The Lucky Years: How to Thrive in the Brave New World of Health (8 page)

BOOK: The Lucky Years: How to Thrive in the Brave New World of Health
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Not everything weakens and becomes more likely to die as it ages. While some species grow stronger and less likely to die through the passage of time, others are practically immune to aging. Put simply, increasing feebleness and infertility with age is not a law of nature, but we humans think of it that way. On one end of the spectrum, a species can live a long time but have increasing mortality, and on the other end, a species can live a short time yet have declining mortality. In the words of the study’s lead author, Owen Jones: “It makes no sense to consider aging to be based on how old a species can become. Instead, it is more interesting to define aging as being based on the shape of mortality trajectories: whether rates increase, decrease or remain constant with age.” He hopes his research spurs more study in this fascinating field to help us address aging in humans.

One barrier to the study of human aging is finding appropriate models in other species that age like we do. Although old people, especially
those who can make it past one hundred, may seem a logical focus for scientists, such an endeavor would move at a glacial pace. Think about it: you’d need to take seventy to eighty years or more to examine people’s aging processes and know the outcome of your intervention. Not very realistic or practical. So instead, we use mice, which live only three to four years but share many of the same characteristics of our DNA and reflect many features of our aging process. From studies in mice, we’ve learned how genes become more or less active with age, and we can even test drugs to make mice live longer and better.

The short-lived killifish, some species of which have a life span of a couple of months and serve as excellent models for aging studies. This killifish can reach a length of about 6.5 centimeters (2.6 inches) at maturity.

Another animal that has proven very useful is the turquoise killifish. It’s a rare fish indeed, found chiefly in the ponds that form during the rainy season in East Africa. Once the eggs hatch from the mud and spring to life, they grow to full size within forty days and measure about 2.5 inches. They live only a few months. But their aging resembles that of humans to a stunning degree. Like us becoming more senile as the years wear on, turquoise killifish lose their ability to learn new things. Their immune systems weaken. Their muscle mass shrinks like ours does as we age. The females become infertile. One team of researchers at Stanford has taken the study of the turquoise killifish (which owes its name partly to the slight shimmering turquoise hue on its scales) to new levels by sequencing the fish’s entire genome, and in the process identifying a number of genes known to influence aging in other species, including mice and humans. They’ve even built molecular tools
to play with the fish’s genes, one of which is the same one I mentioned earlier: CRISPR. As I described, CRISPR acts like scissors to cut out pieces of DNA, literally, so they can be replaced by other pieces of DNA. Using this technique, the researchers have managed to tweak certain genes related to aging and affect how the fish age. Research like this is exciting and offers hope of finding antiaging treatments that can help us age slower and live longer. A compound, for example, that extends the life in the mighty killifish by a mere two weeks may ultimately lead to a substance that adds years to human life.

But context matters. The context of a fifty-year-old is not the same as the context of a twenty-year-old. Similarly, the context of a diabetic with asthma is not the same as that of someone with heart disease and depression. But, ideally, every context can be nurtured and cared for to slow the aging process. If this weren’t true, then we wouldn’t see such immense discrepancies among people of the same chronological age (the age in years) but whose respective “biological ages” are extraordinarily different. At Duke’s Center for the Study of Aging and Human Development, scientists in collaboration with other institutions tracked almost a thousand New Zealanders born between 1972 and 1973 (the Dunedin Study) and calculated their “biological age” twenty years after they turned eighteen.
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Although there’s been a proliferation of age calculators lately, including websites where you can enter a few numbers and share details about your lifestyle to arrive at a “biological age” (as opposed to chronological age), we don’t yet have a standardized clinical measure of biological age.

To reflect the aging process accurately, these researchers based this theoretical biological age on a wide range of parameters, measuring kidney, lung, and liver function, low-density lipoprotein (LDL, or “bad” cholesterol), dental health, metabolic and immune systems, cognitive health, and even the condition of blood vessels at the back of the eye. These tiny eye blood vessels are an established surrogate for the state of the brain’s blood vessels. Eighteen biomarkers in total were tracked, the results of which were checked against tests usually given to older folks to gauge aging, including functions like coordination, muscle strength, gait, balance, and cognitive abilities.

The researchers, who examined the volunteers at age twenty-six, thirty-two, and thirty-eight, found that while the majority aged at a normal pace (one biological year for each chronological year), a few aged shockingly faster or slower.
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In fact, the results indicated that the biological ages of the thirty-eight-year-olds ranged from twenty-eight to sixty-one years old. Some aged as much as three years within the course of just one calendar year. Those who were deemed physiologically older also looked older. And one of the more disturbing findings was that people who were aging the fastest before midlife were already showing signs of cognitive decline and brain aging, and were less physically able. People who showed accelerated aging in the biomarker tests also performed poorly on other tests.

The biological age distribution of the participants of the Dunedin Study in New Zealand. The chronological age of all of the participants was 38 years.

