According to the U.S. Centers for Disease Control, 1,250,000 Americans suffer heart attacks each year, while 710,000 die of heart disease, with most of these following long periods of debilitation. Cardiovascular disease causes 1 of every 2.7 deaths in the United States today. Cancer kills more than 500,000 Americans each year. Strokes account for another 168,000 deaths and diabetes conservatively kills 70,000 more. These sobering statistics are not lost on a growing number of individuals choosing a physician specialized in preventive-aging medicine. Perhaps a close friend, with whom they share a similar lifestyle, has just suffered a heart attack or was diagnosed with cancer. It might be a parent succumbing to the ravages of Alzheimer’s disease. Possibly everyone in their family died at an early age and they, too, are rapidly approaching the same age.

The number-one motivator for looking into the preventive-aging medicine option, however, is one’s personal experience of premature aging. All too often, people have already been diagnosed with measurable signs of aging-related disease – hypertension, high cholesterol, or osteoporosis, for example. Typically, they report a decline in their former physical ability, a personal sense of imbalance in life, or a faltering sense of youthful vitality – loss of strength, fatigue, inability to concentrate, loss of libido or sexual performance, frequent illnesses, and so forth.

Life is truly a marvelous journey; a continuous process of change, followed by growth. Each and every one of us should be able to fully embrace and enjoy every stage of life to its fullest. Sadly, even in this day of modern medical miracles, too many of us have chosen to live in the ‘dark ages.’ By that, I mean the declines that come with aging are far more related to a lifetime of unenlightened choices than they are to the inexorable ticking of a clock.

All things and all phenomena are connected – especially when it comes to physical function and performance, and youthful vitality. Our every choice, thought and action plays a major role in how well or how long we live.

The mission of this program is to demystify the processes of aging and give you the knowledge, tools, and skills needed to live the life you have imagined. Modern science has begun to unlock the long-hidden mysteries of aging, providing hope for a brighter future for the millions of aging baby boomers and those to follow. Ironically, much of the wisdom for avoiding premature disease and death preceded modern medicine by more than 800 years. The twelfth century physician Maimonides understood the importance personal choice has regarding human longevity: “Live sensibly – among a thousand people, only one dies a natural death; the rest succumb to irrational modes of living.” I hope that it won’t take another 800 years for us to heed this sage advice. Think of this program as your personal guide to living sensibly – for living younger.

To know what it means to live younger, we will look at what it means to live older. This section will briefly examine the concepts of human life expectancy and lifespan. To do that let’s travel back in time, and trace the evolution of human lifespan. Your journey to living younger, then, begins in the distant past.

Life expectancy is the average number of years that a person is expected to live in a given population. Some people die following a very long life. Others die quite young.Most, however, fall (sic) somewhere in between. Imagine the shape of a bell curve to describe this life expectancy distribution. Through most of human history, the average life expectancy was actually relatively brief. Early man, through prehistoric times, had a life expectancy of less than 25 years. This is rather brief when compared with the average American, who can expect to live about 78 years – triple that of our earlyancestors. Why was it so short? Animals living in the wild offer a clue.

Very few animals in the wild die of old age. Most often, something causes an early demise. For the most part, predators kill them, or they die from starvation or environmental factors (e.g., drought, climate extremes, infectious organisms, etc). Very few ever escape these life hazards and live long enough to die of old age. Actually, the same thing happened to us in our early history. We, too, were killed by predators or other humans; we died from starvation or significant climate extremes.

Another way to understand the relatively brief life expectancy of early man is by examining the ends of the bell curve distribution for life expectancy. At the beginning of the bell curve are those who die young. Newborn and infant mortality was very high throughout most of human history. When a large proportion of a species dies at a very young age, the overall average life expectancy is reduced significantly. Then, at the opposite end of the life expectancy bell curve are the oldest. Historically, when people became ill, injured, or feeble little could be done to sustain life and they died, driving down the average life expectancy for the species.

It has been only in the past 150 years or so that humans experienced significant gains in life expectancy. In fact, the average life expectancy in the U.S. reached an all-time high of 77.6 years in 2004. That essentially means we have tripled our life expectancy when compared to early man. Such a dramatic increase in life expectancy over an amazingly short period in human history might raise the question whether we have learned to slow or turn back the clock of human aging. Would Ponce de Leon, who searched in vain for the fountain of youth, believe we have found it?

