14.1 Tracing Physical Aging

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Susan has atherosclerosis, or fatty deposits on her artery walls. Her fragile bones and vision and hearing problems are also classic signs of normal aging—body deterioration that advanced gradually over years. Over time, normal aging shades into disease, then disability, and, finally—by a specific barrier age—death.

PRINCIPLE #1 CHRONIC DISEASE IS OFTEN NORMAL AGING “AT THE EXTREME.” Many physical losses, when they occur to a moderate degree, are called normal. When these changes become extreme, they have a different label: chronic disease. Susan’s bone loss and atherosclerosis are perfect examples. These changes, as they progress, produce those familiar later-life illnesses—osteoporosis and heart disease.

The National Health Interview Survey (NHIS), an annual government poll of health conditions among the U.S. population, tells us other interesting illness facts. As you can see in Figure 14.1, arthritis is the top-ranking chronic illness in later life (Centers for Disease Control and Prevention [CDC], 2009). As we get older, our chance of having a variety of illnesses increases. Like arthritis, many age-related diseases are not fatal. They interfere with the ability to function in the world. So the outcome of chronic illness is not just death, but ADL (activities of daily living) problems—difficulties handling life.

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Figure 14.1: Prevalence of selected chronic health conditions among U.S. adults in middle and later life (percentages): As people travel into their seventies and eighties, the rates of common age-related chronic diseases rise. Although every chronic illness can impair the ability to fully enjoy life, many common chronic diseases don’t actually result in death.
Data from: CDC (2009); National Center for Health Statistics (2008).

PRINCIPLE #2 ADL IMPAIRMENTS ARE A SERIOUS RISK DURING THE OLD-OLD YEARS. ADL limitations come in two categories. Instrumental ADL problems refer to troubles performing tasks important for living independently, such as cooking and cleaning or driving. Basic ADL limitations refer to problems with basic self-care activities, such as standing or getting to the bathroom or feeding oneself. When people have these severe disabilities, they typically need full-time caregiving help.

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Although ADL problems can happen at any age, notice from Figure 14.2 that the old-old years are when these problems really strike. Half of all people over 85 living in their homes, have instrumental ADL difficulties. Basic ADL limitations, or fundamental self-care impairments, such as walking to the toilet or dressing, affect 1 in 6 of the oldest old (CDC, 2009). These statistics minimize the true rate of problems because older adults with basic ADL impairments often have to enter a nursing home.

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Figure 14.2: Percentages of people needing assistance with instrumental ADLs and basic ADLs in the young-old years and over age 75: Although in the sixties and early seventies the fraction of people with ADL difficulties is relatively small, the risk of having these problems escalates dramatically over age 75. (Over age 85, roughly 1 in 6 people living in the community have a basic ADL problem.)
Data from: U.S. Department of Health and Human Services, 2009.
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Here, you can see the real enemy in old age: It’s ADL impairments. Moreover, since this 85-year-old man’s difficulties standing are permanent, he was forced to enter a nursing home.
Stockbyte/Getty Images

So, yes, people can arrive at age 85 or 90 virtually disability free. But as we travel further into later life, problems physically coping become a serious risk.

PRINCIPLE #3 THE HUMAN LIFESPAN HAS A DEFINED LIMIT. A final fact about aging is that it has a fixed end. More people than ever are surviving past a century. But a miniscule fraction make it beyond that barrier age. In August 2014, worldwide, there were roughly 75 documented “super-centenarians”—people who lived until 110 and beyond (Gerontology Research Group, n.d.). Unless scientists can tamper with our built-in, species-specific maximum lifespan, soon after a century on this planet, we are all fated to die.

Can We Live to 1,000?

At this point, you might be thinking that many babies will soon make it to be supercentenarians. Due to scientific breakthroughs in extending the lifespan, you may have read the world is poised for the arrival of the first 1,000-year-old human being (As reported in Carnes, Olshansky, & Hayflick, 2013).

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These futuristic forecasts fall on fertile ground because one life-extension strategy has been known for 75 years. By underfeeding rats, researchers can increase the animals’ maximum lifespan by up to 60 percent. The key is what one biologist calls “undernutrition without malnutrition.” The animals are restricted to less food but given a nutritionally rich diet. They are allowed few empty calories (see Belsky, 1999, for review).

Calorie restriction is actually an all-purpose anti-ager, enhancing everything from glucose metabolism (Fok and others, 2013) to cardiac function (Cisiszar and others, 2013). These research findings make excellent sense because obesity, especially via its side-effect of diabetes (impaired sugar metabolism), causes every organ—from our eyes, to our heart, to our kidneys—to prematurely breakdown.

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This species has been the target of almost all of our life-extension research carried out over the past 75 years—but it’s unclear if the rat underfeeding results generalize to human beings.
Sextoacto/Shutterstock

Without denying that it’s important to watch your diet, however, restricting your intake just to live to 110 is a mistake. The calorie reduction research has typically been carried out with rats. The scientific literature is littered with miracle disease-reduction interventions—such as massive doses of vitamin A, supposed to prevent cell damage—that worked with rodents but had toxic effects on human beings!

