Cancer loves sugar, and sugar really loves cancer.  Isn’t that sweet?  Actually, no, it’s more like a match made in hell – because sugar (glucose) makes many types of cancer grow faster.

Scientists have long known that cancers soak up glucose like a sponge; in fact, German physiologist Otto Warburg, who found that tumors extract glucose at a rate 20 to 50 times higher than do normal cells, won the 1931 Nobel Prize for for his research on metabolism.  Lew Cantley told me that.  Cantley, Ph.D., is a world-renowned scientist and Director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.  I recently interviewed him for the Prostate Cancer Foundation’s website, pcf.org.

Cantley has spent much of his career studying the interplay between sugar and cancer.  His studies suggest that it’s not so much the amount of glucose in your bloodstream that helps promote cancer, as it is the level of insulin, the hormone made by the pancreas that controls glucose.  Insulin helps turn glucose into immediate energy, and also helps your body pack it away for longer-term storage.  Briefly, when you eat, your blood sugar goes up; this causes your pancreas to say, “Hey! We need to make more insulin!”  Insulin, like Paul Revere, then travels rapidly throughout the land, telling the cells to let the glucose in, either to be used right away or saved in muscles, fat cells, and the liver.

Why does a tumor suck up more glucose?  “The main reason,” says Cantley, “is that insulin can turn on the glucose transporters (proteins on cell membranes that carry glucose into cells), similar to those in the liver, muscle and fat.  The presence of those glucose transporters on tumor cells is in part regulated by insulin.  That’s why I keep focusing on the insulin.”

Cantley began studying the insulin receptor in the 1980s, when he was on the faculty at Harvard University.  A few years later, after moving to Tufts University, he discovered an enzyme called phosphoinositide-3-kinase (PI3K); PI3K signals cells that insulin is present; the cells, in turn, open the valve that lets in sugar.  Normally, PI3K does good and vital work, helping cells survive, grow and proliferate.  But sometimes it goes awry; in Type II diabetes, this PI3K pathway becomes sluggish, cells don’t respond appropriately to insulin and become insulin-resistant.  But in cancer, even in someone who’s insulin-resistant, PI3K does its job too well; glucose floods in, tumor cells feast on sugar and grow faster.  “What we now know is that mutations in the PI3K pathway make tumor cells hyperactive in response to insulin.”

In many cancers – sugar-loving cancers; not all cancers are addicted to sugar, but many are – PI3K is like a power switch that drives growth“PI3K is the most frequently mutated cancer-promoting gene in humans,” says Cantley.  It may be involved in as many as 80 percent of cancers, including breast cancer, bladder cancer, and certain brain tumors.

What about prostate cancer?  Well, one of the most common genetic events in prostate cancer is the loss of a gene called PTEN; cancer just knocks this gene out.  “PTEN makes an enzyme that reverses what PI3K does.  PI3K makes a lipid, and PTEN destroys that lipid; you have to have a balance between those two enzymes to keep growth under control.  But in prostate cancer, and in breast cancer , the loss of PTEN activates production of this lipid that drives cell growth.

“This tells us we probably should try to keep insulin levels as low as possible if we have cancer, to try to keep the tumor from growing.   If we can keep the diet under control, or exercise to keep glucose levels and insulin levels low, we have a much better chance of slower growth of the tumor.  Our research would also argue that pharmacological intervention would be more effective if we keep insulin levels low.”

Even better:  Keep insulin levels as low as possible anyway, whether you have cancer or not.  “This is a powerful potential cancer-prevention mechanism,” says Howard Soule, Ph.D., Executive Vice President and Chief Science Officer for the PCF.  “Reducing processed sugar may turn out to be even more important for cancer prevention than treatment.”

Can we learn to use cancer’s sweet tooth as a weapon against it?  Cantley’s research has already led to the development of several PI3K-inhibiting drugs: idelalisib, approved by the FDA in 2014 for treatment of lymphoma and leukemia and alpelisib, approved in 2019 for treating breast cancers with mutations in PI3K.  But Cantley also believes that changing the diet – to one low in sugar, but also low in other carbohydrates, which can cause blood sugar to spike – can make cancer-fighting treatments work even better.  In a landmark 2018 paper published in Nature, Cantley and colleagues showed in mice that by severely restricting carbohydrates “and keeping the insulin level low, tumors would respond much more dramatically to drugs that are already approved to treat them.  Tumors we had never been able to shrink in mice, we could shrink with a low-glucose diet.

“That’s my obsession now, to get that message out there.  Endocrinologists tell patients to exercise more and eat less sugar to keep diabetes under control, but for me, it’s even more critical to keep insulin levels low in order to get better outcomes for cancer patients.”  Cantley’s research suggests that “if you have a mutation in the PI3K pathway that causes cancer, and you’re eating a lot of simple carbohydrates, every time your insulin goes up, it’s making the tumor grow.”

How can this knowledge help slow the growth of prostate cancer?  Here’s one example:  “For prostate cancer patients with low Gleason scores who are on active surveillance, it makes perfect sense to pay a lot of attention to what you eat.  Try to keep your consumption of sugary drinks as low as possible.  Keeping sugar down is the best thing you can possibly do.”  It used to be, Cantley notes, Japanese men hardly ever got prostate cancer.  “But second-generation Japanese Americans have prostate cancer in similar rates to Caucasians.  It’s clearly lifestyle,” the Western diet.  “The truth probably is that some Japanese men in their 90s had some level of prostate cancer, but didn’t consume enough sugar for the cancer to advance.”

Here’s another:  If you are on ADT for metastatic prostate cancer, you are more likely to gain weight, and also to develop insulin resistance.  One way to fight this is by limiting your sugar and simple-to-digest carbs.  Bonus: keeping insulin down may also help slow down the cancer.  Watch out for protein drinks, too; many are loaded with sugar.