I don’t think so, at least not yet. How then, can we explain such a dramatic increase in human life expectancy? Recall the fate of the animal in the wild, and that of most of humans throughout our past. Few were lucky enough to survive environmental extremes, other predators, or drought and famine long enough to succumb to old age. Now, let’s look at another scenario. Take an animal out of the wild and place it behind bars in a zoo. Feed it daily and control its environment. It doesn’t take a rocket scientist to realize that the animal is now protected from predators by the cage. And, lack of food or water is no longer an issue. Moreover, the environment ceases to exert a major threat to its survival. As a result, many more animals in a zoo than in the wild will live long enough to die of old age. You know what? The same thing happened to us, too. We learned to protect ourselves from most predators and other environmental threats. Modern agriculture has insured that we always have plenty of food. Therefore, more humans now live long enough to die of old age.

The bell curve of human life expectancy reveals another reason for the dramatic increase in life expectancy. Recently, by human history standards, we learned to improve, effectively and rather significantly, survival for those at either end of the curve – the very young and the old. Beginning at the youngest ages, many more newborns and infants survive today than in the past. Thanks to sanitation, prenatal care, immunizations, antibiotics and numerous other improvements in living conditions during the last century, the chances of surviving birth and early infancy improved dramatically.

Increasing survival of the very young increases the overall average for life expectancy significantly for humans. Now let’s examine the opposite end of the curve. This time, because of many of the same things that improved newborn survival, along with modern medical advances for treating diseases of aging, and organized support systems, many more people formerly near the end of life now continue to survive much longer. Because of this recent phenomenon, it has been said that the majority of people who have ever lived beyond 65 years, in all of history, are living today!

Animals in a zoo are more likely to live to an older age than those in the wild. In other words, the average life expectancy for animals in a zoo is generally greater than that of their wild counterpart. However, the maximum lifespan is the same for a given species, whether in the wild, or in a zoo. Maximum lifespan is the upper limit a given species can live. The maximum lifespan does not change simply because the animal is ‘better off’ in a zoo. Likewise, modern humans live far longer than their ancestors did on average, but the maximum possible lifespan for the human species has not changed throughout history. In other words, average human life expectancy increased but the maximum lifespan did not. Improving living conditions has not increased maximum human lifespan.

Over the course of the next several decades, average human life expectancy in the U.S. could increase to as much as 85 years. Ironically, however, it has recently been predicted that the generation born today may be the first in history to face an average life expectancy that is less than that of their parents. One in three children born today is likely to develop diabetes, and the rate of overweight/obesity continues to climb. If these trends are not reversed, the only way average life expectancy for this new generation could increase will be through major medical breakthroughs to ‘cure’ obesity, diabetes, or simply manage to keep people alive longer but with their existing disease.

The number of centenarians in the U.S., those reaching 100 years, is expected to grow from 140,000 to at least 600,000 within 40 years. How much longer could we actually expect to live? Claims have been made for individuals allegedly living well into their 140s. Myths still circulate about people who are reported to live to an extremely old age – up to 150 years. The problem with such claims is a lack of objective verification.Detailed scientific reports have refuted these claims. The official record for the longest lived human, with verifiable documentation, is held by Jeanne Louise Calment. A French woman, Ms. Calment died in 1997 at the age of 122. Evidence suggests that throughout human history the maximum lifespan for humans has remained constant at around 120 years. A few ancient Romans may have live that long and certainly very few today have reached such an age. Even with recent increases in average lifespan, it does not appear that we have yet found a way to exceed that seeming constant. Does that mean that human lifespan, or the lifespan for any species, is fixed and not amenable to change?

The answer seems to be a resounding “no.” The first evidence surfaced at Cornell University in 1935. What was probably little more than a laboratory curiosity for many years turns out to be a profound discovery into the quest for extension of lifespan. Laboratory rats were fed a diet with a significant calorie restriction – by as much as 40%! Such a significant dietary restriction would ordinarily be expected to induce malnutrition. However, the scientists ensured that the rats received an adequate amount of nutrients, vitamins and minerals. In essence, they were given what we might call a mild starvation diet but without the malnutrition. What the scientists observed was nothing short of remarkable.

Instead of suffering with the kinds of diseases normally found in rats, or the functional decline and premature death associated with malnutrition, nearly the opposite was observed. Compared to the control group of rats, fed a ‘normal’ amount of calories, the calorie-restricted (but not nutrient restricted) group actually experienced fewer aging related diseases. More startling to the researchers, the rats lived longer than the rats in the control group. In fact, they not only lived longer than the control group, they outlived the known maximum lifespan for their species! The experiment proved that maximum lifespan could be greatly extended. Several decades would pass before scientists could begin to explain this phenomenon.

The 1960s ushered in vigorous theories of the aging process, and over the past 40 years scientists have repeated this experiment of calorie restriction with adequate nutrition with more than 1,000 different species, with the same outcome each time. More than 2,000 articles in peer-reviewed journals have documented the significant effects of calorie restriction in animals. Some species have been observed to exceed their previously known maximum lifespan by as much as 50% or more. There is abundant evidence that a calorie restricted, but nutritionally rich, diet can extend average and maximum lifespans, and postpone the onset of most aging-related diseases.

Roy Walford, MD., was one of the leading researchers in the field of calorie restriction. He proposed that human lifespan could be extended significantly with what he called a CRON diet. CRON is an acronym for Calorie Restriction with Optimum Nutrition. Followers of his life extension research established the Calorie Restriction Society (CRS). The CRS offers guidance for those who wish to follow Dr. Walford’s CRON diet.

How does calorie restriction work? It works by slowing the actual processes of aging; it reduces free radical damage, it diminishes insulin levels and the glycation of protein, it inhibits autoimmunity, and it stimulates expression of ‘longevity’ genes. These biological processes of aging will be described later. Is it possible for humans following a similar diet, restricting calories while avoiding malnutrition, to experience a lifespan surpassing the proposed current limit of 120 years? While the evidence from animal studies, so far, is compelling, it is hard to say just yet. One reason we don’t yet have the answer is that humans live a great deal longer than mice and fruit flies; it will be a long time before we have a definitive answer.

In 2004, two articles published in the Journal of the American Medical Association offered tantalizing evidence that calorie restriction seems to have a positive impact on the occurrence of breast cancer and heart disease. Since then, many corroborating reports are finding their way into respected peer-reviewed journals. The evidence does not prove that maximum lifespan will increase with this approach, but the possibility seems likely. While there is no known fountain of youth, it just might be that a nutritionally balanced, calorie-restricted diet may be the next best thing.

What is aging? Simply stated it can be defined as a decline in ability, balance and/or capacity. I call it the ABCs of aging. Ability is the measure of physical and cognitive performance. Loss of ability leads to a loss of the functions of daily living and independence. You may no longer be able to climb stairs, and instead require an elevator. Getting up and down from a chair may become challenging, at best. Once enjoyable activities, such as golf or tennis, may become too painful or even impossible.

A loss of balance can develop at a number of levels in life. At the smallest level, the cellular level, we can experience imbalances in cellular function. If your doctor checks your blood and tells you that your potassium level is low, your hormones are out of balance, or that a liver enzyme is elevated, that represents a cellular imbalance. At the next level, the system level, we can experience imbalances as well. You may develop problems with your cardiovascular system, musculoskeletal system, or immune system for instance. It might become difficult to maintain your physical balance, literally, a frequent cause of falls and premature death in the elderly. At the highest level, we can experience imbalance in the dimensions of our being – physically, mentally and/or spiritually.

Finally, aging can result from a loss of capacity – reserve capacity. In the first few formative, developmental decades of life, we build reserves in all of our body systems to help us resist the slings and arrows of life, such as trauma and infections. Youngchildren are prone to all sorts of infections until the immune system matures and develops the capacity to resist infections. Likewise, children frequently break bones until the musculoskeletal system matures. It is as though a fountain is in you. The fountain is a reservoir to hold something – immune capacity, muscle capacity, neurological capacity, bone density, hormone levels, and so on. When the reservoirs are full during our 20s and 30s, we feel invincible. We have reserve capacity and are more resilient to trauma and infections. If the reservoirs begin to dry up and lose reserves (capacity), as happens after another two or three decades, that is if we aren’t proactive, we become susceptible once again to disease and injury, lacking resilience. Who is more likely to contract infections, break bones, and develop cancers? The young and the old do – when reserves and capacity are lower.

Life is a continuum, from cradle to grave; each moment connected to the collective experiences of all preceding moments, and springing from choices we make. Biologically, this continuum can be distinguished by a gradual, often subtle, transition between two general timeframes, or spans of our life – growth and decline.

The first, growth, is the time when you develop and attain your functional maximum, biologically speaking. Physical capacity increases toward optimum. This is known as your health span. It is when you become physically independent, with the ability to carry out activities of daily living. Reserve capacity is greatest. Biological systems are in balance.

The body is always in a state of growth and decline. Initially, growth exceeds decline. In this regard, during the first few decades of life we all tend to age at a similar rate, in that each of us accumulates reserve capacity at a predictable rate. This is why pediatricians can refer to standardized growth charts and developmental milestones for well-child checkups. Young children will become ill many times per year. Why? Because their immune system is not fully matured. Every infectious organism that comes along stimulates an immune response. The next time the child is exposed to the same organism, he or she now has built-up immune system reserves to offer protection.

By the time the child becomes a young adult he/she is far less susceptible to infections. In a similar fashion, young children frequently break bones because the skeletal system has not yet filled its bone density reserves. Life stressors of various sorts play an essential role in the processes of growth. All of our systems go through a similar process of the accumulation of reserves – endocrine, neurological, cognitive, emotional, cardiovascular, and so forth.

By the time early adulthood arrives, we often feel invincible. This feeling, in part, explains much of the risky behavior exhibited in teens and young adults. It seems that we can be up all night long but are good to go the next day. We endure the insults of vigorous activity and rough sports without fear of breaking a hip or damaging a muscle.

We are less susceptible to infections than we were as a child, and when infections do occur in early adulthood, our body can more readily defeat them. We feel like we can handle anything on our plate. This is the time of life when reserve capacity is generally at its peak. Our biological armor is thick. Our body appears to tolerate the inordinate and unthinking abuse we put it through for the next few decades. The youthful sense of invincibility is a reflection of full reservoirs. Reserve capacity gives us resilience. It is youthful vitality.

At some point in life, reserve capacity begins a gradual decline, imperceptibly at first. We don’t feel poorly and the doctor may tell us we are healthy. Test results remain ‘normal.’ The decline is subtle, making it easy to adapt unconsciously to changes that occur. By our late-thirties to early forties, unless we have been proactive, our health will become suboptimal, meaning that it is not what it once was but at the same time is has not yet declined to a point where true disease is detectable. The damaging processes underlying future, yet undiagnosed, conditions lurk beneath the surface. The armor that protected us is beginning to wear thin. By some estimates, as much as 80% of the adult population in the U.S. has suboptimal health.

Not everyone loses reserve capacity at the same rate or in a similar manner. It is at this point we begin aging at different rates from one another. A divergence occurs, causing some to age biologically and functionally at a more rapid rate than others, while others seem to age more slowly and gracefully. Some body systems may age or lose reserve capacity more rapidly than others. In fact, it is possible to begin aging biologically at a rate equivalent to someone 15-20 years older than your chronological age.

Why is it that we don’t all age at a similar rate? Genetics certainly has something to do with it. However, as you will discover, pathological aging has far more to do with environment and behavioral choices we make in life. Through unenlightened, unhealthy choices we can effectively age more rapidly, or function biologically like someone older than us, developing the largely avoidable pathologic diseases of aging – coronary heart disease, cancers, dementia, and metabolic dysfunction.

Even though we may be aging more rapidly than necessary, it is not always apparent since our physical tests might continue to fall in the ‘normal’ range when compared to others our age, and we still feel that we are capable of continuing our activities of daily living just as we have in the past. On the other hand, it may simply be that we are not tuned in to what our body is trying to tell us. As you will learn, the variance in the rate of decline in our body’s reserve capacity has more to do with the choices we make in life than fate, genetics, or natural aging. Conventional medicine has done little more than pay lip service to this time in our life. Medical interventions begin only after making a diagnosis of disease. However, by this time the diseases of aging, pathological aging that is, have been developing for a long time, in many instances for decades. The central focus of medical intervention then becomes managing the symptoms. Modern medicine helps us to carry on, albeit at a much lower level of reserve capacity. This is the beginning of a transition to the next phase of our life – the disability span. In essence, we begin a downward course of silent degeneration.

Eventually everyone’s functional capacity dwindles enough to give rise to signs and symptoms of disease. These ‘diseases of aging’ finally make us dependent – dependent on drugs, technology or support systems – in order to carry out our activities of daily living. We enter the second time span of our life – the disability span. It is a time associated with reduced levels of reserve capacity, resulting in diseases and morbidity. Conventional approaches to the diagnosed diseases of aging generally involve symptom management, most often with drugs. As far as symptom management goes, modern medicine has been remarkably successful in recent years. People live longer as a result, albeit with their disease and/or at a relatively low level of reserve capacity; with a diminished feeling of vitality. The average lifespan for Americans has increased in recent decades largely because modern medicine has found ways to keep people alive longer, but only after preventable diseases have developed, such as heart disease and cancer. The healthcare system has not been successful preventing disease. Furthermore, the medical establishment has been far less effective improving or replenishing reserves once they have declined. The health care system would be more aptly named the sick care system.

The ideal would be to maintain or even replenish functional reserves to an optimum level, extending our health span, and then at a much later point in life experience a more accelerated decline in morbidity, thus compressing or shortening the disability span of our life. If we happen extend the length of our life in the process, so much the better.

The focus of Living Younger is not longevity. It is primarily about maximizing your health expectancy and making the best of the years you have, however short or long. It is about living fully, with mindful intention. Finally, Living Younger is about celebrating life and the experiences and wisdom that come with growing older. However, in the process of the personal transformation and improvement in health expectancy you will experience from Living Younger, you just might discover considerable years added to your life as well. Longevity might be thought of as the icing on the cake of living younger.

There is a distinction between natural aging and pathological aging. What most of us associate with growing old – heart disease, cancer, stroke, Alzheimer’s disease, diabetes, loss of sexual function, etc. – is actually pathological aging. These diseases rarely occur naturally, and are not a common part of natural aging. It is not to say that we don’t slow down or lose functionality in the normal aging process, or that these diseases never occur naturally. Rather, functionality just declines more slowly, and when we die of natural aging it is usually because everything finally gives out at about the same time. One of the notable observations about centenarians is that while they continue to grow older, they are aging more uniformly than others are. Interestingly, scientists observe that many of the pathological diseases of aging have a window of opportunity; after about 90 years the causes of death are more likely to result from frailty (e.g., falls leading to fractured hips, or infections like pneumonia and urinary tract infections) than from pathological diseases of aging (e.g., cancer, heart disease, Alzheimer's disease, etc.).

In the course of discussing aging and our opportunities to do something about aging, it is important to understand the fundamental biological mechanisms underlying the inevitable declines in ability, balance, and capacity. Let’s address the most important theories for the pathways to biological aging.

The phenomenon known as aging is a result of pathological changes that are somewhat controllable through healthy lifestyle choices and existing technologies. Most of them share one thing in common – lifestyle and environment play a major role in their expression, development, and progression. Fortunately, that implies that they are also amenable to personal intervention. Here are some of the underlying manageable culprits involved in pathological aging.

• Chronic Inflammation

The study of inflammation has evolved rapidly in recent years, and the results have overturned much of what today’s physicians learned in medical school about the origins of diseases as diverse as atherosclerosis, cancer, and Alzheimer’s disease.

The literal definition of inflammation is to “set on fire.” Inflammation has long been recognized as the body’s principal line of defense against infection, causing a constellation of local and systemic signs and symptoms: redness, heat, swelling, and pain. It is the life-saving component of your immune system that helps fend off bacteria, viruses, fungi, and other microbial invaders. It also helps damaged tissue repair itself from injury. Without inflammation, we would be sitting ducks in a very hostile world, with no way to repair the damage constantly being inflicted on us.

Acute Inflammation

Acute inflammation is the body’s initial response to injury, illness, infections, and stress. When you cut yourself with a paring knife, you want:

• To stop bleeding

  • By constricting blood vessels

  • By increasing fibrinogen and clotting factors

• White blood cells to fight infection

• Pain to remind you not to play with knives

Acute inflammation is essential to our survival, and when the inciting event has been resolved, we want acute inflammation to resolve.

Excess Inflammation

Excess inflammation on the other hand, is an over expression of the inflammatory response. Excessive inflammation causes or contributes to asthma, rheumatoid arthritis, systemic lupus erythematosis (SLE), and allergic diseases.

Furthermore, patients with diseases like SLE, characterized by systemic vascular inflammation, tend to develop arteriosclerosis at a younger age and more severely than people without these disorders. Low-level or healed arteritis may hasten the development of atherosclerosis or push existing lesions to growth orcomplications. A clue to the link between inflammation and heart disease comes from the observation that people with chronic inflammatory diseases have earlier and more severe atherosclerosis.

Mediators of Inflammation

Inflammation is mediated by a class of hormone-like substances known as eicosanoids. Eicosanoids are local hormones and do not circulate through the bloodstream. Every cell in the human body produces eicosanoids. They number it least in the hundreds. Eicosanoids control nearly everything from inflammatory processes and immune function, to the brain and heart.

Eicosanoids allow specialized inflammation cells (neutrophils and macrophages) to mobilize and squeeze between the linings of blood vessels. Mast cells, at the first sign of a foreign invader, release the chemical histamine, which signals the immune system that it should launch an attack. Histamine circulates through your bloodstream and attaches onto certain cells, causing a cascade of reactions to occur, starting with a burst of pro-inflammatory eicosanoids. Blood vessels dilate in response to these eicosanoids, allowing more immune cells (neutrophils and macrophages) to reach their target as quickly as possible. This dilation of blood vessels, mediated by eicosanoids, causes the trademark signs of inflammation: swelling, heat, redness, and pain.