Why We Age

Why We Age

The question of why we physiologically age has intrigued scientists for many years. A number of theories have been developed and advanced over time-some have been discarded and others have survived to varying degrees. Current research supports several theories. It is quite likely that there is not just one theory that explains why we biologically age, but rather that our aging is due to a complex interweaving of many processes.

The theories explaining our physiological changes as we get older fall generally into two groups. (Information about these theories is summarized from a National Institutes of Health publication, Aging Under the Microscope [NIH, 2002]). One group is that of the programmed ideas, namely that aging follows a biological timetable, possibly a continuation of the same timetable that controls childhood growth and development. The other group comprises error theories-those ideas that say physiological aging is due to damage to our body systems causing things to go wrong.

While several theories exist to explain physiological aging, there is no one theory which scientists can completely agree. The body and its various systems are extremely complex and intricate, so theories presented still leave many unanswered questions. It is probably that current and future theories will interact with each other in ways that we may never understand.

Some theories promote the role of genetics in determining longevity and aging changes, while others give stronger credence to environment and lifestyle. Evidence appears to exist that would support all of them.

Regardless of the research findings, we can make our own observations of similarities and differences in persons as they age. We may notice changes in appearance, stamina, and stature in some persons but not in others. We may guess one person as being age 60 and another age 80 and we could be right-but we could also be wrong.

We may be surprised by a person's perception of their health status. We may judge based on a conversation that one person is very unhealthy while another is healthy, but realize later that our conclusion was wrong also.

What this tells us is although we can generalize about aging changes, aging is still a process occurring within each individual. Seniors may share common characteristics in theory, but our interactions with each person must reflect a respectful, individualized approach if we are to work successfully with them.

Programmed Theories

The major programmed theories are programmed longevity, the endocrine theory, Hayflick's Limit, and the immunological theories.

Programmed Longevity

According to this theory, aging is the result of certain genes switching on and off in a sequential manner throughout a person's lifetime. Programmed longevity theory presumes that there is a biological clock controlled by a person's genes. Therefore one's longevity and senescence follow a pattern determined by the genetic structure.

Much of the research studying genes has been done with roundworms, fruit flies, and mice, easy to study because their life spans are shorter than those of humans. It is believe, based on these studies, that some genes manufacture proteins that limit life span. But when these genes are tampered with or mutated, they produce either defective proteins or no proteins at all, which actually results in greater longevity. For example, the mutation of one gene, affectionately named the I'm Not Dead Yet gene, doubled the life span of the fruit fly so that by the time 80 to 90 percent of normal flies were dead, those with the mutated genes were still vigorous and reproducing.

The genes that scientists have isolated so far are likely to be only a small percentage of those having an impact on longevity and aging. Further research is needed to determine whether the discoveries about genes of the fruit fly and other species can be applied to humans. Other questions must answer what exactly the genes do, and how and when they are activated.

Endocrine Theory

The endocrine theory is based on the idea that there is a biological clock that acts through hormones to control the rate of aging. Hormones are chemical messengers in the body that move throughout the bloodstream, and attach themselves to and unlock receptors located on the cells in order to carry out their particular action.

Individually and collectively these hormones fulfill numerous functions. While each has a primary action, it appears that the hormones support each other in carrying out their roles. The production and circulating levels of many hormones decline with age, and this has led many to assume that restoring the level of these circulating hormones to levels in young people would be anti aging strategy. However, it may be beneficial to the older organism to have these levels decline. Examples of hormones include estrogen, growth hormone, melatonin, testosterone, and DHEA.