What about the ketogenic diet?  It’s low in carbs and high in fats.  “I’m not preaching the ketogenic diet; I don’t eat it myself,” says Cantley, who says he weighs the same now as he did in high school.  “I eat what my grandparents ate:  a healthy diet, lots of raw vegetables, some animal fat, healthy vegetable fats, an intermediate amount of protein.  I don’t avoid fats, but I prefer olive oil on salads, and healthy fats from fish and avocado,” instead of loading up on butter and cheese.  “I eat more protein than the ketogenic diet would recommend, and I do occasionally eat rice and pasta.”

But here’s the kicker:  “The one thing I’m fanatic about is not drinking anything with sugar:  no orange juice, no apple juice, no soda.  I’ll eat an orange, but I won’t grind it up and drink it.”  Sugar in liquid form is rapidly digested, which results in “glucose peaks, followed by insulin peaks.”

What about alcohol?  “A dry martini is probably safer than wine; there’s not much sugar in there.”  However, Cantley adds, “I do drink wine, but as low in sugar as possible.”

Exercise is a great way to divert sugar into someplace safe:  the muscles.  “Muscle is where you store a lot of sugar in your body.  If you drink a sugary drink after exercising, your insulin goes up, and you drive all that glucose into your muscle.  Whether you’re exercising at the time you drink a sugary drink, or you just put on muscle from exercise in general, there’s still a benefit: insulin won’t spike.”   However, exercise doesn’t make it safer to drink a lot of sugary drinks, because…

Sugary drinks are bad.  It’s not just sodas; sweet teas and coffee drinks have more sugar than you may realize.  Even sports drinks are loaded with sugar.  In 2019, Cantley and colleagues published another landmark paper in Science, involving mice with polyposis syndrome (mice genetically predisposed to developing polyps in the colon).  They demonstrated that sugary drinks can dramatically drive the growth of intestinal polyps.  “We gave mice high-fructose corn syrup, and their polyps grew two to three times faster.”  Fructose is a different sugar from glucose, and although “fructose is not consumed by tumors, it goes straight to the liver and turns into fat.  Fructose makes you fat.  But the other issue is that intestinal epithelial cells can directly consume fructose.  We think this explains why there has been a doubling to tripling rate of colorectal cancer in young adults.”

Consuming sugar in liquid form is worse than having that same amount of sugar in solid form.  Cantley explains:  “If you eat an apple, it takes a long time to get to the colon.  By the time it gets there, all that sugar has leached out.  But if you have that same amount of sugar in a drink, that watery sugar gets to the colon pretty quickly.  That’s independent of the insulin elevation (discussed above), and it’s another scary reason why young people should avoid drinking sugary drinks, no matter how much you exercise.  You may be a champion marathon runner, but if you’re drinking sugary drinks all the time to keep up your energy, this is a real warning that you should pay attention to.”

Now, back to prostate cancer:  Would taking a PI3K-inhibitor help slow cancer’s growth?  As is often the case with prostate cancer, it’s not that simple.  It turns out that there are two different kinds of PI3K, an alpha and a beta form that can contribute to prostate cancer.  “When prostate cancer loses PTEN, it uses PI3K alpha and beta form redundantly to drive the tumor.”  This means that a drug that targets only the alpha form probably won’t be as effective in prostate cancer as in other forms of cancer, where only the alpha form of PI3K is involved.

However, “our preclinical findings are overwhelmingly supportive, and the retrospective data in patients strongly suggests” that one day, in addition to surgery, radiation, hormonal therapy or other treatments for prostate cancer, patients will be prescribed a precision diet to make the treatment more successful.  “The more we learn about cancer metabolism, we are understanding that cancers are addicted to particular things.  For many cancers, that thing is sugar.”

In addition to the book, I have written 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

 

 

Here we are in a global pandemic; we’re all stressed, and we all need to fight it.  If you have prostate cancer, you need to fight it even harder, because the stress hormone, cortisol, may be affecting your cancer, AND because lowering your stress may help your cancer respond better to treatment.  

Having prostate cancer is stressful, even today, when there is more hope of successful treatment than ever before.  But it’s not just the cancer itself.  It’s the hassle of wrangling with an insurance company, and the worry about medical bills or taking time off for treatment; it’s frustration over a slower-than-expected recovery of urinary continence or sexual potency.  It’s anxiety about the next PSA test.  It’s unanswered questions and uncertainty, and worry that life will never get back to normal.  Yes, there’s stress, and plenty of it.    

Does stress make prostate cancer worse?  This one’s not so easy to answer.  “Everybody has an individual response to stress,” says medical oncologist Suzanne Conzen, M.D., Chief of Hematology and Oncology at the University of Texas Southwestern Medical Center in Dallas.  And that’s the key, she adds:  it’s not so much the stress itself but the physiological response that can take a toll, and that may hinder our ability to fight cancer.  Conzen is studying stress pathways in cancers, including prostate cancer.  I recently interviewed her for the Prostate Cancer Foundation (PCF), which is funding some of this research.

The body responds to stress with a surge of corticosteroids; primarily cortisol.  When our ancient ancestors were running for their lives from a savage beast, it was this stress hormone, cortisol – along with adrenaline – that kicked in and saved their bacon.  “We are hard-wired to respond to stress with this ‘fight or flight’ response.”  Unfortunately, many of us react to everyday troubles with the same surge of stress hormone as if we were facing a sabertooth tiger – as if we were under attack.  Our hypothalamus, located in the most primitive part of the brain, tells our adrenal glands, “This is the big one! Go to Defcon 3.”  And cortisol, revving up in its effort to save us – a chemical version of someone running around in a panic, shouting, “Ohmygod, ohmygod,” can cause harm instead, affecting normal functions including the immune system, and even changing genes that are expressed in cancer cells.

“Some people have a higher stress response than others.  It could be an inherited tendency; or they haven’t necessarily developed effective ways of coping with exposure to stressors,” says Conzen.  “However, not all people who have a high stress response get cancer; and a lot of people are under stress and don’t get cancer.  But that’s the complexity: not everybody who smokes gets lung cancer, but smoking is a risk factor.  What you want to do is reduce your risk factors,” and your response to stress – like a bad diet, or smoking, or being overweight – is a risk factor for prostate cancer that can be changed.

