it blocks a protein that cancer cells need to repair themselves, and works especially well in people with defects in the BRCA2 gene. Olaparib and other PARP inhibitors are being studied in clinical trials for prostate cancer.

Cheng also got genetic sequencing of tissue from Mark’s metastatic cancer.

Cancer can change over time. If you have metastatic cancer, there may be different mutated genes than in the cancer that was originally diagnosed from the needle biopsy. This matters because there may be a new medicine that works well with your particular mutated gene or genes. She told him it could get worse before it got better.

It did.  Mark said: “I started olaparib in October 2016. Two months later, “we did a bone scan, and saw that there was cancer all over the place: my ribs, hips, legs, some lymph nodes.”  He became very weak.  He used a cane, then a walker, then a wheelchair. He took a leave of absence from his job. Now he is looking forward to going back.

Starting early in 2017, he says, “I just slowly started to feel better and better.  At some point, I said, ‘Maybe I can go for a walk again. I had a little numbness in my foot, but I said, ‘I’m going to keep walking,’ so I did. I walk my dog every day, a couple of miles. Now even the numbness is gone.”  In a matter of six months, he said, “I’ve gone from shockingly, disastrously ill to feeling – I’m still cautious, still waiting for the other shoe to drop; nobody knows how long this is going to work.  There’s no data on people like me. Now I feel great.”

Mark had known he was BRCA2 positive; after his brother was diagnosed with breast cancer several years earlier, he got genetic testing. But he never expected to get prostate cancer.  In fact, although he’d gotten a PSA test every year, he had stopped. “My doctor said, ‘We don’t need to do PSAs.’ For two years I didn’t get a PSA.”  Which brings us full circle to the Band of Geniuses.

In 2013, Mark developed some urinary symptoms and went to see a urologist. Cancer was found.  He also learned that his father had been treated for prostate cancer when Mark was away in college, and his parents never said a word. “Had I known, I would have kept PSA screening.”

Mark underwent external-beam radiation therapy and a two-year course of ADT, which ended in March 2016. “By July of 2016, something just felt a little off. I went to see a urologist.  A biopsy showed high-grade cancer.

When Mark went to Seattle, Heather Cheng got that biopsy tissue and sequenced it. Cheng told him, ‘Your cancer is very aggressive, but that might work in your favor.’ That turned out to be absolutely correct. It got bad really fast, and it got better really fast.” He says: “The question is, what happens next?  I’m very interested in the five-year survival rate for people like me. They’ve only been using this since 2015, and the studies were on ovarian cancer.  My God, what if this had happened five years ago?”

So, right now, immunotherapy drugs only help men with certain mutated genes: mainly BRCA 1 and 2, and ATM.  But this is just the beginning.

Imagine a waiting room full of 100 men with advanced prostate cancer.  Some of those men have mutated BRCA genes; those genes can also cause breast and ovarian cancer, so let’s color them pink.

Some have a mutated PALB2 gene, also the bad gene in pancreatic cancer.  Let’s color them green.

For about eight of those men, the bad gene is WNT. That’s also the gene involved in 100 percent of aggressive colon cancers.  Let’s color those men blue.

About half have a bad ERG gene.  This is found in children’s leukemia and in sarcoma. Let’s color those men purple.

About one-fourth have a mutated PTEN gene.  That can also cause some brain cancers, endometrial cancer, breast cancer, and ovarian cancer. Let’s color those men orange.

One guy has a mutated IDH1 gene; this only affects 1 percent of men with prostate cancer, but it affects 100 percent of people with a glioblastoma, like Senator John McCain.  Let’s color that man red.

Eventually, our imaginary waiting room looks like an Easter Egg hunt.

Each color represents a subgroupof advanced prostate cancer.  The drug that works best on the men with the bad BRCA genes probably won’t work best on the men with the faulty ERG genes.  The drugs work differently because the men’s cancers are different – but they’re different in groups. A man in the yellow group may not be helped by a drug that works well for the guy in the purple group.  But he probably will be helped by a drug that helps other men in the yellow group.

You know who else will be helped?  People with other cancers who have that same mutated gene. So very good things are happening, and there has never been so much hope for prostate cancer, and cancer in general, as there is now.

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

Just when everything should be getting better – you’ve been diagnosed with prostate cancer, gotten curative treatment with surgery or radiation, and now you’re looking forward to getting your life back – there’s another bump in the road: ED (erectile dysfunction). You don’t need that!

Darn it, here’s yet another “reluctant brotherhood” – a club, like that of prostate cancer, that you never wanted to join. Take heart: You’re not alone, and it’s going to get better.  But your road to success may not be a little blue pill.

Maybe you’re like a lot of men who, before treatment, envisioned themselves boldly striding forward toward recovery of potency – perhaps temporarily using Viagra, Cialis, or another pill in the class of PDE5 inhibitors as a crutch until erections returned on their own.

Unfortunately, for some men, these might as well be sugar pills. They just don’t work as promised. And instead of striding forward boldly, they find themselves making uncertain progress like the Wayfarer, a character painted by Renaissance artist Hieronymous Bosch: a poor guy just trying to get somewhere down a troubled path.

For too many men, the road back to potency is a lot more difficult, confusing, and frustrating than it has to be. This makes me mad, because I have talked to men and their families who just don’t need another health burden to deal with. It makes Johns Hopkins urologist Arthur Burnett, M.D., mad, too, and he is doing something about it.  

Burnett is a surgeon-scientist, a neuro-urologist and pioneer in the understanding of erectile dysfunction (ED). His research on the biochemical mechanisms of nitric oxide in erectile tissue contributed to the development of Viagra and other PDE5-inhibiting drugs.

Burnett is also a world-recognized authority on treating the problems in sexual function that can occur after surgery or radiation for prostate cancer – and there are several. “ED is one thing,” he says, but it’s not the only potential roadblock to sexual recovery. “Some men also develop scarring in the penis, a condition known as Peyronie’s syndrome. Some men have climacturia, where they may release a little urine during sexual stimulation or climax, so that’s problematic. There’s a whole host of things that can go wrong,” and all of these problems can be treated.

