Is There a Limit to Human Life Expectancy?

William Faloon

The journal Science is perhaps the most respected publication in the world. An article in the May 10, 2002 issue of Science¹ discusses gains in life expectancy and states, “There’s no limit in sight.”

According to the researchers who authored this article, the consistency of gains in life expectancy is “astonishing.” Japanese women, for instance, have experienced an almost three months increase in life expectancy per year for the past 160 years!

The article rebuts pessimists who claim that the human life span may soon hit a ceiling. For instance, a calculation was made in 1928 indicating that the average human life span could not exceed 64.75 years. At that time, life expectancy in the United States was only 57 years. What was not considered was the fact that certain populations in New Zealand had already achieved a life expectancy of 65.93 years.

A more recent projection made in 1990 stated that the life expectancy of people reaching age 50 could not go beyond 85 years. Japanese females, however, surpassed that limit six years later (in 1996).

How long will humans live?

 

A historical perspective reveals how far we’ve come in the past 162 years. In 1840 the record was held by Swedish women who lived an average of a little more than 45 years. It took until 1900 for average American life expectancy to reach age 47.3 years and then steadily increase to 76.4 years by year 2000.²

According to the Science article, if the trend of increasing life expectancy continues, female life expectancy in the United States will be between 92.5 and 101.5 in 2070. This is considerably higher than the Social Security Administration’s most recent forecast of 83.9 years.

These new projections for extended life are not predicated on dramatic advances in the biomedical sciences. They are instead based upon the long-term trend of sustained progress in reducing mortality. If anticipated medical breakthroughs do manifest, the increase in life expectancy will be significantly higher.

The Science article points out that average life expectancy has increased 2.5 years per decade for a century and a half. The researchers believe that it is reasonable to expect this trend to continue and that average life expectancy may reach 100 in about six decades. It is striking, the researchers note, that centenarians may become commonplace within the lifetimes of people alive today.

Before 1950, most of the gains in life expectancy were due to large reductions in death rates at younger ages. In the second half of the 20th century, life extension after age 65 propelled the rise in the length of people’s lives. From a practical view, the fact that increases in survival are occurring in older populations substantiates the need for people to take better care of themselves today.

Government underestimates life expectancy

Official government forecasts of how long people are supposed to live have proven to be notoriously inaccurate. The government has incorrectly assumed that life expectancy will increase slowly and not much further, thus giving politicians license to postpone painful adjustments to the funding of social-security and medical-care systems.

The authors of the Science article state that government officials charged with forecasting trends in life expectancy “should base their calculations on the empirical record of mortality improvements over corresponding spans of the past.”

The position of The Life Extension Foundation is that it is not possible to calculate the impact of future medical advances on human longevity. Therefore, any government program that promises a substantive benefit to humans for as long as they live may not be sustainable. This is because life expectancy will most probably exceed the actuarial premise upon which the program was based.

This is good news for life insurance companies, as their payouts will be postponed. Government funding of healthcare and social programs will have to be adjusted because people won’t be dying as soon as the bureaucrats project.

MODERN AVIATION: LESS THAN 100 YEARS OLD

At 10:30 A.M. on Dec. 17, 1903, Orville Wright achieved the first piloted, sustained, powered heavier-than-air flight. His brother, Wilbur, stood by and timed the flight with a stopwatch. The first flight lasted twelve seconds and the aircraft flew 120 feet. The location was near Kitty Hawk, North Carolina. Three more flights were made that day; the longest was nearly a minute and covered more than half a mile.

Even after the Wright Brothers’ flights, experts continued to state that it is impossible for a heavier-than-air vehicle to achieve sustained flight. But further breakthroughs in aviation design and engineering led rapidly to regular air travel and then to rockets and space flight.

Similarly, once the barrier to manipulating genes involved in aging has been broken, there will be a rapid increase in human life expectancy. The “universal” disease of “aging” may soon become a relic of the past, just as infectious diseases such as cholera, diphtheria, polio and smallpox have been largely wiped out.

Will we ever be immortal?

The authors of the Science article predict that “modest annual increments in life expectancy will never lead to immortality.”

We at Life Extension appreciate that mainstream scientists are addressing the immortality issue. History has often shown that, before a major breakthrough occurs, experts go out of their way to deny that it will ever happen. One major breakthrough in genetic engineering could lead to control of the aging process. This could then open up a cascade of new approaches to keeping human beings in a youthful state over the long-term.

Right now, relatively little money is being spent on research to extend the healthy human life span. We believe, however, that even a modest advance in slowing or reversing aging will lead to an enormous outpouring of research funds to further control aging which, in turn, will lead to further advances in extending life span.

Scientists are identifying the genes that control aging. The best program to identify these genes is being conducted at the University of California at Riverside under the direction of Stephen R. Spindler, Ph.D. The Life Extension Foundation is funding this project.³ The program involves the use of “gene chips” to compare the effects of drugs, nutrients and other therapies on the action of thousands of genes at a time in normal aging and in a proven model of retarded aging (caloric restriction).⁴ This revolutionary technology is accelerating the pace of discovery, which will lead to validated anti-aging therapies.

