· ■ BIOLOGY AND ENVIRONMENT Telomere Length: A Marker of the Impact of Life Circumstances on Biological Aging
· ■ SOCIAL ISSUES: HEALTH The Obesity Epidemic: How Americans Became the Heaviest People in the World
· ■ SOCIAL ISSUES: EDUCATION Masculinity at Work: Men Who Choose Nontraditional Careers
The back seat and trunk piled high with belongings, 23-year-old Sharese hugged her mother and brother goodbye, jumped in the car, and headed toward the interstate with a sense of newfound freedom mixed with apprehension. Three months earlier, the family had watched proudly as Sharese received her bachelor’s degree in chemistry from a small university 40 miles from her home. Her college years had been a time of gradual release from economic and psychological dependency on her family. She returned home periodically on weekends and lived there during the summer months. Her mother supplemented Sharese’s loans with a monthly allowance. But this day marked a turning point. She was moving to her own apartment in a city 800 miles away, with plans to work on a master’s degree. With a teaching assistantship and a student loan, Sharese felt more “on her own” than at any previous time in her life.
During her college years, Sharese made lifestyle changes and settled on a vocational direction. Over-weight throughout high school, she lost 20 pounds in her sophomore year, revised her diet, and began an exercise regimen by joining the university’s Ultimate Frisbee team, eventually becoming its captain. A summer spent as a counselor at a camp for chronically ill children helped convince Sharese to apply her background in science to a career in public health.
Still, two weeks before she was to leave, Sharese confided in her mother that she had doubts about her decision. “Sharese,”her mother advised, “we never know if our life choices are going to suit us just right, and most times they aren’t perfect. It’s what we make of them—how we view and mold them—that turns them into successes.”So Sharese embarked on her journey and found herself face-to-face with a multitude of exciting challenges and opportunities.
In this chapter, we take up the physical and cognitive sides of early adulthood, which extends from about age 18 to 40. As noted in Chapter 1 , the adult years are difficult to divide into discrete periods because the timing of important milestones varies greatly among individuals—much more so than in childhood and adolescence. But for most people, early adulthood involves a common set of tasks: leaving home, completing education, beginning full-time work, attaining economic independence, establishing a long-term sexually and emotionally intimate relationship, and starting a family. These are energetic decades filled with momentous decisions that, more than any other time of life, offer the potential for living to the fullest.
We have seen that throughout childhood and adolescence, the body grows larger and stronger, coordination improves, and sensory systems gather information more effectively. Once body structures reach maximum capacity and efficiency, biological aging, or senescence, begins—genetically influenced declines in the functioning of organs and systems that are universal in all members of our species. Like physical growth, however, biological aging varies widely across parts of the body, and individual differences are great—variation that the lifespan perspective helps us understand. A host of contextual factors—including each person’s genetic makeup, lifestyle, living environment, and historical period—influence biological aging, each of which can accelerate or slow age-related declines (Arking, 2006 ). As a result, the physical changes of the adult years are, indeed, multidimensional and multidirectional (see page 9 in Chapter 1 ).
In the following sections, we examine the process of biological aging. Then we turn to physical and motor changes already under way in early adulthood. As you will see, biological aging can be modified substantially through behavioral and environmental interventions. During the twentieth century, improved nutrition, medical treatment, sanitation, and safety added 25 to 30 years to average life expectancy in industrialized nations, a trend that is continuing (see Chapter 1 , page 8 ). We will take up life expectancy in greater depth in Chapter 17 .
Biological Aging Is Under Way in Early Adulthood
At an intercollegiate tournament, Sharese dashed across the playing field for hours, leaping high to catch Frisbees sailing her way. In her early twenties, she is at her peak in strength, endurance, sensory acuteness, and immune system responsiveness. Yet over the next two decades, she will age and, as she moves into middle and late adulthood, will show more noticeable declines.
Biological aging is the combined result of many causes, some operating at the level of DNA, others at the level of cells, and still others at the level of tissues, organs, and the whole organism. Hundreds of theories exist, indicating that our understanding is incomplete (Arking, 2006 ). For example, one popular idea—the “wear-and-tear”theory—is that the body wears out from use. But no relationship exists between physical activity and early death. To the contrary, regular, moderate-to-vigorous exercise predicts healthier, longer life for people differing widely in SES and ethnicity (Ruiz et al., 2011 ; Stessman et al., 2005 ). We now know that this “wear-and-tear”theory is an oversimplification.
This Whitewater kayaker, in his early twenties, is at his peak in strength, endurance, and sensory acuteness.
Aging at the Level of DNA and Body Cells
Current explanations of biological aging at the level of DNA and body cells are of two types: (1) those that emphasize the programmed effects of specific genes and (2) those that emphasize the cumulative effects of random events that damage genetic and cellular material. Support for both views exists, and a combination may eventually prove to be correct.