By far the most common problem after prostate cancer treatment is ED, difficulty achieving or maintaining a penile erection. The American Urological Association has just revised its guidelines on treating this. Burnett, who co-chaired the committee to change these recommendations, says they were brought about by an evolution in thinking. “Treatment should be based on shared decision-making,” he states. “Patients should have the opportunity to have a full discussion on ED with their doctor – the variety of options to treat it, the likelihood of success – and options should exclude those that may have contraindications,” that aren’t recommended in their particular case, or that probably won’t help them.

Makes sense, right? And yet, Burnett has seen thousands of patients from all over the world who have not had such a discussion with their doctor, or whose doctor has continued treatment that not only isn’t working, but never was going to work.  

The old model – the one that emerged close to two decades ago with availability of PDE5 inhibitors – had well-defined steps to follow.   “We initiated therapy along the lines of first line, second line, and third line,” explains Burnett.   The first-line treatment was the pills, “the least invasive form of therapy.”

Erection is a vascular event; it involves blood flowing into the penis, being held inside there, and then flowing back out. The nerves that are responsible for erection lie in fragile neurovascular bundles on either side of the prostate, a discovery made by my co-author on the books, Johns Hopkins surgeon Patrick Walsh, M.D., who found that if men had one or both bundles preserved during prostatectomy, it was still possible for them to recover erectile function. However, he reported that patients who were older or who had one bundle were not always successful in recovering erections, and even men who had both bundles preserved, if they had vascular problems or other health issues, were more likely to have trouble.

Burnett has spent years studying these nerves, and he has found that the surgery itself – the traction on the nerves, and the stress of having an invasive procedure – can damage them. Often they recover, but sometimes they don’t. So even if, theoretically, a man should be able to produce an erection, it’s not guaranteed.

Many men – even though their nerves have been spared – “are not likely to respond to PDE5 inhibitors,” Burnett notes. These patients, particularly men with significant vascular disease, “need to be counseled in realistic terms on their likelihood of responding to these pills, balanced with their preferences, to try to get to the most effective therapy sooner rather than later,” says Burnett.   “Vacuum pumps and injections have traditionally been second-line treatments, but perhaps that should just be put on the table up front. Even penile prosthesis surgery should be put on the table early on for patients with more severe forms of ED. If men are already struggling with erections before surgery, after radical prostatectomy, they’re going to have even more trouble, and more frustration.” In other words, if you were relying on Viagra before treatment, the pill probably isn’t going to have the same effect that it used to.

“I see patients in my clinic who might best have been fast-tracked to a penile prosthesis early.” Burnett even sees men who had “non nerve-sparing” surgery – that is, both neurovascular bundles were removed (which is the right thing to do if cancer has reached these nerves) – who have been “done a disservice,” by being offered medicine that is simply not going to work for them. “Oral therapy depends on a necessary degree of intact nerve function,” Burnett explains. In other words, the pills augment what the nerves are already trying to do. “Their doctor says, ‘Let’s just try PDE5 inhibitors,’ but there are no nerves for penile erection. They start the first-line therapy. Then it’s, ‘Let’s wait another six months; keep trying.’” And that is not acceptable, in Burnett’s opinion. “We have to understand how these different therapies work, think about the clinical presentation of the patient, the variables that may impact his erectile physiology.”

Just having “all guys get first-line treatment, no matter what, and seeing how they do, then ‘maybe we’ll consider vacuum pumps and see how that goes for several months, and if it doesn’t work, we’ll consider injections’ – that’s not good enough. “It’s a much more practical model we’re evolving, one that’s focused on the patient’s desires and what is most likely to be effective.”

Make no mistake, Burnett adds, “if the patient has undergone a good-quality nerve-sparing radical prostatectomy, we should give his nerves the opportunity to recover function,” and not just jump to the third-line treatment, the penile prosthesis, right away. Nerves can continue to recover and erections can continue to improve even as long as four years after surgery. But that doesn’t mean a man should just stoically wait to resume his sex life until the day he achieves a decent erection, either. Maybe try a PDE5 inhibitor and a vacuum erection device, for instance.

Why do so many doctors insist on starting with the pills? Maybe they don’t take the time to find out how well the man’s erections were before surgery; maybe they don’t take heart disease or other health problems (again, some illnesses can hinder blood flow to the penis) into consideration – or maybe, as Burnett suspects, “they think, ‘the pills don’t have much of a negative impact,’ even though the patient will be frustrated for months.” Or maybe “they think, ‘More invasive therapies carry risks. Let’s see how he does,’ and they don’t consider that his sexual dysfunction can have a real impact on his health and wellbeing.” Too many doctors, he adds, “just pat ‘em on the back and say, ‘Things will be fine; you’ll be all right.’”

            But months and months of an unrestored sex life can be demoralizing, Burnett continues. “That’s why I think it’s more humane and appropriate to proceed with effective management of patients – not just treating ED by recipe. If somebody really is not predisposed to do well with PDE5 inhibitors, why push that on him?”

Similarly, injections work very well for some men, but not for others; men who have a large belly or who have poor hand-eye coordination, for instance, have difficulty. Other men simply “don’t feel that doing a needle injection is something that appeals to them. Why would we tell a man that’s all he’s got, instead of referring him to a penile prosthetic surgeon?”

Vacuum erection devices also have their pros and cons. “On the pro side, it’s noninvasive, and it’s fully under the control of the patient,” says Burnett. “But on the downside, it’s cumbersome and mechanical, it involves trying to draw blood into the penis, there’s a constriction band, it feels cold, and it can feel unnatural. Just put it on the table, and try to figure out what will work for one patient at a time – not some rote approach.”

