Why from time to time you need to starve
Health / / December 19, 2019
Fasting can extend life. Scientists have proven not only that, but also found a possible cure for old age, the brain keeps working.
On the dependence of the high life expectancy of the various practices of fasting argue from time immemorial. In the modern world of science and technology of interest in the topic has only increased. And now, a few objective studies have confirmed the link between hunger (at the biochemical level) and longevity.
One of the most striking was the workMouse Study: When It Comes To Living Longer, It's Better To Go Hungry Than Go Running a group of German zoologists led by Derek Huffman (Derek Huffman). Before that it was known that the mouse regularly "involved in sports," live longer representatives of the control group, who are not as active, but get the same food as the first. The fact that physical exercise prevent the development of certain diseases. Accordingly, the active mice increased life expectancy.
But if the mice in the control group (not involved in sports) instead of the standard menu for all subjects received abbreviated portions, they lived much longer than physical activity.
Huffman found out that the whole thing in the level of insulin-like growth factor 1 (IGF-1). This protein is involved in the regulation of cell growth and plays an important role in the aging process. In mice, it increases the level of gluttons and the DNA molecules are destroyed. Animals athletes IGF-1 is small, but there tissue damage or DNA molecules. Fasting slows the process of destruction of DNA molecules, however physically active test group of mice was hungry and the leaders of life expectancy.
There are other scientists studied aspects of fasting. So, Walter Longo (Valter Longo) and his colleagues from the University of Southern California foundFasting triggers stem cell regeneration of damaged, old immune systemThat fasting has a positive influence on the immune system. Within six months, the experimental mice from time to time were deprived of food for 2-4 days. This led to a sharp reduction in the number of leukocytes in blood. When normalization ration levels of immune cells not only restored, but also increased compared to the same.
But research conducted with the participation of a number of cancer patients, showed that during the hunger strike the body eats not only the nutrient reserves accumulated in the form of adipose tissue, but also a part leukocytes. However, the disappearance of the old immune cells contributes to the activation of stem cells, they begin to divide and generate new white blood cells. Younger and stronger than the previous ones.
By the way, this experiment also showed a decrease in the number of hungry people IGF-1 is responsible for the aging process and the emergence of cancer cells (presumably).
Another hypothesis states that a calorie deficit activates certain genes responsible for the deterioration of the body. A group of scientists from the University of Wisconsin, led by Richard Veyndrahom (Richard Weindruch) heldCaloric Restriction Delays Disease Onset and Mortality in Rhesus Monkeys a study, using as experimental rhesus monkeys. Half of the monkeys for 10 years receives a low-calorie diet, the other half eats normally. Animals on a low calorie diet weigh 30% less, have 70% less body fat and low insulin levels. At the moment, 90% of the monkeys alive. In the control group, eat normally, twice the mortality rate of age-related diseases such as heart failure and diabetes, and live here only 70% of the monkeys.
Scientists from the Massachusetts Institute of Technology, working under the direction of Professor Leonard Guarente (Leonard Guarente), establishedUna proteína que promueve la longevidad también parece proteger contra la diabetesThat the gene responsible for this result, - SIRT1 - is the link between longevity and caused starvation mechanism of cholesterol excretion. Low levels of SIRT1 protein encoded by the gene in mouse cells leads to the accumulation of cholesterol. Starvation, enhances the activity of SIRT1, may reduce the risk associated with cholesterol diseases such as atherosclerosis and Alzheimer's disease.
A recent studyIncreased ghrelin signaling prolongs survival in mouse models of human aging through activation of sirtuin1 Japanese scientists from the University of Kagoshima confirmed all earlier assumptions and found that the aging depends on the concentration of hunger hormone - ghrelin. It affects SIRT1, slows the aging process of the body and brain of mice. Thus, increasing the production of ghrelin in laboratory mice and activating of SIRT1, the scientists were able to extend the life of the rodent. By blocking the production of the hormone, the animal was able to wear out.
For these manipulations ghrelin Japanese scientists have used the popular means rikkunsito (rikkunshito), which is made from the roots of plants Atractylodes lancea. This drug was given to mice with mutations that accelerate the process of aging. Admission rikkunsito extended the life of rodents on the 10-20 days for one set of genes and 100-200 days - for the other.
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