Genetically programmed aging receives some support from kinship studies indicating that longevity is a family trait. People whose parents had long lives tend to live longer themselves. And greater similarity exists in the lifespans of identical than fraternal twins. But the heritability of longevity is modest, ranging from .15 to .35 for age at death and from .27 to .57 for various measures of current biological age, such as strength of hand grip, respiratory capacity, blood pressure, and bone density (Cevenini et al., 2008 ; Dutta et al., 2011 ; Gögele et al., 2011 ). Rather than inheriting longevity directly, people probably inherit risk and protective factors, which influence their chances of dying earlier or later.
One “genetic programming”theory proposes the existence of “aging genes”that control certain biological changes, such as menopause, gray hair, and deterioration of body cells. The strongest evidence for this view comes from research showing that human cells allowed to divide in the laboratory have a lifespan of 50 divisions, plus or minus 10 (Hayflick, 1998 ). With each duplication, a special type of DNA called telomeres —located at the ends of chromosomes, serving as a “cap”to protect the ends from destruction—shortens. Eventually, so little remains that the cells no longer duplicate at all. Telomere shortening acts as a brake against somatic mutations (such as those involved in cancer), which become more likely as cells duplicate (Shay & Wright, 2011 ). But an increase in the number of senescent cells (ones with short telomeres) also contributes to age-related disease, loss of function, and earlier mortality (Epel et al., 2009 ; Shin et al., 2006 ). As the Biology and Environment box on the following page reveals, researchers have begun to identify health behaviors and psychological states that accelerate telomere shortening—powerful biological evidence that certain life circumstances compromise longevity.
Biology and Environment Telomere Length: A Marker of the Impact of Life Circumstances on Biological Aging
In the not-too-distant future, your annual physical exam may include an assessment of the length of your telomeres—DNA at the ends of chromosomes, which safeguard the stability of your cells. Telomeres shorten with each cell duplication; when they drop below a critical length, the cell can no longer divide and becomes senescent (see Figure 13.1 ). Although telomeres shorten with age, the rate at which they do so varies greatly. An enzyme called telomerase prevents shortening and can even reverse the trend, causing telomeres to lengthen and, thus, protecting the aging cell.
Over the past decade, research examining the influence of life circumstances on telo-mere length has exploded. A well-established finding is that chronic illnesses, such as cardiovascular disease and cancer, hasten telo-mere shortening in white blood cells, which play a vital role in the immune response (see page 437 ). Telomere shortening, in turn, predicts more rapid disease progression and earlier death (Fuster & Andres, 2006 ).
Accelerated telomere shortening has been linked to a variety of unhealthy behaviors, including cigarette smoking and the physical inactivity and overeating that lead to obesity and to insulin resistance, which often precedes type 2 diabetes (Epel et al., 2006 ; Gardner et al., 2005 ). Unfavorable health conditions may alter telomere length as early as the prenatal period, with possible long-term negative consequences for biological aging. In research on rats, poor maternal nutrition during pregnancy resulted in low birth weight and development of shorter telomeres in kidney and heart tissue (Jennings et al., 1999 ; Tarry-Adkins et al., 2008 ). In a related human investigation, preschoolers who had been low-birth-weight as infants had shorter telomeres in their white blood cells than did their normal-birth-weight agemates (Raqib et al., 2007 ).
Persistent psychological stress—in childhood, abuse or bullying; in adulthood, parenting a child with a chronic illness or caring for an elder with dementia—is linked to reduced telomerase activity and telomere shortness in white blood cells (Damjanovic et al., 2007 ; McEwen, 2007 ; Shalev, 2012 ; Simon et al., 2006 ). Can stress actually modify telomeres? In a laboratory experiment, researchers exposed human white blood cells to the stress hormone cortisol. The cells responded by decreasing production of telomerase (Choi, Fauce, & Effros, 2008 ).
Fortunately, when adults make positive lifestyle changes, telomeres seem to respond accordingly. In a study of obese women, those who responded to a lifestyle intervention with reduced psychological stress and healthier eating behaviors also displayed gains in telomerase activity (Daubenmier et al., 2012 ). In another investigation of men varying widely in age, greater maximum vital capacity of the lungs (a measure of physical fitness) was associated with reduced age-related accumulation of senescent white blood cells (Spielmann et al., 2011 ).
Currently, researchers are working on identifying sensitive periods of telomere change—times when telomeres are most susceptible to modification. Early intervention—for example, enhanced prenatal care and interventions to reduce obesity in childhood—may be particularly powerful. But telomeres are changeable well into late adulthood (Epel et al., 2009 ). As our understanding of predictors and consequences of telomere length expands, it may become an important index of health and aging throughout life.
FIGURE 13.1 Telomeres at the ends of chromosomes.
