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Aging is a progressive, predictable process that involves the evolution and maturation of living organisms. Aging is inevitable, but the rate of aging varies greatly among individuals. This chapter will address the aging process itself. We will explore current aging theories and review exactly what changes we can expect to take place in our bodies.
The maximum life span is the theoretical, species-specific, longest duration of life, excluding premature "unnatural" death. Life expectancy is defined as the average number of additional years of life that is expected for a member of a population. It can be a useful predictor of actual longevity for a given individual. Like most species, humans almost always die of disease or accident before they reach their biologic limit.
The percentage of a population that is alive at any one time is illustrated by the survival curves shown in Figure 1. Curve A, which might be representative of the human population 50,000 years ago in Africa, shows a population in which deaths occur randomly and for whom the probability of dying does not change with age. Curve B, which shows survival that is based on environmental hazards, is the survival curve for animals that live in the wild and perhaps for prehistoric man. As environmental hazards are avoided, curves C and D result, representing the more dominant role that aging plays in mortality. The survival curve that has begun to be characteristic of the population in the United States in the past 50 years is represented by the rectangular shape of curve D.
While life expectancy at birth has increased significantly, life span, which is estimated at 85 to 100 years, has remained about the same. Eliminating the top ten causes of death would increase the life expectancy of people over the age of 65 by about 20 years, but the overall life span would not be affected.
The genetic basis of aging is clear. Even in the best of environmental conditions, various species of animals and plants mature, grow old, and die at widely differing rates. Identical twins, for instance, show much more closely correlated longevity than fraternal twins.
The strong genetic basis for aging is demonstrated by comparing normal aging to the premature aging process caused by the very rare disease of progeria. In this disease, the genetic mechanisms seem to involve just a single gene (or at most, a few genes). Further evidence for genetic influences on aging is provided by the selective breeding in animals for shorter or longer life spans and for various age-related traits. In almost all species, including the human species, females outlive males. This seems to be due to genetic factors, although the mechanism is not known.
Genetic influences seem to be more powerful than environmental factors in determining the enormous differences among species in aging and longevity. However, within a species a wide range of environmental conditions help shape the aging experience. Two groups of factors seem to be involved in determining longevity: those governing the rate of aging and those governing the agedependent vulnerability to disease and death. The latter is much more susceptible to environmental factors.
Random deaths have greatly decreased as a result of improvements in nutrition and sanitation and the decrease of such infectious diseases as tuberculosis, gastroenteritis, typhoid fever, and cholera. Preventive medicine has reduced the disability and mortality in infancy, childhood, and childbirth, and over the past 40 years the availability of antibiotics and other drugs has greatly reduced the death rate. These successes have added years to the lives of millions of people.
In addition to these environmental conditions, a person's lifestyle is an important factor in how we age. Health behaviors such as not smoking, moderation in alcohol use, adequate exercise and rest, a diet high in fiber content, effectively handling stress, and a positive outlook have all been suggested as a means to better health and longevity. Since our bodies are made up of cells, it is useful to explore how these cells age.
The aging of cells can be classified in three ways: cells that are continuously dividing, cells that are resting but can be stimulated to divide, and cells that are past the replicating phase altogether. Examples of continuously dividing cells include cells in the bone marrow that produce red and white blood cells and the cells that line the gastrointestinal tract. Cells in the liver, parts of the kidney, and the cells lining blood vessels are examples of the second type of cells, also called quiet cells, whose function is to respond to tissue injury.
Of the cells that do not reproduce, some have short life spans and others have long life spans. Those with short life spans (weeks to months) such as red blood cells and white cells, require continual replacement. Those with long life spans (years to decades) include nerves, muscles, heart cells, and reproductive cells.
The survival times of red blood cells are correlated with a species' life span. In humans, the survival of a red blood cell averages about four months. Changes in the membrane of these cells help identify the older cells and trigger a mechanism for their removal from the blood. This suggests that there may be a general mechanism for identifying and eliminating older body cells.
Little is known about aging and cell death in long-lived cells. Nerves, which have been extensively studied in humans, are lost at different rates in different parts of the brain. It is difficult to determine what changes are due to age and what changes are due to disease or environmental influences.
Although the cell's ability to reproduce typically declines with normal cellular aging, it is interesting to note that many age-associated processes seem, paradoxically, to involve increases in proliferation. For example, the prostate gland tends to increase its cells with age. One hypothesis is that aging may cause inappropriate cellular responses to signals to proliferate and to signals that tell cells to stop proliferating.