Most men who get a penile prosthesis are happy with the result, says Burnett. “The erection feels natural, and they wonder why they didn’t get it sooner.” Why don’t more men with severe ED choose this option? “Part of it depends on how we in the medical community have presented it to patients.” Many of Burnett’s patients come to him after years of feeling frustrated with the first- and second-line treatments. “All too often, I hear patients say, ‘My internist said never get a penile implant; they get infected, and mechanically they don’t work.’ That’s unfortunate that this is what they’re being told.” In the 1970s and 1980s, penile prosthetics were not as reliable and were more prone to malfunction, but they have vastly improved since then.  

“Just like every other option, the prosthesis has its pros and cons. There is a 1 percent infection risk with prosthetic devices.” Burnett notes that doctors who are “infrequent implanters” tend to have higher infection rates, while “for expert surgeons, high-volume implanters, the infection rate is very low.” Burnett implants 80 or more penile prostheses a year, and “if I see an infection even once a year, it’s very rare.”

Patrick Walsh has told his patients for years, “if there’s a will, there’s a way,” and if they want to have a sex life after surgery, they can. Burnett, Walsh’s longtime colleague, adds to that message of hope from the doctor’s standpoint: “Never give up on a man who wants to preserve and restore his opportunity to be intimate with his partner.   We should try to explore options to help him achieve that.”

There’s one other important message here: Watch out for shysters. “Don’t waste your time or money with over-the-counter treatments or supplements,” says Burnett. They don’t work. Also, be very suspicious of high-cost experimental treatments. “The Sexual Medicine Society has taken a stand about some of this, and in our new ED guidelines for the AUA, we make it very clear that some things are investigational and require further evidence to show that they work.” These include shock wave therapy, stem cells, and platelet-enriched plasma injected into the penis. “Guys are being told, we’ll give you a couple of shots, and you’ll be fine. They pay out of pocket – $10,000 for as yet unproven therapy. It’s reprehensible, people out there trying to exploit these men. It is really terrible.”

It’s particularly terrible when there are medically proven approaches that Medicare and insurance will pay for that can actually restore a man’s sex life.

 

How Common Is ED After Surgery or Radiation?

 

Answering this question is more difficult than you might think, for two reasons: First, every surgeon and radiation oncologist has different results, based on expertise and the number of times the doctor has performed the procedure. So that’s one variable. The other variable is huge – and that’s your personal health. Start with the SHIM score, which is based on a few simple questions. You must be honest here. No one else will see these answers but you and your doctor.

After surgery: “In general,” explains Burnett, “erections are temporarily lost in many men who have a radical prostatectomy. Even with nerve-sparing, the nerves can be traumatized.   It takes a while for these nerves to recover. Although men may have some sporadic erections, it is very common for men not to be able to have consistent erections during the first nine to 12 months after surgery, without help.”

In men who are able to be sexually active without the help of a PDE5 inhibitor before nerve-sparing surgery, the potency rate after surgery gets better over time. “The potency rate at six months is different than at 12 months, and it’s even better at 24 months,” says Burnett. “Most men who had nerve-sparing surgery are going to recover erections in the second year.” Over the long term, he continues, “probably 80 to 90 percent of men who have pre-operative erections have the potential to recover erections without PDE5 inhibitors – if they have no other co-morbidities.”

This is the key. Co-morbidities are other health problems that could affect blood flow – particularly, blood flow to the penis. Major risk factors for not recovering erections, even if you have nerve-sparing surgery, include being a cigarette smoker (cigarettes are vasoconstrictors; they cause your blood vessels to contract); having diabetes, and having cardiovascular disease. There are other conditions and medicines that can affect erections, as well; this is why you need to have an honest discussion with your doctor about your current health and sexual function before treatment.

What about after radiation treatment? It’s kind of the opposite situation. “Unlike surgery, where you have a major loss and then you recover, with radiation you’re pretty much fine and then many men tend to lose erectile function over time,” says Burnett. For these men, PDE5 inhibitors may help. “As many as 50 percent of men who undergo radiation experience a general decline after two or three years – but for the first two to three years, men do not experience any true erection impairment.” Unless, of course, they were already having problems before treatment. The honest SHIM score is important here, too, and so is the discussion of any risk factors that you may already have with your doctor.

Note: None of this means that sex is impossible after you have surgery or radiation treatment for prostate cancer. If you want it, you can absolutely have it, Burnett says – but you may need more than PDE5 inhibitors, especially if you are already experiencing some ED before treatment.

False expectations are cruel. “Patients need to recognize if they aren’t the optimal guy to fully recover potency after surgery without any help,” says Burnett.   “Today, I had a 56-year-old professional athlete in my office, who had a perfect SHIM score and stage T1c cancer.” This man is highly likely to have full recovery of erections after surgery, because his cancer is minimal, and his cardiovascular system is in great shape.

But another man with that same stage of cancer who is diabetic and a smoker might not have such an easy recovery of potency.   That man can still have a full and wonderful sex life, Burnett says, but it might require a penile prosthesis. Knowing this before treatment could spare that man months of frustration.

 

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

This is not about prostate seed treatment, or brachytherapy, by itself.  It’s about giving a short course of hormonal therapy first, to lower testosterone in men with localized prostate cancer to make them eligible for radiation seed treatment. The idea is that a shot of Lupron or Zoladex will shrink the prostate and make it easier to cover the entire area with the seeds.

Don’t get your prostate shrunk just to get seed treatment.  There are three problems here, and one of them is huge.

One: seed treatment, also called brachytherapy, is not a better cure for localized, low-risk prostate cancer than external-beam radiation therapy or surgery. It’s just easier, because it doesn’t require an operation and recovery time, or weeks of daily radiation treatments, and men can go back to work the next day.

Two, no man should undergo hormonal therapy (also called androgen deprivation therapy) unless there is a darn good reason for it. For example, in men with high-risk disease, two to three years of hormonal therapy has been proven to save lives. In men with metastatic cancer, hormonal therapy dramatically shrinks the cancer and eases symptoms, and can be effective at keeping the cancer at bay for many years.  But we’re not talking about that right now.

