Note: Single-source report; awaiting corroboration.
As people age, DNA mutations in blood stem cells can lead to clonal hematopoiesis, a process that increases inflammation and atherosclerosis and raises cardiovascular risk. Researchers investigated how exercise and sleep influence this condition in both humans and mice.
Analysis of data from over 90,000 participants in the UK Biobank and NIH's All of Us program showed that those who engaged in more moderate-to-vigorous physical activity were less likely to have clonal hematopoiesis linked to common mutations in three genes. Exercise was not associated with mutations in DNMT3A.
Mouse experiments with mutations in Jak2, Tet2, Trp53, and Dnmt3 revealed that poor sleep increased mutation accumulation in Jak2 and Tet2 mutants, while exercise reduced this accumulation. Sleep and exercise had no significant effect on mutation accumulation related to Dnmt3a mutations.
Plaque buildup in arteries increased with poor sleep and improved with exercise in mice with certain mutations, but not in those with Dnmt3a mutations. Results suggest that the effects of lifestyle interventions depend on the specific mutation in clonal hematopoiesis.
This NIH-funded study was published in Nature on June 10, 2026.