Fans of the television series Star Trek: The Next Generation may remember an episode entitled "Up the Long the Ladder," in which the star ship Enterprise receives a distress signal from a planet called Mariposa. On this colony all the inhabitants are clones of the survivors of the crashed ship that brought its first settlers, and recent clones had failed to develop to maturity due to a phenomenon called "replicative fading." The clones surreptitiously collected DNA from Commander Riker and other members of the crew, but the officers of the Enterprise finally insisted that the colony replenish its population the old fashioned way, by sex.
It turns out that this episode of Star Trek reflected science that actually had been worked out about 30 years earlier by a researcher named Leonard Hayflick.
Dr. Hayflick's Chicken Cells
In the early 1960's, Dr. Leonard Hayflick was a young professor of anatomy at the University of Pennsylvania. (He is as of the writing of this article still alive, and an emeritus professor at the University of California at San Francisco.) In the early 1960's, it was an accepted scientific principle that organisms, for example, people and animals and plants, die, but cells live forever.
A Nobel Laureate named Alexis Carrell had proved the theory of cellular immortality, or at least so most scientists thought.
Carrell continued to feed chicken cells to his chicken cells and had live chicken cells in the flask for 20 years.
Hayflick, however, noticed that his own experimental culture of chicken cells in fact was not immortal. The cells could divide to continue themselves, but only 40 to 60 times, when they became "senescent," or old. Old chicken cells could live on for a while, but they could not undergo the process of mitosis to produce new chicken cells. Hayflick found that cells actually aren't immortal, that they reach something called a replicative limit, and they die.
The principle also applied to human cells, Hayflick and collaborators determined in the late 1970's. And this finding had profound implications for the science of life extension.
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The Hayflick Limit
From time to time human cells renew themselves by a process called mitosis. The coils of DNA in the center of the cell straighten out so they can copy themselves. Then they make copies of themselves so one cell can become two. The older copy of the cell then can die and be disposed of by the immune system, while the new cell can take its place in the tissue. As long as this process happens on a regular basis, cells and tissues and organs are rejuvenated.
Somewhere between 40 and 60 replications, however, when a cell is between 80 and 120 years old, it simply cannot replicate itself any more. It does not immediately shut down, but it may become quiescent, just "there," rather than performing its vital role in tissue. When this happens, tissues and organs and people malfunction.
All Our Cells Don't Age At The Same Rate
The Hayflick limit tells us that we aren't ever going to find medical methods for becoming immortal. We are all going to die. But the mere fact that our DNA is not capable of being copied indefinitely really is not the problem. The problem is that all our cells do not age at the same rate, and some cells wear out before others.
For example, cells in the localized regions of arteries that are lesioned by calcified, cholesterol-laden plaques are typically filled with non-replicating, senescent (old), or dead cells. The artery wall on either side of them may be in good shape. The linings of the veins may not be affected at all. But that one region of just a few millimeters (usually), just a fraction of an inch, may be the "clog" that stops circulation and causes death--frequently without any warning that death was imminent.
Our cells can be damaged by:
- Pressure. High blood pressure is a killer, but it kills localized cells that accumulate into lesions that cause the problems we recognize as disease.
- Toxins. Not all cells all over the body are affected in the same way by toxins. Nerve tissue, because neurons are "stretched out" over large parts of the body, one part of the nerve cell up to a meter (several feet) from the protective organelles of the nerve cell that could rejuvenated, is especially vulnerable to certain toxins.
- Radiation. Whole-body radiation affects all of the tissues of the body at the same time. Therapeutic radiation, and certain kinds of accidental radiation, may cause certain cells to age rapidly and have no effects on others at all.
- Telomeres. Every strand of DNA has some "junk" DNA, which really is not junk at all, which protects the active DNA it its middle. These protective telomeres can grow shorter with age. When the telomere is too short, the cell won't "risk" replicating itself and getting the sequence of DNA out of order, so it will not become cancerous.
READ Living a Long Life: Genetics or a Way of Life?
For a large part of our lives, our immune systems simply come along and take out the senescent cells, leaving healthy, young cells to do their tasks in tissues. When something compromises the health of the immune system, however, or when they number of aging and dysfunctional cells in a tissue simply becomes too great, the tissue ceases to function. There may be a mass of calcified dead cells, as there is inside atherosclerotic plaques, or there may be a mass of protein the cells that make them simply could no longer regulate, as there is inside cataracts.
Either way, parts of our bodies age and cause us serious illness long before our entire bodies reach their aging limits. And if we really want to live as long as we can, Haylflick tells us, we do not need to try to make all our cells immortal, we need to avoid localized problems commonly lead to disease and death, especially heart disease and cancer.
Sources & Links
- Hayflick L. The illusion of cell immortality. Br J Cancer. 2000 Oct. 83(7):841-6.
- Sills ES, Takeuchi T, Rosenwaks Z, Palermo GD. Reprogramming somatic cell differentiation and the Hayflick Limit: contrasting two modern molecular bioengineering aims and their impact on the future of mankind. J Assist Reprod Genet. 2001 Aug. 18(8):468-70.
- Photos courtesy of SteadyHealth