15

in certain species by retarding the aging of physiological pro-cesses (Masoro, 2010).

Although most experts agree that genetic endowment is a “limiting factor” on the biological and behavioral aspects of aging (Schulz & Albert, 2009, p. 97), two forms of aging— intrinsic and extrinsic—seem to interact to help us understand the mechanisms of this universal process. Intrinsic aging refers to characteristics and processes that occur universally with aging in all members of the same gender within a given spe-cies (Peterson, 1994). Understanding intrinsic aging assists in clarifying the relation between aging and disease, and in spec-ifying how biologists may better identify why and how the body becomes more vulnerable to disease and disability as we age (Kirkwood, 2009a). According to the literature on the biol-ogy of intrinsic aging, this process appears to be driven by a variety of random molecular events that begin early in life and tend to build up in cells and tissues. Busse (1969) used the term primary aging synonymously with intrinsic aging, which he defined as a time-related biological process not contingent on stress, trauma, or disease. In contrast, extrinsic aging refers to outside factors, such as lifestyle, caloric intake, or environ-mental factors that influence the varying degree and rate at which people age. Normal aging can be conceived of as the sum of intrinsic and extrinsic aging plus idiosyncratic or genetic variables unique to each individual (Peterson, 1994). Straus and Tinetti (2009) emphasize that cultural and societal factors influence extrinsic aging and must guide diagnostic and thera-peutic decision making.

In summary, the normal biological aging process has several features that distinguish it. First, the aging process is ubiqui-tous, universal, and developmental, occurring to some extent in everyone after maturation (Evans, 1994; Miller, 2009). It is an individualized and variable process such that organ sys-tems within individuals age at different rates, and thus as people get older the less alike they become (Kirkwood, 2009a; Lewis, 1990; Peterson, 1994; Williams, 1994). Yet aging is char-acterized by a predictable, inevitable evolution and matura-tion until death (Williams, 1994). It is progressive, so that the probability of developing age-related conditions increases with time. Further, normal biological aging processes cause irre-versible changes in cells or organs and permanently increase the probability that a given individual will suffer from harmful consequences (Peterson, 1994). Similarly, there is an increased

Chapter 2The Biology of Aging

Age is a question of mind over matter. If you don’t mind, it doesn’t matter.

—Satchel Paige

RR Learning Objectives

After reading this chapter, you should be able to

RR become familiar with the theories of aging and the distinc-tion between normal aging and disease;

RR apply your knowledge of the physical changes in the organ systems to your audiology practice; and

RR understand the implications of these changes for audiology interventions.

RR What Is Aging?

The terms aging and disease are often used interchangeably when referring to the condition of being old, yet aging is not a disease (Miller, 2009). A determinant of disease that produces many changes, aging is associated with increased risk of physi-cal and cognitive decline. For the purposes of this text, aging is a global, complex, synchronized biological process that occurs across all species at a rate that varies considerably (Galasko, 2009; Miller, 2009). Characterized by a decline in the ability to respond to stress and by an increase in homeostatic imbal-ance, which tends to affect numerous cells, tissues, organs, and systems, the term aging refers to all time-associated events that take place in the life span of an organism (Masoro, 2010; Miller, 2009). It is well established that while aging is a uni-tary, coordinated, and continuous process that takes place gradually over time, the rate at which aging progresses can be decelerated, thereby extending the life span (Kirkwood, 2009a; Miller, 2009). The rate at which and the degree to which aging impacts an individual depends on the interaction among in-trinsic living processes (nature), such as aerobic metabolism; extrinsic factors (nurture) associated with environmental ef-fects; and damage from age-associated diseases (Tremblay & Ross, 2007). Caloric restriction, which involves restricting food intake by close to half of what is typically eaten, is an example of an extrinsic environmental factor that increases longevity

16 I Aging: Normal and Abnormal Aspects

vulnerability to disease with increasing age and a reduced ability to adapt to environmental change (Cristofalo, 1990). According to Cristofalo (1990, p. 6), “aging is a process which is quite distinct from disease; the fundamental changes of aging can be thought of as providing the substratum in which the age-associated diseases can flourish.”

Pearl

Aging is a “process that turns young adults into old ones” (Miller, 2009, p. 4). Aging is not a disease. Age changes occur in all mem-bers of a species and takes place in virtually all species (Hayflick, 2000). Although the underlying mechanisms of aging follow a certain course, there is considerable variability in how aging affects individuals (Kirkwood, 2009a).