“We think high cortisol levels are probably not a good thing in men who have prostate cancer.  At least a subset of those men may have tumors that respond to high levels of stress because the prostate cancer expresses a protein, the glucocorticoid receptor (GR), that is activated by cortisol,” and although Conzen is working on how to determine who these men are, right now, there’s no way to know for sure.

Cortisol, a hormone, attaches to a protein called the glucocorticoid receptor (GR) in cells throughout your body, and this is like flipping a switch that activates stress in all those cells, including cancer cells.  In ovarian cancer, Conzen has shown, higher levels of these receptors in the tumor tissue are linked to more aggressive, even lethal, disease.  And in prostate cancer, she has found that the GR “is more highly expressed in cancer that is resistant to androgen deprivation therapy (ADT).”

But it’s complicated, she adds:  “We think it’s not only how much GR your tumor has, it’s how active it is.”  With PCF funding, Conzen and colleagues in her lab are working to find a way to measure how active cortisol and GR are in a prostate tumor, “whether it’s turning on and off a lot of genes, or just a few genes.  The amount of GR does not necessarily correlate with the activity of the protein.”

So, how to fix it – if a man has aggressive prostate cancer, and high cortisol/glucocorticoid receptor activity?  “One hypothesis would be, deprive that tumor of your body’s stress hormone receptor activity, by keeping the stress hormones relatively low.”  This could happen with some type of medication – or, it could happen with stress reduction.  What is that, exactly?  It could mean making changes in your life, so there are fewer stressful factors in it.   It also could mean making changes in you – with the help of such things as exercise, yoga, meditation, and counseling, and other things to help reduce stress, like having a pet, and reaching out to family, friends or a support group, so you’re not coping with this alone.

Note:  Conzen does not believe that stress, all by itself, causes prostate cancer.  “My guess is that GR-mediated stress signaling in the tumor cells probably has more to do with promoting aggressiveness and progression of cancer,” and perhaps recurrence of cancer.   When Conzen talks about stress, she doesn’t mean a single traumatic incident, such as a car crash:  “The kind of stress we’re talking about is daily unremitting stress.”  Those countless little things that add up, day after day.

Also with PCF funding, Conzen and colleagues are working to identify which genes in prostate cancer cells are involved with the stress response, and what those genes are doing when the tumor cell GR is activated in a man who already has prostate cancer.  “If we knew that, we would know when it would be useful to give a drug (a GR-modulator) to block it,” especially if they could find a drug that would only work in prostate cancer cells.  Glucocorticoid receptors are expressed in a subset (about 20 percent) of castration-resistant prostate cancer.  Conzen and colleagues have initiated clinical trials testing GR-modulating drugs in breast cancer, prostate cancer, and other cancers. In advanced prostate cancer, there are at least three ongoing clinical trials testing GR-modulators: 1) enzalutamide alone vs. with the GR-modulator mifepristone; 2) the GR-modulator CORT125134 plus enzalutamide; and 3) the GR-modulator CORT125181 plus enzalutamide.

In the meantime, stress reduction may help achieve similar results for men with prostate cancer, by lowering circulating cortisol activity.  Clinical trials are needed, Conzen notes, to show the effectiveness of stress response-reducing measures including cognitive behavioral therapy, medication, yoga, and mindfulness in prostate cancer patients.  Such trials have been done in breast cancer, she says, “and have shown that there is a beneficial effect.”

 

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

 

Incontinence after prostatectomy is one of the most feared complications.  The good news is that for nearly all men, it goes away.  For the very small percentage in whom it doesn’t, there is help.  This story is a very strong case in point.

In my work for the Prostate Cancer Foundation’s website,  I was lucky enough to interview JP Mac, who has had a particularly difficult struggle with incontinence after prostatectomy.  JP (real name: John P. McCann) is a novelist and an Emmy award-winning animation writer who worked for Warner Bros. and Disney.

He is also very funny.  So, when he wrote a short ebook (coming soon in paperback form) about his experience with prostate cancer – including his diagnosis in 2014 at age 61, the rush to find the right treatment and get it done before his health insurance was going to expire, his laparoscopic-robotic prostatectomy and the complications afterward, and his five-month battle to recover urinary continence after the surgery – he could legitimately have written a soap opera, or maybe even a tear-jerker; but he didn’t.

Instead, his ebook has a title that sounds like 1950s pulp fiction: They Took My Prostate: Cancer, Loss, Hope.  It’s not “Prostate Cancer Lite,” and it doesn’t minimize what he or anyone else has gone through to get back to normal after radical prostatectomy.  Far from it; in fact, his “short, hopeful essay” is a testament to what it takes to recover from this difficult but life-saving surgery: a balanced perspective, a good sense of humor, a great support system, and plain old hard work and persistence.

Here’s a message you hardly ever hear about prostate cancer, or any illness, for that matter:  It’s okay to laugh!   That doesn’t mean it’s not scary, and that it doesn’t wear you down, or that you’re not afraid you won’t ever get back to normal.

But if it’s laugh vs. cry, Mac would rather laugh.  Although no cancer is great, he says, prostate cancer is “especially seedy,” and in his case, it involved  “bloody urine, black feces, incontinence, impotence, vomiting, and various other bodily malfunctions that shouldn’t be discussed before supper.”  But he does discuss them, with the hope of helping other men and their families.  Mac knows that talking about what’s happening gives the cancer less power over your life, and helps you focus on the light at the end of the tunnel – getting your life back after the cancer is cured.

Mac is speaking out about one area, in particular, that doesn’t get talked about much: urinary incontinence.  For many men who suffer from it, in fact, there might as well be a Cone of Silence over this subject, and that’s a shame, because there is always help for urinary incontinence after radical prostatectomy.

