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The Roadmap to 100
The Breakthrough Science of Living a Long and Healthy Life
By Walter M. Bortz II, Randall Stickrod
Palgrave MacmillanCopyright © 2010 Walter M. Bortz II, MD, and Randall Stickrod
All rights reserved.
AGING, HEALTH, AND THE QUEST FOR LONGEVITY
THE CENTENARIAN IMPERATIVE
Growing old is a relatively recent phenomenon. Until the last century or two, the average life span was less than 30 years. The historical record on aging is so sparse that we have had little information about the aging process, and because so few people had the opportunity to achieve their full aging potential, we are just now learning what our potential life spans are. Prior to the agricultural revolution of 10,000 or so years ago, life was usually cut short by predation, injury, or starvation. The emergence of agriculture led to the formation of villages and cities; with people settling in close proximity, we saw the rise and spread of infectious diseases, which continued to inhibit average life spans. It wasn't until the twentieth century that average life expectancy began to rise appreciably, thanks to the medical successes curing infectious diseases, the widespread availability of food, and fewer hazards of daily life in civilized society. In fact, in the twentieth century alone, we have added approximately 30 years to the average life span, a near doubling over the previous millennia.
A century ago there were only a handful of centenarians on earth. By 1950 their numbers were estimated to be a few thousand. Today there are thought to be 340,000 centenarians worldwide, and it is estimated that that number will increase to 6 million by 2050. The highest concentrations of centenarians are projected to be in the United States and Japan. In 2009 there were approximately 100,000 in the United States and nearly 40,000 in Japan, but by mid-century those numbers are expected to grow to at least 600,000 in the United States and a full million in Japan, making centenarians the fastest-growing demographic, more than 20 times the overall rate of total population growth.
These impressive statistics underscore the viability of 100 as a reasonable objective, a longevity beacon that is demonstrably achievable. And yet we find ourselves in an era when the upward progression of expected life span is seriously threatened by an epidemic of lifestyle-based negative factors. Obesity and diabetes are the scourge of our times, a peculiar regression in a century of generally improving public health and longevity. We are increasingly becoming a bifurcated society, with one segment focused on health, fitness, and nutrition, and the other skewing our public health statistics in the negative direction. Probably the greatest challenge in public health policy today is to provide the education and motivation for the unhealthy to turn their lives around and adopt healthier—and hence more productive—lifestyles.
There is nothing special or magical—or particularly scientific—about the number 100, it should be noted. It is a convenient marker on our decimal-based number system, a "round" number in three digits, that just happens to be statistically significant in life-span studies. But it is a useful symbolic target. What we do know so far is that there seems to be a natural upper limit to the human life span, somewhere around 120 years. The oldest documented person was France's Mme. Jean Calment, who died in 1997 at the age of 122 (and who famously drank two glasses of port wine a day, made a hip-hop record at 121, and claimed to have "an enormous will to live and a good appetite, especially for chocolate").
Not long ago a newspaper item proclaimed the 115th birthday of Los Angeles resident Gertrude Baines and noted the irony in the fact that the world's oldest person would be found in the world's most youth-obsessed city. More remarkable than her age was the fact that, until she was 107, she lived independently and self-sufficiently. Reports of people achieving their 100th birthday are now becoming commonplace. There are nowenough people in the United States who have reached an additional decade, 110 years of age, for us to coin a special term for them, "supercentenarians." At the time of this writing, 75 supercentenarians are being monitored by the Gerontology Research Group of Inglewood, California, and their ranks are slowly increasing.
It is as natural as breathing to want to extend life to its maximum limit. And yet who wants to live infirm, beset with frailty and loss of self-efficacy? Who wants to spend their last years—or decades—bedridden and hooked up to machines? It should be obvious that longevity and health are flip sides of the same coin. Longevity without health is not a desirable outcome for anyone. In fact it's not even an option. It is the convergence of the aging process and the quality of our health that determines our life span.
An extensive study by a Danish research group, covering 30 developed countries, now projects that of the babies born in these countries today, fully half should live to 100 or more. More importantly, these people are expected to encounter less disability and fewer functional limitations as they age, a consequence of presumed healthier lifestyles. The half that will not reach 100 will likely continue the other notable trend of our times, the increasing rate of obesity and diabetes that are tugging longevity statistics in the other direction.
Who wouldn't want to live to 100 or more, to have the longest possible life span? Not everyone, apparently. According to a survey by the Pew Research Group, only 8 percent of Americans actually expressed a desire to live to 100. The reason is that most of us still associate that age with infirmity and a very low quality of life. The image invoked by a 100-year-old person is invariably one dominated by the things that a person can no longer do, of loss of independent living and degraded function. What is desirable about living that long if you can't do the things that seemed to make life worth living in the first place?
