Epigenetic clocks have shown that patterns of DNA methylation from blood cells are strongly correlated with chronological age. Those with accelerated methylation age (methylation age that is greater than expected for chronological age) are at higher risk for several diseases of aging and death, but the biological processes underlying such advanced epigenetic age are incompletely understood. Clonal hematopoiesis of indeterminate potential (CHIP) results from somatic mutations in blood stem cells and may be found in ~20% of the elderly. CHIP most commonly arises due to mutations in the DNA methylation altering enzymes, TET2 and DNMT3A, and also associates with increased risk of death, cancer, and cardiovascular disease. Whether CHIP associates with accelerated methylation age is unknown. We used methylation and whole genome sequencing data from several cohorts in TOPMed together comprising thousands of persons to show that CHIP is strongly associated with increased epigenetic age acceleration. The most consistent association is observed for intrinsic aging (2.8 ± 0.36 years, p < 2.5 x 10-14), which measures epigenetic aging that is independent of changes in cell composition, while a more variable association was seen with extrinsic aging (2.5 ± 0.46 years, p < 4.6 x 10-7), which captures epigenetic aging that is driven by changes in cell composition. We also analyzed the gene-specific effects of CHIP mutations on epigenetic aging, dividing our CHIP carriers into DNMT3A, TET2, and all other CHIP mutations. We found that the increase in intrinsic age acceleration seen in CHIP was very consistent across different genes, while the increase in extrinsic aging was lower with DNMT3A mutations and higher in TET2 mutations. The epigenetic clock software we used can also predict cell type composition and leukocyte telomere length (LTL) from methylation. We observed an increased predicted proportion of CD8+/CD28-/CD45RA- T-cells and decreased predicted LTL. Future experiments should seek to determine whether there is a causal relationship between CHIP and epigenetic age acceleration and whether intrinsic or extrinsic age acceleration is predictive of health outcomes in those with CHIP.