RR Theories of Aging

The scientific study of aging began about 75 years ago, and since that time multiple perspectives on the aging process have emerged. The latest theories on aging have a more inter-disciplinary focus, with emphasis placed on how and why spe-cific changes take place as part of the aging process, and why there is so much variability across individuals in how they age (Bengtson, Gans, Putney, & Silverstein, 2009). In general, the theories of aging can be classified as biological, psychological, and sociological. This chapter addresses primarily the biologi-cal and the psychological; the latter relates to changes within the brain with age. Environmental factors, evolution, techno-logical advances, and public health considerations also have an impact on the aging process and hence the theories of aging.

Biological Theories of Aging

Biological aging can very simply be defined as the gradual and progressive changes in physical function that occur in all species and that begin in adulthood and end at death (Austad, 2009). The biological mechanisms responsible for the aging process include both a stochastic process and a nonstochastic or programmed senescence process (Bengtson et al, 2009). Stochastic (chance) theories posit that aging events occur ran-domly as genetic mutations and accumulate with time, whereas the programmed senescence theories hold that aging is prede-termined and is a function of structured genetic expression.

Evolutionary senescence theory, the immunological theory, the free radical theory, and the programmed longevity theory have garnered the most research over the years and will be discussed below. Table 2.1 categorizes the various theories.

Evolutionary Senescence Theory

In his review of existing biological theories of aging, Austad (2009) concludes that the evolutionary senescence theory has considerable empirical evidence to support it. Evolutionary theorists argue that aging results from a decline in the force of natural selection, and that longevity will be selected if it is beneficial to one’s fitness to survive (Weinert & Timiras, 2003). The evolutionary senescence theory appears to explain why animals of different species age at all; it explains the differ-ent patterns in aging rate across species, and exceptions to the various patterns. The theory posits that antagonistic pleiot-ropy is the form of gene action that determines the rate at which species age (i.e., genes early in life may have good ef-fects but may have deleterious effects later in life). Further, antagonistic pleiotropy theory suggests that late-acting dele-terious genes may be favored by natural selection and be ac-tively accumulated in populations if they have any beneficial effects early in life (Gavrilov & Gavrilova, 2002). An interesting tenet of this theory is that aging evolves only in species that have an age structure (e.g., there is a distinction between re-productive and somatic cells), and in species that have evolved in low levels of environmental hazards. It is worth noting that various classes of gene action mediate the evolutionary biol-ogy theory (e.g., germ-line mutations that one is born with). Further, according to the evolutionary theory, it seems that for each species, the environment and genetics interact such that determining which genes are robust and can withstand nega-tive forces depends in part on the challenges presented by the environment (Bengtson et al, 2009). According to evolutionary biologists, favorable gene actions may take place late in life, thereby escaping the forces of natural selection that will not be passed on to future generations (Martin, 2009). Similarly, some evolutionary biologists suggest that benign mutations with which some people are born may not manifest until late in life, thereby escaping the forces of natural selection yet hav-ing a negative impact on health and, by extension, the life span (Effros, 2009). One final tenet of the evolutionary biology the-ories is that the later a mutation expresses itself, the smaller the probability that it will be removed by the forces of natural selection (Gonidakis & Longo, 2009). In summary, the evolu-

Table 2.1 Biological Theories of Aging

Theory Tenet

Immune system theory (organ system based) As individuals age, the immune system becomes less functional, thereby leading to breakdown.

Free radical theory (stochastic or cellular based) Age-related changes take place due to an accumulation of free radicals.Evolutionary senescence theory Natural selection of a gene is advantageous at one point in life but detrimental at

later points in life.Programmed longevity/aging by design theory The length of one’s life and timing of one’s death are preprogrammed and

influenced by gene switch.

Source: Modified from Pankow, L., & Solotoroff, J. (2007). Biological aspects and theories of aging. In J. Blackburn & C. Dulmus (Eds.), Handbook of gerontology: Evidence-based approaches to theory, practice, and policy. Hoboken, NJ: John Wiley.