(a) Telomeres in a newly created cell. (b) With each cell duplication, telomeres shorten; when too short, they expose DNA to damage, and the cell dies.
According to an alternative, “random events”theory, DNA in body cells is gradually damaged through spontaneous or externally caused mutations. As these accumulate, cell repair and replacement become less efficient, and abnormal cancerous cells are often produced. Animal studies confirm an increase in DNA breaks and deletions and damage to other cellular material with age. Similar evidence is accruing for humans (Freitas & Magalhães, 2011 ).
One hypothesized cause of age-related DNA and cellular abnormalities is the release of free radicals —naturally occurring, highly reactive chemicals that form in the presence of oxygen.
Kinship studies indicate that longevity is a family trait. In addition to favorable heredity, these grandsons will likely benefit from the model of a fit, active grandfather who buffers stress by enjoying life.
(Radiation and certain pollutants and drugs can trigger similar effects.) When oxygen molecules break down within the cell, the reaction strips away an electron, creating a free radical. As it seeks a replacement from its surroundings, it destroys nearby cellular material, including DNA, proteins, and fats essential for cell functioning. Free radicals are thought to be involved in more than 60 disorders of aging, including cardiovascular disease, neurological disorders, cancer, cataracts, and arthritis (Cutler & Mattson, 2006 ; Stohs, 2011 ). Although our bodies produce substances that neutralize free radicals, some harm occurs, and it accumulates over time.
Some researchers believe that genes for longevity work by defending against free radicals. In support of this view, animal species with longer life expectancies tend to display slower rates of free-radical damage to DNA (Sanz, Pamplona, & Barja, 2006 ). But contrary evidence also exists. Experimental manipulation of the mouse genome, by either augmenting or deleting antioxidant genes, has no impact on longevity. And scientists have identified a cave-dwelling salamander with exceptional longevity—on average, 68 years, making it the longest-living amphibian—with no unusual genetic defenses against free-radical damage (Speakman & Selman, 2011 ).
Research suggests that foods low in saturated fat and rich in vitamins can forestall free-radical damage (Bullo, Lamuela-Raventos, & Salas-Salvado, 2011 ). Nevertheless, the role of free radicals in aging is controversial.
Aging at the Level of Tissues and Organs
What consequences might age-related DNA and cellular deterioration have for the overall structure and functioning of organs and tissues? There are many possibilities. Among those with clear support is the cross-linkage theory of aging. Over time, protein fibers that make up the body’s connective tissue form bonds, or links, with one another. When these normally separate fibers cross-link, tissue becomes less elastic, leading to many negative outcomes, including loss of flexibility in the skin and other organs, clouding of the lens of the eye, clogging of arteries, and damage to the kidneys. Like other aspects of aging, cross-linking can be reduced by external factors, including regular exercise and a healthy diet (Kragstrup, Kjaer, & Mackey, 2011 ; Wickens, 2001 ).
Gradual failure of the endocrine system, which produces and regulates hormones, is yet another route to aging. An obvious example is decreased estrogen production in women, which culminates in menopause. Because hormones affect many body functions, disruptions in the endocrine system can have widespread effects on health and survival. For example, a gradual drop in growth hormone (GH) is associated with loss of muscle and bone mass, addition of body fat, thinning of the skin, and decline in cardiovascular functioning. In adults with abnormally low levels of GH, hormone therapy can slow these symptoms, but it has serious side effects, including increased risk of fluid retention in tissues, muscle pain, and cancer (Harman & Blackman, 2004 ; Ceda et al., 2010 ). So far, diet and physical activity are safer ways to limit these aspects of biological aging.
Finally, declines in immune system functioning contribute to many conditions of aging, including increased susceptibility to infectious disease and cancer and changes in blood vessel walls associated with cardiovascular disease. Decreased vigor of the immune response seems to be genetically programmed, but other aging processes we have considered (such as weakening of the endocrine system) can intensify it (Alonso-Férnandez & De la Fuente, 2011 ; Hawkley & Cacioppo, 2004 ). Indeed, combinations of theories—the ones just reviewed as well as others—are needed to explain the complexities of biological aging. With this in mind, let’s turn to physical signs and other characteristics of aging.
During the twenties and thirties, changes in physical appearance and declines in body functioning are so gradual that most are hardly noticeable. Later, they will accelerate. The physical changes of aging are summarized in Table 13.1 . We will examine several in detail here and take up others in later chapters. Before we begin, let’s note that these trends are derived largely from cross-sectional studies. Because younger cohorts have experienced better health care and nutrition, cross-sectional evidence can exaggerate impairments associated with aging. Fortunately, longitudinal evidence is expanding, helping to correct this picture.
