Aging Theories

.. ter a certain number of divisions, the clock genes are triggered and may produce proteins responsible for cell destruction (Keeton, 1992, 50). Cellular Aging In 1961, a discovery made by Leonard Hayflick showed that normal, diploid cells from such continually [email protected] parts of the body as skin, lungs, and bone marrow, divide a limited number of times. Although the cells stop dividing at the point just before DNA synthesis, they do not die. The longer-lived the species, the more divisions the cells undergo.

As the age of an individual increases, the number of potential divisions decreases (Ricklefs and Finch, 1995, 29). This discovery was found using fibroblasts, or cells found in the connective tissues throughout the body. The cells were placed in a laboratory dish under sterile conditions and allowed to grow and divide until they filled the dish. Then some of these cells were placed in a new dish until it was filled. The number of [email protected] necessary until the cells no longer grew and filled the dish represented the number of cell divisions (Ricklefs and Finch, 1995, 29).

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It is not known why the cells stop dividing, but these AHayflick [email protected] may be caused by some genes responsible for halting the division of neurons during developmental stages (Ricklefs and Finch, 1995, 30). This limited number of cell divisions is often thought of as cellular aging (Lafferty et al., 1996, 55), a microcosm of the process of gradual, yet, actual deceleration and deterioration of the body. Though remarkable discoveries support the fact that cells stop dividing, this theory does not seem to recognize why cells stop dividing. Shortened Telomeres The theory that shortened telomeres are involved in aging is an extension of the cellular aging theory. Telomeres are highly repetitive sequences of nucleic bases found at the tips of chromosomes. They contain only a few genes.

Their function is to protect chromosomes in a manner similar to Athe way a plastic cuff protects a [email protected] (Lafferty et al., 1996, 57). After each DNA replication, telomeres on the daughter chromosomes become shorter than those on the parent strand. So after enough replications, which happens to be the Hayflick limit, the telomeres have become strikingly diminished and cell reproduction ceases. It has been theorized that at this point, genes previously protected by telomeres become revealed and produce proteins that aid in the deterioration of tissue, characteristic of the aging process (Lafferty et al., 1996, 57). To back up this theory, researchers have found that cells that do not stop dividing, such as sperm cells and many cancer cells, do not lose telomere DNA.

These cells possess an enzyme called telomerase, which maintain telomeres (Lafferty et al., 1996, 57). If this is true, then with an extra boost of telomerase, DNA may replicate many more times and in turn, we may be able to live longer. Yet instead of slowing or stopping the process of aging, this possibility may only prolong it, since it has already been accepted that damaged, not a shortage of, DNA plays a large role in aging. The Bodys Weakened Immune System During aging, the efficiency of the immune system declines. Normally, novel antigens, foreign molecules found on the surface of viruses and bacteria, activate the production of antibodies secreted by white blood cells, or lymphocytes, called B-cells. The antigens act to neutralize the virus or bacteria, rendering it harmless.

If the novel antigens are missed by the antibodies, a [email protected] process comes into play. Macrophage cells safeguard the body and envelope foreign antigens that they later expose to T-cells for destruction. The pieces of virus that the macrophages pick up trigger the appropriate T-cell, which in turn replicates, producing more copies of itself. These T-cells, called memory T-cells, can recognize and destroy cells infected with the virus (Ricklefs and Finch, 1995, 35). These two methods of protecting the body from invasion make up the primary immune response, and this is the component of the immune system that decreases in efficiency as we age.

The secondary response is the body=s resistance against pathogens it has already met. The reason for the decline in the immune system=s efficiency is that over time, we come in contact with more viral and bacterial infections so that more of our T-cells have been stimulated, converted to memory T-cells, and therefore, used. That is, they cannot be used to fight off any new viruses or bacteria that invade the body. It is possible that the total number of T-cells is set early in life. If this is so, then as we grow older, having already fought off a number of infections, we have a smaller amount of [email protected] T-cells available to fight of infections that come our way (Ricklefs and Finch, 1995, 34).

In addition to the decrease in unused T-cells, antibodies used against the body=s own proteins are occasionally made. This faulty process is common in autoimmune diseases like multiple sclerosis (Ricklefs and Finch, 1995, 36). Whereas this theory of how we age is a very practical one, it almost assumes that older people die as a result of infections, no matter how mild, because of a weakened immune systems. This is often, not so. Wear and Tear Just as machinery and other equipment gets worn down through use, so too do our organs and cells.

It is almost inevitable that once our first cells have developed and our organs begin functioning, they also begin a very gradual deterioration through use. In fact, heavy use of our organs and bodies can accelerate this deterioration we call aging (Ricklefs and Finch, 1995, 33). In typists, for example, carpal tunnel syndrome and other degenerative problems come about faster and more commonly than in those who do not exhibit such specialized use of their fingers. On the other hand, problems can also arise from lack of use. Muscle atrophy, which is noticed in the elderly is the result of a lack of muscle use (Ricklefs and Finch, 1995, 33).