When Mac was diagnosed with prostate cancer, his surgeon told him to buy our book, Dr. Patrick Walsh’s Guide to Surviving Prostate Cancer.  Mac did, and he referred to it a lot – especially our review of the male plumbing, which explains why at least some temporary incontinence is just about inevitable for men after radical prostatectomy.

Note: Long-term urinary incontinence is very rare after radical prostatectomy.  Results differ depending on the surgeon; also, some men have quirky anatomy — very subtle anatomical variations (not like a leg where an arm should be, or anything like that, but even tiny differences can be important in surgery, and good surgeons know this and look for such variations).  This is why, if you are considering radical prostatectomy, it is essential to find out how many of that surgeon’s patients have long-term complications.  If your surgeon doesn’t know, consider this a red flag.

The best surgeons keep track of their patients after radical prostatectomy. “In young (men in their forties, fifties, and early sixties), healthy men operated on by an experienced surgeon,” Walsh says, “about 80 percent should be wearing no pads – or at most, a security pad to catch the occasional drop – by three months after surgery, and at 12 months, 95 to 98 percent should be continent.”  Walsh considers a man continent “if he wears no pad or if he wears a pad that is dry.  “Many men continue to wear a small pad just to be safe,” he explains.  Your surgeon may have a different definition of continence, and you should find this out before surgery.  “Most men, even at three months, are not very wet.  It’s hard to believe, but urinary control does continue to improve over two years, and occasionally, even longer than that.”

But don’t lose hope, he adds:  “For many men, the recovery of urinary control is a slow process. The most important thing you can do is not get discouraged.  If your doctor told you there is only a 2 percent chance that you will have a long-term, serious problem with urinary control, believe it.  This means there’s a 98-percent chance that you’ll be back to normal someday, even if nobody can say exactly when.”

From Three Sphincters to One

Why is urinary control an issue after surgical removal of the prostate?  Normally, Walsh says, men have not one, not two, but three separate anatomical structures to control urine.  There is a sphincter in the bladder neck, one in the prostate itself, and then there’s the external sphincter (also called the striated sphincter), below the prostate. Radical prostatectomy knocks out two of these, leaving only the external sphincter to do the work of three.

Because of the other two sphincters, in most men this external sphincter is never tested or even used much; there is no way to know before radical prostatectomy how strong it really is.  Also, like every other muscle, this sphincter loses its tone with age.  A complicating factor is that older men are more likely to have some benign enlargement of the prostate (BPH), too. This could make the bladder thicker and more muscular – and much more powerful than a sphincter that may not have been that effective to begin with.

Mac didn’t really think about this in a lot of detail until his catheter came out after the surgery.  “A nurse handed me a thick cotton pad to put in my underwear.” Mac’s urologist “warned me that the urine was coming, as surely as a Cambodian rice farmer predicting the monsoon. Little could be done, he explained, until I underwent physical therapy. There I’d learn exercises to strengthen the underused muscles of my external sphincter.”

Mac was so happy to have the catheter out that he thought the worst was over.  Cotton pad in place, he made an appointment to come back in three weeks, and took his wife out for breakfast.  “Rising an hour later after three cups of coffee,” he gushed urine “as if putting out a fire in a wastebasket.”  It turns out that the worst was just beginning.  “Basically, the bladder holds urine until a series of reflexes causes a bathroom urge.  Bladder and sphincters then receive a message from the brain to check flow until an appropriate time. When you’re incontinent, any time is just dandy.  You can experience stress incontinence with activities that suddenly increase pressure inside the abdomen, like lifting or standing. Then there’s urge incontinence, which is a sudden uncontrollable need to leak.  Finally, there’s overflow incontinence when you can’t sense if the bladder was filling.  I had all three.”

Suddenly, Mac’s new normal was a life with absolutely no bladder control.  “Movements gross and subtle, lying on my back, it didn’t matter. Everything ended in a demoralizing urine surge. I really needed that physical therapist. But our new insurance had other ideas.

While he “moped around home like the Incredible Surging Man,” his wife, Joy, spent hours on the phone wrangling with the old and new insurance companies, whose bureaucracies were “sharp as a paper cut,” Mac comments. Meanwhile, he experimented with leakage protection:  “I tried packing my regular underwear with cotton pads. That idea cratered in less than a day. Not only were ‘man diapers’ necessary, but they required cotton pads inside as well. I was soaking through three pads a day minimum. Each morning, I’d wake up drenched, smelling like an interstate washroom.”

Days passed until, Joy finally convinced the insurance company that “we were, indeed, customers and had paid for a specific plan.” Then, the insurance company insisted that the physical therapist wasn’t covered by the plan.  Mac was desperate; his urologist’s office staff stepped in to wrangle with the insurance and finally got the go-ahead for the physical therapist. While all this was happening, “I lived the life of the urine free spirit.  Avoiding coffee or soda mattered little. No internal spigot staunched the constant flow.”  Mac got sick of smelling urine, of feeling that he was “marinating in pee.”

Three or more times a night, he says, “I’d awaken with man diapers soaked and pressure on my bladder. Sitting up, I’d whiz into a hand urinal, change, clean myself, then lie back down and hope for a little sleep before the next voiding.”

At last, Mac could see a physical therapist.  Mac drove to the appointment – his first time behind the wheel since the operation – hopped out of the car, and soaked himself again.  Then he met Eva, his physical therapist, who used biofeedback to help him identify the right muscles to use.

“She hooked my perineal and abdominal muscles to a laptop via adhesive pads, and for the next hour, gave instruction in finding, then clenching and unclenching my striated sphincter in order to control urination. On the computer screen, I could monitor my efforts. A moving graph alerted me when I targeted the correct muscles.”  Mac learned how to do Kegels – clench-and-release exercises to strengthen the pelvic floor muscles below the bladder.