Cardiovascular and Respiratory Systems
During her first month in graduate school, Sharese pored over research articles on cardiovascular functioning. In her African-American extended family, her father, an uncle, and three aunts had died of heart attacks in their forties and fifties. These tragedies prompted Sharese to enter the field of public health in hopes of finding ways to relieve health problems among black Americans. Hypertension, or high blood pressure, occurs 12 percent more often in the U.S. black than in the U.S. white population; the rate of death from heart disease among African Americans is 30 percent higher (American Heart Association, 2012 ).
TABLE 13.1 Physical Changes of Aging
|ORGAN OR SYSTEM||TIMING OF CHANGE||DESCRIPTION|
|Vision||From age 30||As the lens stiffens and thickens, ability to focus on close objects declines. Yellowing of the lens, weakening of muscles controlling the pupil, and clouding of the vitreous (gelatin-like substance that fills the eye) reduce light reaching the retina, impairing color discrimination and night vision. Visual acuity, or fineness of discrimination, decreases, with a sharp drop between ages 70 and 80.|
|Hearing||From age 30||Sensitivity to sound declines, especially at high frequencies but gradually extending to all frequencies. Change is more than twice as rapid for men as for women.|
|Taste||From age 60||Sensitivity to the four basic tastes—sweet, salty, sour, and bitter—is reduced. This may be due to factors other than aging, since number and distribution of taste buds do not change.|
|Smell||From age 60||Loss of smell receptors reduces ability to detect and identify odors.|
|Touch||Gradual||Loss of touch receptors reduces sensitivity on the hands, particularly the fingertips.|
|Cardiovascular||Gradual||As the heart muscle becomes more rigid, maximum heart rate decreases, reducing the heart’s ability to meet the body’s oxygen requirements when stressed by exercise. As artery walls stiffen and accumulate plaque, blood flow to body cells is reduced.|
|Respiratory||Gradual||Under physical exertion, respiratory capacity decreases and breathing rate increases. Stiffening of connective tissue in the lungs and chest muscles makes it more difficult for the lungs to expand to full volume.|
|Immune||Gradual||Shrinking of the thymus limits maturation of T cells and disease-fighting capacity of B cells, impairing the immune response.|
|Muscular||Gradual||As nerves stimulating them die, fast-twitch muscle fibers (responsible for speed and explosive strength) decline in number and size to a greater extent than slow-twitch fibers (which support endurance). Tendons and ligaments (which transmit muscle action) stiffen, reducing speed and flexibility of movement.|
|Skeletal||Begins in the late thirties, accelerates in the fifties, slows in the seventies||Cartilage in the joints thins and cracks, leading bone ends beneath it to erode. New cells continue to be deposited on the outer layer of the bones, and mineral content of bone declines. The resulting broader but more porous bones weaken the skeleton and make it more vulnerable to fracture. Change is more rapid in women than in men.|
|Reproductive||In women, accelerates after age 35; in men, begins after age 40||Fertility problems (including difficulty conceiving and carrying a pregnancy to term) and risk of having a baby with a chromosomal disorder increase.|
|Nervous||From age 50||Brain weight declines as neurons lose water content and die, mostly in the cerebral cortex, and as ventricles (spaces) within the brain enlarge. Development of new synapses and limited generation of new neurons can, in part, compensate for these declines.|
|Skin||Gradual||Epidermis (outer layer) is held less tightly to the dermis (middle layer); fibers in the dermis and hypodermis (inner layer) thin; fat cells in the hypodermis decline. As a result, the skin becomes looser, less elastic, and wrinkled. Change is more rapid in women than in men.|
|Hair||From age 35||Grays and thins.|
|Height||From age 50||Loss of bone strength leads to collapse of disks in the spinal column, leading to a height loss of as much as 2 inches by the seventies and eighties.|
|Weight||Increases to age 50; declines from age 60||Weight change reflects a rise in fat and a decline in muscle and bone mineral. Since muscle and bone are heavier than fat, the resulting pattern is weight gain followed by loss. Body fat accumulates on the torso and decreases on the extremities.|
Sources: Arking, 2006; Lemaitre et al., 2012; Whitbourne, 1996.
Sharese was surprised to learn that fewer age-related changes occur in the heart than we might expect, given that heart disease is a leading cause of death throughout adulthood, responsible for as many as 10 percent of U.S. male and 5 percent of U.S. female deaths between ages 20 and 34—figures that more than double in the following decade and, thereafter, continue to rise steadily with age (American Heart Association, 2012 ). In healthy individuals, the heart’s ability to meet the body’s oxygen requirements under typical conditions (as measured by heart rate in relation to volume of blood pumped) does not change during adulthood. Only during stressful exercise does heart performance decline with age—a change due to a decrease in maximum heart rate and greater rigidity of the heart muscle (Arking, 2006 ). Consequently, the heart has difficulty delivering enough oxygen to the body during high activity and bouncing back from strain.
