The Lucky Years: How to Thrive in the Brave New World of Health (27 page)

Inflammation
is a word and a concept that has gained a lot of notoriety in the past decade. It’s been written about daily in health media, for it seems to have a relationship to virtually all manner of chronic and degenerative disease. Whether it’s the tenderness of a sore throat, the redness that appears after a cut, or the achiness of an arthritic joint, most of us understand that when the body experiences an insult or injury, its natural response is to create swelling and pain, hallmarks of the inflammatory process. But inflammation isn’t necessarily bad. It’s a symptom of the body’s defense mechanisms against something it identifies and responds to as potentially harmful. When the body is tending to an open wound, harmful virus or bacteria, toxins, or sprained ankle, the inflammatory process is ultimately helping it to survive.

The problem with inflammation, and the source of its negative reputation today, is that it can get out of control. A fire hose turned on momentarily to douse nearby flames is one thing, but leave that hose on indefinitely and you’ve got another problem on your hands soon enough. And that’s the case with inflammation gone awry. It’s intended to be a spot treatment, not an ongoing process. If the body
is constantly under assault by exposure to irritants, the inflammatory response stays on. This creates an imbalance in your system that has negative effects on your health as it spreads to every part of the body through the bloodstream; hence, we have the ability to detect this kind of widespread inflammation through blood tests—notably by looking for markers such as C-reactive protein. It can even disrupt the immune system and lead to chronic problems and/or disease.

Inflammation may not seem related to many conditions and afflictions, especially cancer, but volumes of international research prove just how damaging chronic inflammation can be to the body. Certain kinds of inflammation have been linked to most degenerative diseases, including heart disease, Alzheimer’s disease, autoimmune diseases, diabetes, and cancer. It’s also associated with accelerated aging and premature death. At the center of inflammation is the concept of oxidative stress, which, in a rudimentary sense, is like a biological type of corrosion that takes place in our organs and tissues. It can damage our cells’ structures and functionality, stiffen blood vessels, tinker with hormonal switches, and even target DNA, precipitating mutations and mistakes in translation when DNA is used to make various proteins necessary for the body’s operations. Oxidation is actually normal. It happens everywhere in nature, including our bodies. When we digest food, for example, and the body turns it into energy, oxidation is a natural part of the process. But, like inflammation, oxidation becomes a problem when unchecked.

So what does inflammation have to do with the Hopkins study? The road to cancer in any given tissue involves inflammation, which has been correlated with the development of cancer for a long time. In fact, you can’t have a conversation about cancer without talking about inflammation. When you hear that certain infections, such as the human papillomavirus (HPV) or the hepatitis B and hepatitis C viruses, can lead to cancer, much of the reason is rooted in inflammation. Epidemiological studies estimate that nearly 15 percent of the worldwide cancer incidence is associated with microbial infection.
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Why? These infections cause chronic irritation in the body and keep the immune system “on edge,” and this causes ongoing inflammation
that predisposes cells to cancer. The same can be said for anything that continually irritates the body and its immune system: high blood sugar, diabetes, obesity, tobacco use.

The actual process by which chronic inflammation results in cancerous cells is exceedingly complex, and it may be different depending on which type of cell we’re talking about and which type of cancer. But the overall picture is an important one to remember: when the body experiences chronic inflammation, something isn’t right and the body’s attempt to bring things back into balance can be sabotaged by that persistent inflammation, leaving cells—and their inherent DNA—vulnerable.

Cells possess innate mechanisms to prevent rampant, uncontrolled proliferation or the accumulation of DNA mutations (recall the DNA mismatch repair system I described earlier). In the face of DNA damage or the hint of a crazy cell activating tumor growth, cells will either repair their DNA and prevent mutations or the deranged cells will self-destruct. However, when you have an infection or there’s other injury to tissue that leads to inflammation, massive cell death is likely a step in the path to recovery. When a tissue loses such a large number of cells at once, those lost cells must be replaced to keep the tissue functioning, and stem cells often self-renew and divide to fill the gap. So inflammation is used to defend the body, and it’s used to initiate the healing process and repair tissue. But it’s also sending proliferative signals to cells that have the potential to become cancerous.