“I found biofeedback to be of great value,” and for Mac, it helped him start to regain bladder control.  “I know a guy who underwent the same radical robotic prostatectomy,” he says.  “Afterwards, his urologist tossed him a few sheets of diagrammed Kegel exercises and said ‘Vaya con Dios.’ No one told my friend you could overdo these exercises. While other factors may’ve been in play, his continence recovery turned out to be longer and messier than mine. Maybe a little biofeedback could’ve improved his condition quicker.”

Eva gave Mac daily exercises with frequency and duration goals.  She also encouraged him to walk daily.  Psychologically, the Kegels were important,” he notes.  “I lived with a constant dribble that could transform into a flood. Eva’s exercises provided me concrete specific actions. She also warned me against overtraining that could fatigue the striated sphincter, rendering it too tired to work.”

Five days later, at his next PT session, “I saw progress.”  For the first time, he could stand up without urinating.  Next, he learned to anticipate the “go” urge – and not wait until he felt pressure in his bladder.  “I could then reach the toilet with something left in the bladder.”  Mac discovered that, in order to stand up without putting excess pressure on his bladder, he had to walk bent over, “like Groucho Marx.” At first, he could go maybe three or steps without a surge.

Joy noticed improvement before Mac did; so did his urologist, who told him, “a lot of the discomfort you’re feeling now will pass. Once you strengthen the striated sphincter, your bladder urges will stabilize.”

There was some good news:  Two months after surgery, Mac’s PSA was undetectable.  His cancer was gone!  And finally, after much hard work, his bladder control began to return.  “With persistence, I sensed how to locate and activate my new bladder-control muscles.  Eva suggested I aim to eliminate jug peeing (with the handheld urinal at night) and excessive bathroom visits.  Using the striated sphincter, I should school the bladder, aiming for fewer, but more productive, bathroom trips. In the meantime, I discovered a cost-effective method of cutting down on cotton pads out in public. By inserting several sheets of double-ply toilet paper into my man diaper, I caught the wild leaks. Just toss and replace the tissue. It was easier than finding a stall and swapping out cotton pads.”

Then, for two nights in a row, he only urinated once. By mid-November, nearly two months after his surgery, “I’d slept an entire night without awakening to pee.  In the morning, I loped ape-like to the bathroom and urinated. Just after Thanksgiving, I stopped wearing man diapers and returned to underwear, albeit with a cotton pad and toilet paper inside.”

For Christmas, Mac and Joy flew to the Pacific Northwest to visit his sister.  Traveling was “an adventurous time, with me unable to cross forty feet of airport concourse without running into a washroom jackknifed over.  I grew to be an expert at identifying tile patterns.”

But even his “odd potty walk” would not last forever. By March 2015, “ I could check flow and walk upright to the bathroom.  My newly discovered striated sphincter knew the routine and exceeded expectations.  I’d finally turned a corner.

It might not seem like it now, if you’re going through the worst of what Mac endured, but remember: only about 2 percent of men have long-term incontinence after radical prostatectomy, and if you’re in that percentage, there is still hope. Talk to your urologist about biofeedback, which made all the difference for Mac.  Other options include collagen injections, a mesh sling to help take some of the pressure off of the sphincter, and for severe incontinence, an artificial urinary sphincter.

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

Two recent studies bring good news for those of us who either don’t have a lot of time to exercise, or just don’t like it and don’t want to spend an hour working out: bursts of cardiovascular activity matter. A lot.

For those of us who are getting older (which, unless you’re dead or cryopreserved, or both, is everybody), nothing is better at delaying aging than exercise, say Mayo Clinic investigators, who recently published a very interesting study in the journal, Cell Metabolism.  In other words, there is no magic bullet pill or thing you can eat that will do as much as exercise to keep you living longer and healthier.

Well, we kind of knew that. But the really good news here – especially for those of us who don’t just have scads of time or willpower to spend at the gym – is that it doesn’t have to be for a huge chunk of time every day.

The Mayo researchers didn’t just look at the things we usually think of with exercise – weight loss, better endurance, muscle mass vs. fat, maybe improvements in mood or functioning. Instead, they looked at the effects of exercise in younger and older adults at the molecular level. Particularly, they were interested in the effects on the mitochondria – the battery packs that produce energy in our cells.

The study’s volunteers – 36 men and 36 women in two age groups: young (18-30) and “older” (age 65-80) – were healthy but sedentary. They underwent tests to establish baseline levels for their aerobic fitness, blood sugar, and the gene activity and health of the mitochondria in their muscle cells. Then they were randomly assigned either to a control group (no exercise) or one of three different exercise programs: high-intensity interval biking (pedaling hard for four minutes, resting for three, and repeating three more times); vigorous strength training with weights; and a combined program of light weights and exercise bike-riding (at a moderate pace for 30 minutes, a few times a week).

After 12 weeks, all the participants had repeat lab tests. As you may expect, everybody who exercised had better fitness and blood sugar levels. The people who did weights gained more muscle mass, and the people who did interval training had better endurance.

But the really significant changes were invisible to the naked eye. In the under-30 people who did the interval training – the vigorous bike-riding for four minutes, four times – 274 genes showed increased activity; those who did the more moderate exercise had changes in 170 genes, and the weight-lifters had changes in 74 genes.

Think that’s exciting? Well, it is, but it’s not nearly as exciting as what happened to the seniors who did the interval training: nearly 400 genes showed higher activity, compared with 33 genes in the weight-lifting group and a sad 19 genes in the people who just did the moderate exercise. The oldsters who did the bursts of exercise had healthier mitochondria, too.

What do we take away from this study? That you’re never too old to benefit from exercise, for one thing. And for another, just because you’re older doesn’t mean you are past the point of vigorous exercise – especially if it’s just for a few minutes at a time.

If you aren’t already exercising, you should talk to your doctor to make sure it’s okay. Then, if you’re cleared for takeoff, don’t be like that guy at the gym who’s reading a book or watching the TV on the wall and cycling about one mile a minute, pedaling so slowly that if he were on a regular bike, he would fall over because he’d have no momentum. That barely even counts, and I see people like this at the gym all the time. They have no problem carrying on a full conversation, either; they certainly aren’t short of breath.

