Longevity depends on sirtuins and mitochondria

Longevity depends on sirtuins and mitochondria

As early as 1935, a group of researchers from Cornell University in New York showed that the longest-lived mice ate a diet with 30-40% fewer calories and lived 50% longer than their peers who ate in a standard way. Not only that, 50% of long-lived mice did not die of degenerative diseases but simply of natural causes.
The accuracy of this theory is reflected in the longest-lived populations on the planet such as Okinawa, a Japanese island, where many reach 100 years without degenerative diseases, or Vilcabamba in Ecuador, where one arrives in excellent health even at 110 years old or in Ogliastra where many people work the fields or raise animals up to the threshold of 100 years of life.
What is the biological mechanism that relates calorie restriction to longevity?
Caloric restriction induces a faster replacement of damaged mitochondria avoiding cell apoptosis and the appearance of senescent cells. Apoptosis is induced by the worsening of mitochondrial function which, in turn, generates an excess of free radicals, causing the cell to commit suicide. This fact forces the closest cell to replicate with shortening of the telomeres of the same, the appearance of a senescent phase and shortening of life.

The stimulation of the genesis of other mitochondria instead allows the replacement of the most damaged ones, obtaining the improvement of cellular respiration and the reduction of free radicals. Virtually, if we could always produce new mitochondria, our cells would never die, there would be no decrease in telomeres and senescence would go away.
The activation mechanism of mitochondria repair occurs through molecules called “sirtuins”.
Sirtuins are proteins that increase Pgc1-alpha, a gene capable of stimulating the growth of new mitochondria.
Many researches show that the cell, when it has a drop in energy production, activates the sirtuins as if it sensed the need to produce more energy.
Imagine that a cell has 100 mitochondria and each of them produces 34 ATP per minute. This means that the consumption of the cell stands at 3,400 ATP per minute.
If energy production were to decline, how would the cell be able to replenish the energy it needs?
The cell then activates the sirtuins that stimulate the production of new mitochondria that produce the amount of energy it needs by eliminating the damaged / aged ones, which would have produced more free radicals.
What happens when we ingest an excess of simple or complex sugars?
As we have said on other occasions, insulin forces cells to let glucose enter the cytosol, thus activating the alternative energy system called glycolysis.
If the cell is programmed to have a certain number of mitochondria based on energy needs, what happens when it is forced to produce a surplus of energy from glycolysis?
A super energy production is obtained which prevents the cell from understanding if there are damaged mitochondria that must be replaced. When this happens, inefficient mitochondria produce many free radicals with damage to the cell (nucleus and membrane), deterioration of the mitochondria and increased apoptosis.
Some scientific research has found that insulin inhibits sirtuins and therefore reduces the production of new mitochondria.
On the contrary, a diet with very few carbohydrates forces the cells to constantly maintain the mitochondria, replacing the aged or malfunctioning ones. For this reason, calorie restriction induces activation of sirtuins, increases the life of the cells and of the individual they belong to.

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