So much research points to the link between glucose signaling and aging and glucose levels and disease and yet as a country the USA ignores this. The US Government continues to promote a starchy carbohydrate-based diet to satisfy their own financial needs. And more ignorant Americans continue to eat this way predisposing them to Insulin Resistance and the ensuing age-accelerating process. One has to wonder if there isn't another plan at work? Perhaps a thinning of the heard? Why else would a Government promote dietary protocols that ensure the manifestation of chronic disease and aging? Just imagine a country devoid of major chronic disease. One would think this would be the goal. And the cat is out of the bag. We know that all of today's disease is a result of our dietary choices. So why wouldn't a Government act on this and eliminate the culprits? Unless the profits and eventual early demise of SOME people due to bad choices are necessary? - Carl

by Faye Flam

Philadelphia Inquirer

 

Though some people stay energetic and wrinkle-free longer than others, we're all programmed to break down, deteriorate, and eventually, to die.

In our cells are tiny aging clocks made from pieces of DNA called telomeres. Rather than holding genes, the telomeres cap the ends of our DNA strands, preventing them from fatal fraying. Over the years, the telomeres shorten, like candle wicks, until they reach their ends.

Now, scientists are learning how Type 2 diabetes - the most common kind - is linked to the shortening of those telomeres.

On Tuesday at the University of Pennsylvania, medical researcher Mary Armanios spoke about her latest results in telomeres and diabetes - showing how the insulin-producing cells in the pancreas shut down when their telomeres erode to the end.

That understanding, she said, could lead to new approaches to treat or prevent the disease, which is growing more prevalent.

She presented her findings this month in the journal Public Library of Science One.

Armanios, who works at Johns Hopkins Kimmel Cancer Center, said she became interested in studying telomeres after meeting a college-age man with gray hair, lung problems, and bone-marrow failure, all caused by a genetic disease called dyskeratosis congenita. People with the disease have very short telomeres, so their aging clocks run out of time unusually fast.

The telomeres are often compared to caps on shoelaces because, when intact, they protect the parts of the genetic code at the ends of chromosomes.

Every time a cell divides, the telomeres get a little shorter. Once they're gone, a mechanism kicks in that causes the cells to die.

This might seem like something medical science would be scrambling to stop, but the cell death protects us from cancer by eventually stopping malignant cells from growing. So we can't just turn the whole thing off.

In her work, Armanios uses genetically engineered mice with unusually short telomeres, making these already short-lived creatures even quicker to gray and grow old. Besides all their other problems, these mice quickly develop high blood sugar, the hallmark of diabetes.

What seemed to be happening, she said, was that the animals' short telomeres were causing the premature shutdown of insulin-secreting cells. These cells aren't dead but put up a closed-for-business sign and stop doing anything. Armanios said perhaps their research would point to a way to wake them up.

The telomere connection, she said, may explain why scientists haven't found many diabetes-related genes despite strong evidence that the disease runs in families. Though telomeres aren't considered genes, their length is partly inherited.

Telomeres may also explain why those with genetic risk factors don't have the disease when they're, say, 35, but they do when they're 55.

The Johns Hopkins work adds to a growing body of evidence connecting telomeres to diabetes, said Emmanuel Skordalakes, a Wistar Institute researcher who heard Armanios' talk on Tuesday.

"We've sort of implicated telomeres in both Type 1 and Type 2 diabetes," said Skordalakes, who studies the role of telomeres in cancer. From his perspective, the inexorable shortening of our DNA caps is not just a road to decrepitude but also a crucial protective mechanism that keeps cells from going malignant.

In tumors, he said, cells can turn back the clock on their telomeres, building them up. They do this by reactivating a mechanism that normally works only during development, when cells have to divide many times without losing their telomeres.

The rejuvenation process involves an enzyme called telomerase - a substance whose discovery garnered the Nobel Prize in 2009. It might seem like a good youth restorative, but if anyone tries to sell you a bottle, don't buy it.

It's expensive to make telomerase, said Skordalakes, and it might give you cancer.

Most normal adult cells aren't supposed to use telomerase, yet it's active in 98 percent of all cancer cells, he said. They hijack its telomere-saving powers to grow out of control. That's why he's looking for ways to block telomerase as a way to cure cancer.

While you can't buy youth in a bottle yet, there are ways people can keep their telomeres from fraying before their time, he said.

Several years ago, for example, researchers linked exercise to longer telomeres, and now there's evidence that healthy diet also keeps our DNA healthy and our telomeres long.

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