When the Hopkins study suggested that cancer is often due to “bad luck of random mutations,” the researchers left this important cascade of events out of the narrative. What if you’re an overweight smoker who is diagnosed with pelvic bone cancer, a super-rare cancer? Anyone’s lifetime risk of getting this cancer is a mere 0.003 percent; consider that against the lifetime risk for each of us of being diagnosed with lung cancer, which is 6.9 percent. So you might think you were somewhat lucky in that you didn’t get lung cancer as a smoker, but instead you developed this other cancer by the hand of “bad luck.” But let’s connect the dots: smoking kept your body continually fighting that nasty habit’s
negative biological effects. And we know that tobacco and all of its insidious ingredients don’t just affect the lungs in a vacuum. Tobacco affects virtually every cell and system in the body. It’s not a far stretch of the imagination to see how tobacco can trigger genetic mutations that manifest in a cancer anywhere in the body, perhaps in a place where you’re already genetically susceptible to cancer. Maybe you’ve got good genes to protect you from lung cancer, but not so much for bone cancer. We all know people who smoke long past their eightieth birthday and die of something other than lung cancer, or the fellow who gorges on fatty, sugary foods daily but never gets diabetes. These people aren’t necessarily “lucky”; no doubt their habits are fanning flames of inflammation in their body that will manifest in other, less obvious ailments or in conditions that do not at first glance seem to be related directly to their poor lifestyle choices. But we cannot chalk it all up to purely bad luck.

Indeed, life is a genetic gamble to a large degree. We have to play the cards dealt us, but we can stack the odds in our favor by controlling our exposure to environmental and lifestyle factors (e.g., not smoking, eating well, getting our exercise, using technologies to stay on top of our health status, etc.). Suggesting cancer is mostly due to bad luck dilutes the important message that some risk can be modified by behavior. My guess is that future studies and technologies will be able to tell us that even the most elusive, rare types of cancer that seem to be due to bad luck can actually be influenced by our environment and lifestyle. And knowing that cancer is preventable and can be impacted by behavior is, to me, empowering.

Regrettably, most medical studies are wrong; they are biased and flawed, each in its own unique way. By some estimates, on average only 3,000 of 50,000 new journal articles published every year are sufficiently well designed and relevant to inform patient care.
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That’s 6 percent. A whopping 94 percent of studies published do not carry significant
enough valid data to warrant a change in how doctors treat patients, nor will their findings impact patient outcomes. Richard Horton, the current editor in chief of
The Lancet
, has been critical of the reliability in published research despite the fact that he’s at the helm of one of the most well-respected medical journals in the world. In a 2015 comment published in his journal, he went so far as to say, “The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness.”
¹⁷

Other leading physicians and researchers have echoed these critical sentiments, including Marcia Angell, a Harvard doctor and former editor in chief of the
New England Journal of Medicine
. It doesn’t help that studies that appear to be well done have their competition that shows wildly different outcomes. One study will have a conclusion that’s totally opposite to another study’s bottom line. Look no further than the research on foods that cause or prevent cancer to appreciate this disconnect. The truth is somewhere in the totality of the research, but unfortunately the media reports on every study in isolation underneath contradicting headlines.
¹⁸

In 2013, a couple of researchers from Harvard and Stanford teamed up to randomly select fifty ingredients from recipes in
The Boston Cooking-School Cook Book
, then searched PubMed to see which of the ingredients had been linked with either increasing or decreasing the risk of cancer.
¹⁹
They identified forty, including staples like bread, potatoes, tomatoes, wine, tea, milk, eggs, coffee, butter, beef, and corn—foods that we all have heard both positive and negative things about. One of the researchers, John Ioannidis of Stanford, had already delved into this world more than ten years ago when he published “Why Most Published Research Findings Are False,” which became one of the most cited papers in
PLOS Medicine
.
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His latest investigations culminated in his 2013 paper showing that, for the most part, pretty much everything we eat both causes and prevents cancer. And when it comes to things
like milk, eggs, bread, and butter, you can find just as many studies that support their health benefits as their cancer-causing risks.