Cells are only one area that researchers examine in their search for how we age; they also focus on molecular, organic, and individual stages of organization. No single theory has accounted for how we age, but each seems to hold some interesting clues. According to the two main lines of thought, the aging process either results from genetically programmed changes or it occurs because of an accumulation of genetic errors due to environmental damage. Since programmed cell death appears to be a regular feature of human growth and development, it seems reasonable to use this as a model for the aging process. For example, we have to lose our baby teeth to make room for our permanent teeth. But aging could also be viewed as a phase in which the person, having passed his or her reproductive stage, no longer has a genetic program to follow and becomes increasingly vulnerable to random hazards. This process may be analogous to riding a ski life. Genetics (the life) gets you up the mountain, but the ride down is under your control, becoming more hazardous with steeper and longer runs.
One set of theories regarding programmed changes involved in aging suggests that the immune system is the regulator of aging decline and the thymus gland is akin to a biologic clock. The thymus gland is the site where special lymphocytes called T cells mature, and its hormones are important in the development of white blood cells. The thymus gland (located behind the breast bone) is large at birth and continues to grow until adolescence. It begins a rapid withering after adolescence, so that by the time a person is 45 years old, the gland has only 10 to 20 percent of its former cell mass. After people reach the age of 30, the level of thymic hormones goes down; by the time people are 60, thymic hormones can no longer be detected in the blood.
There are a number of theories that attribute aging to the accumulation of various errors in cell functioning and environmental exposures. According to this group of theories, aging results from changes in the information that is provided by the cell nucleus during normal cell function. Aging could result from changes in DNA (deoxyribonucleic acid--the molecule that carries the genetic code of a cell), errors in the synthesis of other nuclear proteins, or alterations in the structures that modify gene expression.
As part of normal metabolism, humans produce chemically reactive substances called free radicals. Free radicals are highly toxic and can damage delicate cellular elements, particularly membrane fats and genetic materials. These chemical-free radicals have been implicated in a number of age-related phenomena, including cancer and arthritis. However, the damage produced by free radicals is so general that the current assumption is that there are some yet undefined intermediates that may cause specific damage to genes and to DNA.
Although compelling evidence suggests that aging is genetically determined, the number of theories tells us that no one knows for sure how this happens. However, a number of environmental factors seem to influence the rate of aging with harsh exposures tending to accelerate the process. Many of these environmental factors have been controlled to such an extent that for the first time in human history people in nations like ours can expect to live into their seventies, eighties, or even older. Old age, once the privilege of the very few, has now become the shared destiny of humankind.
Normal aging in the absence of disease is a remarkably benign process. In terms of body systems, aging involves the steady decline of organ functioning and of the regulation of body systems. We may not even notice these changes except during periods of maximum exertion or stress. We may experience slower reactions to stimuli, wider variations in functioning, and slower returns to resting states. Some biological changes are predictable though. Following are some of the most common changes in our body systems.
Aging is not the accumulation of disease, although aging and disease are related in subtle and complex ways. Several conditions once thought to be part of normal human aging have been shown to be due to disease. For example, heart and blood vessel diseases are less common in populations that eat no meat and little fat, and cataract formation in the eye is largely dependent on the degree of exposure to ultraviolet radiation in sunlight.
The range of individual response to aging deserves emphasis. Biologic and chronologic age are not the same, and body systems do not age at the same rate within any individual. You might have marked arthritis or severe loss of vision while enjoying excellent heart or kidney function. Even those aging changes that are considered usual or normal do not necessarily represent the optimum outcome for an aging individual or society.
The regulation of body systems changes as you age. Progressive changes in the heart and blood vessels impair your body's ability to control blood pressure. Because increases in blood pressure may also impair blood pressure control mechanisms, you have the greatest risk for sudden drops in your blood pressure if you have high blood pressure. Changes in the brain and kidney with aging can amplify these effects.
Your body cannot regulate its temperature as it could when you were younger. This can result in hypothermia if the ambient temperature is low or hyperthermia (heat stroke) if the temperature is high. There may also be aging-related changes in your body's ability to mount a fever in response to an infection. The regulation of the amount and composition of body fluids is diminished in healthy elderly people. Resting levels of the hormones that control fluid volume are unchanged, but abnormalities of fluid regulation frequently occur during illness or physiologic stress. Water regulation involves mechanisms in the central nervous system and the kidneys. The thirst response that follows water deprivation is decreased in elderly people.
What are the relevant implications of these age-related changes in our body systems? First, advancing age results in increasing differentiation and biologic diversity; we become less like each other, and health care must be individualized. Various strategies of diagnostic investigation and the allocation of resources are likely to be far less than optimal if they are based only on chronologic age criteria.