One of the most serious diseases of the cardiovascular system is atherosclerosis, in which heavy deposits of plaque containing cholesterol and fats collect on the walls of the main arteries. If present, it usually begins early in life, progresses during middle adulthood, and culminates in serious illness. Atherosclerosis is multiply determined, making it hard to separate the contributions of biological aging from individual genetic and environmental influences. The complexity of causes is illustrated by research indicating that before puberty, a high-fat diet produces only fatty streaks on the artery walls (Oliveira, Patin, & Escrivao, 2010 ). In sexually mature adults, however, it leads to serious plaque deposits, suggesting that sex hormones may heighten the insults of a high-fat diet.
Heart disease has decreased considerably since the mid-twentieth century, with a larger drop in the last 25 years due to a decline in cigarette smoking, to improved diet and exercise among at-risk individuals, and to better medical detection and treatment of high blood pressure and cholesterol (American Heart Association, 2012 ). And as a longitudinal follow-up of an ethnically diverse sample of U.S. black and white 18- to 30-year-olds revealed, those at low risk—defined by not smoking, normal body weight, healthy diet, and regular physical activity—were far less likely to be diagnosed with symptoms of heart disease over the succeeding two decades (Liu et al., 2012 ). Later, when we consider health and fitness, we will see why heart attacks were so common in Sharese’s family—and why they occur at especially high rates in the African-American population.
Like the heart, the lungs show few age-related changes in functioning at rest, but during physical exertion, respiratory volume decreases and breathing rate increases with age. Maximum vital capacity (amount of air that can be forced in and out of the lungs) declines by 10 percent per decade after age 25 (Mahanran et al., 1999 ; Wilkie et al., 2012 ). Connective tissue in the lungs, chest muscles, and ribs stiffens with age, making it more difficult for the lungs to expand to full volume (Smith & Cotter, 2008 ). Fortunately, under normal conditions, we use less than half our vital capacity. Nevertheless, aging of the lungs contributes to older adults’ difficulty in meeting the body’s oxygen needs while exercising.
Declines in heart and lung functioning under conditions of exertion, combined with gradual muscle loss, lead to changes in motor performance. In most people, the impact of biological aging on motor skills is difficult to separate from decreases in motivation and practice. Therefore, researchers study competitive athletes, who try to attain their very best performance in real life (Tanaka & Seals, 2003 ). As long as athletes continue intensive training, their attainments at each age approach the limits of what is biologically possible.
Many athletic skills peak between ages 20 and 35, then gradually decline. In several investigations, the mean ages for best performance of Olympic and professional athletes in a variety of sports were charted over time. Absolute performance in most events improved over the past century. Athletes continually set new world records, suggesting improved training methods. But ages of best performance remained relatively constant. Athletic tasks that require speed of limb movement, explosive strength, and gross-motor coordination—sprinting, jumping, and tennis—typically peak in the early twenties. Those that depend on endurance, arm–hand steadiness, and aiming—long-distance running, baseball, and golf—usually peak in the late twenties and early thirties (Bradbury, 2009 ; Schulz & Curnow, 1988 ). Because these skills require either stamina or precise motor control, they take longer to perfect.
Research on outstanding athletes tells us that the upper biological limit of motor capacity is reached in the first part of early adulthood. How quickly do athletic skills weaken in later years? Longitudinal research on master runners reveals that as long as practice continues, speed drops only slightly from the mid-thirties into the sixties, when performance falls off at an accelerating pace (see Figure 13.2 ) (Tanaka & Seals, 2003 ; Trappe, 2007 ). In the case of long-distance swimming—a non-weight-bearing exercise with a low incidence of injury—the decline in speed is even more gradual: The accelerating performance drop-off is delayed until the seventies (Tanaka & Seals, 1997 ).
In her early thirties, professional tennis champion Serena Williams recently became the oldest player to be ranked World No. 1 in the history of the Women’s Tennis Association. Sustained training leads to adaptations in body structures that minimize motor decline into the sixties.
FIGURE 13.2 Ten-kilometer running times with advancing age, based on longitudinal performances of hundreds of master athletes.
Runners maintain their speed into the mid-thirties, followed by modest increases in running times into the sixties, with a progressively steeper increase thereafter.
(From H. Tanaka & D. R. Seals, 2003, “Dynamic Exercise Performance in Masters Athletes: Insight into the Effects of Primary Human Aging on Physiological Functional Capacity,” Journal of Applied Physiology, 5, p. 2153. © The American Physiological Society (APS). All rights reserved. Adapted with permission.)
Indeed, sustained training leads to adaptations in body structures that minimize motor declines. For example, vital capacity is one-third greater in both younger and older people who participate actively in sports than in healthy inactive age-mates (Pimentel et al., 2003 ; Zaccagni, Onisto, & Gualdi-Russo, 2009 ). Training also slows muscle loss, increases speed and force of muscle contraction, and leads fast-twitch muscle fibers to be converted into slow-twitch fibers, which support excellent long-distance running performance and other endurance skills (Faulkner et al., 2007 ). In a study of hundreds of thousands of amateur marathon competitors, 25 percent of the 65- to 69-year-old runners were faster than 50 percent of the 20- to 54-year-old runners (Leyk et al., 2010 ). Yet many of the older runners had begun systematic marathon training only in the past five years.
