Theory and Conceptual Models Applied to Gerontology
Theories of aging include those used to explain physical or biological, psychosocial, and developmental changes in the later years. These many theoretical perspectives overlap and offer a framework for promoting health and providing care to older adults.
BIOLOGICAL THEORIES OF AGING
Biological aging is referred to as senescence. Cells do not die; instead they lose their ability to reproduce, a process termed replicative senescence. Three potential pathways for improving the health and well-being of older adults involve telomeres and telomerase, epigenetics, and stem cells (Table 20.1).
Table 20.1 Genetic Pathways of Aging
Telomeres and telomerase
Telomeres are repeated sequences found as “caps” at the end of each chromosome and are essential for cell repair (Figure 20.1).
As telomeres lose capacity for self-preservation, they shorten until the cell eventually dies.
The environment (stress, diet, lifestyle, physical activity, social interactions) can affect genes and turn them “on” or “off.”
The epigenome changes and reacts to signals from the environment.
Stem cells and regenerative medicine relate to the use of infinitely dividing stem cells that can become specialized (organs).
These cells are placed strategically where they can reproduce and restore body parts and functions.
Figure 20.1 Telomere located at each end of the chromosome. This image can be found in color in the app.
378Free Radical Theory
Cellular errors are the result of random damage from free radicals (molecules that contain unpaired ions and an extra electrical charge). Free radical changes mostly affect mitochondrial DNA. In youth, natural vitamins, hormones, and antioxidants neutralize free radicals. With age, production of free radicals increases and the body’s ability to remove them decreases. Adding antioxidants to the diet to counteract the negative effects of free radicals is not definitively supported by research evidence. However, this theory has received strong support, and much corroborating evidence has accumulated over the past four decades.
Aging is the result of accumulated damage from errors involving cross-linked proteins. Cross-linking of new proteins causes advanced glycation end-products, affecting collagen in the lungs, arteries, and tendons. An example is stiffened joints and dry, sagging, less elastic skin. Unsaturated fats and metal ions (e.g., aluminum, zinc, magnesium) may exacerbate cross-linking.
Cellular errors result from “wearing out” over time because of continued use. Internal and external stressors (e.g., pollutants and free radicals) aggravate cells.
Neuroendocrine Control or Pacemaker Theory
Aging is the programmed decline in functioning of nervous, endocrine, and immune systems. It is not that cells die but that they lose their ability to reproduce. Certain hormones (e.g., dehydroepiandrosterone [DHEA] and melatonin), as well as growth factors, estrogen, and testosterone, have been used in studies to prolong longevity and boost immune system response.
Negative, age-related changes in our innate and adaptive immune systems are known collectively as immunosenescence (Table 20.2). With age, there is an increase in autoimmune diseases and systemic inflammation. Inflammation is associated with heart disease, type 2 diabetes, frailty, arthritis, physical disability, and with other chronic conditions.
Table 20.2 Aging and the Immune System