Helping Relationships With Older Adults. Adelle M. Williams
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Название: Helping Relationships With Older Adults

Автор: Adelle M. Williams

Издательство: Ingram

Жанр: Социология

Серия: Counseling and Professional Identity

isbn: 9781483344577

isbn:

СКАЧАТЬ to produce necessary antibodies declines and immune systems become less effective in fighting disease (Bengtson et al., 2005). At the same time, the white blood cells active in immune response become less able to recognize foreign invaders and are more likely to mistakenly attack the body’s own proteins. For example, one hypothesis proposes that cancer rates are higher in older people because the immune system’s surveillance mechanism may not recognize and destroy precancerous cells as it does in younger individuals (Bengtson et al., 2005).

      Additionally, the aging immune system mistakenly produces antibodies against normal body proteins, leading to a loss of self-recognition. An example of this is rheumatoid arthritis, in which the immune system attacks the joints, particularly the hands, wrists, feet, ankles, and knees. While a decline in immune system functioning causes disease, there is no evidence to suggest that a less efficient immune system causes aging (Hayflick, 1996). This theory is unable to account for the mechanism of biological aging, the progressive generalized impairment of functioning that occurs as people grow older. However, the autoimmune theory is another theory that attempts to explain why diseases occur. Its basic premise is that immune reactions normally directed against disease-producing organisms as well as foreign proteins or tissue begin to attack cells of the individual’s own body.

      Free Radical Theory of Aging

      The free radical theory of aging explains the basic chemical process underlying aging. The reaction of active free radicals, normally produced in the organisms, with cellular constituents initiates the changes associated with aging (Herman, 2006). The free radical theory of aging suggests that free radicals, or unstable molecules, are produced when the body transforms food into chemical energy, creating damage that causes aging. This transformation occurs at the individual cell level. Free radicals also may be generated in the body due to cigarette smoke, drugs, and radiation (Dietrich & Horvath, 2010) and are a by-product of normal cells. Most changes associated with aging result from damage caused by free radicals (Bengtson et al., 2005). Free radicals disrupt the normal production of DNA and RNA and alter the lipids, or fats, in cell membranes. They also damage cells lining blood vessels and interfere with the production of prostaglandins, which are derived from essential fatty acids and regulate many physiological functions. Partly as a result of free radical damage, aging leads to alteration of proteins (cross-linking). The prematurely aged, wrinkled skin of smokers is caused by free radical-induced damage that smoking engenders, and cataracts have been linked to free-radical exposure (de Magalhaes, 2014). Free radicals have also been associated with dementia, cancer, and heart disease. Combating free radicals requires the consumption of antioxidants, which can be obtained through food.

      This 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 СКАЧАТЬ