Hubris

Over the Wall: Preserving the Blasts

Dolors & Sense

by Sanford Rose

KISSIMMEE Florida—(Weekly Hubris)—1/23/12—The days of our years are threescore and ten and, if by reason of strength they be fourscore, yet is their strength labor and sorrow . . . .

So says the psalm and, for most people, it rings true. There have been impressive increases in life expectancy, but existence after age 70 is still an increasingly troubled one, plagued by pullulating sarcopenia.

That is progressive muscle wasting, which creates a positive (read negative) feedback loop: Sarcopenia lowers the metabolic rate, which leads to weight gain, which leads to glucose intolerance, which leads to Type II diabetes, which leads to greater inactivity and thus still larger losses in muscle mass.

At around age 70, we seem to hit a wall.

Whereas, once we ran, now we can barely trot.

Whereas, once we lifted, now we must be lifted, often out of chairs.

The villain is our errant myoblasts, muscle-forming cells, which appear to melt away with uncharacteristic suddenness in our septuagenarian decade.

Myoblastic declension is, in turn, powerfully influenced by a failure in the DNA of our mitochondria, an organelle that is responsible for manufacturing adenosine triphosphate, the body’s basic fuel.

And why this failure?

Probably, it is because of the accumulation of mutations.

With age, there are so many cellular copies that a certain and growing number must be bad ones.

That circumstance, incidentally, is also very likely the cause of many cancers: diet-related increases in fat result in chronic inflammation, which leads the cytokine system to heal by generating new cells, thus inevitably creating too many cell copies.

So, because the mitochondrial mutations won’t stop, the muscle wasting is inevitable, right?

Wrong.

Mature mitochondrial DNA may continue to mutate, but this mutant DNA exists side-by-side with another kind of DNA that is far more resistant to, even scorned by, mutation.

So-called wild or non-mutant DNA, which is resident in satellite cells (dormant myoblasts), can be persuaded to awaken, enter the cell cycle and fuse with existing myofibers in order to negate or dilute the impact of the deleterious mutations.

Ergo the myoblasts will revivify and power the body in a youthful fashion for many more years than expected.

And what is principally responsible for such a happy rise in the ratio of wild-type to mutant DNA?

Heavy resistance exercise, of course.

Coenzyme Q 10 and L-arginine can help.

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Sanford Rose, of New Jersey and Florida, served as Associate Editor of Fortune Magazine from 1968 till 1972; Vice President of Chase Manhattan Bank in 1972; Senior Editor of Fortune between 1972 and 1979; and Associate Editor, Financial Editor and Senior Columnist of American Banker newspaper between 1979 and 1991. From 1991 till 2001, Rose worked as a consultant in the banking industry and a professional ghost writer in the field of finance. He has also taught as an adjunct professor of banking at Columbia University and an adjunct instructor of economics at New York University. He states that he left gainful employment in 2001 to concentrate on gain-less investing. (A lifelong photo-phobe, Rose also claims that the head shot accompanying his Weekly Hubris columns is not his own, but belongs, instead, to a skilled woodworker residing in South Carolina.)