The problem of aging and death has always haunted mankind. Men have vainly searched for the “Elixir of Life” and the “Fountain of Youth” to overcome this universal curse. Some deny that death is a curse, saying “death is just a part of life.” This foolishness follows directly from atheistic Darwinism. However, most people are unwilling to accept that idea. They know in their hearts that longer life is a blessing. Advertisers are well aware of this deep human longing, and so we receive promotions for all sorts of anti-aging products. Medical science has also focused much research on the aging process. Several breakthroughs have been made in recent years. One of these advances has surprising implications for the creation-evolution issue.
This breakthrough began fifty years ago, and involved human cells grown in artificial culture. Studies showed that normal cells from a newborn baby could divide and replicate themselves in a culture bottle about 50 times before wearing out and dying. Cells taken from middle-aged adults had lost much of this ability–they could replicate only about 20 times. Cells taken from old people could hardly replicate at all–only 5 or 10 times before dying. This implied that human aging goes on at the cellular level and limits a cell’s ability to replicate. Curiously, it has been found that a select population of human cells does not suffer from this cellular aging process. Could these cells–and some mechanism in them–be a clue to the elusive goal of immortality? Perhaps.
These “deathless” human cells are the original reproductive cells in the male testes and female ovaries. They have been passed on from generation to generation ever since the beginning. It happens like this: each new human being (since Adam and Eve) starts as a single cell, a fertilized egg. The fertilized egg comes from the union of two germ cells, with one coming from each of the parents. This new cell must divide and multiply itself to produce the 100 trillion cells of an adult human.
However, early in embryonic life, a few stem cells separate themselves into a developing gonad, and become the new germ cells that will eventually form the next generation. Meanwhile, the rest of the embryonic cells become the differentiated cells that form specialized organs and tissues. These body cells are called “somatic cells.” However, in the process of maturing, the somatic cells lose much of their replicative ability, and are condemned to wear out and die. It is as though a limit is imposed on their life span. But what of the original germ cells? Do they suffer replicative aging and die? Far from it! If these germ cells wore out and died after only 50 replications, the human race would have been extinct long ago. So, the obvious question is this: why do our somatic cells age and die while our germ cells live on through thousands of generations, seemingly immortal?
A molecular basis for this strange phenomenon was finally found (1, 2). A cellular enzyme complex called telomerase was discovered, which rejuvenates a cell’s chromosomes after cell division takes place. (Chromosomes carry genetic material in all cells except bacteria.) Without telomerase, chromosomes deteriorate successively after each division until cell replication can no longer occur. Single-celled yeasts, the simplest cells with chromosomes, have strong telomerase activity, and are practically immortal. “Higher” organisms also have telomerase–it has been found in all vertebrates tested so far. However, in multicellular creatures, it often does not express full activity. Telomerase is present and highly active in human germ cells, allowing the human race to continue, even though we die as individuals. Its genetic instructions are also present in all other (somatic) cells of the human body. However, in the somatic cells, it is only partially active. Why doesn’t it work fully in all human cells? If it did, we could conceivably live much longer lives. The very personal question for each of us is this: if Darwinian evolution is true, why should our cells have evolved what seems to be a potential fountain of youth, only to keep it mostly hidden away?
[Editors note:]In the second half of this article, Dr. Demick answers evolutionary objections and shows how the creation model of origins is far superior to the evolutionary model in explaining the origin and selective function of telomerase.
1. Bergman, Jerry, “The Life Clock and Paley’s Watch: The Telomeres”,
Creation Research Society Quarterly, v. 37 (2000), p. 176-182.
2. Krupp, Klapper, and Parwaresch, “Review: Cell Proliferation, Carcinogenesis, (This portion – Part 1 – of this article was also included in the July/August 2012 issue of Think & Believe newsletter.) Please call our office or email us at firstname.lastname@example.org for additional resources on these subjects.
and Diverse Mechanisms of Telomerase Regulation, Cellular and Molecular Life Sciences, v. 57 (2000), p. 465.
(This portion – Part 1 – of this article was also included in the July/August 2012 issue of Think & Believe newsletter.)
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