Demography of longevity: past, present, and future trends

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Abstract

Life expectancy at birth has roughly tripled over the course of human history. Early gains were due to a general improvement in living standards and organized efforts to control the spread of infectious disease. Reductions in infant and child mortality in the late 19th and early 20th century led to a rapid increase in life expectancy at birth. Since 1970, the main factor driving continued gains in life expectancy in industrialized countries is a reduction in death rates among the elderly. In particular, death rates due to cardiovascular disease and cancer have declined in recent decades thanks to a variety of factors, including successful medical intervention. Based on available demographic evidence, the human life span shows no sign of approaching a fixed limit imposed by biology or other factors. Rather, both the average and the maximum human life span have increased steadily over time for more than a century. The complexity and historical stability of these changes suggest that the most reliable method of predicting the future is merely to extrapolate past trends. Such methods suggest that life expectancy at birth in industrialized countries will be about 85-87years at the middle of the 21st century.

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Most cited references 21

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Extension of life-span by introduction of telomerase into normal human cells.

A. G. Bodnar, M. Ouellette, M Frolkis … (1998)

Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced straining for beta-galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine.

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Oxidants, antioxidants, and the degenerative diseases of aging.

B. N. Ames, M. Shigenaga, T. M. Hagen (1993)

Metabolism, like other aspects of life, involves tradeoffs. Oxidant by-products of normal metabolism cause extensive damage to DNA, protein, and lipid. We argue that this damage (the same as that produced by radiation) is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts. Antioxidant defenses against this damage include ascorbate, tocopherol, and carotenoids. Dietary fruits and vegetables are the principal source of ascorbate and carotenoids and are one source of tocopherol. Low dietary intake of fruits and vegetables doubles the risk of most types of cancer as compared to high intake and also markedly increases the risk of heart disease and cataracts. Since only 9% of Americans eat the recommended five servings of fruits and vegetables per day, the opportunity for improving health by improving diet is great.

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Rectangularization revisited: variability of age at death within human populations.

J Wilmoth, S Horiuchi (1999)

Rectangularization of human survival curves is associated with decreasing variability in the distribution of ages at death. This variability, as measured by the interquartile range of life table ages at death, has decreased from about 65 years to 15 years since 1751 in Sweden. Most of this decline occurred between the 1870s and the 1950s. Since then, variability in age at death has been nearly constant in Sweden, Japan, and the United States, defying predictions of a continuing rectangularization. The United States is characterized by a relatively high degree of variability, compared with both Sweden and Japan. We suggest that the historical compression of mortality may have had significant psychological and behavioral impacts.