2 The Biology of Aging 17

to work less effectively with age. In short, with age, the body becomes less able to resist the effects of the infinite number of foreign antigens invading it. Finally, the concept of antagonis-tic pleiotropy is integral to the immunological theory. In short, the human body develops many systemic responses to protect itself from foreign antigens, yet this fine-tuned system breaks down in aging, thereby interfering with the ability to resist or fight off these foreign bodies (Bengtson et al, 2009). Hence, this “dysregulated immune system” may account for the de-velopment of cardiovascular disease, Alzheimer’s disease, and other diseases that have an increased incidence with aging.

In summary, T-cell functional capacity or the ability of the immune system to produce the appropriate antibodies in ad-equate numbers declines with age, and this decline in func-tional capacity contributes to a deficiency in cell-mediated immunity as these cells are integral to the body’s ability to fight disease (Hayflick, 1994). The immune system influences critical defense reactions against foreign pathogens and is im-plicated in disease progression (e.g., age-associated loss in bone mass is due in part to immunological factors) (Adler & Nagel, 1994; Effros, 2009). Three examples of the interplay among aging, immunology, and disease are the development of Alzheimer’s disease, diabetes, and cardiovascular disease. It is of interest that changes in T-cell telomere length correlates with the severity of Alzheimer’s disease as determined by scores on the Mini-Mental Status Exam (Effros, 2009). Further, people with shorter telomeres in their blood cells have an increased rate of diabetes, cardiovascular disease, and Alz-heimer’s disease, and individuals with longer telomeres have an increased life expectancy beyond 60 years of age (DePinho, 2010).

Pearl

It has been speculated, and shown in mice that reactivating telom-erase can halt or reverse the shortening of telomeres, thereby es-sentially turning back the clock on aging (DePinho, 2010). This is referred to as the telomere rejuvenation strategy. There is a positive correlation between telomere length and healthy aging (Warner, Sierra, & Thompson, 2010).

The Free Radical Theory

First proposed in 1957, the free radical theory of aging re-mains one of the oldest and most popular mechanistic theo-ries of aging, which posits that wear and tear are the root causes of aging (Bengtson et al, 2009; Warner et al, 2010). A free radical is any molecule with an unpaired electron in its outer ring, and it seems that oxygen-based molecules are predominant in the free radical species (Mattson, 2009). Free radicals are produced during aerobic respiration. Harman (2006) suggests that certain types of mitochondria that gener-ate a disproportionately large amount of reactive oxygen spe-cies (ROS) in cells and are induced by oxidative stress play an important role in aging as well. There is evidence to suggest that aging is associated with an increase in the production and accumulation of oxyradicals in all bodily tissues (Mattson, 2009). The free radical theory of aging posits that aging is due to the deleterious effects of oxidative damage, and that free

tionary theory of aging posits that aging is a balance between wear and tear and prevention and repair, which is genetically controlled (Shringarpure & Davies, 2009).

The Immunological Theory

The immunological theory of aging posits that the adaptive immune system plays an important role in aging. To under-stand this theory, the reader must accept that the role of the immune system is to combat harmful agents that arise early in life and that the success of this process early on will influence one’s life span (Effros, 2009). However, as will become clear from the examination of the many aging theories, what is ben-eficial at an early stage in life may prove to be detrimental or less beneficial as one ages. The immune system theory of ag-ing first proposed by Walford (1969) holds that aging is due in large part to faulty immunological processes (Effros, 2009). It has its basis in biologists’ understanding of the characteristics of the normal immune system. The immune system provides a crucial mechanism for the individual’s interaction with the environment. Considered to have an innate component and an adaptive component, the immune system is the body’s line of defense against parasites, viruses, and bacteria that may enter the body; it also produces antibodies to foreign proteins or chemicals introduced from outside the body (Effros, 2009; Hay-flick, 1994). The immune system comprises several cell types, which form a network of interacting elements (Abrams, Beers, & Berkow, 1995). These interacting elements work together to generate cell-mediated immunity (T lymphocytes or T cells), humoral immunity (B lymphocytes or B cells), and nonspecific immunity (monocytes and polymorphonuclear neutrophil leu-kocytes) (Abrams et al, 1995). Each T and B lymphocyte cell derives from hematopoietic stem cells that have on their sur-face a unique set of receptors that enable it to recognize a for-eign substance, referred to as an antigen (Effros, 2009). The immune system of humans has evolved to a point where it is capable of responding to an infinite variety of foreign antigens that we encounter throughout life.

