www.scientificamerican.com /article/what-a-body-built-to-last-100-years-would-look-like/

What a Body Built to Last 100 Years Would Look Like

S. Jay Olshansky,Bruce A. Carnes,Robert N. Butler 12-15 minutes

We would look a lot different if evolution had designed the human body to work well for a century or more

In Brief

  • The process of human evolution has resulted in bodies that are optimized for successful reproduction and child-rearing but are not necessarily designed for healthy, long lives.
  • Medical problems associated with aging are often described as diseases that are our own fault, but it is unfair to blame people for inheriting bodies that were not designed for extended use. We can shorten our lives, but not prolong them indefinitely.
  • If humans were built primarily for longevity and perpetual health, our anatomies and even our bodies' molecular processes would look very different than they currently do.
  • The single-minded pursuit of life extension could actually be harmful to our species' long-term survival.

Bulging disks, fragile bones, fractured hips, torn ligaments, varicose veins, cataracts, hearing loss, hernias and hemorrhoids: the list of bodily malfunctions that plague us as we age is long and all too familiar. Why do we fall apart just as we reach what should be the prime of life?

The living machines we call our bodies deteriorate because they were not designed for extended operation and because we now push them to function long past their warranty period. The human body is artistically beautiful and worthy of all the wonder and amazement it evokes. But from an engineer's perspective, it is a complex network of bones, muscles, tendons, valves and joints that are directly analogous to the fallible pulleys, pumps, levers and hinges in machines. As we plunge further into our postreproductive years, our joints and other anatomical features that serve us well or cause no problems at younger ages reveal their imperfections. They wear out or otherwise contribute to the health problems that become common in the later years.

In evolutionary terms, we harbor flaws because natural selection, the force that molds our genetically controlled traits, does not aim for perfection or endless good health. If a body plan allows individuals to survive long enough to reproduce (and, in humans and various other organisms, to raise their young), then that plan will be selected. That is, individuals robust enough to reproduce will pass their genes—and therefore their body design—to the next generation. Designs that seriously hamper survival in youth will be weeded out (selected against) because most affected individuals will die before having a chance to produce offspring. More important, anatomical and physiological quirks that become disabling only after someone has reproduced will spread. For example, if a body plan leads to total collapse at age 50 but does not interfere with earlier reproduction, the arrangement will get passed along despite the harmful consequences late in life.

Had we been crafted for extended operation, we would have fewer flaws capable of making us miserable in our later days. Evolution does not work that way, however. Instead it cobbles together new features by tinkering with existing ones in a way that would have made Rube Goldberg proud.

The upright posture of humans is a case in point. It was adapted from a body plan that had mammals walking on all fours. This tinkering undoubtedly aided our early hominid ancestors: standing on our own two feet is thought to have promoted everything from food gathering and tool use to enhanced intelligence. Our backbone has since adapted somewhat to the awkward change: the lower vertebrae have grown bigger to cope with the increased vertical pressure, and our spine has curved a bit to keep us from toppling over. Yet these fixes do not ward off an array of problems that arise from our bipedal stance.

What If?
The three of us have pondered what the human body would look like had it been constructed specifically for a healthy long life. The anatomical revisions depicted on these pages are fanciful and incomplete. Nevertheless, we present them to draw attention to a serious point. Aging is frequently described as a disease that can be reversed or eliminated. Indeed, many purveyors of youth-in-a-bottle would have us believe that the medical problems associated with aging are our own fault, arising primarily from our decadent lifestyles. Certainly any fool can shorten his or her life. But it is grossly unfair to blame people for the health consequences of inheriting a body that lacks perfect maintenance and repair systems and was not built for extended use or perpetual health. Our bodies would still wear out over time even if some mythical, ideal lifestyle could be identified and adopted.

This reality means that aging and many of its accompanying disorders are neither unnatural nor avoidable. No simple interventions can make up for the countless imperfections that permeate our anatomy and are revealed by the passage of time. We are confident, however, that researchers will be able to ease some of the maladies of aging. Investigators are rapidly identifying (and discerning the function of) our myriad genes, developing pharmaceuticals to control them, and learning how to harness and enhance the extraordinary repair capabilities that already exist inside our bodies. These profound advances will eventually help compensate for many of the design flaws contained within us all.

Health and Longevity
Our research interest in redesigning the Homo sapiens body is a reaction to the health and mortality consequences of growing old. We focus on anatomical “oddities” and “design flaws” not only because they would be familiar to most readers, but because they represent a small sample of lethal and disabling conditions that threaten the length and quality of life. It is important to recognize that we live in a world in which human ingenuity has made it possible for an unprecedented number of people to grow old. Our redesign goal is thus to draw attention to the health consequences associated with the aging of individuals and populations.

Even the term “flaw” requires clarification. Living things, and everything they make, eventually fail. The cause of failure is a flaw only when the failure is premature. A race car that fails beyond the end of the race has no engineering flaws. In the same way, bodies that fail in the postreproductive span of life may contain numerous design oddities, but they have no design flaws as far as evolution goes.

