If you’re alive in 20 years, you may be able to live forever. From the moment of birth, we begin the battle against the inevitable. Statistics say that a newborn child can expect to live an average of 76 years. But averages may not be what they use to be.

In 1796, life expectancy was 24 years. A hundred years later it doubled to 48. Right now, it’s 76. “Over half the baby boomers here in America are going to see their hundredth birthday and beyond in excellent health,” says Dr. Ronald Klatz of the American Academy of Anti-Aging. “We’re looking at life spans for the baby boomers and the generation after the baby boomers of 120 to 150 years of age.”

Today’s quest for the fountain of youth is taking scientists from inside the genetic structure of cells to analyzing the role of stress and diet on life spans. Would-be immortals flock to anti-aging clinics and shell out as much as $20,000 a year for treatments that include hormone therapy, DNA analysis, even anti-aging cosmetic surgery. These experimental therapies offer no guarantees — just the promise of prolonging life. “Anti-aging medicine is not about stretching out the last years of life,” says Dr. Klatz. “It’s about stretching out the middle years of life…and actually compressing those last years few years of life so that diseases of aging happen very, very late in the life cycle, just before death, or don’t happen at all.”

The cause of human aging is now being understood.

The cause of what we call “aging” is now finally being understood. This new understanding may soon move anti-aging cosmetics and surgery to the realm of snake oil and Siberian yogurt as life-extension fads. Just when you thought that holographic TV and outer space travel were the future benefits of modern technology, immortality has silently been revealing itself to scientists like Doctor John Langmore of the University of Michigan’s Department of Biology. Dr. Langmore and his group have been looking inside human cells, at the very essence of human life: the DNA molecule. Specifically, Dr. Langmore is looking at the tips of the DNA molecule – a previously overlooked part of the double-helix molecule – that contain a kind of chain of repeating pairs of enzymes.

Telomeres – programmed to die?

Called telomeres, these molecular chains have often been compared to the blank leaders on film and recording tape. Indeed, telomeres seem to perform a similar function in aligning the DNA molecule during the replication process. Protecting the vital DNA molecule from being copied out of synch, these telomeres provide a kind of buffer zone where asynchronous replication errors (that are inevitable) will not result in any of the vital DNA sequences being lost. As a cell gets older, it is under attack by oxides and other so-called free-radical chemicals in the body and environment.

We survive as living beings because our cells have the ability to duplicate themselves before being killed by these natural causes. Each time our cells duplicate themselves, a small portion of the DNA molecule is lost and not copied. The loss is usually to the telomere and so the effect is usually insignificant. Scientists recently noted that the length of these telomere chains were shorter as we grew older. Eventually, the telomeres become so shortened that the losses in replication begin to effect the vital DNA molecule sequence and prevent the cell from being able to duplicate itself. This is why we age.

Dr. Langmore uses physical, biochemical, and genetic techniques to study the structure and function of telomeres. His group has developed a cell-free system to reconstitute functional model telomeres using synthetic DNA, and are studying the mechanism by which telomeres normally stabilize chromosomes and how shortening of the telomeres could cause instability. The protein factors responsible for stabilizing the ends of chromosomes are being identified, cloned, and studied. Electron microscopy is used to directly visualize the structure of the model telomeres.

His group is also using new enzymatic assays to determine the structure of telomere DNA in normal and abnormal cells grown in vivo and in vitro, in order to address specific hypotheses about the role of telomeres in aging and cancer. Viewzone asked Dr. Langmore to give us his thoughts on the role of telomerase, a recently discovered enzyme that seems to repair and lengthen telomeres in human cells. His comments follow:

Telomeres are special, essential DNA sequences at both ends of each chromosome. Each time chromosomes replicate a small amount of the DNA at both ends is lost, by an uncertain mechanism. Because human telomeres shorten at a much faster rate than many lower organisms, we speculate that this telomere shortening probably has a beneficial effect for humans, namely mortality. The telomere hypothesis of aging postulates that as the telomeres naturally shorten during the lifetime of an individual, a signal or set of signals is given to the cells to cause the cells to cease growing (senesce).

At birth, human telomeres are about 10,000 base pairs long, but by 100 years of age this has been reduced to about 5,000 base pairs. Telomerase is actually an enzyme (a catalytic protein) that is able to arrest or reverse this shortening process. Normally, telomerase is only used to increase the length of telomeres during the formation of sperm and perhaps eggs, thus ensuring that our offspring inherit long “young” telomeres to propagate the species.

ViewZone: How is mortality in non-germ line cells a beneficial effect?

The telomere hypothesis of cancer is that the function of telomere shortening is to cause cells that have lost normal control over growth to senesce (i.e. stop growing) before being able to replicate enough times to become a tumor, thus decreasing the frequency of cancer. Immortal cells like cancer have an unfair advantage over normal human cells which are designed to senesce. But nature seems to have planned this human telomere shortening perhaps to prolong life by hindering the otherwise unchecked growth of non-immortal or benign tumors. Malignant, or immortal tumors can simply outlive the rest of the organism.

Malignant cancer cells are being studied because they appear to have altered the shortening of telomeres by turning “on” the telomerase. Thus it appears that some cancers and aging are both connected with the biology of telomeres. It is possible that increasing telomerase activity in normal cells might stop the biological clock of aging, yet the side effect of this intervention might be an increase in the rate of cancer. Further understanding and refinement in the telomere hypothesis might lead to a way to slow the aging process and prevent or arrest cancer.

