Sex-specific aging clocks read organs differently in women and in men

What the research found

Study (multi-cohort clocks). The MULTI Consortium, Z. Song, D. Feng, and colleagues report in Nature Med. (doi 10.1038/s41591-026-04662-6; News-Medical 17 September 2026) on 38 sex-specific biological aging clocks across 15 organ systems, built from genetics, proteomics, metabolomics, MRI, and clinical follow-up in the UK Biobank and checked in ADNI, the Baltimore Longitudinal Study of Aging, and the A4 solanezumab trial. Hepatic proteomic age gap, metabolic metabolomic age gap, and liver MRI age gap were more heritable in women. Immune metabolomic age gap, spleen MRI age gap, and skin proteomic age gap were more heritable in men. In women, higher heart MRI age gap predicted later hypertension, and higher digestive and immune metabolomic age gaps predicted later type 2 diabetes. In men, endocrine and metabolic metabolomic age gaps lined up with hypercholesterolemia, hypertension, and diabetes. Twelve organ-clock pairs raised all-cause mortality risk in women; 14 pairs did so in men, while spleen and liver MRI age gaps looked protective in men. Brain MRI age gap predicted progression from mild cognitive impairment to Alzheimer disease in both sexes, more strongly in women: hazard ratio 1.74 per standard deviation in men and 2.25 in women. It did not clearly predict the step from normal cognition to mild impairment. In A4, women on solanezumab whose brain aging looked slower had higher cognitive scores than men at week 240; that sex gap was absent when brain aging looked faster. Limits named by the authors: many disease genetic studies were not split by sex, UK Biobank had few repeat scans, genetics were mostly European ancestry, and the models left out hormones, pregnancy, and social exposures. Age prediction itself was modest. Educational research notes. Solanezumab here is a completed trial context, not a treatment suggestion.

Evidence level: Human study. A study in people, but an association isn't proof of cause.

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