  • Estrogen hormones are sex hormones primarily found in women, but also in small amounts in men. These hormones have many roles, one of which is to slow thinning of bone as one ages, but they also may help prevent frailty and disability.
  • Growth hormone is a hormone that promotes growth. Growth is the result of the complex interaction of several hormones and growth factors.
  • Melatonin appears to play a part in regulating seasonal changes in the body and assists with sleep. Some believe it can slow or reverse aging, but many questions remain.
  • Testosterone is a hormone primarily found in men, but women also have small amounts. Although production peaks in early adulthood, most men even into older age still produce amounts within normal limits. Studies are now under way to determine whether supplementation can prevent frailty, sharpen memory, or help maintain strong muscles and bones.
  • DHEA is produced in the adrenal glands. Like testosterone, DHEA production peaks in the mid-20's and then gradually declines. It influences other hormones, including testosterone and estrogen, but how it affects the aging process is still not understood. Research is currently under way to study its effects on aging, muscles, and the immune system.

Hayflick's Limit

Leonard Hayflick, a prominent researcher in the 1960's, discovered that fibroblast cells isolated from human skin can reproduce themselves only about 50 times, at which point they stop dividing and enter a state referred to as cell senescence. This Hayflick Limit thus implies that the human body may actually be designed to wear out.

In the early 1990's, this discovery led to yet another important finding. At the ends of each chromosome are structures called telomeres (from the Greek word meaning end body). Telomeres protect the ends of the chromosome, but each time the DNA in the chromosome is replicated, the telomeres at each end get a little shorter. Eventually, after about 50 doublings, the telomeres become so short that the DNA is no longer able to be replicated, so cell division stops.

Thus, one of the most interesting areas of research in gerontology today is how to retain or restore the length of telomeres so that cells will continue to reproduce beyond the Hayflick Limit. However, this does not explain why non dividing cells, such as brain cells, age.

Interestingly, certain cells in the human body, such as germ cells, stem cells, and cancer cells, have telomeres that do not shorten as they reproduce. For instance, cancer cells produce an enzyme called telomerase. This enzyme allows the telomeres on cancerous cells to regrow sufficiently to enable the cancer cell to thrive for as long as the host, or body, is alive. Telomere research could potentially yield numerous advances, such as possible cures for both cancer and HIV/AIDS, as well as slowing the human aging process (Fossel, 1996). The biggest hurdle to overcome in this research is how to selectively maintain telomere lengths in some, but not all, tissue.

Immunological Theories

The immune system is the elaborate defense system that protects our bodies from infection, fungi, parasites and viruses, and other toxins. It is comprised of organs, substances, and cells stationed throughout the body that are designed to recognize intruders not normally a part of the body. It then mobilizes the body's defenses-antibodies-to fight against these intruders.

The system is able to distinguish "non-self" tissue from "self" tissue-those elements normally present in the body-because the molecules of "self" carry markers that the system recognizes. This ability to distinguish "self" from "non-self" prevents the immune system from attacking normal tissue.

As one ages, it is believe there is a programmed decline in the system's ability to function. As a result the body is less able to fight off threats from the "non-self" intruders, resulting in disease and death. Additionally, in a process referred to as autoimmune, the system may produce antibodies that destroy normal "self" tissue. The autoimmune action is believe to be a factor in development of some aging-related disease.

Error Theories

Theories that are part of the error system of biological aging include that of wear and tear, rate of living, cross linking, free radicals, and somatic DNA damage. These theories presume that aging is not due to programming, but to random events that cause damage.

Wear and Tear Theory

In this early theory of aging, the belief is that years of damage to cells, tissues, and organs from toxins, radiation, ultraviolet light, and other stressors repeatedly harm DNA in the genes. Although the body has a remarkable ability to repair itself, many repairs are incomplete or inaccurate, leading to progressive accumulation of damage. This results in eventually killing tissues and organs-and finally the entire body.

Rate of Living Theory

 "Live fast, die young" is sometimes used to describe this theory. It is based on an ancient belief that the body has a finite amount of some substance that, when used up, causes us to age and die. For example, we might be allocated a certain number of breaths or even a definite number of heartbeats. The argument against this is that it is too simplistic and doesn't explain why some people live much longer than others.

