Exhibit 1
Source: Data compiled from Walford (1983); Encyclopædia Britannica (2018); Did You Know? (2019).
Biologists have discovered intriguing relationships among life span, body size, relative brain size, and metabolic intensity. For example, a chipmunk has a maximum life span of 8 years, but an elephant can achieve 78 years. These facts suggest a more general idea known as the rate-of-living concept: roughly, the concept that metabolism and life expectancy are closely correlated. Smaller organisms, which tend to have a more rapid metabolism for each unit of body mass, also tend to have shorter life spans. A short-lived mouse and a long-lived elephant both have approximately the same temperature, but the mouse produces more heat per unit of mass. At the other extreme, slow-moving turtles are likely to have life spans longer than the more active mammals. Another fascinating fact is that no matter their total body mass, mammals have approximately the same number of heartbeats in a lifetime. Still, despite these tantalizing correlations, the rate-of-living theory has largely been rejected by biologists, along with the notion that biological aging is somehow necessary for the good of the species (Austad, 1997).
In comparison with other species of mammals, the human being has the longest life span and also expends more energy per body weight over the total life span than any other mammal. Energy metabolism per body weight across the life span in humans is about four times greater than that for most other species of mammals. Human beings have an average life expectancy and a maximum life span about twice as great as those of any other primate.
Compare the chimpanzee and the human being. The maximum human life span appears to be around 110 to 120 years; the chimpanzee’s is close to 40 years. But when we look at DNA from both species, we find that their DNA is more than 98% identical. These figures suggest that the rate of aging may be determined by a relatively limited part of the genetic mechanism. Calculations suggest that if a cell is determined by around 100,000 genes, then perhaps no more than a few hundred alterations in the genetic code are needed to change the rate of aging.
Scientists have posited that a large increase in maximum human life span occurred fairly recently—probably within the past 100,000 years. The speed of this development suggests that only a tiny portion of the human genome, representing less than 1% of the genetic code, was likely to be involved. If so few genetic mechanisms determine aging, then we can perhaps hope to intervene to delay the process of aging (Finch, 1990).
Biological Theories of Aging
The facts about aging and maximum life span have led many biologists to believe that biophysical aging may have a single fundamental cause. In their efforts to find such a single primary process to explain those time-dependent changes that we recognize as biophysical aging, they have developed many different ideas. Biologist Zhores Medvedev (1972) enumerated more than 300 biological theories of aging. At present, no single theory of aging explains all the complex processes that occur in cells and body systems, but ongoing research is under way that is leading to new insights into why we grow old.
Broadly speaking, we can distinguish between two kinds of theories of aging (Finch & Kirkwood, 2000):
Chance. Some theories see aging as the result of external events, such as accumulated random negative factors that damage cells or body systems over time. For example, these factors might be mutation or damage to the organism from wear and tear.
Fate. Some theories see aging as the result of an internal necessity, such as a built-in genetic program that proceeds inevitably to senescence and death.
In either case, the question remains open: Is it possible to intervene to correct damage to the aging body or modify the genetic program? The most likely interventions are those that would make sense depending on which theory best explains the facts about aging (Ludwig, 1991).
Wear-and-Tear Theory
The wear-and-tear theory of aging sees aging as the result of chance. The human body, like all multicellular organisms, is constantly wearing out and being repaired. Each day, thousands of cells die and are replaced, and damaged cell parts are repaired. Like components of an aging car, parts of the body wear out from repeated use, so the wear-and-tear theory seems plausible.
The wear-and-tear theory is a good explanation for some aspects of aging—for example, the fact that joints in our hips, fingers, and knees tend to become damaged over the course of time. A case in point is the disease of osteoarthritis, in which cartilage in joints disintegrates. Another is cataracts, in which degeneration causes vision loss. Our hearts beat several billion times over a lifetime, so with advancing age, the elasticity of blood vessels gradually weakens, causing normal blood pressure to rise and athletic performance to decline.
The wear-and-tear theory of aging goes back to Aristotle but in its current form was expanded by one of the founding fathers of modern biogerontology, August Weismann (1834–1914). He distinguished between the two types of cells in the body: germ plasm cells, such as the sperm and egg, which are capable of reproducing and are in some sense “immortal,” and somatic cells comprising the rest of the body, which die. Weismann (1889), in his famous address “On the Duration of Life,” argued that aging takes place because somatic cells cannot renew themselves, so living things succumb to the wear and tear of existence.
What we see as aging, then, is the cumulative, statistical result of wear and tear. Consider the case of glassware in a restaurant, which follows a curve similar to that for human populations. Over time, fewer and fewer glasses are left unbroken, until finally all are gone. The life expectancy or survival curve of the glassware follows a linear path over time, but the result for each individual glass comes about because of chance. Nothing decrees in advance that a specific glass will break at a fixed time. Glasses are just inherently breakable, so normal wear and tear in a restaurant will have its inevitable result. Like everyone born in a certain year (e.g., 1880), the “glasses” disappear one by one until none are left.
Some modern biological theories of aging are more sophisticated versions of this original wear-and-tear theory. For example, the somatic mutation theory of aging notes that cells can be damaged by radiation and, as a result, mutate or experience genetic changes (Szilard, 1959). The somatic mutation hypothesis would seem to predict higher cancer rates with age, yet survivors of the atomic bomb at Hiroshima showed higher rates of cancer but no acceleration of the aging process.
Even without actual mutation, over time, cells might lose their ability to function as a consequence of dynamic changes in DNA. According to the so-called error accumulation theory of aging, or error catastrophe theory, decremental changes of senescence are essentially the result of chance or random changes that degrade the genetic code (Medvedev, 1972). The process is similar to what would happen if we were to use a photocopy to make another copy. Over time, small errors accumulate. The errors eventually make the copies unreadable. Similarly, the error catastrophe theory suggests that damaged proteins eventually bring on what we know as aging through dysfunction in enzyme production.
The accumulative waste theory of aging points to the buildup in the cells of waste products and other harmful substances. The accumulation of waste products eventually interferes with cell metabolism and leads to death. Although waste products do accumulate, there is little evidence of harm to the organism. The key to longevity may be the extent to which cells retain the capacity to repair damage done to DNA. In fact, DNA repair capacity is correlated with the metabolic rate and life span of different species. Some studies suggest that DNA damage in excess of repair capacity may be linked to age-related diseases such as cancer.
Autoimmune Theory
The immune system is the body’s defense against foreign invaders such as bacteria.