Now, how can you apply this to your own life? If you ride a bike or use a treadmill, the timer is your friend. You don’t have to program anything; you can just increase the speed to a comfortable running level, and lower it to a brisk walking level. Do it for one minute. If you can’t do it for a minute, start with 30 seconds of running or pedaling harder, then work your way up. My favorite thing to do on the treadmill is walk at a brisk pace for a minute and a half, then run for a minute, then walk for a minute and a half, then run for a minute, etc., for 20 minutes. When I started, my speeds for walking and running were pretty pokey. Then one day, I was running at my customary pace and I thought, “Hmm. I can go faster,” so I did. I was walking at my customary pace, and I thought, “I can go faster,” so I did. You will be amazed at how much better you get over time.

This is similar to the kind of exercise our ancient ancestors got. I’m not talking about grandpa or even great-grandpa, but way back to the hunter-gatherer days. They didn’t go out jogging for the heck of it, and they certainly didn’t spin or do Zumba – but what they did do was put on bursts of speed when they had to, so they could bring down the animal they were hunting. Thus, I think that at some level, we are hard-wired to do this. Try it. Start small – just a few minutes total, at first – and see how you do.

This brings us to the next study, published in the Journal of the American Heart Association.

Scientists from the National Cancer Institute and Duke University looked at records of nearly 5,000 people over age 40 from the National Health and Nutrition Examination Survey from 2003-2006, and followed them for more than six years; during that period, there were 700 deaths. Then they looked at the amount of time those people who died had spent in moderate-to-vigorous physical activity (MVPA).

They found that all MVPA counted: even if it was just a few minutes here and there. It all went toward the daily total.

This is huge, because it goes against all the guilt-inducing exercise recommendations we have been treated to for decades. The conventional medical wisdom has been that exercise only counts if it’s sustained – for 20 or 30 minutes, or more. And the worst result of this is that many people have thought, “Well, I don’t have much time today, so I’ll just have to try to get in a good workout tomorrow,” or the next day, or next week.

Au contraire, say the results of this study: All exercise contributes to helping you not die. “For about 30 years, guidelines have suggested that moderate-to-vigorous activity could provide health benefits,” said the study’s senior author, William E. Kraus, M.D., of Duke University School of Medicine,” but only if you sustained the activity for 10 minutes or more. That flies in the face of public health recommendations, like taking the stairs instead of the elevator, and parking farther from your destination. Those don’t take 10 minutes, so why were they recommended?”

Why, indeed? Because every little bit helps. In this study, Kraus and colleagues at the National Cancer Institute found that the length of each period of exercise was not related to the overall benefit of living longer. Five minutes of jogging counts. Five minutes of riding an exercise bike counts.  Or five minutes of swimming a couple laps, or whatever.

The participants in the survey wore an accelerometer (similar to a Fitbit or the activity tracker on a smart phone) for up to a week. Looking at the data, the researchers looked at the people in two groups: those who had bouts of MVPA for about five minutes at a time, and those who exercised for longer than 10 minutes at a time.

People who got about an hour a day of MVPA – not an hour at a time, mind you, but an hour of little bits of exercise here and there, all added up – were half as likely to die. Those who got 100 minutes of exercise a day cut their risk of dying even more, by about 75 percent. Again, it was the total time they spent moving, not how long at a time they exercised, that mattered.

In this study, there was no distinction between intentional exercise and just plain old physical activity, like walking up a flight of stairs, or vacuuming the floor, or running to catch a bus.

“Despite the historical notion that physical activity needs to be performed for a minimum duration to elicit meaningful health benefits,” Kraus and colleagues reported, “we provide novel evidence that sporadic and bouted MVPA are similarly associated with substantially reduced mortality.”

In other words, it’s all good.

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

 

Hey, guys: If you think exercise is just about pumping iron and getting big traps, six-pack abs and “gun show” biceps, your prostate would like to disagree.

To your prostate, how ripped or shredded you are is not nearly as important as your cardiovascular health.

Now, you may be wondering, why should the prostate even care about cardiovascular exercise? Here’s a very good reason: exercise can lower your risk of getting lethal prostate cancer, or of having cancer come back if it’s already been treated.

Epidemiologist June M. Chan, Sc.D., an expert on lifestyle and cancer, heads a research program at the University of California San Francisco that seeks fixable risk factors for prostate cancer progression – things in your lifestyle that you can change to lower your odds of dying of prostate cancer. I recently interviewed her for the Prostate Cancer Foundation’s website.

In previous work, Chan and colleagues were the first to show that vigorous exercise (such as jogging or bicycling) after diagnosis was associated with a reduced risk of prostate cancer death in men with localized disease. “We observed that three or more hours a week of vigorous activity, as opposed to less than one hour a week, was associated with an approximately 60 percent reduction in the risk of dying of prostate cancer.” Chan and colleagues observed similar results among 1,455 men in the Cancer of the Prostate Strategic Urologic Research Endeavor (CaPSURE). These findings suggest that “engaging in relatively vigorous physical activity and/or having higher cardiorespiratory fitness may protect against prostate cancer progression.”

Now, exactly why is this? That’s what Chan and colleagues are hoping to figure out. “We have a number of studies here at UCSF examining lifestyle and prostate cancer,” she says. “One trial is for men on Active Surveillance, and our main goal is to look at changes in prostate tissue.” Investigators are comparing prostate biopsy samples taken at diagnosis and again after a 16-week period in which men are randomly assigned either to continue their usual activities or to take part in a personalized exercise program that is designed to increase their cardiopulmonary fitness. The researchers also are measuring chemical processes involving circulation and metabolism, looking for specific differences in the two groups.

