18 July 2019

Live longer or healthier?

The "longevity gene" did not add vitality to the worms

Polina Loseva, "The Attic"

Long life and health are usually associated with the body's ability to withstand stress. A group of American scientists discovered that these two properties can be mutually exclusive. Mutant worms deprived of one of the "genes of long life" repelled the attack of Pseudomonas aeruginosa much more successfully than long-lived worms. It turned out that worms pay with their immunity for the opportunity to live longer in ideal conditions. This means that a long life and a healthy life are not necessarily the same thing.

Opponents of interference in the aging process sometimes cite the myth of the immortal Typhon as an argument. Eos, the goddess of dawn, fell in love with a simple young man and begged Zeus for eternal life for her lover. But at the same time she forgot to ask for eternal youth, and Zeus condemned Typhon to an endless old age. In the language of gerontology, this myth can be translated as follows: by prolonging the life of a person as a whole, we cannot be sure that we slow down his aging and improve his health, and do not add extra years of suffering to him.

Examples of Typhons in the animal world are not yet known. However, American researchers in an article published in the journal Nature Communications (Amrit et al., The longevity-promoting factor, TCER-1, widely represses stress resistance and innate immunity) argued that the relationship between health and longevity may be ambiguous. They studied the protein TCER-1 in C. elegans roundworms. It is known about him that he promotes fertility, and the rapid activity of the corresponding gene prolongs the life of nematodes. Mutant individuals with this gene turned off lay fewer eggs, and their offspring are not as viable, that is, in a sense, their reproductive aging proceeds faster.

Usually, "longevity genes" are associated with increased resistance to stress. But with nematodes, everything turned out to be exactly the opposite. The researchers placed control individuals and mutants of the tcer-1 gene in different stressful situations: they were heated to 35 ℃, exposed to ionizing radiation and infected with Pseudomonas aeruginosa. In all cases, the mutant worms proved to be more viable than the control animals. 

Moreover, mutant individuals retained the ease of movement better than centenarians, and when they were forced to produce an analogue of beta-amyloid, which destroys nerve tissue in Alzheimer's disease, they developed paralysis more slowly.

Apparently, TCER-1 suppresses the work of innate immunity, and it does this regardless of the tissue where it started working. The researchers forced different tissues in the body of mutants deprived of TCER-1 to produce this protein anew and found that it was enough for it to form in one organ – be it the intestine, muscle, skin or nervous system to muffle the immune response throughout the body.

Scientists believe that this mechanism is designed to redistribute resources in the body: it reduces the load on the immune system and allows you to spend the released resource on reproduction. However, in stressful conditions, this tactic does not contribute to prolonging life. Based on these data, it can be assumed that a long life under mild stress will not necessarily be healthy.

An analog of the protein TCER-1 also works in human cells, although nothing is known about its relationship with immunity and longevity. This does not prevent the lead author of the study, Arjuman Gazi, from fantasizing about the possible consequences of his work in a conversation with the press service of the University of Pittsburgh. "It will be interesting to understand how the body allocates resources," she says. "Maybe someday women will have the opportunity, after they stop having children, to take a pill that will direct their resources from the reproductive area to stress resistance?"

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