The Future of Old Age

Changing Life Spans

First, let us look at historical changes in the life span. Before 1800, life spans were very short, with life expectancies at birth of 30 to 40 years. However, since 1800, human life expectancy has expanded in developing countries and has more than doubled, whether measured at birth or at age 70 years ( Figure 3-1 ).

About half of those born before 1800 did not reach the age of parenthood, and a mere 10%, at best, reached age 70. Then, during the industrial revolution, country after country developed better living conditions, with increased food distribution and improved hygiene, even before the understanding of infectious disease; after that came pasteurization and vaccination and finally, after WWII, antibiotics. Infectious disease dwindled from the major cause of death before 1900 to less than 5% of total deaths. Now, most of us survive to older ages, where we accumulate the chronic diseases of aging, from atherosclerosis to cancer, and, if we live long enough, a rapidly increasing risk of Alzheimer disease (AD).

These survival data can be further understood when plotted as mortality rates at each age of life ( Figure 3-2 ). These are known as Gompertz curves, first described in 1825 by the Scottish actuary Benjamin Gompertz. After age 40, mortality rates accelerate, with a doubling every 7 to 8 years. Sweden has the most comprehensive data obtained from nationwide household surveys that were initiated in the mid-eighteenth century (see Figure 3-2 ). The mortality rates in 1800 were high in the early years, starting with 10% to 30% infant mortality. Even young adults in the eighteenth century had a 1% annual mortality rate. After about the age of 40, Sweden, like all other countries, shows accelerating (exponentially increasing) mortality rates, which are the basic manifestation of aging.

Note how the slope of the more recent population increases steadily with improving conditions, corresponding exactly to the increase in life expectancy shown in Figure 3-1 . In fact, the curves get progressively steeper; paradoxically, as life spans have increased, the rates of mortality acceleration have also increased. Note also that as infections were progressively minimized as a cause of early-age mortality, mortality at ages 10 to 40 years approached a minimum, below 0.1%/year. Those born most recently may now have an even lower mortality of 0.02%/year (2/10,000). This historically unprecedented low baseline mortality represents deaths from conditions in which significant further reductions are unlikely (e.g., accidents, congenital defects, rare familial diseases). Across all ages, women have slightly lower mortality rates. Nonetheless, both genders incur mortality accelerations by the age of 40 years.

Impact of Biologically Altering Aging Processes

Almost all the diseases that we will discuss are diseases of older ages. The incidence of these conditions increases exponentially with aging, foreshadowing and anticipating the accelerating mortality rates of the Gompertz curve. Some diseases have been accelerating in regard to incidence even faster than the Gompertz curve. For example, AD incidence doubles every 5 years after age 60, and total mortality doubles every 7 to 8 years. Longevity futurists are confronted with the depressing fact that most centenarians have clinical grade dementia. Therefore, before considering expanding life expectancy, we must develop effective interventions to reduce or delay the incidence of AD and slow its course. For example, delaying the onset of AD by 5 years could cut its prevalence in half. Biologists think this is possible because mice that are calorically restricted not only have increased life spans, but also have delayed onset of AD-like brain changes.

Laboratory models have amply documented that every aspect of aging can be manipulated, from DNA damage to cross-linking of connective tissue collagen and elastin to ovarian egg cell loss to arterial lipids to brain amyloid levels. In addition to food intake and exercise, aging processes can be manipulated by regulating gene activity without changing DNA sequence . We believe that it is within reach of the current younger generation of aging researchers to discover the molecular basis for aging fully. However, it is unlikely that aging is controlled by a single gene or single biochemical or cellular mechanism. Thus, we anticipate that multiple interventions will be developed for different aging pathways to slow or possibly reverse aging processes. Aging can be treated, but interventions need to be initiated long before old age.

It is likely that antiaging interventions by specialized drugs and regenerative medicine for damaged organs is likely to be expensive. Already, even in nations with fully socialized medicine, older adults are given lower priority for major organ replacement. Drugs to slow AD and other dementias will be very expensive because of the huge costs in drug development However, those in poverty already age 10 years faster than the general U.S. population. Thus, the so-called health elite, with ample private funds for medical treatment and potential rejuvenating therapy, may further deepen social disparities in health at later ages.