If the sole justification for hormonal therapy is to accommodate one form of treatment when there are two others that have proven more successful, that’s not a very good reason. “This practice of giving three to four months of Lupron or Zoladex before seed treatment has been going on since the early 1990s,” says Anthony D’Amico, M.D., Ph.D., chief of Genitourinary Radiation Oncology at Brigham and Women’s Hospital and Dana Farber Cancer Institute. This is bad, he believes, yet many doctors do it – “despite the fact that we know that even a short course of hormonal therapy can produce irreversible breast growth and other side effects,” such as hot flashes, fatigue, decreased libido, slowing of metabolism, weight gain, cognitive impairment, “and nipple tenderness that can last up to a year; in older men it lasts longer.” (Note: The breast growth can be treated with radiation.)

And three, the huge problem: If you are an African American man, this may shorten your life span. Nobody knew this last part until D’Amico and colleagues conducted a retrospective study looking at the medical records of more than 7,000 patients. Their findings were published in the journal, Cancer. The men, all patients from the Chicago Prostate Cancer Center, all had low- or “favorable- to intermediate-risk prostate cancer, and 20 percent of them were treated with hormonal therapy to shrink the prostate before brachytherapy.

The results of their study were stunning: “We found that African American men being treated with just four months of androgen deprivation therapy were associated with a 77 percent higher risk of death than other men,” says D’Amico. “There is a very strong correlation between the short course of hormonal therapy and shortened survival. The causes of death in this situation were not related to prostate cancer, raising the question of whether a different treatment, such as surgery or external-beam radiation therapy, could easily have been done instead.”

The investigators don’t know how to explain this. D’Amico suspects that “there may be other factors intrinsic to the biology of African American men that make them more susceptible to hormonal therapy.” (This makes sense, and goes along with other research showing other key differences in prostate cancer between men of African descent and other men.)

“These findings should be considered very carefully by all men looking at treatment options for localized prostate cancer,” says D’Amico. “This doesn’t mean that men of other races are not at risk, just that African American men are at more risk. I don’t like the practice of giving hormonal therapy to men of low- or favorable- to intermediate-risk cancer, particularly in older men. It gives them more side effects for a year than they would have experienced if they had just had external-beam radiation or surgery. The metabolic side effects of hormonal therapy are not insignificant, either: it increases glucose, raises blood pressure, and some who are predisposed can get weight gain. In men who already have some of these issues, they can get worse.”

A confounding aspect of prostate cancer treatment is that what works for one man may be harmful for another. If you are an African American man getting screened for prostate cancer or already diagnosed with it, your best bet is to seek care at an academic institution or center that has expertise in personalized treatment of prostate cancer.

One more really important point that I hope you will consider: many men who are diagnosed with one Gleason score actually have higher-grade cancer found after surgery, when a pathologist examines the entire gland. The needle biopsy just samples a tiny percentage of the prostate, and in black men, cancer tends to develop in a different part of the prostate than it does in white and Asian men. Edward Schaeffer, M.D., Ph.D., chairman of urology at Northwestern, recommends that African American patients get an MRI if prostate cancer is suspected. This can help pinpoint areas of cancer that a needle biopsy might have missed, and your doctor may recommend surgery or external-beam radiation therapy instead of seed treatment.

The take-home message here, D’Amico states, is this: “Do not get hormonal therapy unless it has been proven to increase prostate cancer cure rates and prolong your survival. This does not fall into that category: There is no evidence that hormonal therapy followed by seed treatment increases the chance of cure compared to other treatments.” Worse, “it possibly exposes African American men to unnecessary danger, because there are other treatments that have the same cure rate but without this risk. Until we know from further study what is causing this risk and with whom, I would be very cautious about hormonal therapy use just to get seed treatment, or patients accepting it.”

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

 

 

In a matter of weeks, Mark Meerschaert went from being an athlete to someone who could barely walk; metastatic prostate cancer had come from nowhere and spread like wildfire throughout his body.

A highly respected mathematics professor and researcher – the kind who fills up the blackboard in his classroom with labyrinthine calculations to answer questions of probability, statistics, physics and the like – he did what he does best: looked at the numbers. Men with widespread prostate cancer that is not responding very well to standard-of-care treatment don’t live very long.

So then Mark did what I hope everyone with a challenging diagnosis will do: He became his own advocate. He did some research and found a different doctor, Heather Cheng, M.D., Ph.D., a medical oncologist at the Seattle Cancer Care Alliance, University of Washington School of Medicine and Fred Hutchinson Cancer Research Center. She also started the world’s first prostate cancer genetics clinic.

It turns out that Mark has a mutated gene that runs in his family. It’s called BRCA2, and when it is not working as it should, it’s more notorious for increasing the risk of breast and ovarian cancer; recently, scientists discovered that it increases the risk of prostate cancer, too.

Because of Mark’s bad copy of BRCA2, Cheng immediately focused on this gene and suggested a very different type of treatment – off-label use of a drug called olaparib, currently approved by the FDA to treat ovarian cancer. Olaparib is a PARP inhibitor; basically, it blocks a protein that cancer cells need to repair themselves, and has worked especially well in people with defects in the BRCA2 gene. Olaparib and other PARP inhibitors such as rucaparib and niraparib are currently being studied in clinical trials for prostate cancer patients.

I want to pause here just for a moment to make two points. First, among the many very smart things Cheng did was to get genetic sequencing of tissue from Mark’s metastatic cancer.   This is because cancer can change over time. We’ll talk more about this in a minute, but if you have metastatic cancer, there may be different mutated genes than in the younger cancer that was originally diagnosed from the needle biopsy of your prostate. This matters because there may be a new medicine that works well with your particular mutated gene or genes. The other really important point is that, because these new drugs are so specific, they don’t work for everybody. One drug might only help a small percentage of men. But another new drug might help a different small percentage, and a third new drug might target still another small percentage – and you might fit into one of those groups. So take heart! There are entirely new drugs being developed.

