A way to reverse cell aging has been discovered

Scientists at the Fritz Lipmann Institute have uncovered a previously unknown mechanism of mitochondrial aging: with age, levels of a key lipid — phosphatidylcholine — drop sharply in cells, and it is precisely this that triggers the degradation of the "cellular power plants." Most encouragingly, the deficit can be replenished through ordinary diet. The results of the study have been published in the journal Nature Communications (NatCom).

The scientists used C. elegans worms, human tissue samples, and human cell cultures as models. In all three systems, the picture turned out to be the same: phosphatidylcholine synthesis is steadily suppressed as the organism ages. This lipid serves as the primary building material of the outer mitochondrial membranes — without it, the membranes lose their flexibility, the mitochondria begin to fragment, and they become increasingly poor at distributing energy.

"You can imagine the entire system as a branching electrical network that increasingly degrades with age: connections break, currents come to a halt," biologist Maria Ermolaeva figuratively described the process.

When phosphatidylcholine or choline — its dietary precursor — was added to the worms' food, the mitochondria returned to a younger, more flexible state.

"We ourselves were surprised by how strongly this molecule affects the structure, connectivity, and function of mitochondria," noted first author Tatiana Polezhaeva.

Analysis of human tissue samples revealed two important patterns. First, low phosphatidylcholine levels were more frequently recorded in people with diabetes and obesity, while high levels correlated with fast walking speed and good memory — recognized markers of healthy aging. Second, a notable difference between sexes was discovered: in men, the decline in lipid levels occurred gradually, whereas in women it accelerated sharply around the time of menopause. This fact may explain the sudden drop in energy that many women experience during this period of life.

The study authors emphasized that phosphatidylcholine deficiency is only one factor in mitochondrial aging, yet a significant one: its correction through diet opens a realistic and accessible pathway to slowing cellular aging.