Calorie restriction has confusing effects. Sometimes it postpones deaths in youth or allows just a small number of the most long-lived members of a species to survive longer (Gribble & Welch, 2013). There may be an unwelcome fertility trade off. Suppose you lived to 110 but put off puberty to age 25?

Let’s listen to the foremost experts in the biology of aging explain why extending the maximum lifespan in the near future is an unrealistic dream (Carnes, Olshansky, & Hayflick, 2013):

Now let’s turn to two familiar markers that affect our journey toward our expiration date (and every other aspect of our lifespan journey): socioeconomic status and gender.

Socioeconomic Status, Aging, and Disease

The most powerful evidence that poverty affects how long we live comes from scanning a few life-expectancy statistics in the developing versus the developed worlds: Babies born in South Africa can expect on average to survive to age forty years longer. Infants lucky to emerge from the womb in Monaco have a 50/50 chance of living 30 years longer—to 89 (CIA World Factbook, n.d.). This mammoth global difference is mirrored by a socieoeconomic health gap within each country. From Canada to Cameroon and from Sweden to Somalia, affluent and well-educated people live healthier and survive for a longer time.

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These snapshots show visually why babies born in the affluent kingdom of Monaco statistically out-survive South African newborns by a remarkable 40 years.
Marcel Jolibois/Photononstop/Getty Images

When, during adulthood, is the socioeconomic health gap most pronounced? The answer, according to most (but not all) surveys, is during midlife, as normal age changes are progressing to chronic disease. For instance, in one study in Holland, only 5 percent of people in the top quarter of the income distribution reported being in poor health at age 55. For their bottom quarter counterparts, the odds were 1 in 3 (Kippersluis and others, 2010).

You may see these statistics in operation by just looking around. Notice how, by the late thirties people show clear differences in their aging rates. Although there are many exceptions, notice also that low-income adults are apt to look physically older than their chronological age. In fact, for disadvantaged Americans, “old-age” ADL impairments, not infrequently, qualify as problems of midlife (Health United States, 2009).

How far back in development can we trace this accelerated aging path? Unfortunately, based on the fetal programming hypothesis, its roots might emerge in the womb. Remember from Chapter 2 that low birth weight—which is linked to poverty—is epigenetically associated with premature heart disease and earlier death. Now recall from Chapters 4 and 5 that obesity and elevated levels of cortisol (the stress hormone) are more common among preschoolers at the low end of the socioeconomic scale. Therefore, the many health-impairing forces linked to early childhood poverty—from obesity, to chronic anxiety, to being born small—accumulate to increase our allostatic load, that overall marker of body breakdown signaling disease (Umberson and others, 2014; O’Donovan and others, 2013).

Now compound this with the poisonous adult lifestyle forces linked to poverty—from social-class differences in smoking (Boykin and others, 2011); to lack of exercise (who has time to work out if you are working two jobs to survive?); from poor eating habits (as high-fat foods are less expensive than fish or fresh fruit, what choices would you make if you had to save every dime?); to the stress-inducing impact of unemployment or living in crime-ridden neighborhoods.

So far, I’ve spelled out a dismal scenario. But, socioeconomic status involves both education and income. And, as you will see in Figure 14.3 below, the educational component of SES looms large in predicting life expectancy, especially for men (OECD, 2014; Mazzonna, 2014).

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Figure 14.3: Life-expectancy gaps between older people with high and low levels of education in selected European countries in 2010: Notice that, while the size of the gap differs in interesting ways from nation to nation, depending partly on the given country’s income inequalities, in the European Union, being well-educated gives people—mainly men—a considerable longevity boost.
Data from: OECD, 2014, p. 19.
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This compelling photo offers one reason for the “Hispanic paradox” (the fact that disadvantaged Latino-heritage adults tend to live a surprisingly long time): a culture immersed in intergenerational adoration and respect. The lesson: As a caring, involved grandchild of any cultural background, you might be “working” to help extend a beloved elderly family member’s life!
© Jose Luis Pelaez, Inc./CORBIS

Fascinating evidence that education directly affects aging involves research on telomeres, DNA sequences at the end of our chromosomes. Telomere shortening is a benchmark of cellular aging, as it shows that a particular cell has reached senescence and can no longer divide. Among a huge group of U.S. older adults, researchers found that high school graduates had shorter telomeres than people who attended college, a difference that was particularly striking among Black men (Adler and others, 2013; Mazzotti, Tufik, & Andersen, 2013). Therefore, in addition to (or due to) its other benefits, college can extend our lives!

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Another life extender is close relationships. In one landmark study, researchers found that caring social connections were as—or more—important than good health practices in predicting how long people survived (Berkman & Breslow, 1983).

Being embedded in nurturing communities may explain “the Hispanic paradox,” the fact that poverty-level U.S. Latinos outlive low-income Whites (Turra & Goldman, 2007). It accounts for why loving marriages are correlated with longevity, too (Choi & Marks, 2013). While caring attachment figures do everything from encouraging us to eat well (Friedman, 2014), to insisting we go to the doctor when we are ill, love stimulates oxytocin production, which, in itself, mutes the anxiety response to stress (Myers and others, 2014).