This was among the first studies to look at young adults in the hopes of understanding why people grow old at different rates, a phenomenon we’ve only just begun to explore. The authors of the study, published in
Proceedings of the National Academy of Sciences
in 2015, wrote: “Our findings indicate that aging processes can be quantified in people still young enough for prevention of age-related disease, opening a new door for antiaging therapies.”
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They also stressed the importance of studying the young in searching for the secrets to prolonging healthy life, and that we “may
be focused on the wrong end of the lifespan” when we look solely at people in the second half of life. Tests like the one these researchers came up with will only get more data driven, precise, and useful in the future, as biomarkers are added, dropped, and given different weights or importance. Such calculators can translate to medical savings as well. If you find out at fifty that your body is biologically behaving like a forty-year-old’s, then you might not need a routine mammogram or colonoscopy as frequently as someone biologically older might.

Other, more specific calculators will also be developed and become more sophisticated. Do you know, for example, how “old” your heart is? You can find out using an online calculator developed by the National Heart, Lung, and Blood Institute and Boston University. You might be surprised to learn that your heart is not as youthful as your chronological age. In a 2015 report by officials at the Centers for Disease Control (CDC), 3 out of 4 adults between the ages of 30 and 74 in the United States were found to have a predicted “heart age” older than their actual age.
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Specifically, men had a predicted heart age of nearly 8 years older than their chronological age; women had a heart age that was 5.4 years older. This was determined using data from the large and well-established Framingham Heart Study and involved information from more than 570,000 participants. The calculator takes into consideration various risk factors such as smoking, blood pressure, diabetes status, and weight as measured by body mass index. A riskier profile means an “older” heart.

The study also found geographic differences. Those with the “oldest” hearts live primarily in the South, with Mississippi, West Virginia, Kentucky, Louisiana, and Alabama having the highest percentage of adults with a cardiovascular age of 5 years or more over their real age. Younger hearts are found in places like Utah, Colorado, California, Hawaii, and Massachusetts. Note that people tend to have younger hearts where there are lower rates of smoking and obesity, both of which are huge risk factors for cardiovascular challenges.

The purpose of the calculator is not to discourage, but to inspire people to take steps to de-age their hearts by quitting smoking, losing
weight, and considering certain drugs (e.g., blood pressure medication and statins). We know that people who calculate their heart age are more likely to try to improve their cardiovascular health, compared to those who receive only general information or who wait until their first cardiovascular event to learn about their risk factors.

As much as youth—and oldness—is a state, so is health. If we think along these lines, addressing matters of health and wellness becomes simple. Coley didn’t understand why his toxins were working, and for him—and his patients—that didn’t really matter. Similarly, Metchnikoff didn’t understand the exact mechanism by which gut bacteria were contributing to healthy physiology. But that didn’t matter, either. Both physicians observed results that benefited their patients.

It’s important to maintain a perspective about your health that appreciates your body’s complexity and mystery. You may never be able to understand or know everything about its inner workings or why, for example,
X
is said to cause
Y
. As I always like to emphasize, honor the human body and its relationship to disease as a complex, emergent system that you’ll probably never fully comprehend. By
emergent
, I’m referring to the notion that we are more than the sum of our individual parts and even our parts’ individual properties.

To understand this concept, which appears in subjects as diverse as philosophy, science, and art, consider your heart, which is obviously made of heart cells. But heart cells on their own cannot pump blood. You need the whole heart to be able to do that. The pumping property of the heart is an
emergent
property of the heart—an outcome caused by intricate interactions among smaller or simpler entities that by themselves do not exhibit such properties. Heart disease, diabetes, cancer, autoimmune disorders, and neurodegenerative ailments all reflect breakdowns in that complex system. Cancer, for instance, isn’t something the body “has” or “gets”; as defined earlier, it’s the result of something that the body
does
with its own cells and machinery. And this is why prevention is the most important tool in aging like an oak tree (or tortoise, take your pick). Through prevention, we tip the scales
in favor of choosing what the body does today and later on. What happens to us at the end of life has its roots early in life.

Cheating Cancer and Death

The human body is tremendously resilient. When faced with illness or infection, it will adapt to preserve life. With most diseases, the body waxes and wanes alongside the progression or remission of a disease. Cancer is one of the only diseases that can be aggressive and outsmart the body’s resiliency. Whatever you throw at it, the cancer gets more hostile, and there’s less of a chance that it will respond to anticancer therapies. Childhood cancers, on the other hand, are usually curable. So there’s a switch somewhere that distinguishes cancers that are fragile and can be conquered from those that are hardy and, ultimately, lethal. Relatively few cancers happen to people between the ages of twenty-five and fifty. Future research will likely bear out the reasons for this difference and offer some new therapies to turn deadly cancers into weak, combatable ones. Or ones that we can quarantine somehow and babysit with drugs so they don’t misbehave or harm the body.

In the past I’ve criticized my field of medicine for its lack of progress in finding meaningful treatments that can delay the progress of cancer or prevent it entirely with proven therapies. But now we’re finally seeing some hope with new technologies such as sequencing tumors and targeting cancerous growths molecularly with pills that essentially turn off the switch that makes a cell go rogue. This buys one of the most precious commodities: time. For a patient with a terminal illness, an extra few weeks or a month can be significant—especially if there’s hope of a new therapy around the corner. Molecular targeting is used much more commonly now than it was when we employed it for Steve Jobs’s therapy, but it doesn’t work in everyone; it is currently helping about 20 to 30 percent of cancer patients, across all types of cancers. And it can be expensive, but I predict this will change as various economic forces drive costs down. To get a closer sense of how molecular targeting
works, take a look at the following. This particular example is from a tumor DNA sequencing company called Foundation Medicine.
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