The B and T cells evolved so that they perfectly complement each other in terms of their functional activities (Effros, 2009). The B cells secrete antibodies that inactivate pathogens in the bloodstream, whereas the T cells serve as effector cells, recog-nizing and responding to infected cells or pathogens in the bloodstream. In light of the small number of cells that can rec-ognize and respond to a single antigen, the cytotoxic T cells that recognize a particular virus must undergo clonal expan-sion as a way of proliferating (cell division). Hence, clonal ex-pansion is critical to T-cell responses. It is noteworthy that as people age, the level of telomerase, an enzyme that makes or synthesizes telomeres (e.g., small units of DNA that seal the tips of chromosomes, the structures at the end of chromo-somes) decreases, and in turn this is associated with the short-ening of the telomeres (ends of the chromosomes). Interest-ingly, telomeres can be considered a kind of a clock that keeps track of the number of divisions a cell has undergone such that when a critical length is reached, the cell enters a stage of “irreversible growth arrest” (Effros, 2009, p. 166). It seems that T cells undergo dramatic changes with age (e.g., shortened telomere length), often referred to as replicative senescence of T cells, which explains in part why the immune system tends

18 I Aging: Normal and Abnormal Aspects

are equipped with lines of defense against oxidative stress, thereby minimizing the release or formation of free radicals. Several small molecules produced by the human body acts as antioxidants or “scavengers of free radicals,” including vita-min E, ascorbic acid (i.e., vitamin C), and glutathione (GSH) (Shringarpure & Davies, 2009); the latter can also be raised by taking vitamins orally. It is important to note that while most organisms are equipped with antioxidant defenses, dam-age to cellular macromolecules cannot be avoided, increasing with age.

Although the free radical theory enjoys considerable pop-ularity as a theory of cellular aging, a causal relationship between oxidative stress and aging has not been proven cate-gorically as a major theory of human aging and longevity (Bengtson et al, 2009; Hayflick, 1994). It is safe to say, how-ever, that oxidative damage is related to aging and age-related disease.

Pearl

The aging process is associated with a gradual accumulation of damage to cells and tissues that begins early and is due to multiple processes, including genetic and nongenetic factors (Kirkwood, 2009a).

Programmed Longevity

Programmed longevity is considered by some authorities to be an evolutionary theory. I consider it to be a hybrid theory providing a link between the evolutionary and mechanistic theories of aging. It holds that the healthy portion of an indi-vidual’s life is programmed to optimize fitness (Gonidakis & Longo, 2009). Further, proponents agree that aging produces tangible effects on an individual or members of a given species without producing an ailment per se. Stated differently, as organisms age, systems break down; there are age-associated markers for cell damage and death, and the organisms become less likely to survive. These theorists hold that aging is intrin-sically programmed, and the genome in large part determines life expectancy (Shringarpure & Davies, 2009). For example, with time age changes take place in the DNA, and the DNA has reduced repair capabilities. Further, proponents of the concept that aging is genetically programmed suggest that the expres-sion of genes is specifically programmed to either extend life or to trigger senescence. Although it is enticing to think that DNA is encoded for a lifetime, this type of thinking conflicts with evolutionary theorists (Pankow & Solotoroff, 2007). Kirk-wood (2005) is not of the opinion that there are specific genes for aging, and he argues that this theory is flawed. He does acknowledge that underlying the aging process is a lifelong, bottom-up accumulation of molecular damage and cellular defects that are both intrinsic and occur at random, and that genetic mechanisms contribute to maintenance and repair of the organism throughout life. According to Kirkwood (2009b), support for the theory that there are genes that actively underlie aging and are specifically programmed to “end life” is weak.

radical reactivity inherent in biology results in cumulative damage and senescence (Warner et al, 2010; Weinert & Ti-miras, 2003). Regarding the term oxidative, it is important to keep in mind that the processes essential to life, including respiration and metabolism, are oxidative, so it is noteworthy that according to this theory the accumulation of “oxidative stress leads to disease” (Bengtson et al, 2009). Having origi-nated in radiation biology, the seed for the free radical theory was first planted by Gerschman, Gilbert, Nye, Dwyer, and Fenn (1954); Denham Harman is a chief proponent of this theory of aging (Hayflick, 1994). Harman (2006) speculates that one’s life span is determined, in large part, by the rate of oxidative damage to mitochondrial DNA.

