Why Do Our Bodies Grow Old? Controversy 2 Why Do Our Bodies Grow Old? (c) 2011, SAGE Publications, Inc.

Why Do Our Bodies Grow Old? The maximum lifespan for the human species appears to be around 120 years We have no valid records of people living much beyond 120 years Over recent years, life expectancy (e.g., average number of years lived) has risen; but lifespan (e.g., maximum possible length of life) hasn’t changed at all Compression of Morbidity theory—believes we should aim for a healthy old age, followed by a rapid decline and death, which would likely: Enhance the quality of life Extend life expectancy and “health span” Reduce health care costs and caregiver burden (c) 2011, SAGE Publications, Inc.

The Process of Biological Aging Normal Aging (Senescence)—an underlying time-dependent biological process that, although not itself a disease, involves functional loss and susceptibility to disease and death. Gompertz Law—death rates for contemporary humans double every 8 years (ex., a 38-year-old would be twice as likely to die as a 30-year-old) Additionally, at any given age, men are twice as likely to die as women (c) 2011, SAGE Publications, Inc.

The Process of Biological Aging (cont.) Comparative Anatomy—the study of the structure of different species Helps us understand differences in aging and lifespan across species The rate of aging can be correlated with the amount of time it takes the death rate of a species to double e.g., the doubling time for humans is 8 years, but it is 10 days for a fruit fly and 3 months for a mouse (c) 2011, SAGE Publications, Inc.

The Process of Biological Aging (cont.) Rate-of-Living Concept—the concept that metabolism and life expectancy are closely related Smaller organisms, which have faster metabolisms, also have shorter life expectancies Human beings have an average lifespan and maximum life expectancy about twice as great as those of any other primate (c) 2011, SAGE Publications, Inc.

Biological Theories of Aging No single theory of aging explains all the complex processes that occur in cells and body systems But ongoing research is finding new insights into why we grow old Two basic kinds of theory of aging: Chance—the result of external events Fate—the result of an internal necessity The question remains whether or not it’s possible to intervene to correct damage to the aging body or modify the genetic program (c) 2011, SAGE Publications, Inc.

Biological Theories of Aging Wear-and-Tear theory—sees aging as the result of chance A good explanation for some aspects of aging, such as the fact that our joints and bones become damaged over time as an outcome of living Somatic Mutation theory—notes that cells can be damaged by radiation, and as a result, mutate or experience genetic changes A more modern and sophisticated version of the wear-and-tear theory, but little science evidence to support it at this point (c) 2011, SAGE Publications, Inc.

Wear-and-Tear Theory (cont.) Error Accumulation theory (aka error catastrophe theory)—says that decremental changes of senescence are the result of chance or random changes that downgrade the genetic code Over time, small errors in genetic coding occur and eventually make the later copies unreadable (e.g., like using a photocopy to make another copy) Accumulative Waste theory—theorizes that the accumulation of waste products eventually interferes with cell metabolism and leads to death According to scientific research, although waste products do accumulate, there is little evidence of harm to the organism (c) 2011, SAGE Publications, Inc.

Biological Theories of Aging (cont.) Autoimmune theory—the system may eventually become defective and no longer distinguish the body’s own tissues from foreign tissues The body may then begin to attack itself, as suggested by the increase with age in autoimmune diseases, such as rheumatoid arthritis Aging-Clock theory—claims that aging is programmed into our bodies like a clock ticking away from conception (c) 2011, SAGE Publications, Inc.

Biological Theories of Aging (cont.) Cross-Linkage Theory—claims that the bodily changes that we see as we age result from the accumulation of cross-linking compounds in the collagen, which gradually becomes stiff Collagen—a natural protein found in the skin, bones, and tendons Free Radicals—damage created by free radicals (molecules that appear as a byproduct of oxygen metabolism in cells) eventually gives rise to the symptoms we recognize as aging The body produces anti-oxidants—substances that protect against free radicals that prevent damage to cells (c) 2011, SAGE Publications, Inc.

Biological Theories of Aging (cont.) Cellular Theory—argues that aging ultimately results from the progressive weakening of capacity for cell division, perhaps through exhaustion of the genetic material Hayflick limit—the finite number of cell divisions that normal human cells in tissue culture go through Named after discoverer Leonard Hayflick (1961) (c) 2011, SAGE Publications, Inc.

(c) 2011, SAGE Publications, Inc. Is Aging Inevitable? The biological aging process may not be the result of a rigid genetic program: It may simply be the complex and indirect result of multiple traits in the organism tied to normal development But aging is not a disease Rather, it’s a normal process of change, part of which may make us more vulnerable to disease (c) 2011, SAGE Publications, Inc.

Environmental and Genetic Approaches There is only one environmental intervention that has scientifically been shown to be connected to longevity in mammals: restricting food intake When caloric intake is reduced—by up to 40% fewer calories than normal—age-related deterioration slows down, and age-related diseases are diminished This is possibly because caloric reduction slows metabolism—the rate at which food is transformed into energy For any individual, length of life will be the result of both genetic and environmental factors (c) 2011, SAGE Publications, Inc.

Compression or Prolongation of Morbidity? Various environmental and genetic alterations have been shown to increase lifespan among simple organisms But human beings are more complex, and there is still no conclusive evidence from research on humans According to the textbook, the compression of morbidity theory stands out as an important reminder of how critical biological research will be for the future of an aging society (c) 2011, SAGE Publications, Inc.

Reading 5: Why Do We Live as Long as We Do? Discuss Hayflick's basic premise regarding the increase in longevity of the human species. What are the key aspects—and implications—of his premise? (c) 2011, SAGE Publications, Inc.

Reading 6: Vitality and Aging Fries and Crapo, writing in the 1980s, provided a “new syllogism” about human aging. What are the key components of their model of biophysical aging? Is there any indication that what they propose in their model has been borne out in the past two decades as more people reach later life? (c) 2011, SAGE Publications, Inc.

Reading 7: The Compression of Morbidity Hypothesis What are the key components of the “compression of morbidity hypothesis”?  While author Mor agrees that there have been improvements in the rate of late life morbidity, he questions whether this trend will continue into the future. What are some of the reasons for his concern? (c) 2011, SAGE Publications, Inc.

Reading 8: Health Trends in the Elderly Population Parker and Thorslund assert that “a concept of general morbidity is not sufficient when discussing health trends and the need for care services in the elderly population.” What do they propose as an alternative? (c) 2011, SAGE Publications, Inc.

Reading 9: We Will Be Able to Live to 1,000 If Aubrey de Grey’s proposal for curing aging were to come to pass, what would aging and later life look like?  What would society look like? (c) 2011, SAGE Publications, Inc.

Reading 10: Don’t Fall for the Cult of Immortality Olshansky provides a counter argument to de Grey’s agenda to “cure aging.” What are the key ideas in Olshansky’s argument? Taken together, which side of the debate do you find to be more compelling? More realistic? (c) 2011, SAGE Publications, Inc.