Changing how we see aging

Are We Meant to Live Longer?

Our bodies are designed to live longer.

The late Sherwin Nuland in his 1995 book How We Die described the process of extreme old-age death very eloquently: “Whether it is the anarchy of disordered biochemistry or the direct result of its opposite—a carefully orchestrated genetic ride to death—we die of old age because we have been worn and torn and programmed to cave in. The very old do not succumb to disease—they implode their way into eternity.”

Stem Cells in the human body
The most persuasive argument for the biology of death is the Hayflick Limit. In 1961, going against the thinking at the time, biologists Leonard Hayflick and Paul Moorhead noticed that their cell cultures were dying after replicating a certain number of times. At the time Alex Carrel—a Nobel Prize winner in surgery—held the thinking that cells are naturally immortal. We do bad things to them to kill them. Taking a direct leaf from the biblical story of Adam and Eve, we are held responsible for our own mortality.

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In contrast, Hayflick demonstrated that normal human fibroblasts cells divide about 70 times in 3 percent oxygen—which is the same as human internal conditions—before stopping replicating.  Refuting the idea that normal cells are immortal. The mechanism was not yet known at the time of this observation. But a Russian scientist Alexey Olovnikov hypothesized in 1971, and later confirmed in 1984 by Nobel Prize winners Elizabeth Blackburn and Carol Greider for the necessity of proteins called telomeres at the end of the DNA which get shorter with every division until they get too short to allow for more replication.

Although this is an eloquent theory, there is large variance in correlating telomere length with aging. The telomeres are not proportional to longevity. Nuno Gomez from the University of Texas Southwestern Medical Center and his colleagues, undertook the largest comparative study involving over 60 mammalian species, reported that telomere length inversely correlates with lifespan, while telomerase (an enzyme that promotes the growth of telomeres) correlates with size of the species.

Assuming human fibroblasts endure 70 divisions—as Hayflick says in his 1994 book How and Why We Age—there are more than enough cells for several lifetimes. Biologically it is feasible that individual cells in our body can maintain their level of division and renewal for at least 150 years. And yet no one has lived beyond 122 years.

In addition, it seems that telomeres do not provide us with a complete picture. The Italian biologist Giuseppina Tesco and her colleagues in 1998—refuting earlier studies—found that fibroblast taken from centenarians showed no difference in the number of replications compared to cells from younger donors.  It could be that within the body, cells can be replaced with new ones—rather than simply renewed.

Adult stem cells have been identified in many organs and tissues of older adults, including brain, bone marrow, peripheral blood, teeth, heart, gut, liver, blood vessels, skeletal muscle, skin, ovarian epithelium, and testis. They are thought to reside in a “stem cell niche" which is a specific area within each tissue. We all have these and yet some of us seem to use them up quickly, perhaps we started with fewer stem cells, or perhaps the environment that we live in degraded them faster.

Older people are more likely to have experienced more environmental stressors that damage stem cells, and utilized more of their stem cells. Once they run out or become disabled, stem cells cannot be replaced.

And then this might be the symphony that Sherwin Nuland talks about. Because dying cells secrete chemicals that disrupt other cells in their immediate environment even a small percentage dying cells, can have a much broader domino effect on neighboring cells. There is a tipping point before an implosion into eternity.

 © USA Copyrighted 2014 Mario D. Garrett

Mario Garrett, Ph.D., is a professor at the school of social work, San Diego State University.


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