So assuming that moderate use of our bodies is healthy and will not promote any degenerative problems seems safe. Still, even regular, moderate use of one=s body, however long it can prevent certain problems, does not hold the body=s performance at the same level for very long. As aging continues, a loss of elasticity from the connective tissues in various parts of the body is experienced, and muscle performance, among other things, is reduced (Ricklefs and Finch, 1995, 33). In 1900, the life expectancy in the U.S. was 47 years. It may be thought that this was the length of time the human body could withstand *wear and tear= before it Abroke [email protected] Today, the life expectancy in the U.S.

is about 76 years because of modern technology, and many beneficial medical breakthroughs (Lafferty et al., 1996, 55). This large increase in life expectancies does not necessarily mean that human bodies can endure heavier use, or more wear and tear, but that it takes longer for our bodies to deteriorate now than it did in previous years. At the molecular level, lipofuscins, or aging pigments, appear with increasing frequency in non-dividing cells. Because they contain oxidized lipids, it has been theorized that they are products of oxidative chemical reactions such as those involving free radicals (Ricklefs and Finch, 1995, 34). Modifications in Hormonal and Neuroendocrine Systems The pituitary, ovaries, and testes are part of a system of glands that secrete hormones into the blood stream and which are controlled by the brain. This system is called the neuroendocrine system. At puberty, a signal is sent by the pituitary gland to the ovaries and testes, telling them to produce more sex hormones such as estrogens and progesterone in women and androgens in men.

In women, menopause, a stage in which the reproductive system is shut down, is reached. From this point in a woman=s life these hormones are no longer produced and many changes are experienced. Because some neurons can become [email protected] to estrogens, the absence of these hormones induces the brain to respond in different ways, such as sending a surge of blood to the skin. This is sometimes called a Ahot [email protected] (Ricklefs and Finch, 1995, 37). Unlike hot flashes, a woman may experience harmful or dangerous changes because of menopause: osteoporosis, or the loss of compact bone is accelerated because bone-mineral metabolism is dependent on estrogen.

Once this condition has reached a certain stage, it reduces the ability of bones to support body weight. It also immensely elevates the risk of bone fractures. In fact, as a woman increases in age, her risk of bone fracture due to osteoporosis increases exponentially (Ricklefs and Finch, 1995, 43). In men, the number of abnormal sperm, incidence of lower testosterone production, and incidence of impotence have been found to increase with age. Because the brain controls the pulses of testosterone, it can be said that some of these changes arise because of different signals in the brain (Ricklefs and Finch, 1995, 44).

The hormonal and neuroendocrine theory collects evidence mostly from a female way of life, yet both men and women experience the aging process and many of the same characteristics that go with it. The knowledge that the process of aging is very complex can be deduced from the simple fact that there are many entirely different, yet plausible, theories of how aging works. In fact, the possibility that several of these theories are connected, or play a combined part in aging is not far fetched. Yet because the process of aging is so multifarious, just how humans complete or even begin the transition from youth to old age remains a mystery to some extent. However, with new evidence and proof supporting some of these hypotheses, opportunities for a healthier, longer life may arise. Bibliography Allis, S.

et al., 1996. Older, Longer. Time Magazine. Fall 1996:60-64 Keeton, K. 1992. Longevity: the Science of Staying Young.

Penguin Books USA Inc., New York, NY. Kronhausen, E. et al. 1989. Formula for Life.

William Morrow and Company, Inc., New York, NY. Lafferty, E. et al., 1996. Can We Stay Young?. Time Magazine. 25/11/96:53-62 Ricklefs, R.E.

and Finch, C.E. 1995. Aging; A Natural History. W.H. Freeman and Company, New York, NY. Bibliography Aging, The Concise Encyclopedia of Science and Technology, 1978 ed.

Allis, S. et al., 1996. Older, Longer. Time Magazine. Fall 1996:60-64 Keeton, K. Longevity: the Science of Staying Young. New York, NY: Penguin Books USA Inc., 1992.

Kronhausen, E. et al., Formula for Life. New York, NY: William Morrow and Company Inc., 1989. Lafferty, E. et al., 1996. Can We Stay Young?.

Time Magazine. 25/11/96:53-62 Ricklefs, R.E. and Finch, C.E. Aging; a Natural History. New York, NY: W.H. Freeman and Company, 1995. Segall, P. and Kahn, C. Living Longer, Growing Younger.

Toronto, ON: Random House of Canada Limited, 1989. New York, NY: Random House Inc., 1989.