In this study, Chan is not as interested in studying the men who are already exercising a lot. “We anticipated that the biggest benefits would be observed in individuals who are relatively sedentary and who adopt moderate exercise. If men are already highly fit, they’re probably already exercising several hours a week, and we thought it would be harder to ask them to do more or spend more time, so that we could observe a relative change in fitness,” she says. “Our main goal is to increase the fitness levels gradually through a walking program in men who are at low to intermediate levels of fitness at the beginning of the study.”

The idea here is that even moderate exercise can help lower the risk of lethal prostate cancer. We’re talking about the kind of exercise that almost everyone can do. It is “purposely scaled to be relative to someone’s baseline fitness, and we are choosing men who are low- to moderate-fit,” Chan notes. Men in this study start out just by walking, and then walking faster, and then escalating – literally – to walking uphill.

The men aren’t going flat-out, like someone in a high-intensity workout. They’re just doing a little more than they could, and after they get used to that, they do a little bit more – slowly building up their fitness.

Chan speculates that the tissue samples in the exercise group will show changes in indicators of angiogenesis (cancer’s ability to build a scaffolding of blood vessels and other infrastructure so it can grow and move beyond the prostate); in inflammatory processes; in insulin and insulin-like growth factor signaling; in androgen receptor signaling pathways; and in oxidative stress mechanisms. “Biochemically, exercise could help deter metastasis of the tumor by changing the environment for the cancer” – in effect, 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 confined to its current location.

Making 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 medical oncologist Jonathan Simons, M.D., CEO of the Prostate Cancer Foundation. “There is no form of treatment that has this effect, and certainly not one as beneficial to the entire body as exercise.”

It may be, Simons adds, that what exercise does – just as it improves blood flow in the arteries – is give 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, continental breakfast, and a pool. It’s content to stay there indefinitely, ordering room service. “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 found in research at Johns Hopkins, not only pipes in more blood to supply the tumor; it gets rid of waste products – the cancer cells’ sewage, in effect. “When tumors try to turn on blood vessel growth to get more nutrients, they also build their own plumbing for both intake and waste disposal. Angiogenesis is not just about getting oxygen and food – glucose and protein – to the cancer. It’s getting rid of byproducts, too. That kicks off a genetic program so the cancers can relocate” – start to spread.

But giving the cancer a better blood flow might subvert 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, of course, 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 have proved fatal,” notes Simons. 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. “What if you have a Gleason 8 cancer, you had surgery, your PSA was undetectable, and now it’s starting to creep up. And what if you could exercise and delay its colonizing in your bones by eight or nine years, because you so shifted the chemistry in your body that the cancer cells just sat there? That’s a very abstract concept, one that’s still not widely appreciated. But if we could get even three times as many men right now exercising, we could change the overall survival of the disease.” And if scientists like Chan can figure out precisely why this is happening, it may lead to development of new treatments that could make exercise even more effective in deterring the return or spread of prostate cancer.

Is it ever too late to start to exercise? No!

In other trials, including one funded by Movember, Chan and colleagues from around the globe are studying the benefit of aerobic exercise and also strength training in men with castrate-resistant prostate cancer, to see if these interventions can help men at a later stage of cancer live longer. “There are data in men with advanced disease also suggesting that exercise may impart not only quality of life but also clinical benefits” she says.

Body Size and Prostate Cancer

Prostate cancer loves fat. Fat increases inflammation in the body, lowers insulin resistance, and just generally makes a more inviting environment for prostate cancer.

But exercise burns fat. And this, in turn, lowers your body mass index (BMI).   “Increasing evidence suggests that being overweight, either before or at the time of diagnosis with prostate cancer, is strongly associated with the risk of cancer progression and of dying from prostate cancer,” says Chan. “For example, among 2,546 men diagnosed with localized prostate cancer in the Physicians’ Health Study, a one-unit increase in BMI before cancer diagnosis was associated with about a 10-percent increase in a man’s risk of dying of prostate cancer.”

BMI calculators are available on the internet, but briefly, if you are at a healthy weight, your BMI is between 19 and 24.9 kg/m2.  In the Physicians’ Health Study, having a BMI of 30 kg/ m2 or greater “was associated with a nearly twofold increased risk of prostate cancer death,” notes Chan. Further, “a meta-analysis of six studies in prostate cancer patients reported that a 5 kg/m2 increase in BMI raised the risk of dying of prostate cancer by 20 percent, and of biochemical recurrence (having the PSA start to rise again after treatment) by 21 percent.”

 More of this story and much more about prostate cancer are on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.” The PCF is funding the research that is going to cure this disease, and they have a new movement called MANy Versus Cancer that aims to crowd-fund the cure, and also empower men to find out their risks and determine the best treatment. 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 for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

 

In 1993, I actually wrote that sugar and carbs were fine. Want to be healthy? Eat more pasta and healthy grains, I wrote. Fats were the big evil. I was so wrong – but this was what the studies showed. This is what many doctors believed. Fat was our enemy. Fat was the reason we were becoming – not nearly so much as we are now, I might add – a nation of lard butts.

For decades, this was reflected in packaged “healthy” foods. Eat as many cookies as you want: yes, they’re chock full of carbs and junk calories, but no worries! They’re LOW FAT. This was the new food gospel, and we saw it proclaimed on our grocery store shelves – low-fat chips, ice cream, cakes. Guilt-free! Breakfast cereal – great! It’s got NO FAT! We saw the birth of olestra, which not only had no fat – it was indigestible! Side effects included gas, cramps, bloating, diarrhea, and, most appalling of all, “anal leakage.” Lays potato chips, Ruffles, and Doritos at the time that were “FAT FREE” and contained olestra had the word “WOW” in huge letters right there on the bag. I guess they meant the taste, but maybe they were referring to what happened when you ate it, as in: “Wow! I just pooped my brains out!”

In 1967, Nancy Sinatra had a hit song called “Sugartown.” She sang, “I got some troubles, but they won’t last. I’m gonna lay right down here in the grass, and pretty soon all my troubles will pass” (most likely, she did not mean “pass” in the olestra way) “ ‘Cause I’m in shoo-shoo-shoo, shoo-shoo-shoo, Sugar Town.” There were about five more “shoos” in that line, but you get the drift.

