genes with a negative impact, such as a shorter lifespan. In contrast, the genes that determine maximum lifespan could turn out to be linked to genetic factors that forestall the degenerative diseases of late life. Thus, under the most favorable scenario, if we were to discover and intervene in the genetic causes of longevity, we might also find the key to reducing the disabilities and dysfunctions of old age.
Scientists studying genetic influences on aging and longevity have moved in a number of suggestive research directions. From an evolutionary point of view, for example, there is no obvious reason that human beings should live beyond 30 or 40 years, which gives them enough time to reproduce. There seems to be a trade-off between the biological investment made in survival for reproduction and maintaining organs and tissues beyond the end of the reproductive period.
In fact, we see from population studies of animals in the wild that aging rarely exists. The sea anemone, for example, seems to exhibit no physiological losses with chronological age at all. Animals in the wild exhibit survival curves similar to those of human populations; that is, most individuals die during a certain age range, but others die when very young or when very old. What follows from this evolutionary argument is that there is no intrinsic biological necessity for aging, and thus no reason why raising the maximum lifespan would be impossible.
According to one optimistic view, most of the decremental changes associated with aging—including potentially preventable diseases, such as Alzheimer’s—are not the result of any preprogrammed, built-in requirement for decline, but are the result of environmental causes (Cutler, 1983). However, maximum lifespan seems to be largely shaped by specific genetic endowment, rather than environmental factors. Perhaps, then, aging is a passive or indirect result of biological processes, whereas maximum lifespan is a positive or direct result of evolution. From this perspective, it follows that both the rate of aging and the maximum lifespan of a species could change—and change relatively quickly.
Some provocative questions follow: Would it be possible by direct intervention to alter the genetic code and thus delay the onset of age-dependent illnesses and perhaps to slow down the rate of aging itself (Austad, 2015)? With deeper biological knowledge, could the maximum lifespan be extended to 150 or 200 years or beyond? Even to ask these questions shows just how far we have come from a traditional view of the human life course, in which birth, aging, and death were facts simply taken for granted as part of the unalterable nature of things (Aaron & Schwartz, 2004; Pew Research Center, 2013).
Mechanisms of Physical Aging
We sometimes think of aging as a process applying uniformly to the whole organism, yet physiological studies show that different parts of the body age at different rates. For example, white blood cells die and are replaced within 10 days, but red blood cells last 120 days. The stem cells that produce all blood cells reveal no signs of aging at all. Cells in the brain last as long as the body lives; once the brain is fully formed, neurons do not exhibit significant cell division, and unless damaged by illness, they remain largely intact. But apart from long-living stem cells and brain cells, most parts of the body are constantly subjected to damage and repair. The mechanisms that contribute to this process of aging include wear and tear, the effects of free radicals, and the decline of the immune system.
Wear and Tear
The organic process of life is a delicate balance between forces that wear down structures—forces that lead to cell death, for instance—and those that repair damage at the molecular and cellular levels. The structure and metabolism of each living thing maintain this balance over time. But over time, the balance begins to shift: Damage occurs faster than it can be repaired. Moreover, repair capacity is not unlimited; mechanisms for maintenance and repair can be maintained only at a certain cost. In other words, there are trade-offs involved in longevity. As a result, damage tends to accumulate with age, and the body gradually loses its capacity to repair that damage.
Like other components of the body, DNA in the nucleus of cells is always being damaged and repaired, although not always perfectly. Among mammals, the longer-lived species are the ones that have greater capacity to repair damaged DNA. But as DNA replicates over and over, those small errors, or mutations, progressively alter the organism’s genetic code.
Can we conclude that we could possibly control aging by reprogramming our genes? Perhaps, but manipulating genes to slow down aging might not increase the human lifespan. Imagine that an older person starts to exhibit signs of arteriosclerosis, and so we “fix” the individual’s DNA. We might prolong one person’s life, but we haven’t really done anything to prolong the lives of that person’s children or successive generations; they will also need DNA fixes when they become older. The problem is that a harmful mutation expressed at an advanced age, only after reproduction, will not be removed from the gene pool. In fact, we may want to leave a mutation that contributes to aging in place for the next generation because the mutated gene could have positive effects at an earlier age. In other words, the same biological processes promoting health and vigor among young organisms can have a negative impact in later life.
Free Radicals
Like the effects of wear and tear, the action of free radicals contributes to physical aging (Halliwell & Gutteridge, 2015). As they engage in metabolism, all cells produce waste products. Among those waste products are free radicals, or molecules of ionized oxygen, which have an extra electron. Those ionized oxygen molecules cause damage because they more readily bond with proteins and other physiological structures. Sometimes the proteins become inactive and unable to carry out their functions. Even oxygen, the essential element required for energy transformation in living organisms, can become a destructive force.
Certain physiological processes can fight the effects of free radicals, but over time the reduction of functional capacity damages the organism. Free radicals have been implicated in many processes of physical aging (Armstrong et al., 1984). A similar mechanism of physical aging is glycosylation. Among the most universal of all chemical changes in living things are those involving sugar (glucose). Along with oxygen, glucose is the basis for metabolism in all organisms. When foods such as meat and bread are heated, the proteins combine with sugar and turn brown, in a process known as caramelization. In our bodies, the sticky by-products of this chemical reaction can literally gum up our cells. Glycosylation is behind much of the damage created in adult-onset diabetes as well as stiffened joints and blocked arteries.
Is it possible to reverse the signs of aging caused by free radicals or glycosylation? Perhaps so, but that intervention is not likely to be simple—at least not as simple, for instance, as taking an “antiaging pill.”
The Immune System
The decline of the immune system is another important mechanism of biophysical aging (Muller & Pawelec, 2015). It has even received a name: immunosenescence, which notes that age brings increasing susceptibility to diseases as well as weaker response to treatments. The immune system’s job is to defend the body from invaders like viruses, bacteria, and parasites. To perform this job, it sends a variety of cells, which are categorized as T cells, B cells, and accessory cells, coursing through the body. These cells interact in complex ways to destroy or neutralize antigens, the foreign organisms that trigger an immune response. The cells of the immune system also remove damaged and mutant cells produced within the body, which may become cancers.
With normal aging, the immune system’s ability to fight off invaders and mutants gradually declines; it may even begin mistakenly attacking healthy cells. The process begins at puberty, when components of the immune system, particularly the T cells, gradually lose their efficiency.
The aging immune system leaves the body increasingly vulnerable.