However telomeres function, they are an integral part in the very complex process of cell growth, involving many other factors as well. Telomerase might be the Achilles Heal of aging and cancer, but as our understanding of factors that interact with telomerase, factors that are responsible for telomere shortening in the first place, and non-telomerase mechanisms for increasing the length of telomeres, we might find that one of these factors is more easily manipulated to slow aging or prevent cancer. Also there are additional factors that affect aging and cancer, which might prove in the end to be more important than telomeres and telomerase.

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ViewZone: Are telomeres unique to individual DNA? If so, does this preclude any universal treatment for aging?

Different individuals have telomeres with exactly the same DNA sequence but of different lengths. It is too early to say whether there is any relationship between telomere length in an individual and his or her life expectancy, or whether a treatment that would artificially lengthen telomeres would arrest (or reverse) the aging process. One problem is that even in one individual the telomeres of different chromosomes have very different lengths. Therefore an individual might have on average long telomeres; but, he might have one chromosome with a very short telomere that could affect cell growth.

ViewZone: In the work of Shay and Wright (see below), increased telomere length was positively associated with telomerase. How significant is this?

Shay, Wright and all their many collaborators stimulated telomerase activity in normal cells. This was expected to 1) Increase the length of telomeres and 2) Prolong the lifetime of the cells in tissue culture. The treatment did both, in perfect agreement with the telomere hypothesis of aging.

ViewZone: How much was cell lifetime prolonged due to this treatment that reactivated telomerase?

The increased proliferation of the cells was perhaps equivalent to hundreds of years of human life.

Dr. Langmore received his Ph.D. degree from the University of Chicago in 1975. He has held postdoctoral fellowships at the Laboratory of Molecular Biology in Cambridge and at the University of Basel.

A link to cancer:

In the March 15 issue of the European Molecular Biology Organization (EMBO) Journal, Dr. Jerry Shay and Dr. Woodring Wright, both professors of cell biology and neuroscience at UT Southwestern Medical Center at Dallas, report manipulating the length of telomeres to alter the life span of human cells. Shay and Wright are the first to report this important finding. They received an Allied-Signal Award for Research on Aging to explore this line of research last year.

“By lengthening the telomere, we were able to extend the life of the cell hybrids,” Wright explained. “This study is strong evidence that telomere length is the clock that counts cell divisions.” “The expression of the enzyme telomerase maintains stable telomere length. Telomerase is not detected in normal cells and telomeres shorten and then the cells stop dividing and enter a phase called cellular senescence. “

Shay and Wright have shown in earlier studies that telomeres maintain their length in almost all human cancer cell lines. This correlated with inappropriate expression of telomerase and as a consequence allowed the cell to become “immortal.” Cell immortality is a critical and perhaps rate-limiting step for almost all cancers to progress. Previous work by the UT Southwestern investigators showed that in a special group of advanced pediatric cancers the lack of telomerase activity correlated with critically shortened telomeres and cancer remission. Consequently, an idea gaining momentum is that the ability to measure and perhaps alter telomere length and/or telomerase activity may give physicians new diagnostic and treatment tools for managing the care of patients with cancer.

Shay and Wright tried to alter already-immortal cells by attempting to inhibit telomerase activity and cause telomeres to shorten. “Unexpectedly, we found the opposite result. Rather than inhibiting telomerase, our treatment caused the immortal cells to develop longer telomeres,” Shay explained. “Although we were surprised with the result, we now know there is a causal relationship between telomere length and the proliferate capacity of cells.

“Essentially, we combined the tumor cells containing experimentally elongated telomeres with normal cells and extended the life span of those cell hybrids compared to similar hybrids using cells without experimentally elongated telomeres.” Shay and Wright said the mechanism that causes telomeres to lengthen is still unclear. However, Shay said, “Our observations increase confidence in the hypothesis that immortal cells and reactivated telomerase are essential components of human tumors. Ultimately, we may be able to regulate tumor cells by inhibiting telomerase activity.”

The potential implications for research on human aging also are significant. “It is still speculative, but understanding the role of telomere shortening in cell aging may give us the information we need to increase the life span of an organism,” Wright said. (News Releases from UT Southwestern)

Other factors that make us “rust”…

DNA damages occur continuously in cells of living organisms. While most of these damages are repaired, some accumulate, as the DNA Polymerases and other repair mechanisms cannot correct defects as fast as they are apparently produced. In particular, there is evidence for DNA damage accumulation in non-dividing cells of mammals. These accumulated DNA damages probably interfere with RNA transcription.

It has been suggested that the decline in the ability of DNA to serve as a template for gene expression is the primary cause of aging. Most damage comes in the form of oxidative damage – the same “rusting” process that oxidizes iron – and hence is likely to be a prominent cause of aging. Arteriosclerosis and heart disease are the results of this type of damage to the cells lining our blood vessels.

Without the ability to duplicate itself before being “rusted” to death, a cell is sentenced to senesce, or death. As we gradually lose members of our cumulative body, we wear out and become a mortal. Understanding the biology of telomeres and telomerase hold the potential of unlimited duplication and unlimited life.

The twenty-first century may well be the era in which humans learn the secrets of eternal life, but it may also be a time to be reminded of the many dangers inherent in exploring these god-like abilities. From every tree in the garden did he grant them to eat, save but one. And that tree, in the center of the garden, was called the tree of life.

And the Snake said to Eve, “Eat of this fruit and you will become as God.”

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