Sue E. Meiner, EdD, APRN, BC, GNP On completion of this chapter, the reader will be able to: 1. Define aging from a biologic, sociologic, and psychologic framework. 2. Analyze the prominent biologic, sociologic, and psychologic theories of aging. 3. Discuss the rationale for using an eclectic approach in the development of aging theories. 4. Develop nursing interventions based on the psychosocial issues and biologic changes associated with older adulthood. 5. Discuss several nursing implications for each of the major biologic, sociologic, and psychologic theories of aging. Human aging is influenced by a composite of biologic, psychologic, social, functional, and spiritual factors. Aging may be viewed as a continuum of events that occur from conception to death (Ignatavicius & Workman, 2005). Biologic, social, and psychologic theories of aging attempt to explain and explore the various dimensions of aging. This chapter explores the prominent theories of aging as a guide for developing a holistic gerontologic nursing theory for practice application. No single gerontologic nursing theory has been accepted by this specialty, which requires nurses to use an eclectic approach from other disciplines as the basis of clinical decision making (Comfort, 1970) (Box 2–1). Theories of aging attempt to explain this phenomenon of aging as it occurs over the life span, which is thought to be a maximum of approximately 120 years (Cetron & Davies, 1998). Several basic assumptions and concepts have been accepted over the years as guiding research and clinical practice related to aging. Human aging is viewed as a total process that begins at conception. Because individuals have unique genetic, social, psychologic, and economic factors intertwined in their lives, the course of aging varies from individual to individual. Senescence, defined as a change in the behavior of an organism with age, leading to a decreased power of survival and adjustment, also occurs. The recognition of the universal truths is what we attempt to discover through the theories of aging. Biologic theories are concerned with answering basic questions regarding the physiologic processes that occur in all living organisms as they chronologically age. These age-related changes occur independent of any external or pathologic influence. The primary question being addressed relates to the factors that trigger the actual aging process in organisms. These theories generally view aging as occurring from a molecular, cellular, or even a systems point of view. In addition, biologic theories are not meant to be exclusionary. Theories may be combined to explain phenomena (Hayflick, 1996; Hayflick, 2007). The foci of biologic theories include explanations of the following: (1) deleterious effects leading to decreasing function of the organism, (2) gradually occurring age-related changes that are progressive over time, and (3) intrinsic changes that can affect all members of a species because of chronologic age. The decreasing function of an organism may lead to a complete failure of either an organ or an entire system (Hayflick, 1996; Hayflick, 2004; Hayflick, 2007). In addition, according to these theories, all organs in any one organism do not age at the same rate, and any single organ does not necessarily age at the same rate in different individuals of the same species (Warner, 2004). The biologic theories can be subdivided into two main divisions: stochastic and nonstochastic. Stochastic theories explain aging as events that occur randomly and accumulate over time, whereas nonstochastic theories view aging as certain predetermined, timed phenomena (Box 2–2). As a cell ages, various changes occur naturally in its deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), the building blocks of the cell. DNA, found in the nucleus of the cell, contains the fundamental genetic code and forms the genes on all 46 human chromosomes (Black & Hawks, 2005). In 1963, Orgel proposed the Error Theory, sometimes called the Error Catastrophe Theory. This theory’s hypothesis is based on the idea that errors can occur in the transcription in any step of protein synthesis of DNA, and this eventually leads to either the aging or the actual death of a cell. The error would cause the reproduction of an enzyme or protein that was not an exact copy of the original. The next transcription would again contain an error. As the effect continued through several generations of proteins, the end-product would not even resemble the original cell and its functional ability would be diminished (Sonneborn, 1979). In recent years the theory has not been supported by research. Although changes do occur in the activity of various enzymes with aging, studies have not found that all aged cells contain altered or misspecified proteins, nor is aging automatically or necessarily accelerated if misspecified proteins or enzymes are introduced to a cell (Hayflick, 