We also need to consider how our biologic systems that are minimally affected by age are often profoundly influenced by lifestyle circumstances such as cigarette smoking, physical activity, nutritional intake, or economic advantage. Although the precise mechanisms by which these environmental and lifestyle factors induce changes in body systems are unknown, some exposures seem to accelerate the aging process. The potential interactions of environmental and physiologic conditions are shown in Figure 2. The upper line represents the maximum potential performance for a given organ system such as the musculoskeletal or cardiovascular system. Ideally, this line is almost horizontal with minimal decrements in maximum function occurring over time. The position and slope of this line may be affected by various environmental factors. For example, cigarette smoking in youth may reduce optimal respiratory potential in later years. The lower line represents the rate of atrophy when the system is put at complete rest (never stressed); the system always functions at some point between these lines.
The third consequence of aging physiology is the prospect of living with diminishing resources with which to meet increasingly complicated environmental demands. The decline of functional capacity is often compounded by losses of social status, income, family support (for example, through death), and self-esteem. Diseases may reduce physical and mental capabilities, which are magnified by rapidly changing social expectations, especially for people who have accepted a self-reliant lifestyle.
However, the capacity to learn and adjust continues throughout life, strongly influenced by interests, activity, motivation, health, and income. With years of rich experience and reflection, some of us can transcend our own circumstances. We call this wisdom. Old age, despite the physical limitations, can be a time of variety, creativity, and fulfillment.
This section will review various age-related changes that influence our bodies' ability to resist and control infections.
The skin and mucous membranes that line body cavities are primary barriers to infection. Some of the barrier and antimicrobial properties of the skin may be impaired with age. In addition, certain skin conditions that predispose one to infection--pressure ulcers and trauma (wounds, lesions, bruises, etc.), for example--become common.
The lining surfaces of body tissues, the mucosal surfaces, help prevent infection by trapping organisms in secreted mucus and removing them by a process called ciliary transport. This transport system works like a tiny escalator conveying the trapped material toward a body opening such as the mouth. Aging may compromise this barrier function, which commonly occurs in the mouth, urethra, and vagina.
Disturbance in swallowing, a common and age-related change, predisposes individuals to aspiration (drawing substances into the lungs instead of swallowing them through the esophagus), which is a common cause of pneumonia in older people. (Aspiration and pneumonia are each addressed in Chapter 21.) Our cough mechanism decreases as we age, further reducing our ability to eliminate organisms. Changes in the lung, especially the collapse of small airways and the overall loss of lung elasticity, also increase the risks of infection.
In the gastrointestinal system, the stomach secretes reduced amounts of acid, the bowel's contractions can change, and out-pouchings called diverticula often form in the bowel lining. (See Chapter 22 for a discussion of diverticula.) Each of these changes makes it easier for bacterial populations to increase in the stomach and intestines. Changes in the urinary tract lower resistance to infection: the chemistry of the urine; decreased prostatic fluid (with reduced ability to kill organisms); diminished flushing mechanism of the bladder; backward flow of bladder contents toward the kidney; and the potential obstruction of urine flow by prostate enlargement, bladder prolapse, narrowings in the urethra, or stones.
In general, white blood cells do not appear to change as we age. Their ability to attack organisms does not seem to be impaired, and they respond normally to signals that they are needed in order to combat infecting organisms. While you can probably develop fever with infections, reduced or absent fever responses are not rare.
Declines in immune responsiveness as we age may explain our increased likelihood of infections, cancer, and various immune diseases. Our body's production of antibodies is impaired in old age.
The changes in the thymus (see page 13) play a crucial role in impairment of the immune system. An impaired response to a stimulus, a fundamental defect in immunity, appears to be due to reduced numbers and diminished responsiveness of certain lymphocytes and other cell lines. Older people show less vigorous skin test reactions, suggesting that the response to antigens is impaired.
Decreases in physical activity and accompanying changes in body composition may cause some of the declines in body metabolism and cardiovascular function that occur with advancing age. In addition, aging produces several changes in the ability of our body to acquire and deliver oxygen to the tissues. These changes include increasing stiffness of the chest wall, impaired blood flow through the lungs, diminished strength of each contraction of the heart, and decreased muscle mass. It is not surprising that because of these changes the physical work capacity of the average 70-year-old person is about half that of a 20-year-old. Although the decrease over this 50-year age span is progressive, the rate of loss accelerates after our mid-fifties.
Total body metabolism declines slightly but steadily. The maximum oxygen consumption with exercise, a measurement of fitness, declines more rapidly because of the decrease in lean muscle mass and a fall in maximum heart rate. While there is considerable variability among older individuals, the maximum oxygen consumption tends to be higher in physically active people than in sedentary individuals. It may be higher still in older athletes who are in training. Even after correction for height, weight, and other differences, maximal oxygen consumption is higher in men than in women.