Sugartown was the place to be. We believed it because of review articles like one that appeared in the New England Journal of Medicine (NEJM) the same year as “Sugartown” – 1967. It discounted evidence that linked sucrose consumption to coronary heart disease. Doctors believed it. They told their patients. Their patients believed them.

It turns out that this particular study was secretly funded by the Sugar Research Foundation (SRF). Now we know, thanks to a bombshell article recently published by University of California-San Francisco scientists in the journal, PLoS Biology, that the SRF (now defunct) was completely evil. It manipulated the science.

It not only “discounted evidence linking sucrose consumption to blood lipid levels and hence coronary heart disease,” report the study’s authors, Cristin Kearns, Dorie Apollonio, and Stanton Glantz. It also “withheld information from the public” linking sugar to changes in the microbiome that can lead to bladder cancer.

But it’s not just the SRF, which later became the International Sugar Research Foundation (ISRF); it’s a bunch of sugar industry trade associations. And it wasn’t just back in the 1960s. All of these groups have “consistently denied that sucrose has any metabolic effects related to chronic disease beyond its caloric effects,” Kearns, Apollonio and Glantz state. In other words, the main side effect these groups are willing to acknowledge is that sugar makes you gain weight.

Let’s take a moment here for me to say that I love sugar. I do. I love cookies, and chocolate cake, and coconut custard pie, and Mexican Coke with real cane sugar instead of corn syrup.  But I really limit it.  I don’t like food Nazis, who tend to be snarky and condescending and who alienate people who really could benefit from what they’re trying to say by making snide statements like, “What’s next, a deep fried stick of butter?” (I actually read that this week in a nutrition magazine that means well, but its tone is so snotty that it’s off-putting.)

That’s not what I’m trying to do at all. What I’m writing about here is the disturbing idea that sugar has been linked to serious illnesses and that the sugar industry has suppressed this information. If we had known six decades ago, maybe a lot more people would be alive now, and maybe our country wouldn’t be struggling so hard with obesity, heart disease, and diabetes.

In case you’re wondering, Kearns, D.D.S., M.B.A., is an assistant professor at the University of California San Francisco (UCSF) School of Dentistry. Stanton Glantz, Ph.D., is Distinguished Professor of Tobacco Control in the Department of Medicine at UCSF. He’s seen this same kind of twisting and distorting of medical evidence a lot; the tobacco industry did it for years. Dorie Apollonio, Ph.D., is an associate professor in the Department of Clinical Pharmacy at UCSF. Together, these UCSF researchers make a formidable team.

Now, back to the 60 years of manipulating the science and hiding the harmful effects of too much sugar. As recently as 2016, the Sugar Association issued a press release blasting findings from a study published in Cancer Research. In that study, done in mice, scientists found that dietary sugar induces increased tumor growth and metastasis when compared to a non-sugar starch diet. But instead of saying, “Hey, you know, maybe you might want to consider not eating so much sugar – all things in moderation,” the Sugar Association doubled down, stating that “no credible link between ingested sugars and cancer has been established.” Nothing to see here, move along, move along. Look over there – doughnuts with sprinkles!

In this PLoS paper, the UCSF scientists lay out a trail of damning evidence. In that first project in the 1960s, one group of rats was given a diet of 75 percent fat but no sugar. A second group of rats ate a diet of less fat, just 15 percent, but 60 percent sucrose, and their little bodies metabolized all that sugar as a carbohydrate. The sugar-eating rats developed thiamine deficiency, which then led to heart failure. But in the rats that ate more complex carbohydrates and no sugar, the gut bacteria, or microbiome, changed and actually started synthesizing thiamine.

This study intrigued SRF scientists, who thought that maybe, if the microbiome could be adjusted, the gut could tolerate sugar better. This idea led to Project 259, in which scientists led by W.F.R. Pover at the University of Birmingham in the UK studied the effect of sugar in the gut between 1967 and 1971. Pover’s team showed, in rats and guinea pigs, that eating more sugar led to higher levels of triglycerides; in turn, this led to higher levels of beta-glucoronidase in urine a finding that’s linked to bladder cancer and in an internal document, scientists described this research as “one of the first demonstrations of a biological difference” between rats that eat a lot of sugar and rats that don’t.

Project 259 didn’t just link sugar consumption to cancer, but to hypertriglyceridemia, an elevated level of triclycerides (a type of fat) that raises the risk of heart disease, say the UCSF scientists, and these findings stayed hidden for decades until the UCSF scientists uncovered them. Also suppressed was evidence linking higher doses of sugar to other “renal disorders, urinary tract infections, and renal transplant rejection.” Eat sugar – reject your donor kidney!

Even worse, the sugar industry did what every good magician knows how to do: misdirect. In previous research, published in the Journal of the American Medical Association (JAMA), Glantz and Kearns, with colleague Laura Schmidt, examined SRF internal documents and historical reports and found that the SRF secretly funded studies, including one published in 1965 in the NEJM, “promoting fat as the dietary culprit in coronary heart disease.”

Imagine there’s a gunshot, and the killer quickly places the murder weapon in somebody else’s hands and starts shouting, “He did it! It’s that guy!” and then slinks away. That’s what the sugar industry did.

For six decades, we have blamed fat – and as a society, we now look more and more like the tubby earthlings on the big spaceship in the Pixar movie, “Wall-e.” We’re huge, and we’re unhealthy.

Sugartown is not so sweet.

©Janet Farrar Worthington

 

If an illness can have a stereotype, gout has one: its poster boy is a portly, wealthy gentleman who drinks too much red wine and eats too much rich food. In literature, gout is an Epicurean affliction, the runoff of opulence and “disease of kings.”

In fact, gout attacks the poor as well as the rich; it’s more like a creepy shadow that follows other diseases, piggybacks off of their risk factors, and kicks sick people when they’re down. It is also becoming more common. Read more