In sum, although athletic skills are at their best in early adulthood, biological aging accounts for only a small part of age-related declines until advanced old age. Lower levels of performance by healthy people into their sixties and seventies largely reflect reduced capacities resulting from adaptation to a less physically demanding lifestyle.
The immune response is the combined work of specialized cells that neutralize or destroy antigens (foreign substances) in the body. Two types of white blood cells play vital roles. T cells, which originate in the bone marrow and mature in the thymus (a small gland located in the upper part of the chest), attack antigens directly. B cells, manufactured in the bone marrow, secrete antibodies into the bloodstream that multiply, capture antigens, and permit the blood system to destroy them. Because receptors on their surfaces recognize only a single antigen, T and B cells come in great variety. They join with additional cells to produce immunity.
The capacity of the immune system to offer protection against disease increases through adolescence and declines after age 20. The trend is partly due to changes in the thymus, which is largest during the teenage years, then shrinks until it is barely detectable by age 50. As a result, production of thymic hormones is reduced, and the thymus is less able to promote full maturity and differentiation of T cells (Fülöp et al., 2011 ). Because B cells release far more antibodies when T cells are present, the immune response is compromised further.
Withering of the thymus is not the only reason that the body gradually becomes less effective in warding off illness. The immune system interacts with the nervous and endocrine systems. For example, psychological stress can weaken the immune response. During final exams, for example, Sharese was less resistant to colds. And in the month after her father died, she had great difficulty recovering from the flu. Conflict-ridden relationships, caring for an ill aging parent, sleep deprivation, and chronic depression can also reduce immunity (Fagundes et al., 2011 ; Robles & Carroll, 2011 ). And physical stress—from pollution, allergens, poor nutrition, and rundown housing—undermines immune functioning throughout adulthood (Friedman & Lawrence, 2002 ). When physical and psychological stressors combine, the risk of illness is magnified.
The link between stress and illness makes sense when we consider that stress hormones mobilize the body for action, whereas the immune response is fostered by reduced activity. But this also means that increased difficulty coping with physical and psychological stress can contribute to age-related declines in immune system functioning.
Sharese was born when her mother was in her early twenties. At the same age a generation later, Sharese was still single and entering graduate school. Many people believe that pregnancy during the twenties is ideal, not only because of lower risk of miscarriage and chromosomal disorders (see Chapter 2 ) but also because younger parents have more energy to keep up with active children. Nevertheless, as Figure 13.3 on page 438 reveals, first births to women in their thirties have increased greatly over the past three decades. Many people are delaying childbearing until their education is complete, their careers are well-established, and they know they can support a child.
Nevertheless, reproductive capacity does decline with age. Between ages 15 and 29, 11 percent of U.S. married childless women report fertility problems, a figure that rises to 14 percent among 30- to 34-year-olds and to over 40 percent among 35-to 44-year-olds, when the success of reproductive technologies drops sharply (see page 54 in Chapter 2 ) (U.S. Department of Health and Human Services, 2012b ). Because the uterus shows no consistent changes from the late thirties through the forties, the decline in female fertility is largely due to reduced number and quality of ova. In many mammals, including humans, a certain level of reserve ova in the ovaries is necessary for conception (Balasch, 2010 ; Djahanbakhch, Ezzati, & Zosmer, 2007 ). Some women have normal menstrual cycles but do not conceive because their reserve of ova is too low.
FIGURE 13.3 First births to American women of different ages in 1970 and 2010.
The birthrate decreased during this period for women 20 to 24 years of age, whereas it increased for women 25 years of age and older. For women in their thirties, the birthrate increased six-fold, and for those in their early forties, it doubled. Similar trends have occurred in other industrialized nations. (From U.S. Census Bureau, 2012b.)
In males, semen volume, sperm motility, and percentage of normal sperm decrease gradually after age 35, contributing to reduced fertility rates in older men (Lambert, Masson, & Fisch, 2006 ). Although there is no best time in adulthood to begin parenthood, individuals who postpone childbearing until their late thirties or their forties risk having fewer children than they desired or none at all.
CONNECT How do heredity and environment jointly contribute to age-related changes in cardiovascular, respiratory, and immune system functioning?
APPLY Penny is a long-distance runner for her college track team. What factors will affect Penny’s running performance 30 years from now?
REFLECT Before reading this chapter, had you thought of early adulthood as a period of aging? Why is it important for young adults to be aware of influences on biological aging?