Regular physical exercise is the best antidote to many of the effects of aging. The major benefits from regular exercise include favorable effects on fats in the blood, better handling of blood sugar, increased maximal oxygen capacity, greater strength, denser bones, an improved sense of well-being, and better sleep. It has not yet been proven, however, that an exercise regimen reduces the chance of eventual disability or prolongs life expectancy. Nonetheless, these benefits are likely to be demonstrated in the next several years as a result of current studies.
We have just reviewed how aging affects our bodies' control systems and defense systems, and that regular physical exercise may well forestall some of these changes. Let us now consider some of the more visible manifestations of aging.
Difficulties in making health care decisions result when normal aging changes are not appreciated or are misinterpreted. Because of this, a knowledge of the anatomy of aging is fundamental to our care. While the cause of most of the aging changes remains unknown, many changes are not inevitable.
We all lose height as we age but with great variability both in the age of onset and the rate of loss. Generally, before the decline begins, our height increases until our late forties, then approximately two inches are lost by age 80. Changes in posture, changes in the growth of vertebrae, a forward bending of the spine, and the compression of the disks between the vertebrae cause a loss in trunk length. Increased curvature of our hips and knees, along with decreased joint space in our trunk and extremities, contribute to a loss of stature. The length of the bones in our legs shows little change. In our feet, joint changes and a flattening of the arches can also contribute to the loss of standing height.
In men, body weight increases until the mid-fifties; then it declines, with the rate of weight loss accelerating in the late sixties and seventies. In women, body weight increases until the late sixties; it declines thereafter at a rate slower than in men. People of less technologically developed societies do not show this sequence of weight change, which suggests that reduced physical activity and changes in eating patterns may be causes of the change in body weight rather than the aging process.
Total body fat as a proportion of the body's composition doubles between the ages of 25 and 75. Exercise programs may prevent or reverse much of the proportional decrease in lean muscle mass and the increase in total body fat. Because the fat just beneath the skin decreases with age, fat accumulation is presumed to occur in our muscles and body organs. These changes in body composition have important implications for nutritional planning and metabolic activity. They also strongly influence the distribution and disposition of various drugs. For example, because of this increase in our body fat, drugs that are dissolved in fatty tissues remain in our body much longer than in a younger person's body.
The loss of lean body mass is due to a decrease in arm and leg muscle mass, with some decrease in our bones and body organs. Hormone changes seem to influence these losses: In women the decrease of estrogens that occurs with menopause is proportionally much greater than the fall of total androgens in men. Other organs also show losses; our liver and kidneys, for example, lose about a third of their weight between the ages of 30 and 90. The prostate gland, however, doubles in weight between the ages of 20 and 90.
The aging changes in normal human skin are shown in Figure 3. Little change occurs with aging in the outer layer of the skin called the stratum corneum. The contact area between the dermis and the epidermis decreases, and the number of deeper cells called basal cells and pigment-producing cells, called melanocytes, is reduced. With advancing age, the number of Langerhans' cells, cells that come from the bone marrow and provide assistance to the immune system, is also modestly reduced. The reduction of these cells is striking in skin that has been exposed to sunlight; this reduction is thought to contribute to the development of sun-related skin cancers. The graying of hair reflects the loss of pigmented cell (melanocyte) function.
The dermis thins by approximately 20 percent as we age, and the number of cells decreases. The blood supply is reduced. The collagen, a basic chemical building block of skin, decreases with age, which results in less skin elasticity. The collagen fibers in younger skin exhibit an orderly arrangement similar to fibers in a rope. These fibers become coarser and more random with aging, resembling a mass of unstirred spaghetti. Alterations in elastic tissue cause a loss of resiliency and produce wrinkles.
Skin changes caused by excessive sunlight exposure compound these changes. The main features of sun-damaged skin include irregularity in the cell membranes with loss of the organization of skin cells, damage to the lower levels of skin, a loss of collagen, and a modest infiltration of inflammatory cells. Generally speaking, normally aged skin shows thinning, a loss of elasticity, and the deepening of normal expression lines whereas sun-damaged skin is characterized by wrinkled, yellowed, rough, leathery, and spotted skin.
The tissues below the skin may undergo site-specific atrophy or enlargement. A well-recognized occurrence is the relative increase of fat along the waistline in men and the thighs in women. Locations that show atrophy include our face, the back of our hands, our shins, and the soles of our feet.
Hair changes play a prominent role in the perception of age. Hair graying results from a progressive loss of pigment cells from the hair bulbs. The loss of these pigment cells is more rapid in the hair than in the skin, possibly because of the rapid proliferation of cells during hair growth. The graying of hair in the armpit is thought to be one of the most reliable signs of aging. There is a decrease in the number of hair follicles of the scalp. Changes in the growth rate of hair depend upon the site. The growth rate of scalp, public, and armpit hair declines; however, possibly because of changes in hormones, an increased growth of facial hair is sometimes seen in elderly women. An increased growth of eyebrow and nostril hair occurs in elderly men.