1996; Hayflick, 2004; Schneider, 1992; Weinert & Timiras, 2003). Harman (1956) was the first to suggest that the administration of chemicals terminating the propagation of free radicals would extend the life span or delay the aging process. Animal research has demonstrated that administration of antioxidants did increase the average length of life, possibly because of the delayed appearance of diseases that may have eventually killed the animals studied. It appears that administration of antioxidants postpones the appearance of diseases such as cardiovascular disease and cancer, two of the most common causes of death. Antioxidants also appear to have an effect on the decline of the immune system and on degenerative neurologic diseases, both of which affect morbidity and mortality (Hayflick, 1996; Weinert & Timiras, 2003; Yu, 1998, 1993). This primarily involves collagen, which is a relatively inert long-chain macromolecule produced by fibroblasts. As new fibers are created, they become enmeshed with old fibers and form an actual chemical cross-link. The end result of this cross-linkage process is an increase in density of the collagen molecule but a decrease in the capacity to both transport nutrients to the cells and remove waste products from the cells. Eventually, this results in a decrease in the structure’s function. An example of this would be the changes associated with aging skin. The skin of a baby is soft and pliable, whereas aging skin loses much of its suppleness and elasticity. This aging process is similar to the process of tanning leather, which purposefully creates cross-links (Bjorkstein, 1976; Hayflick, 1996; Hayflick, 2004). Cross-linkage agents have been found in unsaturated fats; in polyvalent metal ions like aluminum, zinc, and magnesium; and in association with excessive radiation exposure. Many of the medications ingested by the older population (such as antacids and coagulants) contain aluminum, as does the common cooking ingredient baking powder. Some research supports a combination of exercise and dietary restrictions in helping to inhibit the cross-linkage process, as well as the use of vitamin C prophylactically as an antioxidant agent (Bjorkstein, 1976). One researcher, Cerani, has shown that blood glucose reacts with bodily proteins to form cross-links. He has found that the crystallin of the lens of the eye, membranes of the kidney, and blood vessels are especially susceptible to cross-linking under the conditions of increased glucose. Cerani suggests increased levels of blood glucose cause increased amounts of cross-linking, which accelerate lens, kidney, and blood vessel diseases (Schneider, 1992). Cross-linkage theory proposes that as a person ages and the immune system becomes less efficient, the body’s defense mechanism cannot remove the cross-linking agent before it becomes securely established. Cross-linkage has been proposed as a primary cause of arteriosclerosis, a decrease in efficiency of the immune system with age, and the loss of elasticity often seen in older adult skin. The cross-linkage theory has emerged from deductive reasoning, and aside from the previous examples, there is little empiric evidence to support its claims (Hayflick, 1996). This theory proposed that cells wear out over time because of continued use. When this theory was first proposed in 1882 by Weisman, death was seen as a result of tissues being worn out because they could not rejuvenate themselves in an endless manner (Hayflick, 1988). Essentially, the theory reflects a belief that organs and tissues have a preprogrammed amount of available energy and wear out when the allotted energy is expended. Eventually this leads to the death of the entire organism. Under this theory, aging is viewed as almost a preprogrammed process—a process thought to be vulnerable to stress or to an accumulation of injuries or trauma, which may actually accelerate it. “Death,” said Weisman, “occurs because a worn out tissue cannot forever renew itself” (Hayflick, 1996; Weinert & Timiras, 2003; Holliday, 2004). Hayflick and Moorehead’s study showed that functional changes do occur within cells and are responsible for the aging of the cells and the organism. The study further supported the hypothesis that a cumulative effect of improper functioning of cells and eventual loss of cells in organs and tissues are therefore responsible for the aging phenomenon. This study contradicted earlier studies by Carrel and Ebeling in which chick embryo cells were kept alive indefinitely in a laboratory; the conclusion from this 1912 experiment was that cells do not wear out but continue to function normally forever. An interesting aspect of the 1961 study was that freezing was found to halt the biologic cellular clock (Hayflick & Moorehead, 1961). Based on this 1961 study, unlimited cell division was not found to occur; the immortality of individual cells was found to be more an abnormal than a