Health and Fitness
Figure 13.4 displays leading causes of death in early adulthood in the United States. Death rates for all causes exceed those of other industrialized nations (OECD, 2012b ). The difference is likely due to a combination of factors, including higher rates of poverty and extreme obesity, more lenient gun-control policies, and historical lack of universal health insurance in the United States. In later chapters, we will see that homicide rates decline with age, while disease and physical disability rates rise. Biological aging clearly contributes to this trend. But, as we have noted, wide individual and group differences in physical changes are linked to environmental risks and health-related behaviors.
SES variations in health over the lifespan reflect these influences. With the transition from childhood to adulthood, health inequalities associated with SES increase; income, education, and occupational status show strong, continuous relationships with almost every disease and health indicator (Braveman et al., 2010 ; Smith & Infurna, 2011 ). Furthermore, SES largely accounts for the sizable health advantage of white over ethnic minority adults in the United States (Phuong, Frank, & Finch, 2012 ). Consequently, improving socioeconomic conditions is essential for closing ethnic gaps in health.
FIGURE 13.4 Leading causes of death between 25 and 44 years of age in the United States.
Nearly half of unintentional injuries are motor vehicle accidents. As later chapters will reveal, unintentional injuries remain a leading cause of death at older ages, rising sharply in late adulthood. Rates of cancer and cardiovascular disease rise steadily during middle and late adulthood. (Adapted from U.S. Department of Health and Human Services, 2011b.)
Health-related circumstances and habits—stressful life events, crowding, pollution, diet, exercise, overweight and obesity, substance abuse, jobs with numerous health risks, availability of supportive social relationships, and (in the United States) access to affordable health care—underlie SES health disparities (Ertel, Glymour, & Berkman, 2009 ; Smith & Infurna, 2011 ). Furthermore, poor health in childhood, which is linked to low SES, affects health in adulthood. The overall influence of childhood factors lessens if SES improves. But in most instances, child and adult SES remain fairly consistent, exerting a cumulative impact that amplifies SES differences in health with age (Herd, Robert, & House, 2011 ).
Why are SES variations in health and mortality larger in the United States than in other industrialized nations? Besides lack of universal health insurance, low-income and poverty-stricken U.S. families are financially less well-off than families classified in these ways in other countries (Wilkinson & Pickett, 2006 ). In addition, SES groups are more likely to be segregated by neighborhood in the United States, resulting in greater inequalities in environmental factors that affect health, such as housing, pollution, education, and community services.
These findings reveal, once again, that the living conditions that nations and communities provide combine with those that people create for themselves to affect physical aging. Because the incidence of health problems is much lower during the twenties and thirties than later on, early adulthood is an excellent time to prevent later problems. In the following sections, we take up a variety of major health concerns—nutrition, exercise, substance abuse, sexuality, and psychological stress.
Bombarded with advertising claims and an extraordinary variety of food choices, adults find it increasingly difficult to make wise dietary decisions. An abundance of food, combined with a heavily scheduled life, means that most Americans eat because they feel like it or because it is time to do so rather than to maintain the body’s functions (Donatelle, 2012 ). As a result, many eat the wrong types and amounts of food. Overweight and obesity and a high-fat diet are widespread nutritional problems with long-term consequences for adult health.
Overweight and Obesity.
In Chapter 9 , we noted that obesity (a greater than 20 percent increase over average body weight, based on age, sex, and physical build) has increased dramatically in many Western nations, and it is on the rise in the developing world as well. Among adults, a body mass index (BMI) of 25 to 29 constitutes overweight, a BMI of 30 or greater (amounting to 30 or more excess pounds) constitutes obesity. Today, 36 percent of U.S. adults are obese. The rate rises to 38 percent among Hispanics, 39 percent among Native Americans, and 50 percent among African Americans (Flegal et al., 2012 ). The overall prevalence of obesity is similar among men and women.
Overweight—a less extreme but nevertheless unhealthy condition—affects an additional 33 percent of Americans. Combine the rates of overweight and obesity and the total, 69 percent, makes Americans the heaviest people in the world. TAKE A MOMENT… Notice in these figures that the U.S. obesity rate now exceeds its rate of overweight, a blatant indicator of the growing severity of the problem.
Recall from Chapter 9 that overweight children are very likely to become overweight adults. But a substantial number of people show large weight gains in adulthood, most often between ages 25 and 40. And young adults who were already overweight or obese typically get heavier, leading obesity rates to rise steadily between ages 20 and 65 (Flegel et al., 2012).
Causes and Consequences.
As noted in Chapter 9 , heredity makes some people more vulnerable to obesity than others. But environmental pressures underlie the rising rates of obesity in industrialized nations: With the decline in need for physical labor in the home and workplace, our lives have become more sedentary. Meanwhile, the average number of calories and amount of sugar and fat consumed by Americans rose over most of the twentieth and early twenty-first century, with a sharp increase after 1970 (see the Social Issues: Health box on pages 440 – 441 ).