Aging changes in our muscles include a decrease in muscle strength, endurance, size, and weight relative to total body weight. However, the late onset of these changes and their unpredictable rate of appearance suggest that they may not be due to aging but rather due to inactivity, nutritional deficiency, disease, or other long-standing conditions.
Older muscles appear to have a reduced blood supply, although the utilization of oxygen appears to be unchanged. Curiously, both the diaphragm and the heart, two muscles that work continuously, appear to be relatively unchanged by aging.
Age-related chemical changes occur in cartilage, the substance that provides the lubricating surface of most joints. Because cartilage contains no blood vessels, it depends upon the blood supply of the synovium (the tissue that produces joint fluid) for nutrients that pass through the joint fluid. The water content of cartilage decreases, and changes in the deeper structures such as the underlying bone may influence the cartilage and may reduce its ability to adapt to repetitive stress.
Bone loss is a universal aspect of aging that occurs at highly individual rates. (The section on osteoporosis and osteomalacia in Chapter 17 provides further information on bone loss.) Aging affects and reduces the bone cells that produce bone more severely than those cells that reabsorb bone. While bone-remodeling occurs throughout life, the balance between the amount of bone reabsorbed and the amount of bone formed is impaired with aging; the growth of bone slows and the bone begins to thin and become more porous. The internal latticework of bones loses its horizontal supports, which significantly compromises its strength. These changes mean that the smallest trauma may cause the bone to collapse.
Our skull appears to thicken with age. All of our skull dimensions increase, but greater increases are noted deep in the skull and in the frontal sinuses located just over the eyes. Bone growth has also been demonstrated well into advanced age in the ribs, the fingers, and the femur (the large bone in the hip and thigh). These changes in the hip may be important, because growth in the midportion of the bone results in a wider but weaker bone.
Conditioning, nutrition, vascular and neurologic abnormalities, and hormones influence the degeneration in our muscles and bones. Conditioning is the most significant because disuse or underuse produces marked declines in bone and muscle structures. Nutrition affects bone and mineral metabolism, and blood vessel and neurologic abnormalities accelerate muscle degeneration. In addition, a variety of hormones--growth hormone, estrogens, androgens, and many others--modifies our musculoskeletal integrity.
The brain's weight declines with age, but this decline appears to be in a few specific places rather than overall. Atrophy of the outer surface of the brain, called the gray matter, is usually moderate in healthy older people, as compared with a more extensive loss of cells in older people with dementia. From ages 30 to 70, the blood flow to our brain decreases by 15 to 20 percent.
With aging there is a loss of neurons in the gray matter, the cerebellum, and the hippocampus, a structure deep in the brain resembling a seahorse (hence the name), that seems to be involved in some aspects of memory function. Less dramatic losses occur in deeper brain structures.
For some nerves, the density of their interconnections seems to be reduced with aging. However, there is slow and continued growth of the very end connections between nerves, which suggest a possible repatterning of the nervous system.
Brain proteins, including an impressive number of enzymes, generally decline, notably, those that involve glucose breakdown and a key enzyme in carbon dioxide detoxification. Not all proteins are reduced, however. Some abnormal proteins increase with age.
Aging changes in brain structure and biochemistry do not necessarily affect our thinking and behavior. (Chapter 3 has more information about thinking and behavioral changes.) Our basic language skills and sustained attention are not altered with aging, but some aspects of our cognitive ability do seem to change, the earliest being the ability to retain large amounts of information over a long period of time. Naming tasks and abstraction are altered late in life. However, none of these changes develops uniformly or inevitably, and many older people continue to perform at levels that are comparable to, or even exceed, those of much younger people.
Sight. The normal anatomy of the eye is shown in Figure 4. With age, the tissues around our eyes atrophy and fat around the eye is lost; this may result in the upper lid drooping and the lower lid turning inward or outward. The decreased production of tears combined with atrophy around the eye increases the chance of eye infection. Changes in the cornea can also occur, although they are usually related to disease and not aging. The iris, or the colored part of the eye, becomes more rigid, the pupil becomes smaller, and changes around the lens occur, predisposing us to glaucoma.
What changes in the lens? As newer lens fibers proliferate at the periphery, older fibers migrate to the center to form a denser central section. This process is like continually forming a ball of yarn. The lens progressively accumulates yellow substances, possibly from a chemical reaction involving sunlight with amino acids in the lens. These substances reduce the amount of light and color entering the eye, and this yellow filtering causes the lens to become less transparent to the blue part of the color spectrum. To older eyes, blue appears greenish blue.