There has been a flurry of research over the past two de-cades documenting the impact of oxidants on reactive oxygen species in aging (Beckman & Ames, 1998). Free radicals, which are unstable molecular fragments formed by complex chem-ical reactions, are produced during aerobic respiration and other physiological processes including mitochondrial electron transport (Cristofalo, 1990; Hayflick, 1994; Martin, 1992). Free radicals are highly reactive elements that lead to cumulative oxidative damage, ultimately resulting in aging and death in humans (Shringarpure & Davies, 2009). As free radicals con-tain an unpaired electron or are missing an electron from the outer shell, they are capable of and eager to react or pair with available molecules from any part of the cell, including in the DNA, protein, and lipids (Martin, 1992). Free radical damage to lipids has been noted in the aging heart, liver, and kidney. Free radicals can quickly be destroyed by protective enzyme sys-tems, yet according to the free radical theory, some escape de-struction and cause damage in important biological structures (Cristofalo, 1990). Upon uniting with neighboring molecules, free radicals can cause considerable destruction because the molecules to which they attach are prevented from perform-ing their designated function in the cell (Martin, 1992). This accumulation of damage, which ultimately interferes with function, can cause death.

Pearl

Mitochondria are the main sites for the generation of reactive oxy-gen species, and the rate of mitochondrial damage may determine one’s life span. It is widely accepted that mitochondrial DNA dam-age tends to increase with age (Shringarpure & Davies, 2009).

Examples of the damage created by free radicals include the accumulation of lipofuscin, an “age pigment” that accumulates in aging cells, such as those in the inner ear, and the formation of the neuritic plaques characteristic of dementia of the Alz-heimer’s type (Hayflick, 1994). Skeletal muscle is vulnerable to oxidative stress, and it has been hypothesized that deterio-ration of muscle function is associated with oxidative damage of muscle proteins (Warner et al, 2010). Evidence in support of the free radical theory of aging is the observation that chemi-cals, known as antioxidants, can inhibit the formation of free radicals by preventing unpaired oxygen electrons from attach-ing to susceptible molecules (Hayflick, 1994). Most organisms

2 The Biology of Aging 19

associated with the passage of time, which occurs in biological as well as nonbiological systems. (2) There is no single theory that explains why or how we age. (3) Aging is unavoidable, universal, and has many causes. (4) Aging is an extremely variable phenomenon across biological, cognitive, personality, and social characteristics. (5) There is no specific gene for ag-ing, and in fact it seems clear that multiple genes contribute to the aging phenotype. (6) Natural selection and environment play an important role in aging. (7) The aging process is pro-gressive and deleterious (Blass, Cherniack, & Weiss, 1992; Kirk-wood, 2009a).

Kirkwood (2009a,b) proposed a model for the mechanism of aging that I support. Kirkwood (2009b) suggests that aging is driven by a lifelong accumulation of random molecular dam-age that increases the number of cells that carry defects. This accumulation of cellular defects leads to age-associated frailty, disability, and disease, which can be delayed by environmen-tal factors such as good diet, exercise, and other lifestyle fac-tors, but can be accelerated by stress, poor diet, and adverse environmental conditions. It seems also from evolutionary biol-ogy that genetic factors are influenced by the mechanisms (e.g., environmental accumulation) listed in Fig. 2.1, which attempts to capture Kirkwood’s conception of the mechanisms of aging. It is important to add that chance figures into the individuality of the aging process (Kirkwood, 2009b).

Discussion of the Various Biological Theories of Aging

Biological aging, which is associated with major losses, is a progressive process, associated with gradual impairment of function and susceptibility to environmental stressors, which ultimately is associated with disease and death (Kirkwood, 2005). My review of the major biological theories of aging, in-cluding the rate of living (wear and tear), programmed aging, and evolutionary senescence, suggests that empirical evidence may not support any of the theories as acting independently to explain the phenomenon of aging, nor does it support the idea that any of the theories exist in a vacuum (Austad, 2009). The evidence is compelling that genes that have deleterious effects later in life accumulate because of evolutionary pro-cesses whereby they escaped natural selection (Austad, 2009; Bengtson et al, 2009). However, it also seems clear that aging may in fact be “a balance between wear and tear and geneti-cally controlled mechanisms of prevention and repair” (Shrin-garpure & Davies, 2009, p. 229). The sentiment of Harman (2006) that aging is the accumulation of changes that one can attribute to development, genetic defects, the environment, disease, and an inborn aging process is probably the most sound.