Gender, Aging, and Disease

Their wider web of social connections could be one reason why women outlive men, sometimes by an incredible decade or more (OECD, 2014). Still, the main reason for women’s superior survival is biological. Having an extra X chromosome makes females physically hardier at every stage of life.

During adulthood, the main reason for this gender gap can be summed up in one phrase: fewer early heart attacks. Illnesses of the cardiovascular system (the arteries and their pump, the heart) are the top-ranking killers for both women and men. In 2014, cardiac arrests accounted for roughly 1 in 6 U.S. deaths (Go and others, 2014). However, because estrogen helps to slow the process by which fat deposits clog the arteries, men are roughly twice as likely as women to die of a heart attack in midlife (American Heart Association, 2001).

Their biological susceptibility to early heart attacks means that men tend to “die quicker and sooner.” For women, the worldwide pattern is “surviving longer but being more frail” (OECD, 2014; Tareque, Begum, & Saito, 2013; Rohlfsen & Kronenfeld, 2014; Onadja and others, 2013).

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It makes sense that disability is the price of traveling to the lifespan train’s final stops. However, the phrase “living sicker” applies to women throughout adult life. During their twenties and thirties and forties, only women experience the physical ailments related to pregnancy and menstruation. As they age, females have higher rates of arthritis, vision impairments, and obesity—illnesses that produce ADL problems but (except in the case of obesity) don’t lead to death (Whitson and others, 2010).

This male/ female disability distinction brings me to a statistic called healthy-life years—the age at which we can expect to survive without ADL limitations. Notice from Figure 14.4, in the European Union, healthy-life years are much shorter than overall life expectancy for both sexes. But, if you look just at the length of the blue bar, notice that elderly men live healthy comparatively longer than women do. In fact, considering just healthy-life years, EU females’ average six-year longevity advantage shrinks to a single year! (See OECD, 2014.)

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Figure 14.4: Life expectancy (blue plus magenta bars) and healthy life years (blue bar) at 65, for women and men in a few European nations in 2012: Notice that in each E.U. nation, overall life expectancy at age 65 is considerably longer than the years older people can expect to live in health. However, the gap between the two measures is wider for women than men. Bottom-line message: The statistical price of surviving into your older years is disability during the final years of your life, particularly if you are a female.
Data from: OECD, 2014, p. 19.

INTERVENTIONS: Taking a Holistic Lifespan Disease-Prevention Approach

How can we increase our healthy-life years and get closer to the biological limit of life? As I mentioned in Chapter 5, with regard to obesity, one route is to alter our epigenetic path by changing the environment from day one. Specifically:

  • Focus on childhood. As I’ve been stressing throughout this book, we need to prevent premature births, make inroads in child poverty, and improve early childhood education. Now we understand that encouraging teens to enroll in and finish college can also have health benefits in middle and later life!

  • Focus on constructing caring communities. Let’s commit to making cities senior-citizen friendly (Barusch and others, 2013); and construct walkable, planned communities that allow people to exercise without going to gyms. Let’s build in services that reach out to isolated neighbors and provide the nurturing social relationships that extend life.

Finally, let’s appreciate the realities in Figure 14.4. Without minimizing old age’s emotional benefits, even in the most health-conscious European nations, the price of living to the upper ends of the lifespan is frequently disease. Given that running for miles at age 90 is unrealistic, and we are decades from tampering with our DNA, let’s use our human ingenuity to make the world user-friendly for normally aging people marching into later life. With this goal in mind, it’s time to confront the conditions causing ADL problems in the flesh—sensory-motor declines and major neurocognitive disorders, or dementia.

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Tying It All Together

Question 14.1

When she was in her late fifties, Edna’s doctor found considerable bone erosion and atherosclerosis during a checkup. At 70, Edna’s been diagnosed with osteoporosis and heart disease. Did Edna:

  1. suddenly develop these diseases?

  2. have normal aging changes that slowly progressed into these chronic diseases?

  3. have both above events occur?

b

Question 14.2

Marjorie has problems cooking and cleaning the house. Sara cannot dress herself or get out of bed without someone’s help. Marjorie has_____ problems and Sara has_____ problems.

Marjorie has instrumental ADL problems, and Sara has basic ADL problems.

Question 14.3

Laura brags that her newborn is likely to live to 120. Using the points in this section, convince Laura that she is wrong.

Tell Laura that physical aging has such complex causes that finding any single life-extension intervention will be virtually impossible. Moreover, even if we can replace individual body parts, such as our heart, other vital organs such as our kidneys are programmed to wear out. The fact that only a tiny percentage of twenty-first-century babies is projected to live to 100 makes it unlikely that her child—or any child—can live to 120.

Question 14.4

Nico and Hiromi are arguing about men’s versus women’s health. Nico says that women are basically “healthier”; Hiromi thinks that it’s men. Explain why both Nico and Hiromi are each partly correct.

Nico and Hiromi are both correct, because although women live longer (meaning that they must be healthier), they also live “sicker” (meaning that they are more apt to be ill) throughout adulthood.