The jellylike substance inside of the eye, called the vitreous body, tends to shrink, causing traction, or pulling, on the retina. It also becomes more liquid, and densities may form in it that produce visual images called floaters. Changes in the retina have not been clearly identified, although blood vessel disease involving the retina is common. Changes in the blood supply of the retina and possibly the pigmented layer of the retina can cause macular degeneration, one of the most common causes of vision loss in older people. (Macular degeneration is discussed in Chapter 18 in the section on vision problems.)
The most common change in our vision associated with aging is called presbyopia, a condition in which it becomes harder to focus on nearby objects. This is mainly due to decreased elasticity of the lens and atrophy of the muscle that controls the lens shape. It affects men and women equally and begins in our early twenties, although it is usually not noticeable until 20 or 30 years later. Eyeglasses usually correct the problem.
With age, the sharpness of our vision when looking at static objects, called static visual acuity, shows a gradual and steady decline. This decline is due to change in the diameter of the pupil, loss of the focusing power of the lens, and increased scattering of light. Much of this loss of vision is correctable by glasses. Dynamic visual acuity, or the ability to discriminate detail in a moving object, decreases more rapidly as we age than static acuity. This decline seems to be at least partially attributed to a loss of the cells along the visual pathway in the brain.
Changes in the shape of our eyes and the formation of cataracts reduce visual acuity, and both increase in likelihood as we age. Women are more likely than men to have cataracts. Unprotected exposure of the eyes to the sun is a major cause of cataracts. Chapter 18 contains additional information on cataracts.
As we age we adapt more slowly to an abrupt change from light to dark areas. So consistent is this correlation with age that a person's age may be predicted to within three years on the basis of this performance. These changes are not trivial: After two minutes of reduced illumination, young people's eyes are almost five times as sensitive as older people's eyes; after 40 minutes, there is a 240-fold difference.
The discrimination of objects in the presence of a source of glare declines so that older people require 50 to 70 percent more light than younger people to recognize an object near a source of glare. The increased effect of a glaring light is due to the scattering of peripheral light caused by the more opaque lens in the older eye. When the lens is removed because of a cataract, the amount of glare perceived is decreased.
Older people need greater contrasts between the object of focus and its background in order to identify it accurately, especially in dimmer light. Other changes in vision are discussed in Chapter 18.
Hearing. Changes in our ears also occur with aging. The ear canal atrophies, resulting in thin walls and decreased production of earwax. Our eardrum thickens, often appearing dull and white to the physician. Degenerative changes and even arthritis can develop in the small joints connecting the bones in the middle ear. Significant changes take place in the inner ear. Whether aging alone produces these changes or whether they are due to excessive noise exposure is unknown. Noise exposure apart from aging can clearly cause diminished hearing.
These changes in ear structure significantly affect hearing. Presbycusis is the name for hearing loss for pure tones, which increases with age in men and women. Higher frequencies become less audible than lower frequencies; overall the loss is slightly less severe in women than it is in men.
The decrements in our hearing occur not only in the absolute threshold of tones of varying frequency but also in the point at which a change in pitch is detectable. Between the ages of 25 and 55, our pitch discrimination decreases, but after age 55 the decline is steeper. This is especially true for very high and very low frequencies. Combined with this loss in sensitivity is a distortion of signals that makes the localizing and understanding of sounds more difficult.
Pitch discrimination plays an important role in our speech perception. As we age, speech discrimination declines, even when pure tone hearing loss is taken into account. From the ages of 6 to 59, our intelligibility declines less than 5 percent. Thereafter it deteriorates rapidly, dropping more than 25 percent from peak levels after the age of 80. When exposed to loud background noise or indistinct speech, older people hear less, but at the same time they may be very sensitive to loud sounds. Hearing impairments are discussed further in Chapter 18 on hearing disorders.
Taste. The evidence regarding taste sensitivity is inconclusive and varies both among individuals and the substance tested. The tongue atrophies with age, which may result in diminished taste sensation; however, the number of taste buds remains unchanged and the responsiveness of these taste buds appears to be unaltered.
Smell. Our sense of smell declines rapidly after the age of 50 for both men and women, and the parts of our brain that are involved in smell degenerate significantly. By age 80, the detection of smell is almost 50 percent poorer than it was at its peak. Taste and smell work together to make the discrimination and enjoyment of food possible. As we age we may have trouble recognizing a variety of blended foods by taste and smell.
Touch. In general, our response to painful stimuli is diminished with aging. Sensitivity of the cornea of the eye to light touch declines after the age of 50 (touch sensitivity to the nose declines by age 15). Pressure touch thresholds on the index finger and the big toe decline more in men than in women.
Our cardiovascular system changes in ways that affect its overall function. With aging, our hearts tend to show disease in the heart muscle, heart valves, and coronary arteries. It is unclear whether any age-related changes of the heart occur in the absence of disease. The cells responsible for producing heartbeats become infiltrated with connective tissue and fat. Similar but less dramatic changes occur in other parts of the heart's electrical system. Poor blood supply does not seem to be an underlying cause.
