The Lucky Years: How to Thrive in the Brave New World of Health (26 page)

• moderate aerobic exercise (walking 30 minutes 6 days weekly)

• stress-management techniques (gentle yoga-based stretching, breathing, meditation, imagery, and progressive relaxation for a total of 60 minutes daily)

• participation in a weekly 1-hour support group to enhance adherence to the intervention

The diet of the intervention group was predominantly fruits, vegetables, whole grains (complex carbohydrates), legumes, and soy products. It also was low in simple carbohydrates and included approximately 10 percent of its calories from fat.

The results looked at a common marker in evaluating the progression of prostate cancer: PSA, prostate-specific antigen, a protein produced by prostate gland cells. Elevated levels of PSA in the blood can signal changes in the prostate, including prostate cancer. Here’s what Ornish’s experiment found: the serum PSA decreased an average of 0.25 ng/ml, or 4 percent of the baseline average in the experimental group. But in the control group PSA levels increased an average of 0.38 ng/ml or 6 percent of the baseline average. Now, what does this really mean? Despite the slight “increase” and “decrease,” the change was not clinically significant in medical terms. And here’s the kicker: a change in PSA doesn’t mean you change the disease or the disease outcome at all. Ornish published no follow-up to his study, so we have
no idea what happened to these men. We don’t know if they lived longer or not. We also don’t know if the cancer progressed more or less in the lifestyle group.

Put another way, disease wasn’t measured in this experiment—only the PSA. My guess is the PSA was lowered due to the estrogenic effects of the dietary soy; soy notoriously reduces PSA in men but has no bearing on the actual cancer. This same problem crops up in studies done on the effects of saw palmetto, a popular over-the-counter herbal remedy touted to lower PSA. It does, but artificially, by lowering testosterone. It doesn’t touch the cancer! A change to one marker, in these cases a lower PSA, may not be meaningful. And weight loss may have been a huge factor, if not the main game changer. The lifestyle group participants lost an average of 10 pounds on the study.

And yet bold, sweeping statements were made in the media about Ornish’s results: “Lifestyle Changes May Slow Prostate Cancer Progression” and “Improving Diet, Lifestyle Slows Prostate Cancer.” The other weird thing about the Ornish paper, published in the
Journal of Urology
, is that it reported only the average PSA of each group, which is meaningless when managing patients on an individual basis. One outlier in a small study, for example, can move the entire number and thereby alter the results dramatically. I know of no other cancer studies that report results like that. Usually the number reported is the percentage of patients who have a PR (partial response), meaning greater than 50 percent shrinkage of a tumor or 50 percent lowering of PSA.

I get scared when anyone makes broad statements like “Lifestyle can reverse cancer,” but it’s especially alarming when these come from people who are considered leading experts. While I can concede that lifestyle may in fact impact cancer outcomes, there is currently no hard evidence of this. And let me push the envelope a little further by asking the question: Was this study looking at lifestyle factors? Who defines “lifestyle”? I count five medications, in the form of vitamins and supplements, taken by the experimental group. Even more worrisome is that vitamin E was used, and we now have solid evidence from large-scale studies clearly showing that vitamin E supplementation can
increase
the incidence of prostate cancer. One multicenter study led by Fred Hutchinson Cancer Research Center has found that high-dose supplementation with both the trace element selenium and vitamin E increases the risk of high-grade prostate cancer.
¹¹
These findings, published in 2014 in the
Journal of the National Cancer Institute
, are based on data from the Selenium and Vitamin E Cancer Prevention Trial, or SELECT, a well-designed trial conducted by the SWOG cancer research cooperative group that involved more than 35,000 men. The scientists behind the study wanted to determine whether taking high-dose vitamin E (400 IU/day) and/or selenium (200 mcg/day) supplements could protect men from prostate cancer.

The trial began in 2001 and was supposed to last twelve years. But it was halted early, in 2008, because it found no protective effect from selenium, and there was a hint that vitamin E increased risk. Even though the use of the study supplements ended, the researchers continued to follow the men. After an additional two years, those who had taken vitamin E had a statistically significant 17 percent increased risk of prostate cancer.