“She said, ‘Let’s try something else,’” Mark recalls. Cheng told him that the medicine may take a few months to kick in fully. “I started olaparib in October of 2016. At the end of 2016, we did a bone scan, and saw that there was cancer all over the place: my ribs, hips, legs – I can’t remember all the places – some lymph nodes. One day, I walked my dog, and I had to sit down,” right in the middle of the walk, “and rest for 20 minutes.”   That fall, Mark – on the faculty in the Department of Statistics and Probability at Michigan State University in East Lansing – organized a conference.   He was the moderator, and was supposed to stand up for five minutes between talks and moderate discussions. “I couldn’t stand up for five minutes.”

He used a cane, then a walker, then a wheelchair. He took a leave of absence from his job. Now he is looking forward to going to work. “The great thing is,” starting early in 2017, “I just slowly started to feel better and better,” he says. “At some point, I said, ‘Maybe I can go for a walk again. I had a little numbness in my foot, but I said, ‘I’m going to keep walking,’ so I did. I walk my dog every day, a couple of miles. Now even the numbness is gone.

“In the last six months, I’ve gone from shockingly, disastrously ill to feeling – I’m still cautious, still waiting for the other shoe to drop; nobody knows how long this is going to work,” Mark told me when I interviewed him for the Prostate Cancer Foundation’s website, pcf.org. “There’s no data on people like me. Now I feel great.”

Unexpected Family History

Mark is one of the pioneers of gene-targeted treatment for prostate cancer – medicine that, as Cheng explains, “is tailored to the weakness of his cancer resulting from a specific gene mistake in that cancer, rather than just treating it the same as all prostate cancers.” In other words, treating the gene, not the cancer.

“I knew that I was BRCA2 positive before I was diagnosed with prostate cancer,” he says; after his brother was diagnosed with breast cancer, several members of Mark’s family got genetic testing. But he never expected to get prostate cancer. In fact, although Mark had gotten a PSA test every year, he had stopped. “My doctor said, ‘We don’t need to do PSAs.’ For two years I didn’t get a PSA.”

Mark believes the policy of not screening men – which recently was revised – because of a fear of overtreatment is misguided. “A PSA costs almost nothing. To me it’s a misreading of the statistics,” somehow saying it’s worse for some men to get unnecessary biopsies than for other men to miss their shot at an early cancer diagnosis.

In 2013, Mark developed some urinary symptoms and went to see a urologist. Cancer was found.  Around this time, he received some bombshell news: “My dad had prostate cancer. But I never knew that until after I was diagnosed. Had I known, I would have kept PSA screening.” Mark’s father had been treated for prostate cancer when Mark was away in college, and his parents never said a word. “I’m a big fan of sharing knowledge with your family, even though it might be a little embarrassing. You might not feel comfortable talking to your kids about things like impotence, but they really need to know.”

Mark underwent external-beam radiation therapy and a two-year course of androgen deprivation therapy (ADT), which ended in March 2016. “By July of 2016, something just felt a little off. I went to see a urologist. He said, ‘I don’t think it’s anything to worry about, I saw something kind of weird, so I sent it off for a biopsy.’ It came back as high-grade cancer,” Gleason 9. The prostate cancer had come back with a vengeance.

Genetic tumor sequencing: When Mark went to the Seattle Cancer Care Alliance, “they got the tissue from last July and sequenced it.” As Cheng suspected, the genetic makeup of the cancer in Mark’s first prostate biopsy in 2013 was not the same as the tissue removed in 2016, after the cancer had time to mutate and become more dangerous. “They found out that I have the BRCA2 mutation in one of the two copies in my germline, but in the metastatic cancer cells, it was mutated in both copies.

“Dr. Cheng said, ‘Your cancer is very aggressive, but that might work in your favor going the other way.’ That turned out to be absolutely correct. It got bad really fast, and it got better really fast.” He is still taking the olaparib. “I guess I’ll keep taking it as long as it works.   The question is, what happens next?

“I’m very interested in things like the five-year survival rate for people like me. Nobody knows. They’ve only been using this since 2015, and the studies were on ovarian cancer.”

So there are no guarantees. However, Mark says, “I can deal with that. I do feel like this is something pretty remarkable. My God, what if this had happened five years ago?”

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

 

Take Back Your Sex Life! Here’s How to Make it Happen.  It’s the side effect that men fear most: Erectile dysfunction (ED) after surgery or radiation treatment for localized prostate cancer. As urologist Patrick Walsh, M.D., the great Johns Hopkins surgeon and my coauthor on several books about prostate cancer, always says: The first thing is to cure the cancer. Second is to preserve urinary continence. ED is third, because there are many ways to restore sexual function.

You deserve to be not only cancer-free, but to have all your parts in working order. So, if you’ve had a radical prostatectomy or radiation therapy for prostate cancer and you’re having some ED, take heart! This doesn’t mean that your sex life has to be over!

But a big part of this is up to you. If you’re having trouble and you don’t say anything, hoping for the best probably isn’t going to cut it. Ask your urologist for extra help. If you don’t get it, find another urologist.

I recently interviewed Trinity Bivalacqua, M.D., Ph.D., the R. Christian B. Evensen Professor of Urology and Oncology at Johns Hopkins, for the Prostate Cancer Foundation’s website (you can read more at pcf.org.) Here are some key points he wants you to know.

First: A lot of urologists don’t give their patients the most accurate picture of what to expect after prostate cancer treatment. There may be several reasons for this: Maybe they don’t want to admit that their results aren’t that good, or they don’t want to discourage patients from getting their prostate cancer treated by worrying them about their future sex life. We’ll get to some of that in a minute.

Second: Way too many men suffer in silence. These men – leaders at the office or in the community, respected, take-charge, tough guys – don’t ask for help. They push sex over to a quiet corner of their lives, and they’re miserable, because they assume that ED is a done deal. It’s their fate. Some things are just not meant to be, they sigh.

They give up.  They tell themselves that this is how it’s always going to be – partial erection, or no erection, forever.

Come on, men: This is rehab. If you had trouble walking after a car accident or a stroke, you would accept that it’s a step-by-step process to get you back on your feet. Maybe you’d start with a wheelchair, but graduate to a walker, and then a cane. You would understand this. It would make sense to you.

