2024 Author: Malcolm Clapton | [email protected]. Last modified: 2023-12-17 03:44
Fasting can prolong life. Scientists not only proved this, but also found a possible cure for old age, keeping the brain working.
The dependence of high life expectancy on various fasting practices has been debated since time immemorial. In the modern world of science and technology, interest in this topic has only increased. And now, several objective studies have confirmed the connection between hunger (at the biochemical level) and longevity.
One of the most illustrative was the work Mouse Study: When It Comes To Living Longer, It's Better To Go Hungry Than Go Running by a group of German zoologists led by Derek Huffman. Before that, it was known that mice that regularly "play sports" live longer than representatives of the control group, who are not so active, but receive the same nutrition as the former. The fact is that physical activity prevents the development of certain diseases. Accordingly, active mice have a longer lifespan.
But if mice from the control group (not involved in sports) received reduced portions instead of the standard menu for all subjects, they lived significantly longer than physically active ones.
Huffman found it was all about the (IGF-1) level. This protein is involved in the regulation of cell growth and plays an important role in the aging process. In gluttonous mice, its level rises, and DNA molecules are destroyed. In animal athletes, IGF-1 is low, but there is damage to tissues or DNA molecules. Fasting slows down the process of destruction of DNA molecules, so the test group of physically active and starving mice was among the leaders in terms of life expectancy.
There are other aspects of fasting that scientists have studied. For example, Valter Longo and his colleagues at the University of Southern California discovered Fasting triggers stem cell regeneration of damaged, old immune systems that fasting has a positive effect on immunity. For six months, the experimental mice were deprived of food from time to time for 2–4 days. This led to a sharp decrease in the number of leukocytes in the blood. With the normalization of the diet, the level of immune cells not only restored, but also increased in comparison with the previous one.
But a study carried out with the participation of several cancer patients showed that during a hunger strike, the body eats not only the reserves of nutrients accumulated in the form of adipose tissue, but also part of the leukocytes. However, the disappearance of old immune cells promotes the activation of stem cells, they begin to divide and generate new white blood cells. Younger and stronger than the old ones.
By the way, this experiment also showed a decrease in the amount of IGF-1 in starving people, which is responsible for the aging of the body and the appearance of cancer cells (presumably).
Another hypothesis is that a calorie deficit activates certain genes responsible for wear and tear in the body. A group of scientists from the University of Wisconsin led by Richard Weindruch conducted Caloric Restriction Delays Disease Onset and Mortality in Rhesus Monkeys, using rhesus monkeys as test subjects. Half of the monkeys have been receiving a low-calorie diet for 10 years, the other half have been eating normally. Animals on a low-calorie diet weigh 30% less, have 70% less body fat and have low insulin levels. At the moment, 90% of the monkeys are alive. The normal-eating control group has twice the death rate from senile diseases like cardiac arrest and diabetes, and only 70% of macaques are alive.
Scientists at the Massachusetts Institute of Technology, led by Professor Leonard Guarente, have established Una proteína que promueve la longevidad también parece proteger contra la diabetes that the gene responsible for this result, SIRT1, is the link between fasting-related longevity and mechanism for removing cholesterol from the body. A low level of the protein encoded by the SIRT1 gene in mouse cells leads to the accumulation of cholesterol. Fasting, which increases SIRT1 activity, may reduce the risk of cholesterol-related diseases such as atherosclerosis and Alzheimer's disease.
The recent study Increased ghrelin signaling prolongs survival in mouse models of human aging through activation of sirtuin1 by Japanese scientists from the University of Kagoshima confirmed more and more earlier assumptions and found that aging depends on the concentration of the hunger hormone - ghrelin. It affects SIRT1, slows down the aging process of the body and brain of mice. So, by increasing the production of ghrelin in laboratory mice and activating SIRT1, scientists were able to extend the life of rodents. By blocking the production of the hormone, the animal was able to age.
For these manipulations with ghrelin, scientists used the Japanese folk remedy rikkunshito, which is made from the roots of the Atractylodes lancea plant. This drug was given to mice with mutations that accelerate the aging process. Taking rikkunshito extended the life of rodents by 10–20 days for one set of genes and by 100–200 days for another.
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