There are countless other aspects of human biology that would merit modification if health and longevity were nature's primary objective. For example, gerontologists theorize that aging is caused, in part, by a combination of the molecular damage that inevitably arises from operating the machinery of life within cells and the imperfect mechanisms for molecular surveillance, maintenance and repair that permit damage to accumulate over time. If this view of the aging process is correct, then modifying these molecular processes to lessen the severity or accumulation of damage, or to enhance the maintenance and repair processes, should have a beneficial impact on health and longevity. These wondrous modifications, however, would have little effect unless the common sense that is needed to avoid destructive lifestyles becomes more widespread among people.

Living things are exceedingly complex, and experience teaches us that undesirable consequences invariably arise whenever humans have taken over the reins of evolution to modify organisms (microbes, plants and animals) to suit their purposes. The most worrisome trade-off for genetic manipulation directed toward living longer would be an extension of frailty and disability rather than an extension of youthful health and vitality.

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Though cobbled together by the blind eye of evolution, humans have proved to be a remarkably successful species. We have outcompeted almost every organism that we have encountered, with the notable exception of microbes. We have blanketed the earth and even walked on the moon. We have even figured out how to escape premature death and survive to old age.

At this point in history, we need to exploit our expanding knowledge of evolution to enhance the quality of our lives as we grow older because the single-minded pursuit of life extension without considering health extension could be disastrous.

Our fanciful designs of anatomically “fixed” humans are not intended as a realistic exercise in biomechanical engineering. Given what is known today about human aging, if the task of designing a healthy, long-lived human from scratch were given to a team comprising the father of evolution, Charles Darwin, the great painter Michelangelo, and the master engineer and scientist Leonardo da Vinci, they most certainly would have fashioned a living machine that differs from the one we now occupy. Indeed, anyone who tries his hand at redesign would probably construct a human body that would look unlike the ones we have created on these pages. Yet we invoke this approach as an instructive way of communicating the important message from evolutionary theory that, to a significant degree, the potential length of our lives and, to a lesser degree, the duration of health and vitality are genetic legacies from our ancient ancestors, who needed to mature quickly to produce children before they were killed by the hostile forces of nature.

This article was originally published with the title "If Humans Were Built to Last" in SA Special Editions 24, 1s, 106-111 (March 2015)

doi:10.1038/scientificamericansecrets0315-106

MORE TO EXPLORE

Aging: A Natural History. Robert E. Ricklefs and Caleb E. Finch. Scientific American Library, W. H. Freeman, 1995.

Cheating Time: Science, Sex, and Aging. Roger Gosden. W. H. Freeman, 1996.

A Means to an End: The Biological Basis of Aging and Death. William R. Clark. Oxford University Press, 1999.

Aging: The Paradox of Life. Robin Holliday. Springer, 2007.

How Long Must Humans Live? Bruce A. Carnes and T. M. Witten in Journals of Gerontology: Biological Sciences, Vol. 69, No. 8, pages 965–970; August 2014.

ABOUT THE AUTHOR(S)

S. Jay Olshansky, Bruce A. Carnes and the late Robert N. Butler shared an enduring interest in the processes that underlie human aging. Olshansky is professor in the School of Public Health at the University of Illinois at Chicago. Carnes is professor in the Donald W. Reynolds Department of Geriatric Medicine at the University of Oklahoma Health Sciences Center. Olshansky and Carnes collaborate on studies—funded by the MacArthur Foundation, the National Institute on Aging and NASA—of the biodemography of aging (examining the biological reasons for age-related patterns of disease and death in populations). They are co-authors of The Quest for Immortality: Science at the Frontiers of Aging (W. W. Norton, 2001). Butler, who died in 2010, was president of the International Longevity Center in New York City and founding director of the National Institute on Aging.
S. Jay Olshansky, Bruce A. Carnes and the late Robert N. Butler shared an enduring interest in the processes that underlie human aging. Olshansky is professor in the School of Public Health at the University of Illinois at Chicago. Carnes is professor in the Donald W. Reynolds Department of Geriatric Medicine at the University of Oklahoma Health Sciences Center. Olshansky and Carnes collaborate on studies—funded by the MacArthur Foundation, the National Institute on Aging and NASA—of the biodemography of aging (examining the biological reasons for age-related patterns of disease and death in populations). They are co-authors of The Quest for Immortality: Science at the Frontiers of Aging (W. W. Norton, 2001). Butler, who died in 2010, was president of the International Longevity Center in New York City and founding director of the National Institute on Aging.
S. Jay Olshansky, Bruce A. Carnes and the late Robert N. Butler shared an enduring interest in the processes that underlie human aging. Olshansky is professor in the School of Public Health at the University of Illinois at Chicago. Carnes is professor in the Donald W. Reynolds Department of Geriatric Medicine at the University of Oklahoma Health Sciences Center. Olshansky and Carnes collaborate on studies—funded by the MacArthur Foundation, the National Institute on Aging and NASA—of the biodemography of aging (examining the biological reasons for age-related patterns of disease and death in populations). They are co-authors of The Quest for Immortality: Science at the Frontiers of Aging (W. W. Norton, 2001). Butler, who died in 2010, was president of the International Longevity Center in New York City and founding director of the National Institute on Aging.