Based on my review of aging theories, it appears safe to con-clude the following: (1) Aging is a series of biological changes

Fig. 2.1 Mechanism of aging. [Modified from Kirkwood, T. (2009b). Genetics of age-dependent human disease. In J. Halter, J. Ouslander, M. Tinetti, S. Studenski, K. High, & S. Asthana (Eds.), Hazzard’s geriatric medicine and gerontology (6th ed.). New York: McGraw-Hill.]

20 I Aging: Normal and Abnormal Aspects

standing could be stressors that interfere with interpersonal relations, resulting in negative outcomes for the individual. Interestingly, as shown in Fig. 2.2, self-efficacy, or the belief that one can master a situation, appears to mediate the sup-port–health relationship (Antonucci et al, 2009). Specifically, Fig. 2.2 illustrates how personal characteristics, situational characteristics, and self-efficacy interact to impact mental and physical well-being.

RR Structural and Functional Changes Associated with Aging

Several changes in organ systems occur gradually as people age. Many of the changes can be explained on the basis of the theo-ries of aging previously discussed. Although several thousands of age changes have been identified, this discussion focuses on morphological changes in the organ systems and on those functional implications that may have a potential impact on hearing status and on the delivery of comprehensive audiology services to older adults.

Consistent with Kirkwood’s perspective on aging, the con-voy model of social relations provides a life span perspective on how personal, situational, and environmental factors may shape and impact the health and well-being of individuals (Antonucci, Birditt, & Akiyama, 2009). The word convoy refers here to the close social relationships that surround individ-uals, providing them with the base for personal development and exploration. According to this model, social networks and social relations are central to development, with the quality and quantity of social relations influenced by personal and situational variables. Interestingly, a personal assessment of one’s satisfaction or dissatisfaction with one’s social networks contributes to the understanding of how social relations im-pact psychological and physiological health and well-being. Hence, negative social interactions, which may ensue from im-paired hearing, according to the convoy model, may have neg-ative outcomes for the individual. Similarly, stress mediates the impact of personal and social factors on relationships and ultimate well-being. Hence, for example, social relations can buffer the effect of stress on well-being. In my view, untreated hearing impairment and associated deficits in speech under-

Fig. 2.2 Interplay among personal factors influencing biological aging. [Modified from Antonucci, T., Birditt, K., & Akiyama, H. (2009). In V. Bengtson, M. Silverstein, N. Putney., & D. Gans (Eds.), Handbook of theories of aging (2nd ed.). New York: Springer.]

2 The Biology of Aging 21

and a decrease after 70 years of age. Significant decreases in lean body mass are also known to occur in both men and women with increasing age. Such changes to body composi-tion may occur as early as 40 years of age (Andreoli et al, 2009). Weight stability is also important for maintaining health with advancing age, as weight loss or gain could be indicative of ill-ness and an increase in the inability to perform activities of daily living (ADL), and could increase mortality (Newman et al, 2001). Elderly individuals with stable weight tend to maintain an optimal health status and lower disability status as com-pared with those who are prone to lose or gain weight. Aging is also associated with a progressive decline in the ability to sense absolute temperature (e.g., hot and cold), and in the abil-ity of the body to generate heat and to dissipate heat (Masoro, 2010). The deficits in regulation of body temperature render older adults very vulnerable to the effects of high and low temperatures.

Pearl

An audiologist’s index of suspicion should be aroused when a hearing-impaired client suffers from a dramatic weight loss, and the appropriate referral should be made.

The Skin

Human skin has several major roles. It serves as a protective barrier against homeostatic regulation and against mechani-cal, thermal, or chemical injuries and from loss of fluid; as an interface with the external environment; as a thermoregulator; and as a window through which the body reveals its internal pathology (Kaminer & Gilchrest, 1994; Veysey & Finlay, 2010). Specialized mechanoreceptors in the skin register pressure, touch, and vibration; hence, it is critical for sensory perception (Frick, Leonhardt, & Starck, 1991; Veysey & Finlay, 2010). The skin also participates in immunobiological defense reactions. In general, the skin shows dramatic changes with age. In fact, some of the changes in the skin lining the external ear canal are of particular relevance to audiologists during selected pro-cedures (e.g., cerumen management, earmold/hearing-aid impressions, and diagnostic tests including immittance testing and otoacoustic emissions). A brief overview of skin anatomy will facilitate the discussion.

