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Prolongevity Update


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Shorter telomeres mean shorter life
    A University-of-Utah study (Shorter telomeres mean shorter life - New Scientist) of 143 seniors 60 or over indicated that those with the shortest telomeres were eight times as likely to die of infectious diseases and three times as likely to die of heart attacks as those with the longest telomeres. The article says,

    "In healthy people, telomeres do not shrink significantly until old age because the enzyme telomerase ensures regeneration. But eventually telomeres get so short that the DNA strands either stop replicating or, worse still, start fusing together, often encouraging tumours to grow.
    "White blood cells rely on their ability to replicate quickly to mount attacks on infections. Retarded replication caused by shorter telomeres might explain why those patients were much more likely to die of an infectious disease, says Cawthon.
    "He admits that it is not clear whether short telomeres actually cause age-related diseases and death or whether they are just a symptom of some other process responsible for aging. Either way, there are other forces at work - earth worms and fruit flies get old long before their telomeres shrink significantly.
    "Inducing telomere growth by somehow injecting telomerase might seem like a potential way to extend life. But this would risk causing cells to replicate uncontrollably, leading to cancer."

    Another, related article (Chromosome shrinkage may promote age-related disease, study suggests  - Nando Times) says,
    "Scientists found that people older than 60 who showed shorter-than-average chromosome tips were nearly twice as likely than others to die over the next 15 years or so, especially from heart disease and pneumonia.
    "Experts called the finding intriguing but cautioned that the study was far too small to let anybody draw conclusions.
    "In 1998, researchers made headlines by showing they could block that process and keep cells young and dividing indefinitely by giving them an enzyme called telomerase. While that led to public speculation about making people live dramatically longer, scientists are focusing on prospects for treating specific diseases by rejuvenating certain tissues.
    "The new work impressively bolsters the case that telomeres might play a role in human aging, said one expert, Dr. Woodring Wright of the University of Texas Southwestern Medical Center at Dallas. But like other scientists, he said the study must be repeated with many more participants to get a firmer result.
    "In all, 101 donors died. People with shorter telomeres showed an 86 percent higher death rate. They ran a threefold higher risk of dying from heart disease and an eight-fold higher risk of death from infectious disease, almost entirely pneumonia.
    "Their rates of death from stroke and cancer were higher, but by too little to be considered meaningful."

    The conclusion I draw from this is that greater telomere lengths don't raise one's likelihood of dying of cancer. It seems to me that this is in opposition to the theory of antagonistic pleiotropy.  The antagonistic pleiotropy model implies that nature has optimized telomere lengths in a way that maximizes life span. This would lead us to expect that people with longer telomeres wouldn't live any longer, or as long as, people with shorter telomere, because people with longer telomeres would be more apt to present with cancer than would people with shorter telomeres. If nature has optimized telomere length to give maximum life span, then when we moved away from that optimum in either direction, average life span would be shortened.
    One possible flaw in my argument could be that people with longer telomeres had a greater likelihood of dying of cancer when they were younger than did people with shorter telomeres. Since this study examines only individuals who are already at least 60, we aren't told what earlier filtering may have occurred with each of the two groups in their earlier years.
    It's interesting that people with longer telomeres seemed to live longer because they were much more resistant to pneumonia and heart disease, with neither protective nor deleterious effects evinced with respect to stroke and cancer. 

Why don't we get cancer of the heart or of the arteries?
    I've mentioned this before, but how does the body protect so well against cardiovascular cancers? Fatty plaques have been likened to tumors, but unrestrained proliferation and metastasis doesn't occur. How do organisms prevent it from ever happening? What are the protective mechanisms? (This might be a lead to more effective cancer prevention.)

The paragraph,
    "Inducing telomere growth by somehow injecting telomerase might seem like a potential way to extend life. But this would risk causing cells to replicate uncontrollably, leading to cancer."
seems to me to be the opposite conclusion