A way to reverse cell aging has been found

Scientists at the Fritz Lipmann Institute have identified a previously unknown mechanism of mitochondrial aging: with age, levels of the lipid phosphatidylcholine drop in cells, and it is precisely this that leads to the degradation of "cellular power plants." The supply can be replenished through nutrition. The study was published in the journal Nature Communications (NatCom).

The models used were C. elegans worms, human tissue samples, and human cells. In all three systems, the scientists observed the same thing: phosphatidylcholine synthesis is gradually suppressed with aging. This lipid is the primary building material of the outer mitochondrial membranes: without it, membranes lose flexibility, mitochondria fragment, and energy distribution deteriorates.

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

When phosphatidylcholine or choline (its dietary precursor) was added to the worms' food, their 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 the study's first author, Tatiana Polezhaeva.

Analysis of human tissue samples revealed two important features. First, low phosphatidylcholine levels were more commonly found in people with diabetes and obesity, while high levels correlated with fast walking speed and good memory — markers of healthy aging. Second, in men the decline in lipid levels was gradual, whereas in women it accelerated sharply around the time of menopause — which may explain the sudden drop in energy that many women experience during this period.

The authors emphasized that phosphatidylcholine deficiency is only one factor in mitochondrial aging, but a significant one: correcting it through diet opens a realistic pathway to slowing cellular aging.