Many scientists believe that rate of living involves the rate of oxygen metabolism, not finite numbers of other factors, and that perhaps some species die sooner because they have a faster rate of metabolism. Other studies are researching the relationship of total weight of body organs to increased oxygen metabolism. This had led to testing how caloric restriction and reduction of total organ weight could slow metabolism and again and lead to longer life.

Investigators have found that rats and mice fed a nutritionally balanced diet with 30 percent fewer calories live up to 40 percent longer, appear to be more resistant to age-related diseases, and demonstrate a delay of usual age-related degeneration of almost all their physiological systems. These researchers are unclear about why this happens but speculate that there is reduced oxidative damage to the cells, the immune system functions at a more youthful level, and the cells more effectively retain their capacity to proliferate (NIH, 2002). 

Cross Linking Theory

As we age, protein, DNA, and other structural molecules develop inappropriate and excessive attachments between each other, similar to the rungs of a ladder. These excessive attachments, or cross links,lead to decreased mobility and elasticity of these structures. Effects are more easily seen in the skin where protein cross links lead to skin wrinkling and less pliability, arteriosclerosis, in rib cartilage create less flexibility, and in kidneys are responsible for decreased kidney function.

While the protein cross links in organs such as the skin can be identified based on experimental evidence, the cross linking as a biochemical reason for aging is one of many explanations for aging, but not the most important one. (Haylick, 1996).

Free Radical Theory

Oxygen is metabolized in our cells to provide energy for the body. During the metabolism process toxic byproducts, called free radicals,  are released. Natural substances-for example, antioxidants-absorb and neutralize the toxic radicals so they can't harm the body. However, some radicals manage to escape capture by the antioxidants and harm the cells anyway. According to the free radical theory, accumulated damage caused by oxygen free radicals causes the cells and, eventually, the organs to stop functioning.

Scientists who support this theory believe that the free radicals cause DNA damage, protein cross linking, and formation of age pigments. They point to studies showing the effects of antioxidants in slowing the aging process in animals. Other scientists argue that slowed aging happens because antioxidants suppress the animals' appetites and lead to calorie restriction.

Somatic DNA Damage Theory

This theory is based on the belief that changes or mutations of our gene structure occurring in egg or germ cells will be passed on to future generations, but the mutations that occur in other cells of the body will affect only that particular individual instead. While most of those mutations will be either corrected or eliminated, others will not and will go on to cause malfunction and death of cells.

Those who argue against this theory say that shorter life spans should result from inbreeding of animals with mutations and longer life spans of inbred animals without the mutations. But in reality, any inbreeding results in shorter life spans.

How Do Aging and Disease Differ?

From the discussion of theories of biological aging presented above, we learn that there are changes occurring in our bodies as we get older. Some "normal" changes-such as decreased muscle strength or stamina, hearing loss, or lessened immune response, to name a few-may be visible and apparent, while others are not so noticeable. But the changes that accompany the aging process are not the same as disease or sickness. Aging is a predictable process that occurs in all of us over time, while a disease is an abnormal process not present in everyone. One theorist argues that to distinguish it from disease, a normal aging change must meet three criteria: it is universal, it comes gradually from within the body, and it has a negative effect on body functioning (Atchley & Barusch, 2004).

However, the presence of these changes in organs and cells from the normal aging process makes us more vulnerable to becoming ill and suffering age related diseases. We may suffer a stroke because of changes in blood vessels as we age. Fractures occur more easily because of loss of bone mass following menopause. With declines in our immune system, we may not fight off an infection as quickly or easily. Our immune system may even malfunction, mistake our own cells as the invaders, and lead a fight against them, resulting in an autoimmune disorder.

Hayflick argues that while it is important to distinguish between normal aging changes and disease, it is not always easy. Sometimes, in fact, it is impossible to do for several reasons. For example, protein changes in the lens of the eye result in cataract formation, while the same protein changes elsewhere in the body cause no discomfort.

Although scientists can detect the differences between aging and disease in the higher levels of cells, tissues, and organs, they really don't know the differences between an aging cell and a diseased cell at the molecular level. But they do believe that the physiological losses characterizing aging are universal in all older members of a species, while changes attributable to disease are found only in some of the species (Hayflick, 1996).