Let’s take a look at one more study, this one more recent and which really hit a nerve in my medical community after it was published in
Science
. The headline from Johns Hopkins University media department said it all: “Bad Luck of Random Mutations Plays Predominant Role in Cancer, Study Shows.”
¹²

In early 2015, during the holiday lull around New Year’s, a study by mathematician Cristian Tomasetti and cancer geneticist Bert Vogelstein of Johns Hopkins suggested “bad luck”—random mutations accumulating in healthy stem cells—could explain about two-thirds of cancers.
¹³
In other words, the media reported, cancer occurs mostly by chance—arbitrary, unexplained mutations lead to most cancers rather than the risks conferred by environmental and genetic factors combined (so go ahead and keep eating your potato chips, smoking, and avoiding exercise).
They also seemed to suggest, based on their findings, that some cancers could not be prevented and that detecting them early was key to combating them. It didn’t take long for there to be a backlash against the implied message. Tomasetti and Vogelstein were accused of focusing on rare cancers while leaving out several common cancers that indeed are largely preventable. The International Agency for Research on Cancer, the cancer arm of the World Health Organization, published a press release stating it “strongly disagrees” with the report.

To arrive at their conclusion, Tomasetti and Vogelstein used a statistical model they developed based on known rates of cell division in thirty-one types of tissue. Stem cells were their main focal point. As a reminder, these are the small, specialized “mothership” cells in each organ or tissue that divide to replace cells that die or wear out. Only in recent years have researchers been able to conduct these kinds of studies due to advances in the understanding of stem-cell biology. Cells that divide must make copies of their DNA, and errors in this delicate process, as you know by now, can spark the uncontrolled growth that leads to cancer.

The researchers sought to answer the following: Do higher rates of stem-cell division up the risk of cancer simply by providing more room for error? More chances for mistakes? Dr. Vogelstein, who is one of Hopkins’s most prolific and esteemed cancer researchers, said the question of what causes cancer had bothered him for decades, ever since he was a young intern and one of his first patients was an impressionable four-year-old girl with leukemia. Like any distraught parents with a sick child, hers wanted to know what had brought on the disease. He didn’t know and couldn’t provide a reasonable, acceptable answer. He’d be asked this same troubling question from patients and their families repeatedly, particularly from parents of children with cancer. Parents of children who die of cancer can be somewhat comforted knowing that it might have happened by chance, that there was nothing they could have done, and that it didn’t come from them. But cancer in children might work differently than cancer in adults. Clearly, children haven’t had a lifetime to accumulate risk factors for genetic mutations that can
lead to cancer. So their cancer’s narrative is probably not the same as that for most adults.

This wasn’t the first time scientists had discovered different cancer rates in different tissues. After all, you rarely hear about someone getting ear cancer or heart cancer. Cancers of the small intestine’s lining are three times less common than brain tumors, even though the cells that line the small intestine are exposed to much higher levels of environmental toxins that can cause cellular mutations than are cells within the brain, which are largely protected by the blood-brain barrier. So what explains this discrepancy?

More than one hundred years ago it was observed that some tissues are far more susceptible to developing cancer than others. But we didn’t know why and we couldn’t give a reason for it. That observation motivated Tomasetti and Vogelstein to dig a little deeper and try to understand why, for example, the lifetime risk for cancer in the large intestine is 24 times higher than in the small intestine. What they found is that the large intestine houses more stem cells than the small intestine. Moreover, the large intestine’s stem cells divide four times more frequently than do the stem cells in the small intestine. This relationship between rates of stem-cell division and risk of cancer was also seen in many other tissues. Unfortunately, their analysis didn’t include two of the most common types of cancer—breast and prostate—because there wasn’t enough information on rates of stem-cell division in those tissues, an omission that was criticized by others upon their reporting.

