Beginning to Taste the Fountain of Youth

The biggest causes of death have always been part of the aging process. If you live long enough, you will develop a cancer. The longer you live, the more likely you are to develop heart disease, stroke, osteoporosis and Alzheimer’s, to list only a few.

That may seem like the normal inevitable fact of human existence, but it is not normal or inevitable to scientists and researchers. Aging is caused by genetic triggers in the human body, so scientists have long speculated that figuring out which genes cause aging could lead to much longer lives, if not an aging process that approaches immortality.

The problem has been that it looks like many genes are involved in aging, and the complex interplay between them and other environmental factors is so difficult to untangle that we may be far from anything approaching a fountain of youth.

Until recently, that is. On April 30, researchers at the Salk Institute for Biological Studies and the Chinese Academy of Sciences announced they found a shortcut in research that reveals the key driver in the aging process. The shortcut was to study a strange disease called Werner syndrome, which rapidly and prematurely ages the body.

Fewer than 1,500 people have been diagnosed with the disease, which usually begins to advance after puberty. People with Werner syndrome die in their 40s and 50s, and almost always of cancer and heart disease. The disease is genetic and occurs more often in Japan than anywhere else — about 20 times more frequently there than in the United States.

The Salk scientists studied the genetic mutations in Werner syndrome cases and focused on heterochromatin, bundles of DNA that deteriorate in these patients.

Juan Carlos Izpisua Belmonte, a senior author of the study, said in a press release that “The gene mutation that causes Werner syndrome results in the disorganization of heterochromatin, and this disruption of normal DNA packaging is a key driver of aging. This has implications beyond Werner syndrome, as it identifies a central mechanism of aging — heterochromatin disorganization — which has been shown to be reversible.”

Using human stem cells and state-of-the-art gene editing methods, researchers at Salk created a line of cells that mimicked the genetic mutation found in Werner patients. As if they were a more modern equivalent of lab rats, the cells allowed scientists to study the disease and discover changes as the stem cell line began to age prematurely. Researchers were able to establish that a mutated WRN gene’s protein will lead to destabilization of heterochromatin.

Izpisua Belmonte says this suggests that “accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging. This begs the question of whether we can reverse these alterations — like remodeling an old house or car — to prevent, or even reverse, age-related declines and diseases.” He added that further studies could show how heterochromatin is involved with shortening the ends of human chromosomes, called telomeres. Shortened telomeres are known to be part of the aging process. Each time a cell replicates itself, the telomeres are shortened.

Last month, researchers at Harvard and Northwestern Universities announced results of a long-term study of telomeres that may make it possible to predict human cancers with a simple test that measures telomere shortening, which cancer cells can somehow survive indefinitely.

The Salk study may be the clearest, most direct leap in understanding aging in the history of medical research and opens extraordinary possibilities for slowing down or even halting the aging process in humans.

To your health and wealth,

Stephen L. Petranek
for The Daily Reckoning

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