What Factors Affect Aging and Longevity?

Scientists don't agree on the degree of influence that genetics, environment, and lifestyle each have on our aging and, ultimately, our life spans. However, most believe that all three factors likely play roles in determining whether someone will lead a long and healthy life.

Research on theories of biological aging appears to demonstrate that genetics plays a strong role. Madame Calmet of France could give some credit for her longevity to her genes. She had numerous ancestors who had lived long lives and had several descendants who did the same. Studies of twins have found that the life spans of fraternal (nonidentical) twins vary more than that of identical ones.

Dr. Thomas Perls and his colleagues at Boston University Medical School have been studying centenarians since 1994 to determine why they live to an old age, much of it in excellent health. Approximately 1,000 subjects are enrolled in their New England Centenarian Study, the largest genetic study of centenarians in the world. The study looks not only at the centenarians, but also their siblings, children, and some control subjects. Knowledge gained from the study will help others understand how to age well for a long life span. Although the centenarians differ from each other in such characteristics as education, socioeconomic status, religion, ethnicity, dietary habits, and exercise, they do share a number of other characteristics. It has been found that at least 50 percent of the centenarians have first-degree relatives or grandparents that also lived to an old age. Many of the subjects have sibling achieving advanced years. Other common characteristics include:

  • a rarity of significant obesity
  • rare history of smoking
  • low score of neuroticism in personality testing
  • high functioning (90 percent of the centenarians retained high functioning to an average of 92 years; 75 percent had high functioning until age 95)
  • bearing children after age 35, and even after age 40-a woman bearing a child beyond age 40 had four times the chances of living to age 100 compared to one who gave birth before age 40, a finding that likely indicates that the reproductive system is aging well
  • centenarians' children aged 65 to 82 years showed significantly lower rates of age-related diseases, including such conditions as high blood pressure, diabetes, and heart disease, as well as lowered susceptibility to stress (Boston University, 2002).

Researchers stress the difficulty of separating the purely genetic influence of aging and health from environmental and lifestyle influences. Heredity plays a strong role in the development of some diseases-Huntington's disease, certain forms of cancer, or familial high cholesterol syndromes, for example. Other families show strong histories of hypertension, diabetes, hypothyroidism, heart disease, or arthritis. Some researchers say genetics play a part in promoting a disease, but this is probably only have the story, Just because family members share similar characteristics may not mean that genetics is responsible for the characteristics. Rather the habits they share-diet, exercise, stress management, where they live-can make a difference, and, in fact, may be more important than heredity (Rowe & Kahn, 1998).

The MacArthur Research Program on Successful Aging studied both identical and fraternal twins raised apart to determine the importance of heredity and environment on their mental and physiological changes as they aged. They found that only about 30 percent of physiological aging was attributable to genetics. Furthermore, when they studied Swedish twins who were older than 80, they found that only about half the changes in mental functioning were related to genetics.

Researchers with the MacArthur Program believe that the role of genetics becomes less important ass we get older. They found that the likelihood of being fat, having hypertension, having high cholesterol and triglyceride levels, and having decreased lung function was largely not inherited but instead was due to lifestyle and environmental factors. They concluded that greater importance should be attached to where and how we live in determining age-related changes in organ function throughout the body (Rowe & Kahn, 1998).

The role of regular psychological activity in promoting healthy aging is supported by numerous studies. The NIA stresses that it may be the most important factor, and that the more one exercises in later life, the better off one will be. Not only can regular, sustained exercise help prevent or delay disease and disability, but it may actually improve these conditions once they have developed. One study showed that subjects ages 80 and older discarded their walkers and adopted canes instead after 10 weeks of simple muscle building exercises (NIGH, 2002).

Endurance, strength, balance, and stretching exercises all can improve overall health. Brisk walking has an effect on the heart, lungs, and circulatory system by enhancing stamina. Muscles are improved by doing strenght exercises. Balance exercises help prevent falls. Stretching keeps the body limber (NIH, 2002).