The skin is composed of several interrelated functional lay-ers that tend to undergo changes with age. The layers include the epidermis, the dermis, the subcutaneous fat, and the cuta-neous appendages (Balin, 1990). The layers are shown in Fig. 2.3. The epidermis is the outer or most superficial layer of the skin. The epidermis serves as the cutaneous surface of the skin. It comprises several layers, and it functions primarily to protect the deeper tissues from drying, invasion by organisms, and trauma. The epidermis is composed primarily of keratino-cytes, with smaller populations of Langerhans’ cells and mela-nocytes (Veysey & Finlay, 2010). Keratinocytes are constantly being reproduced after being pushed to the surface, replacing other keratinocyte cells that have died and are subsequently shed (Kaminer & Gilchrest, 1994). It takes about 28 days for the turnover of keratinocyte cells to take place; however, the

Special Consideration

For the most part, aging changes are highly specific to the individ-ual and the organ system, and thus the rate of decline or failure varies dramatically across individuals (Hayflick, 1994).

Body Configuration and Composition

As humans age, there are several changes taking place that contribute to overall declines in body systems. Most notable is the loss of body water or decline in the proportion of body weight attributable to water. Water makes up two thirds of the body weight, and is found in extracellular and intracellular compartments and in the form of plasma, lymph fluid, and spinal fluid. Accordingly, changes in water metabolism con-tribute to several changes within organ systems (Morley, 1990). Further, as will become evident, aging is associated with re-ductions in lean body mass, in protein synthesis and protein degradation rates, and in the amount of potassium in the human body (Morley, 1990). On average, by age 75, the num-ber of cells in the human body may have declined by as much as 30%, exacting a toll on major systems. Bone mineral density (BMD), which accounts for close to 70% of bone strength, de-clines as we advance from middle age to old age (Masoro, 2010). These changes in body composition, structure, and function contribute to many of the changes within the human body that are described below.

Changes in Appearance and in Body Temperature

Overall, there is a gradual decrease in height in both genders as we age, along with a decrease in weight after age 55. Re-ductions in height are attributable to changes in the skeleton, including calcification of tendons and ligaments; thinning of vertebral disks associated with osteoporosis; and weakening and shrinkage of muscle groups (Tideiksaar & Silverton, 1989). Characteristically, as people age they assume a more stooped posture with the head and neck bent slightly forward and the hips and knees flexed. It is likely that normal aging changes in height contribute to instability and an increased prevalence of falls among older adults.

Declines in weight are due to a decline in lean tissue mass, a decrease in total body water, a decline in muscle mass, and bone loss (Kane, Ouslander, & Abrass, 1994). Whereas slight weight loss is common with increasing age, significant weight loss may be symptomatic of an active disease process. For ex-ample, it is well recognized that weight loss is common in individuals who are undernourished or malnourished, have Alzheimer’s disease, suffer from depression, undergo drug-nutrient interactions, or have cancer. The changes in body composition can have a significant effect on level of function.

Overall, aging is associated with a decline in bone mass, skeletal muscle mass, strength, and work capacity. Loss of skeletal muscle mass has been known to occur with advancing age in both men and women (Andreoli, Scalzo, Masala, Taran-tino, & Guglielmi, 2009). Yet studies have shown that elderly men lose more skeletal leg muscle than do women, and such skeletal mass muscle loss is often masked by weight stability due to an increase in total body fat mass through middle age

22 I Aging: Normal and Abnormal Aspects

elastin provides it with its elasticity and resilience (Veysey & Finlay, 2010). With few exceptions, throughout the body the dermis contains hair follicles and the major sensory fibers that help humans distinguish among pain, touch, heat, and cold. Sebaceous glands, such as those located in the outer third of the ear canal, have primary responsibility for protecting the skin against dryness through the production of an oily sub-stance known as sebum. In contrast, sweat glands produce perspiration, allowing for the elimination of water and elec-trolytes (Falvo, 1991). The dermis has an extensive microvas-culature network that contributes to thermoregulation and the inflammatory response of the skin (Kaminer & Gilchrest, 1994).