Scientists can have difficulty getting their papers accepted into prestigious journals. In a world of “publish or perish,” this has created a market for bottom-feeding journals with impressive-sounding names but absolutely no standards. The number of published medical studies has skyrocketed accordingly, with a 300 percent increase over the last twenty-five years.
²¹
And the so-called open-access model, which allows anyone to access certain journals freely online without paying a fee, has given rise to a slew of online publishers, many of which are unscrupulous and exist only to make money off the authors who pay to have their papers published. The authors’ reports (and research results) are not filtered or challenged by the scientific rigors of traditionally published peer-reviewed journals that maintain high-quality standards in accepting papers and making them available to the research community. Most respectable studies involve several leading experts and many months of editorial and scientific scrutiny, and back and forth discourse, before they are published. With some rare exceptions, anything can get published relatively quickly by these open-access journals regardless of the quality and validity of the research methods, data, and conclusions. In 2011, the number of predatory publishers was only 18; by 2014, that number had ballooned to 477.
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What all this really means is that information not driven by real data is seeping into the medical literature, and mainstream media journalists will often base their articles and arguments on these shoddy papers that should never have made it to publication. The need for skepticism has never been greater.

The lesson: seek multiple sources that arrive at the same answer. Until we have better curators of medical wisdom in our country for the benefit of all, each one of us must play the curator role in our individual lives.

In my first book, I condemned vitamin D supplementation alongside taking vitamins in general. At the time, millions of Americans had been told they were deficient in vitamin D and were taking megadoses of it in a bid to bring their levels up to what was considered “normal.”
To most people, this seemed like an obvious problem to remedy, for previous research claimed that vitamin D deficiency in adults could cause fractures, falls, functional limitations, cancer, diabetes, cardiovascular disease, depression, and higher risk of death in general. We get vitamin D through certain foods but mostly through UV exposure to the sunlight, which stimulates a reaction in the skin to produce this important hormone that’s involved with a multitude of physiological functions. But given our use of sunscreen today and living at high latitudes, the thinking went, we probably weren’t getting enough. Really? The body is much cleverer than that. It always has been.

Some advertising for the supplement went so far as to suggest that vitamin D could alleviate obesity, autoimmune disease, insomnia, and even autism. The jig was up following more research and meta-analyses of research to determine what should be considered “normal.” The original definition was quite arbitrary and not many people, if any, who were deemed below “normal” were getting diagnosed with rickets, the soft-bone disease associated with a true deficiency. Yet so many blanket statements had been made about the benefits of vitamin D that people who hadn’t even gotten their levels tested were taking it. New brands of vitamin D supplements flooded the market.

In the past few years, the whole idea of there being a widespread vitamin D deficiency and a need to test vitamin D levels, let alone supplement, has been called into question. Two new studies emerged in late 2013 that added to the growing body of evidence against the so-called sunshine vitamin. In one, a large review by Philippe Autier and colleagues at the International Prevention Research Institute in Lyon, France, it was found that taking supplemental vitamin D has no effect on a spectrum of diseases and conditions, from osteoporosis and bone diseases to heart disease, weight gain, multiple sclerosis, depression and other mood disorders, and metabolic disorders such as diabetes.
²³
After looking at more than 450 studies, Autier and his colleagues concluded: “The absence of an effect of vitamin D supplementation on disease occurrence, severity, and clinical course leads to the hypothesis that variations [in vitamin D levels] would essentially be a result, and
not a cause, of ill health.” Put another way, we’ve had the cause and effect backward. Low vitamin D is the
result
of poor health—not the cause. The study stated: “Associations between 25(OH)D and health disorders . . . are not causal. Low 25(OH)D [vitamin D] could be the result of inflammatory processes involved in disease.” In other words, low vitamin D levels could very well be signs of inflammation in the body, and correcting the alleged “low” vitamin D is just addressing a symptom—not a root cause of disease causing the inflammation.