It’s the same thing with your penis. There are steps. You can escalate.

Don’t give up. This is practical stuff here. If your doctor is not telling you this, print the article and take it in for your next appointment. Ask for help. If you want this to happen, help make it happen. Don’t give up.

And partners: Give the guy a break. Have some empathy. Yes, it’s frustrating for you, and it will take a lot of patience and encouragement on your part, but keep your eye on the prize: long-term success. This man just beat cancer. With your help, he can get all of his life back. It’s not going to be this way forever. Recovery of erections after surgery can take a long time – even years – to return fully. In the meantime, there are many options here. Hang in there, people.   You’re not alone.

Rehabilitating Your Penis

Will your sex life be the same after surgery? The absolute honest answer is, probably not, or at least, not for a while. But the other absolute truth is just as important: You can have a good sex life after surgery.

It’s essential to know these two facts, because a lot of men don’t hear the whole truth from their doctor – or maybe they do hear it, but then focus on statistics for younger men who have never had erectile dysfunction (ED) and think the results will be the same for everybody. They won’t.

If you are in your sixties or older, have already experienced ED, and maybe you also have some other health issues, like diabetes or heart disease, then most likely you will have some ED after surgery. It happens after radiation, as well; the onset is more gradual, but the basic problem is the same – damage to the nerves and blood supply that control erection (see below).

“Erections are going to be altered from what you had before surgery,” says Bivalacqua. “Unfortunately, many doctors never provide this information; in fact, some men believe that if their erections before surgery are not as rigid as they would like, that a radical prostatectomy may actually improve them. This is definitely not the case. You may go on the Internet and find some doctor who says that 98 percent of his patients are continent and have excellent erections after surgery – but nowhere does that doctor tell you that he or she is just reporting on his youngest and best post-op cases, not on every single patient. I can’t tell you how many men come to see me and expect the same results. When they’re older and already have some trouble with ED, that’s just not going to happen.”

Bivalacqua cites a recent study in the Journal of the American Medical Association led by Harvard urologist Martin Sanda, M.D., based on data from 1,027 men with clinical stage T1 and T2 prostate cancer who had either radical prostatectomy or external-beam radiation therapy. “For a 50-year-old man with good sexual function before surgery, the probability of having good sexual function 24 months after surgery ranged from 21 to 70 percent, depending on their pre-surgery PSA and whether the nerve bundles (see below) were spared.” And for a man of any age with good sexual function before external-beam radiation therapy, “the probability of having good sexual function 24 months later ranged from 53 to 92 percent, depending on their PSA level and whether they received a short course of hormones along with their radiation therapy.”

Hold that thought.  We need to take a very brief detour and have a mini-crash course in prostate anatomy. On either side of the prostate – think of Mickey Mouse’s ears, except extremely tiny and hard to see – are two bundles of nerves.   They are called neurovascular bundles (that just means there are a bunch of nerves and blood vessels all clustered together). These nerve bundles were discovered by Pat Walsh, who invented the “nerve-sparing” radical prostatectomy.

Although these nerves are not in the penis itself, they are responsible for erection. They’re like junction boxes that control the wiring in a different room. Inside the penis are blood vessels; they’re like the plumbing. Basically, the erection happens when blood flows inside the penis – think of a water balloon filling up. If you have heart disease, and plaque in the arteries that can hamper blood flow, the penis (which depends on blood flow for erection) can be affected, too. This has nothing to do with the prostate, or prostate cancer, or surgery or radiation. This is just a problem you may already have.

In a nerve-sparing radical prostatectomy, if cancer is well confined within the prostate, your surgeon may be able to save one or both of those nerve bundles. You can have an erection with just one bundle. If you have both bundles removed, because your cancer is too close to that edge of the prostate, you can still have a sex life; you just will need some help with erections, and there are several options.

But first, back to your own situation: “If you have strong erections already and the nerves that control erections are spared during surgery, your chances of achieving a full recovery are excellent,” says Bivalacqua. But if, before prostate cancer treatment, you already had some mild ED, “this means that even if the nerves are spared, you will need some medication to help with erections after surgery.”

By medications, he means pills like Viagra, Cialis, Stendra, or Levitra.

Before we get into the specifics of sexual function after prostate cancer treatment, here’s one more very brief detour:

What kind of cancer do you have? If your doctor says you are a candidate for active surveillance, and you don’t have a family history of cancer and you are not of African descent, you may want to consider it, because it won’t affect your sex life or your urinary continence. However, it is not fun to get repeat biopsies, and if you are the kind of man who will constantly worry about having cancer – even if it seems unlikely to progress – this may not be for you.

If you are likely to choose surgery after a few years of active surveillance because you don’t want to live with the cancer and you want peace of mind, then please understand that your chances of recovery of potency are better sooner rather than later. Younger men who are potent before surgery do better, for the reasons discussed above.

Next, and this is huge: If you have cancer that is likely to progress beyond the prostate, you should get treatment now. Active surveillance is for a highly selected group of men with cancer that’s considered “safe.” It is completely different from not having surgery because you don’t want to have ED and hoping the cancer won’t spread. That’s actually more like denial than a good treatment strategy, and here’s why:

If you wait to have treatment, you might have more trouble than if you get treatment now. Not just because you’re more likely to recover your potency if you’re younger, but because if you don’t get treated for prostate cancer when you need it, and if that cancer progresses, you will lose much more than the ability to have an erection. If you have advanced cancer, the mainstay of treatment for metastatic disease is hormonal therapy, the shutdown of testosterone. One of the most difficult side effects of hormonal therapy is that it causes loss of sexual desire. (Note: Testosterone comes back if you stop taking the hormonal therapy, so a short course of hormonal therapy with radiation is different from taking it for the rest of your life.)

