an enzyme that could hold the secret of longevity and healthy aging

Low calorie diets have been shown to increase the lifespan and health of everything from yeast to monkeys – as long as there was no malnutrition. And while no long-term study has proven the benefits of caloric restriction on human life, short-term studies suggest that it actually improves health. Here is how it could work.

Our body monitors and detects the amount of nutrients available through specific molecules in our cells. Depending on the amount of food we eat, these molecules alter our metabolism to regulate the way we use available nutrients. One of these molecules is an enzyme called TOR.

When there is a lot of food, the TOR enzyme tells the body's cells to grow. If there is less food, TOR asks the body to be on the alert – a condition that scientists call a "moderate stress response".

Many experiments have shown that when animals eat a lot, especially for long periods, TOR detects it and their life span is shorter. But do all foods have this effect on the TOR?

The TOR enzyme is particularly activated when cells detect large amounts of amino acids (building blocks of the protein) or proteins. A low-protein, malnutrition-free diet can have the same effects on the metabolism and lifespan of laboratory animals as a calorie-restricted diet.

Age-related illness

Age-related diseases are known to be caused by genetic mutations, but could there be a link between RPT, nutrition and old age diseases? We know that nutrition is badociated with cancer and heart disease, and that RPT overdose is known to be involved in these diseases, but recent studies show that it is also directly related to neurodegenerative diseases. For example, the activity of the TOR enzyme in the brains of people with Alzheimer's disease is much higher than that of a healthy brain. In addition, simulation of these diseases in mice and other laboratory animals has shown that the elimination of excess TOR prevents death of brain cells.

There may be a connection between what we eat, how our body perceives it and the risk of neurodegenerative disease. Scientists are exploring different possibilities to prevent neurodegeneration. If more protein means more TOR, we can safely change our diet or develop a drug that induces our body into believing that it absorbs less protein.

Work in many labs, including ours, has shown that caffeine and a drug called rapamycin do exactly that. Although cells contain an abundant amount of protein, their metabolism and lifespan are similar to those of protein-restricted cells. We are currently studying this in human neurons and the first results are in the same direction.

Not that easy

Does this mean we should change our diet and protein intake? What about other nutrients such as sugars? Unfortunately, as expected, things are not so simple. Many other molecules in our body participate in the detection of nutrients, including carbohydrates, which affect longevity and age-related diseases.

That's why we have to be very careful. First, each person's nutrient needs vary by stage of development, age, bad, or level of activity, to name a few important factors. In addition, while evidence from the laboratory using human cells and tissues is accumulating, we need large population studies that can record specific diets, including protein intakes. , in lipids and carbohydrates, with parallel badyzes of relevant molecular and health markers. Such studies take decades to generate solid data and valid conclusions.

Nevertheless, with the development of new technologies and scientific approaches, we are taking steps to understand the underlying causes of aging and age-related diseases. Combined with targeted clinical trials and population studies, we may soon be able to achieve healthy aging and a longer life span.