We believe that this view of late life is demonstrably wrong. One's later years are not fated to catastrophic decline and decrepitude, and we can now assert with the support of solid science that a great deal of the aging process is within our personal control. But first we have to understand just what the aging process is—and is not.
AGING IS NOT A DISEASE
A browse through the obituary pages of any major newspaper today reveals a subtle change that has taken place in the vernacular of dying over the last generation or two. It used to be commonplace, when almost anyone over the age of 60 succumbed, to attribute their death to "old age" or at least "natural causes." Today it is rare to see death reduced to such simple, non-clinical terms. If an 88-year-old's heart stops beating, it will likely be referred to as "cardiac failure," on the presumption that something went wrong, presumably the result of cardiac disease and not the programmed exhaustion of heart function, the predictable wear and tear of aging. Dying no longer requires disease as a handmaiden.
The urge to defy aging and its negative consequences seems as fundamental as the urge to procreate. That is understandable. What is not understandable is the notion that we can find a "cure" for aging and simply use a pill, an injection, or a surgical procedure as soon as medical science unlocks that secret. If aging were a disease, it's one that we were all born with and are destined to succumb to.
Aging is an inescapable reality, as immutable as the fundamental laws of physics. But its effects can be mitigated through conscious choices we make in everyday life. Aging does not have to imply infirmity, disease, frailty, or the inability to live full, productive, satisfying lives.
Our current remedial approach to aging is derived from the disease model of the medical profession. We look to potions, pills, medications. We look to gene therapies and radical surgeries. All of these approaches derive from the medical model that began with the French scientist Louis Pasteur in the mid-nineteenth century. From the time of the agricultural revolution until just a few decades ago, the primary threat to our health was infectious diseases: bubonic plague, smallpox, cholera, polio, tuberculosis, malaria, to name a few. Pasteur's discovery that the agents of these diseases were tiny microbes was a breakthrough that allowed us to combat them effectively. Ever since, medical science has been remarkably successful at finding remedies and preventive strategies for these diseases, and in many cases actually wiping them out. These successes have effectively entrenched the disease model as the de facto operating model of medicine for the past 150 years.
Surprisingly, aging has historically been poorly understood in the medical science community. Or perhaps not so surprisingly. Medicine can be considered in many ways our youngest science—physics, chemistry, and biology were established disciplines long before Pasteur and long before we had an accredited school of medicine with a science based curriculum. The sheer complexity of living processes presents a daunting challenge, and requires not only a solid platform of the core sciences, but also a way of bringing them together to synthesize these disciplines into a new, emergent science of life. Aging has for too long been considered a process that is in opposition to living; and perhaps even more to the point, it is a process that has been largely shrouded in mystery.
Everything ages. It is the nature of our universe to change over time. Some 14 billion years from the Big Bang, time still ticks off its metrics, marking not just living things, but all matter. Even our fundamental particles—neutrons, electrons, protons—decay over time. Change is constant, everywhere, and inescapable. Without change, in fact, the concept of time would be meaningless. The arrow of time points in one direction only, an anomaly of physics, where everything else can go either forward or backward. Time, as a variable, frequently appears in most of the mathematical equations used to describe the physical world. Whether time flows backwards or forwards usually makes no difference in mathematics. But in our everyday world we never see time flowing backwards—from the present into the past. The fact that time is observed to flow inexorably only in one direction in real life is known as "time's arrow." The reason we experience time in only one direction, from past to present to future, is a consequence of the second law of thermodynamics, which is central to all life processes.
Thermodynamics is the science of energy production and exchange. Its laws govern everything associated with living and being alive, particularly our metabolic processes, those mechanisms of energy production and conversion that literally define what it means to be alive. The first law is often called the law of conservation of energy. It says that energy cannot be created or destroyed, that the amount of energy available in the universe is a constant. Einstein's famous equation, E = mc2, can be thought of as part of this same concept, that energy and matter are interchangeable. The second law, simply stated, says that energy tends to spontaneously disperse. Entropy is a way of measuring that dispersal. Though the second law is the one we associate with the aging process, the first law is notable as the ironclad principle of all diet and weight loss systems—that weight loss happens only when the number of calories expended exceeds calorie intake, no matter what the source of calories.
The second law has become famous as the reason that such concepts as perpetual motion machines and "free energy" sources are impossible. It is the law from which the principle of entropy is derived. Entropy describes how things in nature tend toward increasing disorder, a scattering of available energy.
Our bodies age because, over time, things, including our internal structures, tend to become increasingly disordered. By analogy, we build things such as buildings, cars, and machines in orderly, systematic structures according to specific design criteria and with an investment of energy. But over time they tend to decay, to fall apart, and their components disperse. This is why, among other things, our skin may start out taut and smooth and over decades accrue wrinkles and begin to sag. Our DNA programs our structure, but entropy tends to work against the orderliness of our programmed form over time.