During aging, the epidermis becomes structurally thinner; there is a flattening of the dermo-epidermal junction, and the corneocytes adhere less to one another, causing a reduction in their water-binding capacity, which leads to skin dryness. With age there is a depletion of certain types of melanocytes; hair graying is also a consequence of aging of the epidermal layer of the skin. Similarly, decreased blood flow slows healing and provides pathogens the opportunity to enter broken skin. Overall, the skin becomes dry and itchy, and its integrity de-creases over time (Scheinfeld, 2005).

The dermis undergoes significant anatomical and physio-logical change with age as well. Many of these changes may impact considerably on audiological practice. Overall, there is an approximate 20% loss in dermal thickness with age that can account for the paper-thin appearance of the skin of some older adults (Kaminer & Gilchrest, 1994). There are changes in the collagen and elastin fibers, which degenerate, resulting in less bulk and structure to the dermis (Giangreco, Qin, Pintar, & Watt, 2008). Further, the number of mast cells, which serve a protective function, and fibroblasts, which help to heal wounds, decreases, resulting in a diminished ability for healing (Law-ton, 2007). The most pertinent anatomical and physiological changes are displayed in Table 2.2. There is a reduced vascular response of old skin to chemical irritants and microbial inva-sion. Apocrine gland activity is diminished, and the sebaceous glands in the dermis become larger, hyperplastic, and less ac-tive (Veysey & Finlay, 2010). Changes in the dermis with age account in large part for the tendency for people to be prone to wrinkle formation as they age. In sun-exposed sites there tends to be more abnormalities in the collagen and elastin fibers in the dermis. With age (>70 years), most elastin fibers in the dermis appear abnormal, and thus the skin loses the elasticity and resilience provided by these fibers (Veysey & Finlay, 2010). The latter age-related changes have implications for hearing-aid fittings and for pure-tone hearing sensitivity. With age the density of Langerhans’ cells in the skin decreases, and there is a decline in their number. In light of their role in immune function, age-related changes in the Langerhans’ cells are associated with delayed hypersensitivity reactions. Further, older adults have a diminished capacity to manifest character-istic reactions when exposed to known allergens, and they are more susceptible to skin infections. Finally, age-related changes in the skin and its vasculature contribute to a decrease in sen-sory perception and an increase in the pain threshold, which places older adults at risk for burns and infections. Further, the diminished tensile strength of the dermis, which is produced by the decrease in collagen, and the reduction in microvascu-

turnover time of these epidermal cells is reduced dramatically as people age (Kaminer & Gilchrest, 1994). As a result of the decrease in epidermal cell turnover with age, there is a de-crease in the rate at which wounds heal (Veysey & Finlay, 2010). In addition to keratinocytes, the epidermis contains melanocytes and Langerhans’ cells. The melanocytes contain melanin, which is responsible for defining skin color and serves as the body’s protection against solar radiation (Ka-miner & Gilchrest, 1994). There is a steady decrease in mela-nocytes with each decade, which occurs in both sun-protected and sun-exposed skin. The loss of melanin in the skin that occurs with age means that as people age they have less pro-tection against the negative effects of ultraviolet (UV) radia-tion. Graying of hair, for example, is a manifestation of loss of function of the melanocytes (Balin, 1990). The Langerhans’ cells, which derive from the bone marrow, are important for antigen recognition. With age, there is a dramatic decrease in the number of Langerhans’ cells. This decrease is greatest in photo-aged skin.

The dermis or inner layer of skin lies beneath the epidermis. It consists predominantly of connective tissue and contains blood vessels, lymphatics, sweat glands, and sebaceous glands. It serves to provide a tough layer that supports the epidermis and binds to the subcutaneous layer (Veysey & Finlay, 2010). The dermis also contains specialized cellular components that are produced by fibroblasts and include collagen (a protein) and elastin. Collagen gives skin its strength and support, whereas

Fig. 2.3 Functional layers of the skin: 1, epidermis; 2, dermis; 3, subcutaneous connective tissue; 4, sweat gland; 5, apocrine sweat gland; 6, hair root sheath; 7, sebaceous gland with hair root sheath. [Data from Frick, H., Leonhardt, H., & Starck, D. (1991). Human anatomy 1. General anatomy, special anatomy: limbs, trunk wall, head and neck (1st ed.). New York: Thieme Medical Publishers. Reprinted by permission.]