Interestingly, they noted that some cancers, such as those of the lung and skin, develop more often than would be expected from their rates of stem-cell division. But this makes sense when you consider the impact of environmental forces in the risk of those diseases, namely smoking and UV exposure from the sun, respectively. Other cancers found to be more common than expected given their stem-cell division rates were linked to genes that cause cancer, which again helps explain that surprising difference. Dr. Tomasetti used an apt analogy when he described his results in an addendum to the original news release from Hopkins that created such a stir: Think of your risk of a car accident. In general, the
more you drive or the longer the trip, the higher the odds of a crash. But other forces are also at play that add to and/or compound the risk, namely environmental ones like awful weather and poor roads (bad habits), as well as defects in the car itself (bad genes). The researchers finally got their message right when they stated the following:

Some risk factors may be outside of our control, but others are not. The fact that much of the risk of traveling by car is due simply to the trip distance doesn’t mean that accidents cannot be prevented. Distance is one factor, but even if the distance of a trip cannot be changed, traveling can be made safer by driving well-maintained vehicles, using safety devices, such as seatbelts and airbags, and choosing a particular route. Controlling the risk of accidents associated with bad cars and bad roads prevents accidents and reduces overall risk.

In the same way, we can prevent many cancers. Like car accidents, cancer is caused by a combination of factors—random DNA changes made during stem cell divisions that are not within our control, environmental exposures and inherited gene mutations. As a result, there are many opportunities for cancer prevention . . . by eliminating environmental factors and by changing lifestyles.
¹⁴

This addendum, which also underscored the importance of detecting and treating cancer early to prevent death, was published within days of the original news release. But I’m not sure many people read it or got the message through those same journalists who misinterpreted the original report.

Where critics and journalists went wrong in their analysis of the study was that Tomasetti and Vogelstein weren’t suggesting that two-thirds of all cancers are due to chance. They were showing that two-thirds of
the variation in cancer rates in different tissues
could be explained by random bad luck. Put another way, some tissues are more vulnerable to cancer than others, and mutations piling up in stem cells can explain
two-thirds of that variability. A subtle but very important distinction, one that many of the journalists reporting on the study missed, hence the misleading headlines suggesting most cancer is random and not influenced by heredity or lifestyle choices.

To say that a “bad luck” component explains a far greater number of cancers than do hereditary and environmental factors is doing a disservice to public health, especially since the lay public doesn’t have the expertise to tease out the nuances and finer details of this complex study and its even more complex conclusions. And what really infuriates me, as someone who stares cancer in the face daily, is that people have begun to take advantage of this inaccuracy for profit. My dear friend Esther Dyson, a prominent journalist and technology leader whose focus lately, ironically, has been none other than improving efficacy in health care, became the target of predatory practices in health care. She forwarded the sales pitch in a message to me with the following remark: “This wretched Hopkins study is now being used by sleazy marketers.” Indeed, it was:

Hi Esther,

I am writing to bring your attention to new research from Johns Hopkins, which demonstrates that
²
/
₃
of cancers are due to bad luck, thus making it difficult to avoid solely through lifestyle modifications (e.g., not smoking, diet, etc.). Therefore, the best prevention remains intensive surveillance. That’s why we provide the most comprehensive preventive physical possible including upgraded imaging and laboratory screening. . . . It is the same program of care as received by the President of the United States, and a 2011 study in the
Journal of the American Medical Association
(
JAMA
) has already proven that Presidents live much longer than expected. We would like to ensure that you have the same opportunity for good health and longevity. Therefore, we are expanding our membership capability with the addition of other highly qualified physicians who specialize in preventive medicine.

We would be glad to welcome you as a member of our program . . .

In a word: unbelievable. I wonder how many other marketers sold people on expensive services they probably don’t need, reinforcing their desire to leave their health in the hands of others rather than make their own daily choices. Don’t get me wrong: there’s always a place for preventive screenings and, sometimes, “intensive surveillance,” but we cannot ignore the power of prevention through a combination of lifestyle habits and other therapies. Just as cancer is likely a result of a constellation of forces—genetic, environmental, behavioral—our efforts to prevent it should take all those factors into account. And we can’t forget one of the most powerful forces of all underlying most diseases, cancer included: inflammation. This word was surprisingly left out of the entire dialogue about the Hopkins study, including the authors themselves and the critics who threw tomatoes.