normal occurrence. Therefore this study seemed to support the Hayflick Limit Theory. Life expectancy was generally seen as preprogrammed, within a species-specific range; this biologic clock for humans was estimated at 110 to 120 years (Gerhard & Cristofalo, 1992; Hayflick, 1996). Based on the conclusions of this experiment, the Hayflick Limit Theory is sometimes called the “Biologic Clock,” “Cellular Aging,” or “Genetic Theory.” Essential components of the immune system are T lymphocytes, which are responsible for cell-mediated immunity, and B lymphocytes, the antibodies responsible for humoral immunity. Both T and B lymphocytes may respond to an invasion of the organism, although one may provide more protection in certain situations. The changes that occur with aging are most apparent in the T lymphocytes, although changes also occur in the functioning capabilities of B lymphocytes. Accompanying these changes is a decrease in the body’s defense against foreign pathogens, which manifests itself as an increased incidence of infectious diseases and an increase in the production of autoantibodies, which lead to a propensity to develop autoimmune-related diseases (Hayflick, 1996; Weinert & Timiras, 2003) (Box 2–3). Immunodeficient conditions, such as the human immunodeficiency virus (HIV) and the immune suppression of organ transplant recipients, have demonstrated a relationship between immunocompetence and cancer development. HIV has been associated with several forms of cancer, such as Kaposi’s sarcoma. Recipients of organ transplants are 80 times more likely to contract cancer than the rest of the population (Black & Hawks, 2005). The neuroendocrine theory examines the interrelated role of the neurologic and endocrine systems over the life span of an individual (Box 2–4). The neuroendocrine system regulates and controls many important metabolic activities. It has been observed that there is a decline, or even a cessation, in many of the components of the neuroendocrine system over the life span. The reproductive system, and its changes over the life of an individual, provides an interesting model for the functional capability of the neuroendocrine system. Research has shown there are complex interactions between the endocrine and the nervous systems. It appears that the female reproductive system is governed not by the ovaries or the pituitary gland but by the hypothalamus. Men do not experience a reproductive event such as a menopause, although they do demonstrate a decline in fertility. The mechanisms that trigger this decline may offer a template for understanding the phenomena of aging (Hayflick, 1996; Weinert & Timiras, 2003). Another hormone that has been receiving attention is dehydroepiandrosterone (DHEA). This hormone, secreted by the adrenal glands, diminishes over the lifetime of an individual. Administration of this hormone to laboratory mice showed it increased longevity, bolstered immunity, and made the animals appear younger. These mice also ate less, so there is some question whether DHEA-fed mice exhibit the effect of calorie restriction (Cupp, 1997; Guardiola-Lemaitre, 1997; Hayflick, 1996; Hayflick, 2004). The belief that melatonin has a role in aging comes not only from its effect on the immune system and its antioxidant capability but also from studies on rodents that demonstrated an increased life span when melatonin was administered. These studies also found that rodents fed supplementary melatonin restricted their calorie intake. More research needs to be performed regarding the safety and efficacy of melatonin. However, in the United States melatonin can already be sold as a dietary supplement, so there is little financial incentive for conducting research. In Europe melatonin is considered a neurohormone, so there would be more financial gain to determining its role in the aging process. At this time, no individual should take melatonin without his or her primary health care provider’s knowledge (Guardiola-Lemaitre, 1997; Hayflick, 1996). This theory proposes that all organisms have a finite metabolic lifetime and that organisms with a higher metabolic rate have a shorter life span. Evidence for this theory comes from research showing that certain fish, when the water temperature is lowered, live longer than their warm water counterparts. Extensive experimentation on the effects of caloric restriction on rodents has demonstrated that caloric restriction increases the life span and delays the onset of age-dependent diseases (Hayflick, 1996; Schneider, 1992).
Theories of Aging
Biologic Theories of Aging
Stochastic Theories
Error Theory
Radical Theory
Cross-Linkage Theory
Wear and Tear Theory
Nonstochastic Theories
Programmed Theory or Hayflick Limit Theory
Immunity Theory
Emerging Theories
Neuroendocrine Control or Pacemaker Theory
Metabolic Theory of Aging/Caloric Restriction
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Theories of Aging