Age-related declines in the ability of the heart to contract include a prolonged contraction time, decreased response to various medications that ordinarily stimulate the heart, and increased resistance to electrical stimulation (normally these changes do not result in disease). The elastic properties of the heart muscle are altered.
Changes in the blood vessels also occur as we age (see Figure 5). Irregularities in size and shape develop in the cells that line blood vessels, and the layers in the blood vessel wall become thickened with connective tissue. Our large arteries increase in size and thickness.
The cardiovascular system responds less efficiently to various stresses with age. The maximum heart rate changes in a linear fashion and may be estimated by subtracting our age from 220. The resting heart rate and the amount of blood pumped by the heart over time (cardiac output) do not change. The cardiac output with work may increase, even though there is a decrease in the maximum heart rate. This increase in cardiac output occurs because the amount of blood pumped with each beat increases to compensate for the decreased heart rate with age. The extent of blood flow within various organs varies: In the kidney it may decrease by 50 percent, and in the brain by 15 to 20 percent. Following stress, it takes longer for our heart rate and our blood pressure to return to resting levels.
Whether blood pressure increases as an inevitable consequence of aging is unknown. Several studies have shown that aging is associated with an increase in the blood pressure. Stiffness within the blood vessels is thought to be the reason for these increases; however, an age-associated increase in blood pressure is not found in individuals who live in isolated, less technologically developed societies or in people who grow old in a special environment such as a mental institution.
The trachea (windpipe) and large airways increase in diameter as we age. Enlargement of the very end units of the airway results in a decreased surface area of the lung.
Decreased lung elasticity contributes to the increase in lung volumes and to the reduced amount of surface area. The decreased elasticity causes the chest to expand and the diaphragm to descend. The end of our ribs calcifies to our breastbone producing stiffening of the chest wall, which increases the workload of the respiratory muscles.
The consequences of these aging changes are an increased likelihood that we will have lung disease and progressive declines in measurements of lung function. From the ages of 20 to 80, our vital capacity declines linearly. The amount of residual air left in our lungs after each breath increases from about 20 percent of the total lung capacity when we are 20 to 35 percent at age 60.
The amount of oxygen dissolved in the blood decreases, largely as the result of impaired matching of blood flow with the parts of the lung that contain air. Aging does not cause any problems in our ability to get rid of carbon dioxide.
Well-conditioned older people may reach levels of lung function that exceed those of much younger people. Endurance training can produce a striking increase in the lung capacity of sedentary older persons. Of all the factors that influence lung function, smoking continues to produce the greatest amount of disability. Because smoking seems to accelerate aging changes, older smokers should stop smoking--now.
On the whole, the gastrointestinal tract shows less age-associated change in function than other systems. The lining of the gut maintains an extraordinary capacity for replacing itself.
Age-related dental changes do not necessarily lead to the loss of teeth. Poor dental hygiene is a more important factor than age in this dental loss. Usually the losses have been caused by cavities or periodontal (gum) disease, both of which can be prevented by good care. With age, the location of cavities changes, and an increasing amount of root cavities and cavities around existing sites of previous dental work are seen. Tooth loss leads to changes in diet and can increase the likelihood of malnutrition. False teeth reduce taste sensation and do not completely restore normal chewing ability. Alterations in swallowing are more common in older people without any teeth. As we age we do not chew as efficiently as younger people and tend to swallow larger pieces of food. Swallowing takes us 50 to 100 percent longer, probably because of subtle changes in the swallowing mechanism.
The word presbyesophagus refers to normal aging changes in the muscle contractions of the esophagus. The principal abnormality is in the size of the contraction during swallowing. All other measures of esophageal contraction do not differ as a result of age. Moreover, the decreased size of the these contractions does not appear to cause any symptoms. Because of this, disorders of the esophagus are not due to aging but rather to diabetes mellitus, central nervous disorders, malignancy, or other diseases.
Continuing down our aging gastrointestinal system, stomach contractions appear to be normal, although according to some reports, we may need more time to empty liquids from our stomach. The amount of stomach acid secreted declines, probably as a result of a loss of the cells that produce gastric acid.
The small intestine shows a modest amount of atrophy of the lining. Changes in the large intestine include atrophy of the lining, changes within the muscle layer, and blood vessel abnormalities. Approximately one in every three people who are 60 years or older has diverticula, or outpouchings, in the lining of the large intestine, the likelihood increasing with age. The condition results from increased pressure inside the intestine, which is caused by a disorder of intestinal muscle function. Weakness in the bowel wall is another contributing factor. (For more information on diverticula, see page 371.)
