Studies Of Caloric Restriction, Resveratrol And Sirt1 Demonstrate A ?Metabotype’ Continuum From Cellular Rejuvenation To Aging To Cancer
|
To a rather remarkable degree, the aging cell and cancer cell metabotype have recently been reverted to normal with dramatic increases in life extension and incidence reduction in cancer, from groups of apparently unrelated experiments that only share their fortunate results by viewing them from a shared metabolic perspective. By life extension, it is meant to mean ‘age beyond its normal well nourished maximum’ This not to be confused with achieving the natural maximum by delaying premature death, but instead, by going beyond its natural healthy maximum by a considerable extent. Also, it is far too early to talk of cancer ‘cure’, but the early data point to a significant cancer renormalization or kill. But first, there is a need for a bit of a preamble. Until recently, the only technique known to cause genuine life extension is to initiate a condition known as caloric restriction. Caloric restriction and its life extension affects hails back seven decades, but its many manifold mechanisms of action are just now coming to light, due to new technologies grown out of the genomics revolution. Studies had shown that caloric restriction rejuvenated cells, by virtually every measure, and in virtually every tissue and organ of the body, from neuroregeneration, to delayed and reversed muscular wasting, visual impairment, skin wrinkling etc. These rejuvenation-like phenomena occurred in organisms, as lowly as yeast, upward through the multicellular organism evolutionary chain ranging from roundworms to mice. Just this past year, a 25 year caloric restriction study on rhesus monkeys extended these findings to the primate order, of which humans are a member. Preliminary results on humans are yielding parallel results. By hindsight, such findings make evolutionary sense, because feast and famine cycles go back to the dawn of time. There is a distinct survival advantage in being able to sweat out the lean times until nutrient availability of fat times allows energy availability to support cell division in single cell organisms or procreation in multicellular organisms. Hibernation or estivation may work for periodic circumstances such as winter snow or summer drought, as it does for northern bears or desert toads, but variable and unforeseen conditions have led to a much more ancient and flexible metabolic solution, as observed by caloric restriction. It seems apparent that untold millions of generations have been honed by caloric restriction to utilize it as a generic life extender as a means of avoiding extinction. In just the last couple years, the genetic mechanisms behind the caloric restriction phenomenon have become much more elucidated. First, caloric restriction turns on a gene called SIRT1 that activates a suite of, at least, 745 genes that is normally turned on in juveniles, but is turned off in adults. At the very least, SIRT1 is turning on a hugely complex gene system in adult cells that is normally only operational in juveniles, tempting the notion of ‘rejuvenation’, especially since life extension is the result of their activation. It appears obvious that this must be an ancient system for it to be composed of such a high number of orchestrated components, and in such a pan specific manifestation, with a particular bent toward extending organism life length by mimicking, or attempting to mimic the juvenile period and imposing it on adult cells. The impact seems to be most pronounced on metabolic efficiency.
Related posts:
|