Current evidence suggests that there are specific genes involved in aging. Some of these genes may become active (turn on) at some point in the human life span, thus programming cells to malfunction and die. Other genes responsible for maintaining youth may become inactive (turn off), thus preventing cells from performing metabolic functions necessary to sustain vitality and survival.^5-8 There is also evidence that some genes necessary for youthful function may become lethal later in life.⁹

For the first time in history, scientists have access to data that can provide clues about which anti-aging genes to stimulate and which pro-aging genes to suppress. The manipulation of genes is expected to lead to the greatest medical breakthroughs of all time, eclipsing all previous discoveries related to human longevity.

Genetic engineering is just one technology that could produce a healthy human life span of thousands of years, with no end in sight. Stem cell technologies also promise to lead to therapies to maintain youth and extend the healthy life span indefinitely.

There are historical analogies that provide a basis for projecting that human populations may be on the verge of dramatic increases in life expectancy. It took mankind hundreds of years to figure out how to build a heavier-than-air vehicle that could achieve sustained flight. Once the basic concepts were known, however, aviation technology advanced quickly and dramatically.

When reviewing the history of medicine, it is apparent that once a fundamental discovery has been made, such as the role that bacteria plays in many infectious diseases, it doesn’t take long to turn that discovery into practical benefits for humans. We know that genes are a major cause of aging and many age-related diseases. Once we learn how to manipulate the appropriate genes, it shouldn’t be long before we develop therapies to slow and reverse human aging.

Genetic medicine could increase life span rapidly. The authors of the Science article state that, based upon historical increases in longevity, centenarians will become commonplace while many of us are still alive. One major anti-aging breakthrough, on the other hand, could lead to an explosion of new discoveries that could remove the limits on how long we can live in good health.

Extending your life expectancy

Mainstream scientists are optimistic that the average human life span will continue to increase. In the life extension research community, advances in genetic engineering and other technologies could lead to a significant prolongation of maximum life span. To personally take advantage of these upcoming breakthroughs, we have to maintain our health.

One of the most frightening diseases of aging is senility. Be it dementia of the Alzheimer’s type or cerebrovascular dementias, diseases of the brain are now occurring at epidemic levels as people age. The good news is that many studies now show that the risk of vascular dementia and Alzheimer’s disease can be reduced.^10-15

In this issue, we discuss new European research showing that a form of choline used by many Life Extension members may be more effective in preventing brain diseases than previously thought. Protecting cognitive function against age-related disease should be a paramount objective for those seeking to enjoy ever-increasing life expectancy.

For longer life,

William Faloon

Note: The authors of the Science article are J. Oeppen and J. W. Vaupel. J. Oeppen is with the Cambridge Group for the History of Population and Social Structure, Cambridge University, Cambridge, CB2 3EN, UK. J. W. Vaupel is at the Max Planck Institute for Demographic Research, Doberaner Strasse 114, D-18057 Rostock, Germany.

References

1. Jim Oeppen and James W. Vaupel. “Broken Limits to Life Expectancy.” Science VOL 296; 10 May 2002.
2. Freireich EJ. Can we conquer cancer in the twenty-first century? Cancer Chemother Pharmacol 2001 Aug;48 Suppl 1:S4-10.
3. Spindler SR. “Reversing Aging Rapidly with Short-Term Calorie Restriction.” Life Extension magazine December 2001 pgs 40-54.
4. Spindler SR. Calorie restriction enhances the expression of key metabolic enzymes associated with protein renewal during aging. Ann N Y Acad Sci 2001 Apr;928:296-304.
5. Perls T. Aging and susceptibility to diseases associated with aging are likely to be influenced by thousands of genes. Genetic and environmental influences on exceptional longevity and the AGE nomogram. Ann. N.Y. Acad. Sci. 959: 1-13 (2002).
6. Wolkow CA. Life span: getting the signal from the nervous system. Trends Neurosci 25, 212-6 (2002).
7. Lee CK, Klopp RG, Weindruch R & Prolla TA. Gene expression profile of aging and its retardation by caloric restriction. Science 285, 1390-1393 (1999).
8. Cao SX, Dhahbi JM, Spindler SR and Mote PL. Genomic profiling of short- and long-term caloric restriction effects in the liver of aging mice. Proc. Natl. Acad. Sci., USA 98, 10630-10635 (2001).
9. Williams GC. Pleiotropy, natural selection, and the evolution of senescence. Evolution 11, 398-411 (1957).
10. Kivipelto M, Laakso MP, Tuomilehto J, et al. Hypertension and hypercholesterolaemia as risk factors for Alzheimer’s disease: potential for pharmacological intervention. CNS Drugs 2002;16(7):435-44.
11. Postiglione A, Milan G, Ruocco A, et al. Plasma folate, vitamin B(12), and total homocysteine and homozygosity for the C677T mutation of the 5,10-methylene tetrahydrofolate reductase gene in patients with Alzheimer’s dementia. A case-control study. Gerontology 2001 Nov-Dec;47(6):324-9.
12. Scott HD, Laake K. Statins for the prevention of Alzheimer’s disease. Cochrane Database Syst Rev 2001;(4):CD003160.
13. Scott HD, Laake K. Statins for the reduction of risk of Alzheimer’s disease. Cochrane Database Syst Rev 2001;(3):CD003160.
14. White AR, Huang X, Jobling MF, et al. Homocysteine potentiates copper- and amyloid beta peptide-mediated toxicity in primary neuronal cultures: possible risk factors in the Alzheimer’s-type neurodegenerative pathways. J Neurochem 2001 Mar;76(5):1509-20.
15. Mattson MP. Existing data suggest that Alzheimer’s disease is preventable. Ann N Y Acad Sci 2000;924:153-9.