The MacArthur Study looked beyond exercise as a factor in maintaining physiological functioning. They utilized a variety of tests and measurements with a group of more than 4,000 older persons from Massachusetts and North Carolina to identify "successful agers" in terms of their mental and physiological functions. Some of the factors that contributed to the subjects' successful aging were predictable-younger age group, higher income, high lung function, male, normal weight, and moderate activity, but other findings were quite surprising. They found that those who had higher mental function were more likely to retain more physiological function than others. Most surprising was that the frequency of emotional support strongly predicted enhanced physiological functioning over a period of time. Based on these finding, they believe that having someone around who can provide cheering up and "talk therapy" can actually promote better physiological status (Rowe & Kahn, 1998).

The National Institute on Aging continues to study the effects of caloric restriction on longevity in monkeys. Both rhesus and squirrel monkeys in their study consume nutritionally sound diets, but are fed 30 percent less food. (A control group gets as much food as desired.) As expected, the restricted monkeys' maturation as measured by onset of puberty and skeletal development has been delayed by approximately one year. Now the monkeys, moving into midlife and smaller in size, are just as active as the controls. Early findings point to the possibility of less heart disease and cancer in the restricted monkeys, although more years of observation are needed (NIH, 2002).

We can't ignore the environmental factors affecting longevity and again. In earlier decades, individuals with shorter life expectancies faced epidemics of influenza, polio, diphtheria, and other infectious diseases for which there were no antibiotics. Overcrowding, poor water supply, hazardous working conditions, malnutrition, and contaminants in the environment took their toll. But many of these environmental hazards have been overcome for a substantial segment of the population. So while some may still assume that genes play the dominant role, new research suggests that environment and lifestyle may in face be more important in terms of risk factors associated with aging and longevity (Rowe & Kahn, 1998).

Calculating Your Expected Longevity

Tools are available for those who wish to estimate their longevity based on genetics, lifestyle, and environment. One tool, developed by researchers at the New England Centenarian Study, is built on the assumption that we are born with a set of genes that allow us to live to age 85 or more. However, positive behaviors can add as much as 10 more quality years, while a lack of preventive behaviors will subtract a substantial number of years. Questions in the longevity calculator address issues of personal data, lifestyle and environmental factors, nutrition and exercise, medical check-ups, and family history. The calculator has been published by the Alliance for Aging Research and its available online at http://www.agingresearch.org.

What is Your True Age?

Researchers have posed this interesting question as they attempt to find a correlation between our physiological aging and our chronological age. So far, scientists know that age in years and physiological aging aren't necessarily the same. It is obvious in looking at a group of persons of roughly the same chronological age that their physiological characteristics may be very different.

By collecting data on various organ functions, researchers hope to establish markers of physiological aging. They believe these markers would be more precise indicators of aging than chronological age and would make it easier to study normal aging, diseases, and interventions. So far their efforts to identify markers have been unsuccessful (NIH, 2002).

In pondering the question of how old we are, researcher Hayflick raises some interesting thoughts. One's exact age is difficult to determine if we base it on the age of our body cells, he theorizes. Since some cells turn over at short intervals but others live longer, our exact age is elusive. For exa;mple, many of the cells of the skin and the digestive tract, as well as red and white blood cells, divide constantly. That makes these parts of our bodies potentially different each day and perpetually newborn. Other cells are replaced in 7 to 10-year cycles, so those parts of our bodies are always less than 10 years old.

Our molecules, whether they have turned over or not, at their very basic level, are composed of atoms. Most of these atoms have been around since our planet was formed, and since we are simply unique rearrangements of this immortal material, parts of our bodies may be many years old (Hayflick, 1996).

The information above is reprinted from Working with Seniors: Health, Financial and Social Issues with permission from Society of Certified Senior Advisors® . Copyright © 2009. All rights reserved. www.csa.us