Help for ED after Prostate Surgery: The Basics

What’s the secret to having a good sex life after prostate cancer? It’s very simple, says Bivalacqua: “You use prescription erection pills. If they don’t work, you move to injectable medications. If they don’t work, you get a penile prosthesis. Also, having a loving and understanding partner always helps.” There’s also the vacuum erection device (VED).   It is not a first-line treatment for ED because there’s a high drop-out rate, Bivalacqua says. However, the VED can play a very important role in another aspect of surgical recovery: penile rehabilitation (see below).

First, the pills: “When one of my patients leaves the hospital after a radical prostatectomy, he takes home a prescription for Viagra,” says Bivalacqua. Does he take it every day, like a vitamin? No. Although some doctors prescribe the pills this way, it’s not what physicians call an “evidence-based” practice; that is, the medical literature doesn’t back it up conclusively.   Instead, Bivalacqua tells his patients to take it as needed. “It is very difficult for me to tell a man that he should spend $600 a month to take a daily erection drug, because the evidence of a quicker return of erections is just not there.” However, he adds, “taking a pill daily may provide a benefit, and a lot of prostate cancer patients want to take a proactive approach. If that’s the case, then I encourage them to go ahead.”   Pat Walsh gives his patients samples of different types of ED medications, because each one works a little differently, so his patients can find the one that’s best for them.

Don’t just take a pill once and give up if it doesn’t work.

Taking an ED pill can boost confidence as well as help with erections, but even so, the first try might be frustrating. “I tell men that it often takes three or four attempts with Viagra to have a true response that will allow penetrative sex.” This doesn’t usually occur within the first couple of months after surgery. “Usually men see the most meaningful recovery around 9 to 12 months after surgery,” Bivalacqua notes. Just to recap here: Don’t be discouraged if the first time after surgery is not that great. And don’t give up.

Hear these words: “The penis works. The blood supply to the penis is still good.” So basically, it’s like a car that is having trouble starting. What you may need is a jump-start to get it going. That doesn’t mean you will always need this. Your body is going to continue to recover. It just means that at least right now, you might need a little help.

Now, here’s a question Bivalacqua asks all of his patients a couple months after surgery, when they are healing and are no longer having any problems with urinary leakage. (Note: not every man has urine leakage after surgery, but some men do and it is usually temporary.) “How important is it to you to have penetrative sex?” If that is very important to the man and his partner, “then I ask how often he has tried Viagra over the last four weeks.” If the man has tried it multiple times with no success, “I recommend that he start injection therapy immediately.” Remember, the penis works. “By injecting a medication that will increase the blood flow to that area, the man has a very good chance to restore erections and get that important part of his and his partner’s life back.”

Injection therapy? You mean, sticking a needle in the penis? Well, yes. But it’s a tiny needle, and your doctor won’t just hand it to you and say, “Good luck, buddy.” You will be taught how to use it. “Injection therapy allows a man to have sexual intercourse again,” says Bivalacqua. Very important: “We know that the more blood flow there is throughout the penis following a nerve-sparing radical prostatectomy, either with a pill like Viagra or with an injection of a pharmacological agent, the better the chances of regaining erections.”

Bivalacqua explains: “If you don’t have enough blood flow within the penis after surgery, it becomes ischemic; it does not get the nutrients it needs to stay healthy.”

Let’s take a moment to think about rehabilitation – say, after a bad injury. Maybe a man needs to learn to walk again, or use his hands, or how to talk again. If that guy just sits around and hopes it will happen and gets frustrated when it doesn’t, you may agree that he’s not taking the approach most likely to guarantee success. To put it bluntly, your penis needs rehab, too: “By increasing the flow of oxygenated blood to the penis, whether it is from a pill or an injection, we are able to preserve the erectile bodies (these are chambers where blood flows to provide a rigid erection), so they will respond once those nerves start to work again.”

How injection therapy works: As its name suggests, Tri-mix is actually three drugs (papaverine, phentolamine, and prostaglandin E-1). “The specific formulation of these drugs is based on the type of erection achieved with test dosages in the doctor’s office,” says Bivalacqua. “We teach the patient how to self-inject,” and understandably, this may take some getting used to. “The medication is shot into the base of the penis with a small hypodermic syringe,” and it works pretty quickly – within five to 20 minutes. What happens is that the Tri-mix causes the smooth muscle tissue in the penis to relax; it also dilates the main arteries and allows blood to fill the penis. “The erection can last between 30 and 90 minutes, and it becomes more rigid with sexual stimulation.” However, it may not always disappear right away after orgasm. (Note: After prostatectomy, there is no ejaculation, because the organs that contribute fluid for semen are gone.)

How well does it work? Pretty well; the success rate is between 70 and 80 percent.   However, the main cause of failure is poor blood flow to the penis, Bivalacqua says. “Sometimes, although the shot produces an initial erection, it doesn’t last because the veins in the penis are damaged,” because of heart disease, diabetes, or other health problems, in addition to the surgery.

Each shot costs about $7, and even though it works, about half of men abandon it within a year. Bivalacqua speculates that one reason is that these men didn’t get good or detailed enough instruction for them to feel confident injecting themselves. Also, it may take two or three visits for an experienced urologist to determine the optimum combination and dosage of the medication.

The Vacuum Erection Device (VED) and penis-stretching: One fact about the penis: It needs activity. The nerves in those neurovascular bundles are also responsible for nighttime erections (in your sleep), and those “are responsible for penile health and strength.” Think of tiny push-ups happening in your sleep. After surgery – temporarily if one or both nerve bundles (the nerves to the penis) are spared – these erections don’t happen. If these bundles are damaged or removed during surgery, scar tissue can develop. When any part of the body is injured, a scar forms. This is because as it heals, tissue gets fibrosis (it hardens; this is the more rigid tissue that makes up a scar). There is extra collagen in there, and this contracts over time. This contraction can shrink the penis by as much as half an inch. Now, before you say, “That’s it! I’d rather have the cancer!” or make any hasty decisions, please read this next sentence: “The good news is that there is a way to prevent the loss of length in the penis: using a vacuum erection device,” Bivalacqua says.

Please note this important point: We’re focusing on stretching, not shrinking.

