Helping Relationships With Older Adults. Adelle M. Williams
theory helps to explain why some individuals are at a greater risk of certain diseases than others, and it attempts to explain why aging occurs. Aging occurs when cells become permanently damaged from the life-long and unrelenting attack of charged molecular fragments, known as free radicals. The cellular damage inflicted by this uncontrolled oxidative stress inexorably spreads outward to the level of tissues and organs, where it eventually manifests itself as some form of degenerative disease. Over 80 degenerative diseases are now known to be linked to free radicals. Some of these diseases include heart disease, cancer, diabetes, arthritis, senile dementia, and Alzheimer’s disease. It is now believed that when people age, their ability to make sufficient amounts of antioxidants (substances that fight free radicals) declines, and then free radicals begin to accumulate and damage the cells. This is how the aging process ensues (MacWilliam, 2002).
Cross-Linkage Theory of Aging
The cross-linkage theory of aging proposes that the physical changes seen on the body result from the accumulation of cross-linking compounds in the collagen, which gradually become more numerous. Cross-linking is side-by-side (lateral) linking in which two or more adjacent molecules of a polymer (substance made up of a large number of smaller molecules) join to form a bigger molecule. Collagen is the most abundant protein in the human body and is the substance that holds the whole body together. The piling up of harmful molecules is thought to eventually impair cell function (Moody & Sasser, 2012). The accumulation of cross-linked collagen is responsible for such changes as the loss of skin elasticity, hardening of the arteries of the circulatory system, and stiffness of joints throughout the body. This accumulation also plays a role in the formation of cataracts and is connected to the decline of kidney function (Mitteldorf, 2010).
This theory contributes to our understanding of aging, but it does not explain the totality of the process. It explains that it is the binding of glucose (simple sugars) to protein (a process that occurs under the presence of oxygen) that causes various problems. Once this binding has occurred, the protein becomes impaired, and it is unable to perform as efficiently. Living a longer life is going to lead to the increased possibility of oxygen meeting glucose and protein. Also, in persons with diabetes, 2–3 the times the numbers of cross-linked proteins when compared to their healthy counterparts has been observed (Anti-Aging Today, 2013). This theory proposes that reducing the risk of cross-linking by reducing sugar (and also simple carbohydrates) in one’s diet would be helpful in the aging process.
Genetic Control Theory of Aging
The genetic control theory of aging suggests that the genetic information in our cells provides a blueprint for the aging process and that different cells may be programmed to divide a set number of times. This theory of aging assumes that the life span of a cell or organism is genetically determined—that the genes of an animal contain a program that determines its life span, just as eye color is determined genetically (Encyclopaedia Britannica, 2015). This theory finds support in the fact that people with parents who have lived long lives are likely to live long themselves. Also, identical twins have life spans more similar in length than do nontwin siblings (Encyclopaedia Britannica, 2015). For example, the cells from an embryo will divide approximately 50 times before dying, but similar cells from an adult will divide only 20 times (Cristofalo, 1988). Genes influence life expectancy and place some people at risk for certain diseases, but despite the fact that some older persons are more susceptible to diseases than others, it is not definite that they will develop the disease.
The genetic theory of aging centers on telomeres, which are repeated segments of DNA (deoxyribonucleic acid) occurring at the ends of chromosomes. The number of repeats in a telomere determines the maximum life span of a cell, since each time a cell divides, multiple repeats are lost. Once telomeres have been reduced to a certain size, the cell reaches a crisis point and is prevented from dividing further. As a consequence, the cell dies. This may be an important mechanism of aging in tissues like bone marrow and the arterial lining where active cell division is necessary (Block, 2015). This theory contributes to our understanding of aging by attempting to explain a genetic foundation for why individuals live as long as they do. However, other factors may be operating in the aging process, so it cannot be explained purely by genetics.
Somatic Mutation Theory of Aging
The somatic mutation theory of aging proposes that harmful or deleterious mutations (genes that are incorrectly copied) will accumulate with advancing age, leading to an increase in pathological changes (disease altering) in body systems (Bengtson et al., 2005). Over a lifetime, a person’s body is exposed to many external insults from air pollution, chemicals in food and water, and radiation, which cause mutations or genetic damage to somatic (body) cells. Air pollution has been linked to respiratory illnesses (bronchitis, emphysema, asthma), chemicals in food and water have been linked to gastrointestinal disorders (stomach and liver problems), and radiation has been linked to cancer.
This theory is helpful in understanding variations between body systems in the aging process, but fails to explain basic processes of normal change. As cells grow and divide, a small proportion of them undergo mutations. This change in the genetic code is then reproduced when the cells again divide. The somatic mutation theory of aging assumes that aging is due to the gradual accumulation of mutated cells that do not perform normally. Genetic mutations occur and accumulate with increasing age, causing cells to deteriorate and malfunction (Jin, 2010). This leads to cellular dysfunction such as cancer. Different organs may develop diseases and some may be spared; however, these mutations are uncontrolled.
Wear and Tear Theory of Aging
The wear and tear theory of aging is an early theory that proposes that the body wears out (Cristofalo, 1988). This theory is difficult to test, as normal wear and tear has not been defined, and the breakdown of various body systems cannot be predicted (Hayflick, 1996). The wear and tear theory postulates that the daily grind of life, in particular abuse or overuse, literally wears the body out, leading to disease states. This theory proposes that vital parts of our cells and tissues wear out resulting in aging (Jin, 2010). Wear and tear is an accumulation of errors and damage due to natural use (MacWilliam, 2002). The degeneration of cartilage and eventual grinding of bone on bone is an example of the aging process on body joints, as wear and tear exceeds the body’s ability to repair. This theory was the first theory that attempted to explain aging as a result of damage accumulated over time and laid the foundation for other scientists to explore additional explanation as to why and how the body ages.
Table 1.1
Though none of these major biological theories encapsulate the aging process on its own, they are each an important piece of the aging puzzle. Table 1.1 provides a brief overview of the theories and what they contribute to the knowledge of aging.
The various theories identified are an attempt to explain why the body ages from the biological perspective and causes the physical changes that older persons experience.
Physical Changes That Accompany Aging
Adulthood is a time of life characterized mostly by personal growth and stability, but over the adult life span, loss and decline begins (Heckhausen, 2001). Age-related declines in physical function are observed from midlife onward, even in the absence of disease, as a result of normal age-related changes in the musculoskeletal system and other body systems (Cooper, Kuh, & Cooper, 2011). It is important to remember that no two people age at the same rate. Levels of stability or decline differ greatly in areas of physical, sensory, and cognitive functioning.
Physically, some of the most noticeable signs of aging include the loss of pigmentation leading to the graying of hair, thinning of hair caused by hair germination center destruction, rigidity of the skin’s dermal layer leading to wrinkling, and changes in the strength and tone of voice (Whitbourne, 2001). Less noticeable signs of aging, which may affect most individuals in