Adding some weight between ages 25 and 50 is a normal part of aging because basal metabolic rate (BMR), the amount of energy the body uses at complete rest, gradually declines as the number of active muscle cells (which create the greatest energy demand) drops off. But excess weight is strongly associated with serious health problems (see page 291 in Chapter 9 )—including type 2 diabetes, heart disease, and many forms of cancer—and with early death.
SES variations in health in the United States—larger than in other industrialized nations—are in part due to lack of access to affordable health care. This Los Angeles free clinic helps address the problem by offering preventive services, including eye exams, to over 1,200 patients per day.
Furthermore, overweight adults suffer enormous social discrimination. Compared with their normal-weight agemates, they are less likely to find mates, be rented apartments, receive financial aid for college, or be offered jobs. And they report frequent mistreatment by family members, peers, co-workers, and health professionals (Ickes, 2011 ; Puhl, Heuer, & Brownell, 2010 ). Since the mid-1990s, discrimination experienced by overweight Americans has increased, with serious physical and mental health consequences. Weight stigma triggers anxiety, depression, and low self-esteem, which increase the chances that that unhealthy eating behaviors will persist and even worsen (Puhl & Heuer, 2010 ). The widespread but incorrect belief, perpetuated by the media, that obesity is a personal choice promotes negative stereotyping of obese persons.
Social Issues: Health The Obesity Epidemic: how Americans Became the Heaviest People in the World
In the late 1980s, obesity in the United States started to soar. As the maps in Figure 13.5 show, it quickly engulfed the nation and has continued to expand. The epidemic also spread to other Western nations and, more recently, to developing countries. For example, as noted in Chapter 9 , obesity was rare in China 30 years ago, but today it affects 7 percent of Chinese children and adolescents and 11 percent of adults; an additional 15 percent of the Chinese population is overweight (Xi et al., 2012 ). Yet China is a low-prevalence country! Worldwide, overweight afflicts more than 1.4 billion adults, 500 million of whom are obese. American Samoa leads the globe in overweight and obesity, with a staggering 94 percent of people affected (World Health Organization, 2013a ). Among industrialized nations, no country matches the United States in prevalence of this life-threatening condition.
A Changing Food Environment and Lifestyle
Several societal factors have encouraged widespread rapid weight gain:
· ● Availability of cheap commercial fat and sugar. The 1970s saw two massive changes in the U.S. food economy: (1) the discovery and mass production of high-fructose corn syrup, a sweetener six times as sweet as ordinary sugar and therefore far less expensive; and (2) the importing from Malaysia of large quantities of palm oil, which is lower in cost than other vegetable oils and also tastier because of its high saturated fat content. Use of corn syrup and palm oil in soft drinks and calorie-dense convenience foods lowered production costs for these items, launching a new era of “cheap, abundant, and tasty calories”(Critser, 2003 ).
· ● Portion supersizing. Fast-food chains discovered a successful strategy for attracting customers: increasing portion sizes substantially and prices just a little for foods that had become inexpensive to produce. Customers thronged to buy “value meals,”jumbo burgers and burritos, and 20-ounce Cokes (Critser, 2003 ). Research reveals that when presented with larger portions, individuals 2 years and older increase their intake, on average, by 25 to 30 percent (Fisher, Rolls, & Birch, 2003 ; Steenhuis & Vermeer, 2009 ).
· ● Increasingly busy lives. Between the 1970s and 1990s, women entered the labor force in record numbers, and the average amount of time Americans worked increased dramatically. Today, 86 percent of employed U.S. men and 66 percent of employed women work over 40 hours per week—substantially more than in most other countries (Schor, 2002 ; United Nations, 2012 ). As time for meal preparation shrank, eating out increased (Midlin, Jenkins, & Law, 2009 ). In addition, Americans became frequent snackers, tempted by a growing assortment of high-calorie snack foods on supermarket shelves. And the number of calories Americans consumed away from home doubled, with dietary fat increasing from 19 to 38 percent (Nielsen & Popkin, 2003 ).
· ● Declining rates of physical activity. During the 1980s, physical activity, which had risen since the 1960s, started to fall as Americans spent more time in sedentary transportation and jobs—driving to and from work and sitting throughout the work day, often behind a computer. At home, a rise in TV viewing to an average of more than four hours per day has been linked to weight gain in adults and children alike (Foster, Gore, & West, 2006 ).
Combating the Obesity Epidemic
· Obesity is responsible for $150 billion in health expenditures and an estimated 300,000 premature deaths per year in the United States alone (Finkelstein et al., 2009 ; Flegal et al., 2007 ). Because multiple social and economic influences have altered the environment to promote this epidemic, broad societal efforts are needed to combat it. Effective policies include
· ● Government funding to support massive public education efforts about healthy eating and physical acti