Briefly, the VED is what you might suspect; an actual vacuum. The device costs between $200 and $500, and is available from the pharmacy with a prescription. You place a clear plastic cylinder over the penis, and use either a manual or electrical pump to create negative air pressure (a vacuum). It takes about two minutes to achieve an erection; then you slip a flexible tension ring from the bottom of the cylinder around the base of the penis. This keeps the blood from flowing back out. “No matter what is specifically causing the erection, the vacuum causes the vessels in the penis to fill with blood, just as they would during a normal erection.” There’s a downside, though: “The big complaint of all men using the VED is that the penis becomes cold and semi-rigid, and this makes intercourse difficult.”

Granted, it may not be the best way for you to have sex. However, you may want to think of it more in the category of an exercise bike: It can help you get back in shape. A recent study from the Cleveland Clinic evaluated the early use of a VED after radical prostatectomy. There were 109 men in the study. “One group of 74 men used the VED at least twice a week, starting one month after surgery, for a total of nine months,” says Bivalacqua. “The second group of 35 men did not receive any erection treatment.” The study’s investigators found that “only about 23 percent of men who used the VED properly complained of decreased length and girth of the penis, compared with 85 percent in the group who did not use it as directed, twice weekly. And 63 percent of the men in the control group – who didn’t use a VED at all – reported a decrease in the length and girth of the penis. To sum up: “What the VED does is stretch the penis. It is this stretching that will prevent the penis from contracting, or shrinking, after surgery.”

If You Still Need Help

MUSE: Meh. There is another type of therapy, called MUSE. Bivalacqua doesn’t recommend it, but your doctor might talk to you about it, so here’s what it is: MUSE stands for “Medicated Urethral System for Erections.” Basically, you take a small plastic plunger, and use it to press a tiny pellet (about the size of a grain of rice) into the tip of the penis. When it dissolves, it triggers an erection. It can also burn. “Many men complain of a burning pain in the penis after inserting the pellet,” says Bivalacqua.   Also, “the erection that you get is soft; it is not very rigid.” And, just as with the Tri-mix used in injection therapy , your urologist will need to determine the right dosage for you. “Some men may need double or triple the standard dose, but other men are so sensitive to the medication that they have actually fainted with the highest test dose.” Compared to an injection, “MUSE is nowhere near as effective.”

Penile Prosthesis

Instead, if pills or injections are not a good long-term solution, Bivalacqua recommends a penile prosthesis. “The device is just phenomenal,” he says. “Pills like Viagra are popular, because they’re easy to take, and when they work, they’re great. But the next most popular option is the penile prosthesis, and it works as advertised 100 percent of the time.”

It also looks 100 percent natural. It’s not some cyborg penis. For all practical purposes, it is your actual penis – just more reliable.

A penile prosthesis is an implant. It requires surgery to put it in. The procedure takes about an hour, and although it can be done on an outpatient basis, many urologists have their patients stay overnight.

How it works: Hydraulics. “The device is made up of two extremely compact, hollow cylinders,” explains Bivalacqua. These come in a variety of widths and lengths. “A small container that holds fluid is inserted in the lower part of the abdomen, and a pump is implanted in the scrotum. “ To get an erection, you squeeze the pump several times. This sends fluid from the reservoir to the inflatable cylinders, which then expand, making the penis get longer and wider – just as in a regular erection. Afterward, you squeeze a valve at the top of the pump, the fluid returns to the container in the abdomen, and the erection goes away. “The device is extremely durable and reliable,” says Bivalacqua.

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

 

American men need a baseline PSA test and rectal exam to check for prostate cancer in their forties, and then they need follow-up screening at regular intervals – maybe every five years, if the PSA number is low and nothing feels abnormal in the exam, or maybe more often, depending on the number. Men who are at higher risk – men with a family history of prostate cancer and other forms of cancer, and African American men – need to start screening earlier, ideally at age 40.

Have you been screened yet? If not, why not? Read more

We are living longer, and 75 is not the ripe old age it used to be.  But it’s a cutoff age for PSA screening – and this is missing cancer in men who really need to be treated, say Brady investigators.  “There is increasing evidence that this age-based approach is significantly flawed,” says Johns Hopkins urologist Patrick C. Walsh, M.D.  Walsh and I have written several books on prostate cancer, and this new information is being added to the upcoming 4th edition of our book, Dr. Patrick Walsh’s Guide to Surviving Prostate Cancer, which we’re writing now.

 doctor medicineWalsh is the senior author of a recent Johns Hopkins study that looked at high-risk prostate cancer in older men.  The study’s interdisciplinary group of investigators also includes first authors Jeffrey Tosoian and  Ridwan Alam, and Carol Gergis; Amol Narang, Noura Radwan, Scott Robertson, Todd McNutt, Ashley Ross, Danny Song, Theodore Deweese, and Phuoc Tran.   

The U.S. Preventive Services Task Force recommends against screening for men over 75.  “There’s no question that there has been overtreatment of prostate cancer,” says urologist Tosoian. “However, that is getting better; more men are taking part in active surveillance programs, and we are much better at interpreting PSA and other biomarkers to rule out aggressive disease.”

But PSA can’t be interpreted if a man doesn’t get his PSA tested.  Population studies have shown that “men diagnosed at 75 years or older account for 48 percent of metastatic cancers and 53 percent of prostate cancer deaths, despite representing only 26 percent of the overall population,” says Tran, clinical director of Radiation Oncology and Molecular Radiation Sciences at Hopkins.  

Why are older men more likely to die from prostate cancer?  To find out, the team studied 274 men over age 75 who underwent radiation therapy for prostate cancer. “We found that men who underwent PSA testing were significantly less likely to be diagnosed with high-risk prostate cancer, and that men with either no PSA testing or incomplete testing (either a change in PSA was not followed up, or a biopsy was not performed when it was indicated); had more than a three-fold higher risk of having high-risk disease at diagnosis, when adjusted for other clinical risk factors,” says Tran.

Although this was a small study and more research is needed, Walsh says, “we believe that PSA screening should be considered in very healthy older men.”

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington