Why Do We Age?

Who hasn’t dreamed what it might be like to live forever young? Over the centuries, many have sought a fountain of youth, a way to delay or escape the debilitating effects of aging and death. They’ve tried countless diets and chemicals. They’ve studied the oldest surviving people, looking for common threads. Yet even with the benefits of twenty-first-century science, the secret of eternal youth eludes us.

The oldest verified person, outside the biblical record, died in 1997 at age 122. She ate two pounds of chocolate a week and smoked until she was 117. Other centenarians have sworn by their daily portion of chicken soup and asparagus, or two eggs a day and cookies, or any number of other notions. No consistent lifestyles have emerged to explain their longevity.

While the genetic revolution has improved our understanding of aging, we have learned that aging is a complicated process. It is predictable yet highly individualized. And it begins with innumerable events in molecules and cells throughout the body.

Christians need to have a clear, biblically based understanding of the causes and proper responses to aging. Rather than rushing to the latest fads and cure-alls, we need to have informed answers based first on God’s Word and then on the latest and best research.

Not the Original Plan

We were not designed to die. We learn from Scripture that, because of sin’s curse, death awaits us all.

As in every great question of life, including science, God’s Word is the place to start. It gives the big picture and reveals key facts we can’t find anywhere else. First off, Genesis informs us that we were not designed to die. God created Adam and Eve to live forever. Their rebellion brought death into the world—death typically preceded by years of aging.

We also learn that before the worldwide flood, people lived for around 900 years. After the flood, our lifespan was shortened. While Noah lived to be 950, Abraham died at 175. Moses made it to 120 but observed in Psalm 90:10 that people typically lived 70–80 years. The same is true today.

We learn from Scripture that, because of sin’s curse, death awaits us all. And unless our lives are untimely cut off, we age. The effects of aging are well known in every people group. For instance, in Deuteronomy 34:7, we learn that Moses was exceptional for a 120-year-old man because he did not lose his strength and vision like other older people. Ecclesiastes 12 poetically describes the familiar miseries that accompany old age.

The stages are predictable, though specifics vary. Hair grays and skin wrinkles. Vision, hearing, muscle mass, and mobility diminish. Arthritis afflicts the majority. Cardiac output drops. The lining of our arteries becomes more brittle. Bones contain less blood-making marrow. Our brain mass decreases as much as 10% between ages 20 and 90, and it loses some of the synapses that connect nerves. And these are things to expect if we are healthy!

No one wishes to become frail and dependent. Modern researchers want to improve our understanding of aging so we can do something about it.

Why Did the Patriarchs Live So Long?

Genesis records that most early patriarchs lived for over 900 years. By Moses’ day, the average had fallen to 70–80 years (see Psalm 90:10). What happened?

After the flood, the human life span plunged. When you graph the ages of Noah’s descendants, the line resembles an exponential decay curve, which biologists frequently see in nature. This “natural” decline hints that the flood may have coincided with changes in our genetic programming.

But since we don’t fully understand how aging works today, how can we reconstruct what happened then? We don’t have access to any pre-flood humans to examine, so we can’t know exactly how the biology of aging changed.

Note: Some people wonder whether our current life span limit fulfills Genesis 6:3: “My Spirit shall not abide in man forever, for he is flesh: his days shall be 120 years.” In context, this verse refers to God’s plan to send the flood in 120 years. It cannot refer to life span, for many people subsequently lived past 120.

Long Life Spans Before the Flood

Life spans changed dramatically after Noah’s flood destroyed the earth. Before the flood, the average recorded life span was over 900 years. Immediately after the flood, they plummeted. Why the sudden change?

Exponential Decline of Life Spans

The decline of life spans after the flood was not random, but something called an exponential decay curve. This mathematical phenomenon is common in nature. Did the genetic effects of the dramatic population reduction—or some other effects of the catastrophic worldwide flood—trigger a rapid, permanent change?

The Endpoint of Aging

If modern experience is any indicator, there seems to be a hard-and-fast endpoint. Jean Calment, the oldest known modern person, died at 122. The oldest people alive today are a Japanese woman, age 115, and a Japanese man, age 113. Modern medicine has increased average life expectancy but not the maximum lifespan, which seems to be about 120. Most researchers now accept this and want to help people live well for as long as possible.

But they run into a fundamental question. Are we programmed to run down, in which case we might be able to tinker with the clock? Or do we age because of accumulated wear and tear, in which case we should focus on decreasing cellular damage?

In Your Genes?

Aging itself is not a disease. Instead, it’s a slow deterioration of the whole body—beginning with our DNA and cells and affecting every part of the body. However, aging increases our body’s vulnerability to many ailments, such as heart disease, stroke, diabetes, cancer, pneumonia, or Alzheimer’s. Thanks to these age-associated diseases, our risk of dying increases each year until we hit 80. Interestingly, after 80, the yearly odds of dying diminish, plateauing at 105.

The predictability of the aging process suggests it is somehow internally controlled. But how much of aging is “in our genes”? To determine this, doctors have studied aging twins. They’ve learned that about 20–30% of the variation in human life expectancy is under genetic control.

That’s huge. No matter how well you take care of yourself, your genes may have the final say.

Then which genes are to blame? Scientists have found that no single gene controls aging. As a person ages, various genes switch on and off, affecting a complex web of biochemical and physiological processes.

Biological events, not the calendar, trigger the changes associated with aging. In other words, our genes don’t dictate a specific day on which we’ll die. Instead, the body gradually makes subtle changes throughout our lives, timing these changes in response to many internal and external factors. So where does aging start?

It Starts in Our Cells

When we think of aging, we think about the visible signs like sagging skin. But, in fact, it begins at the cellular level throughout our body. A series of predictable, progressive, cumulative small changes are ultimately harmful to the whole body. Aging results from a gradual deterioration in the ability of cells to maintain a stable, efficient internal environment and function efficiently.

We know that some cells, such as neurons in the brain, are permanently lost to time, toxins, or accidents. But most cells divide. Why can’t other cells keep dividing indefinitely? Is there an intrinsic limit on cell division?

The answer came in the 1960s when Leonard Hayflick showed that normal cells replicate only a finite number of times. Normal cells are not, as previously thought, immortal.

Since then, scientists have tried to figure out why (and how) cell reproduction is limited. Eventually, scientists learned that the caps on the ends of chromosomes are not copied during DNA replication. Those caps—telomeres—get shorter each time DNA is copied.

But scientists have discovered that this can be reversed. It turns out that a cell can rebuild telomeres if a gene for the enzyme telomerase is activated. In fact, this happens in cancer cells, making them effectively immortal.

Could activating telomerase in “good” cells immortalize them? Well, things are not so simple. How to control telomerase production in normal cells, first in the laboratory and then in people, hasn’t been worked out. Moreover, some animals with long telomeres die young, while mice with deficient telomeres age normally. Therefore, there is no guarantee such therapy would work.

Clearly, there is more to aging than short telomeres.

Telomeres (white), which protect the ends of our chromosomes (gray), get shorter as we age. Telomere shortening is thought to contribute to aging.

Faltering Hormones

Scientists began to wonder what other genetically controlled mechanisms, in addition to Hayflick’s cellular clock, might preprogram the body to shut down. One likely candidate is hormones. Hormones are the body’s chemical messengers, and, among other things, they cause many age-associated changes.

That’s logical. Hormonal changes accompany both puberty and menopause. Doctors have found that replacing the hormones women stop producing at menopause diminishes their symptoms and reduces the risk of osteoporosis (loss of bone mass) and hip fractures. Unfortunately, long-term therapy is associated with an increased risk of breast cancer. People must weigh the benefits and risks of hormone replacement in the battle against aging.

Other chemical messengers, such as growth and adrenal hormones, also decrease with time. Could replacing them slow aging? Therapies under investigation include medications to decrease resistance to hormones that help the body utilize sugar as well as adrenal hormone replacement. However, these treatments have risks too. Moreover, they have not slowed the aging process. Worse yet, recent studies suggest that the natural decrease in some of these hormone levels accompanies a longer lifespan, making attempts to boost them potentially counterproductive!

Faltering Immune System

Another familiar effect of aging is the increased risk of infection. Just think of the push to get the elderly to update their vaccinations before flu season. And many of us have had aged relatives succumb to pneumonia. Aging affects our immune system. Perhaps restoring our immune system, which fights off deadly diseases, could lengthen life.

The immune system changes throughout life. Early in life, the body produces a generous supply of T cells in our bloodstream to fight foreign invaders. By puberty, our stock of T cells is well established, so production slows. These T cells remember the things to which they’re exposed, equipping the immune system for fast responses. By the time a person is old, however, his or her immune system has seen a lot, so most of its T cells are now targeted against a specific disease. Only an ever-shrinking number remain available to respond to new challenges.

Furthermore, as we age, our T cells often fail to properly cooperate with the other cells that produce antibodies. Age also decreases the production of new immune cells. Moreover, the immune system may malfunction, turning on when it should remain off, causing chronic inflammation. This unhealthy inflammatory environment makes life difficult for all other cells in affected tissues.

At the moment, we don’t have a way to fix the immune system. We just know that it breaks down at different times for different people. So doctors must tailor advice, case by case, to address the inevitable deterioration of our immune system.

Photo: SciencePhoto Library/Steve Gschmeissner

Scanning electron micrograph (SEM) of a lymphocyte, a type of white blood cell and part of the immune system that helps our body fight off deadly disease. As we age, various factors lead to the inevitable deterioration of our immune system.

Looking Outside the Body—Those Pesky Free Radicals

Thus far we’ve considered internal systems that seem programmed to self-destruct in our sin-cursed world. But what about the accumulating effects of unrepaired damage? Could they be a major cause of aging?

One of the most popular culprits, if you believe all the marketing, is free radicals. These are highly reactive molecules that destroy organic molecules. Normal metabolic processes in the body produce them. Many contain oxygen, which is harmful to organic molecules. To clean them up, the body employs antioxidants, such as vitamin A, vitamin C, and a naturally occurring enzyme. Could aging be largely the result of accumulated damage caused by free radicals?

Much of this damage afflicts the energy factories of the cell, mitochondria, where lots of free radicals are normally produced. Research has shown, however, that free radicals serve some important functions and are not uniformly evil actors. Their contribution to aging remains unsubstantiated.

So beware. Many anti-aging arguments sound convincing on the surface, but there is usually more to the story.

Accumulation of Damaged Proteins and DNA

Here’s another popular candidate: damage to proteins and DNA.

Proteins can fold incorrectly, suffer damage from metabolic byproducts, or simply deteriorate. Sure, cells have systems to remove damaged proteins, but these systems become less efficient with age. Damaged proteins can build up in cells and even link with other molecules. Are these a cause of aging or just something we see in the aged? Scientists do not know for sure. What about damage to DNA? Cells have repair systems to deal with these too, and most are corrected. But when the genes responsible for this repair suffer mutations, it can impair a cell’s ability to police its own genes. Such mutations appear to increase with aging.

Many biomolecules floating in our bodies are fragile because of their own chemical instability. Impaired molecules can interfere with normal metabolic processes in innumerable ways and cause some of the deterioration seen with aging. While a number of cases have documented that impaired molecules cause harm, no evidence incriminates any particular molecule in the aging process.

Too Many Calories and Aging

Tiny mammals such as mice have a high metabolic rate and die young. Could burning lots of calories cause cellular damage that leads to aging and death? Might starvation be a path to a longer life?

Researchers have learned that severe calorie restriction improves longevity in some small laboratory animals, as do drugs that interfere with energy metabolism. Many people have jumped on these findings to conclude we need to eat less—a lot less—to live longer.

However, the effect of starvation on lifespan certainly cannot be tested on people! So we need to be careful. We know for a fact that extreme calorie restriction risks decreased muscle mass, osteoporosis, and the life-threatening aberrations that come from anorexia. Furthermore, drugs that interfere with metabolism have dangerous side effects.

Some have suggested that intermittent fasting or calorie restriction—a few days every now and then—might allow cellular damage time for repair. Such an approach is safer than starvation, and it is under active investigation, although no research has demonstrated its potential for improving human lifespan or quality of life in the twilight years.

Epigenetics and Aging

Some external influences impact the expression of genes in our aging cells. We call the study of this vast new field epigenetics. Scientists have discovered that epigenetic (“outside the genes”) factors influence the expression of genes without changing the genetic code itself. If epigenetic factors get modified as we age, could this reduce the cell’s ability to function and cope with the challenges of life? Quite likely.

Just one example should suffice: DNA methylation. Attaching a “methyl” molecular subunit to a strand of DNA will prevent the transcription of the affected gene. This modification changes the way genes are expressed without changing the genes themselves.

Researchers have already discovered that epigenetic changes like methylation are associated with some age-related diseases. However, more research is needed to understand how these epigenetic factors vary among healthy people as they age. We are far from knowing enough to begin interfering with these processes.

A Hopeful Future?

Aging is a natural process of deterioration in this sin-cursed world. We have learned much. Yet with each new piece of knowledge, we unearth further complexities and more questions. Isn’t that the case with so many things in life?

Part of the wisdom of old age is not to rush to conclusions. We need to slow down and compare everything against Scripture (Acts 17:11). God made life challenging so that we would have compassion on others but ultimately look to him.

No single discovery will reverse the complex processes that the Creator apparently unleashed when he judged mankind’s sin.

Modern medicine has done a laudable job of reducing the scourge of many age-associated diseases and improving life expectancy. Let’s hope the trend continues. But we should be wary of marketing hype. No single discovery will reverse the complex processes that the Creator apparently unleashed when he judged mankind’s sin. Meanwhile, we must care for people as they age—whether they suffer debilitating problems or escape them—with Christlike compassion and patience.

Even as we seek to help the elderly maintain the best possible quality of life and love them to the end, we see that God seems to have imposed aging as an ever-present and inescapable reminder of sin’s curse, including the vanity of life on earth and our need for him. Jesus Christ paid the price for sin and defeated death so that through him alone, we find the sure hope for life eternal.