Living systems are "open" systems that continuously exchange matter and energy with their environment. When our cells replicate, they use our DNA as a blueprint to create new cells. Entropy is not just about the dispersal of energy, but about the loss of information in the process. Entropy ensures that the process of cell replication is not perfect, that over time the organism is going to experience changes as the result of a subtle loss of information from one cycle to the next.
THE LIFE—AND DEATH—OF A CELL
Cells are the structural and functional units of living organisms, the "building blocks" of life. All of our life processes begin at the cellular level, and our health and wellness originates in our cells. The word cell comes from the Latin cellula, meaning "a small room," a designation given by the seventeenth-century polymath and inventor of the microscope, Robert Hooke, when he compared the cork cells he saw through his microscope to the small rooms monks lived in.
Mitochondria are the energy factories of the cells. They produce energy-rich molecules called adenosine triphosphates (ATPs). ATPs are produced in the mitochondria using the energy stored in food. Just as the chloroplasts in plants act as sugar factories for the supply of ordered molecules to the plant, the mitochondria in animals act to produce the ATP molecules as the energy supply for the processes of life. The conversion from food to energy molecules is a chemical reaction, fueled by oxygen. The reaction also produces free radicals as byproducts. These ionized molecules are highly reactive, and in turn create oxidative stress within the mitochondria. Oxidative stress leads to mitochondrial mutations, a kind of vicious cycle in which enzymatic abnormalities are created, leading to further oxidative stress. This is what signals the cumulative breakdown process we call "aging."
A number of changes occur to mitochondria during the aging process. Tissues from elderly patients show a decrease in key enzymatic activities. Large deletions in the mitochondrial genome can lead to high levels of oxidative stress and trigger the neuronal death that leads to Parkinson's disease. Hypothesized links between aging and oxidative stress are not new and were proposed over 50 years ago; however, there is much debate over whether mitochondrial changes are causes of aging or merely characteristics of aging. Regardless, we know that to effectively deal with the effects of aging, it is necessary to understand mitochondrial processes.
Free radicals are a by-product of normal metabolism, but they also come from smoking, pollution, toxins, and fried foods among other things. Free-radical damage is associated with an increased risk of many chronic diseases. Antioxidants such as vitamin C, carotenes, and vitamin E can reduce the damage caused by free radicals. Fortunately for us, those antioxidants are commonplace components of a normal, healthy diet.
Every cell at rest carries on its base activity. All of the cell's hundreds to thousands of receptor sites—proteins in the cell walls—are continually scanning the environment for energetic cues, whether chemical, thermal, mechanical, electrical, or magnetic, which initiate a repertoire of cellular reactions, both functional and structural. The genes listen in to this cueing, and turn on or turn off according to their programmatic function.
As you read this, millions of your cells are dying. Most of them are either superfluous or potentially harmful, so you're better off without them. In fact, your health depends on the judicious use of programmed cell death. The cells even come primed for self-destruction, equipped with the instructions and instruments. First, the cell shrinks and pulls away from its adjacent cells. Then, the surface of the cell begins to decompose, fragmenting and breaking away.
There is another kind of cell death, necrosis, that is unplanned. Necrosis can result from a traumatic injury, infection, or exposure to a toxic chemical. During necrosis, the cell's outer membrane loses its ability to control the flow of liquid into and out of the cell. The cell swells and ultimately bursts, releasing its contents into the surrounding tissue. Immune cells then flood the affected tissue, but the chemicals the cells use cause the area to become inflamed and sensitive. Burns from a hot stove are a commonplace example, with resulting redness and pain.
Many different kinds of injuries can cause cells to die via necrosis. It is what happens to heart cells during a heart attack, to cells in severely frostbitten fingers and toes, and to lung cells during a bout of pneumonia.
Within our cells, our DNA molecules reside in our chromosomes, carrying the codes that define our nature. Each DNA strand is capped with telomeres, which cover the ends of the chromosome, much like the plastic caps on the ends of shoelaces protect the shoelace from unraveling. In the course of normal cell growth and replication, the telomeres are progressively shortened until they reach a built-in limit. At that point the cell can no longer divide (the process known as mitosis), and it will begin to die. The limit of the number of times a telomere can shrink is known as the Hayflick limit, after microbiologist Leonard Hayflick, who discovered the phenomenon.
The enzyme telomerase, which is produced both naturally and synthetically, has been found to inhibit the shortening of telomeres and hence has generated intense research activity to determine if it might be a way of extending life. The 2009 Nobel Prize in medicine was awarded to researchers doing pioneering work in this very area. Unfortunately, telomerase is also associated with cancer cells and their unregulated growth. A great deal of research and discovery remains to be done in this area.
Excerpted from The Roadmap to 100 by Walter M. Bortz II, Randall Stickrod. Copyright © 2010 Walter M. Bortz II, MD, and Randall Stickrod. Excerpted by permission of Palgrave Macmillan.
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