THEORIES OF AGING

The lifestyle changes that occur with aging have been de­scribed in various developmental theories. Probably the most widely known is Erikson's eight stages of development. According to this theory, the first seven developmental stages span the period from childbirth through middle adulthood. The eighth stage, in older adulthood, focuses on "ego integrity versus despair." Ego integrity is the ac­ceptance of one's life in relation to humanity and one's place in history. Lack of ego integrity leads to despair, sig­nified by nonacceptance of one's lifestyle and a fear of death. Despair may be manifested as apathy, depression, or decreased life satisfaction.³,⁴

The stages of physical change that occur as part of the aging process are less well articulated. Several theories at­tempt to explain the biology of aging through a variety of scientific observations at the molecular, cellular, organ, and system levels. No one theory explains all of the aging processes, but each holds some clues. In reality, it is rea­sonable to suppose that there are multiple influences that affect the aging process. The various theories of aging can be categorized as either programmed change theories or stochastic theories. Developmental-genetic theories propose that the changes that occur with aging are genetically pro­grammed, whereas stochastic theories maintain that the changes result from an accumulation of random events or damage from environmental agents or influences.⁵ It is ac­cepted now that the process of aging and longevity is mul-tifaceted, with both genetics and environmental factors playing a role. In animal studies, genetics accounted for less that 35% of the effects of aging, whereas environmen­tal influences accounted for more than 65% of the effects.⁶

The developmental-genetic theory resides with genetic influences that determine physical condition, occurrence of disease, age of death, cause of death, and other factors contributing to longevity.⁵,⁷ At the cellular level, Hayflick and Moorhead observed more than 35 years ago that cul­tured human fibroblasts have a limited ability to replicate (approximately 50 population doublings) and then die.⁸ Before achieving this maximum, they slow their rate of di­vision and manifest identifiable and predictable morpho­logic changes characteristic of senescent cells. Another explanation of cellular aging resides with an enzyme called telomerase that is believed to govern chromosomal aging through its action on telomeres, the outermost extremities of the chromosome arms. With each cell division, a small segment of telomeric deoxyribonucleic acid (DNA) is lost, unless a cell has a constant supply of telomerase. In the ab­sence of telomerase, the telomeres shorten, resulting in

senescence-associated gene expression and inhibition of cell replication. It is thought that in certain cells, such as cancer cells, telomerase maintains telomere length, thereby enhancing cell replication. Currently, there is interest in developing telomerase therapy that could be used to initi­ate cell death in selected targets such as cancer cells and preventing cell senescence in other cell types, such as the chondrocytes in joints, the retinal epithelial cells in the eye, and the lymphocytes in the immune system.^5,9

The stochastic theories propose that aging is caused by random damage to vital cell molecules.⁵ The damage eventually accumulates to a level sufficient to result in the physiologic decline associated with aging. The most prom­inent example of the stochastic theory is the somatic mutation theory of aging, which states that the longevity and function of cells in various tissues of the body are de­termined by the double-stranded DNA molecule and its specific repair enzymes. DNA undergoes continuous change in response both to exogenous agents and intrinsic pro­cesses. It has been suggested that aging results from con­ditions that produce mutations in DNA or deficits in DNA repair mechanisms. The oxidative free radical theory is a stochastic idea in which aging is thought to result partially from oxidative metabolism and the effects of free radical damage (see Chapter 5). The major byproducts of oxida­tive metabolism include superoxides that react with DNA, ribonucleic acid, proteins, and lipids, leading to cellular damage and aging. Another damage theory, the wear and tear theory, proposes that accumulated damage to vital parts of the cell leads to aging and death. Cellular DNA is cited as an example. If repair to damaged DNA is incom­plete or defective, as is thought to occur with aging, declines in cellular function might occur.⁵,⁷

Although these theories help to explain some of the biologic phenomena of aging, many questions remain. It seems likely that the human genome project will begin to explain some of the questions regarding the genetics of aging, but many questions need to be answered regarding the effects of environmental influences on aging.

In summary, aging is a natural, lifelong process that brings with it unique biopsychosocial changes. Aging is not synony­mous with disease or ill health. The aging body can accomplish most or all of the functions of its youth, although they may take longer, require greater motivation, and be less precise.

The older adult population is typically defined in chrono­logic terms as individuals 65 years of age and older and can be further defined as young-old (65 to 74 years), middle-old (75 to 84 years), and old-old (85+ years). The number of older persons has increased and is expected to continue to grow in the future, with an anticipated 70 million Americans older than age 65 by the year 2030.

There are two main types of theories used to explain the biologic changes that occur with aging: programmed change theories, which propose that aging changes are genetically programmed, and stochastic theories, which maintain that aging changes result from an accumulation of random events or damage from environmental hazards.