Slowing ageing itself

This driver follows the attempt to prevent or slow ageing itself. Curing any single cause of death adds a few years to a population, because those saved are still old and die of something else soon after. Acting on ageing, if it could be done, would move every cause at once. That is the claim, and it is why the field exists.

The human evidence is thin, and improving. Senolytics have cleared small human trials on safety and biomarkers, not on outcomes. Metformin's effect on ageing rests largely on a retrospective comparison whose control group was in worse health, and the trial designed to test it properly has spent years seeking funding. Rapamycin has the strongest animal evidence in the field and almost no human data at doses anyone would use. Partial reprogramming has restored function in mice and has not been given to a person. Caloric restriction changes biomarkers in humans, and its effect on human survival is not known.

Measurement is in better shape, and is where the near-term interest sits. Epigenetic, proteomic and phenotypic clocks give a number for how old a body looks against how old it is. That number predicts death more sharply than most single risk factors. That said, the clocks disagree with one another, and they are trained on the outcomes they then predict. No clock has yet been shown to move in response to an intervention and to carry a mortality benefit with it. Until one does, a clock is a measurement rather than a target.

Trackers