The field pivots from mechanism to measurement
The strongest new evidence this cycle is human and randomized: a placebo-controlled RCT showing semaglutide slows epigenetic aging, and the one-year PEARL rapamycin trial reporting real healthspan gains. Against that, a Science paper dismantles taurine as a reliable aging biomarker. The through-line: the field is maturing from mechanism to measurement, and epigenetic clocks are becoming the currency of proof.
Semaglutide pace of aging (PCGrimAge, RCT)
Where the human evidence is
Count by statusEvidence-stage map
Evidence stage × investigator promise (1–10)Metabolism & nutrient sensing
Semaglutide slows epigenetic aging — first RCT evidence
First randomized, placebo-controlled evidence a GLP-1 drug slows biological aging on validated epigenetic clocks. In adults with HIV-associated lipohypertrophy, semaglutide slowed pace of aging ~9% on PCGrimAge, strongest in inflammation-, cardiometabolic-, brain- and kidney-linked methylation. Authors stress this is an early signal in a specific population, not proof of rejuvenation.
Read the paperPEARL: longest human rapamycin healthspan trial reports out
48-week double-blind placebo-controlled trial of intermittent low-dose rapamycin (5/10 mg weekly) in normative-aging adults. Relatively safe; significant improvements in lean tissue mass and pain in women (10 mg) and wellbeing (5 mg). Among the first controlled human healthspan signals for the ITP's flagship molecule.
Read the paperTaurine is NOT a reliable aging biomarker
Longitudinal reversal of the 2023 taurine-decline story: across three human cohorts, primates and mice, circulating taurine stayed flat or rose with age. Variation tracked diet, sex and species more than aging — a corrective to the supplement hype.
Read the paperSenescence, SASP & inflammaging
Senolytics (D+Q) clear senescent cells and cut kidney injury
Dasatinib + quercetin reduced senescent-cell burden, macrophage infiltration and systemic inflammation; a single 5-day oral regimen improved kidney function in diabetic kidney disease, building on prior human pilot data. Indication-specific but the clearest translational senolytic story.
Read the papercGAS-STING as a driver of inflammaging
Cytosolic (largely mitochondrial) DNA in senescent cells activates cGAS-STING, remodeling immunity toward a pro-aging state; STING blockade in aged mice improved cognitive and motor performance. Relevant to the cGAS partial-LOF therapeutic-window question — protection vs antiviral tradeoff.
Read the paper