Direct measurements of the speed with which substances are transported through the small intestine have not shown any age-related changes when people are not eating. However, upon eating, elderly people show reduced intestinal muscle contractions. Since the food transport in the large intestine slows down, constipation is common. Subtle changes occur in the coordination of large intestinal muscle contractions. The number of certain narcotic (opiate) receptors increases as we age, and this increase may lead to significant constipation when we ingest narcotics. Our intestines' ability to absorb foods as well as drugs generally does not change significantly. Changes can occur in the metabolism and absorption of some sugars, calcium, and iron. Highly fat-soluble compounds such as vitamin A appear to be absorbed faster as we get older. The activity of some enzymes such as lactase, which helps us digest some sugars (particularly those found in dairy products), appears to decline, but the levels of other enzymes remain normal. The absorption of fat may change, but this may relate more to changes in the pancreas and the digestive enzymes it produces rather than the ability of the intestine to absorb fat.
With age, the liver decreases in size and blood flow declines. There is reduced capacity to regenerate damaged liver cells. The shape of the liver adjusts to the contours of the adjacent organs, and the common bile duct that drains into the intestine enlarges. However, the portion of the bile duct just at the opening to the intestine narrows somewhat.
The pancreas commonly drops a little in the abdomen and the pancreatic ducts gradually increase in size. Atrophy is common in the pancreas as is scar tissue and fat. The liver and pancreas maintain adequate function throughout life, and, thankfully, age-related failure in the liver or pancreas does not occur. The metabolism of specific compounds, including numerous drugs, can be significantly prolonged in elderly people. (See Chapter 9 on how our body handles drugs.)
With aging, there is a 25 to 30 percent decrease in kidney mass. There is probably a steady age-related decline in our kidney function; nevertheless, absolutely no fall in kidney function was observed in some older people who were studied for as long as 18 years; a few even showed an increase.
The reduced kidney function leads to decreased clearance of some drugs. The kidneys' hormonal response to dehydration is reduced, as is the ability to retain salt under conditions when it should be conserved. The ability of our kidneys to modify vitamin D to a more active form may also decline.
Like the cells lining our intestines, the bone marrow cells have remarkable restorative capacity. The normal values for red blood cells in terms of number, size, and hemoglobin concentration remain essentially unchanged throughout life. The average life span of red blood cells remains constant at about 120 days, although these cells may be more fragile. The blood volume is also usually well maintained throughout old age.
Despite the continuing production of bone marrow cells, the amount of active bone marrow diminishes whereas marrow fat increases. While anemia is commonly seen in older people, it is not a normal consequence of aging and is always caused by something other than age, most frequently malnutrition, blood loss, or a malignancy. In some situations, however, the cause of the anemia is never found. (See the section on anemia in Chapter 20 for more details.)
The number of white blood cells and platelets remain unchanged, and the white blood cells continue to be effective in fighting off bacteria.
While women lose the capacity to reproduce well before they reach the average life span, men maintain this ability in extreme old age. In women, the rapid decline in eggs produced by the ovary is precisely and quantitatively age related. After menopause very few, if any, eggs can be seen in the ovary, which becomes scarred and withered.
At menopause, the production of ovarian estrogen is markedly reduced. This is responsible for the "hot flashes" felt by some women and changes in the uterus and the vagina. The lining of the uterus (endometrium) thins and the connective tissue increases. This thinning of the vaginal lining and reduced secretions can cause pain with sexual intercourse and can contribute to urinary incontinence. Changes in breast tissue are attributed to hormonal changes, and cysts may appear. The stretching of ligaments and the loss of muscular tone alter the contour of the breast.
In men, the decline in reproductive ability is a gradual process since sperm cells continue to be formed. The prostate tissue is replaced by scar tissue. The gland enlarges, particularly around the urethra. Changes in the concentration of testosterone, particularly its conversion to dihydrotestosterone, appear to cause the enlargement. (For more on this, see the section on prostate disease in Chapter 25.) Changes in the penis include progressive decline in blood flow and the formation of scar tissue in the inner compartments.
The frequency of sexual activity generally declines with age, but how much this is due to aging and how much to circumstance is not known. The most important factor may be the presence of a willing and able partner. Social and cultural circumstances tend to reinforce the decline in sexual activity, especially for older women.
Biologic changes that affect reproductive function, such as reduced responsiveness to erotic stimuli, may also influence sexual activity. It is not possible to predict how menopause will influence a woman's sexuality, although vaginal lubrication diminishes. In men, the ability to develop and maintain an erection can be impaired. Older men may also notice a decreased sensitivity of the penis, thus requiring more stimulation.
To sum up, bodily changes associated with aging generally increase our vulnerability to environmental conditions, to side effects of medical treatment, and the complications of medical procedures.