A 2026 primate study from the same group that performed The return of the free radical theory of aging investigated effects of vitamin C on bone marrow cells:

“We map the single-cell transcriptomic landscape of primate bone marrow aging and demonstrate that long-term oral vitamin C (VC) supplementation attenuates selected molecular and progenitor-level decline. Aging drives severe common lymphoid progenitor (CLP) depletion, myeloid-biased hematopoietic stem and progenitor cell (HSPC) output, and anatomical site-specific molecular adaptations.

VC administration partially offsets these phenotypes, expanding the CLP pool and rebalancing lineage commitment trajectories. This aligns with a ∼4-year reduction in transcriptomic age estimates, cross-validated by an epigenetic clock. Cell-cell communication analyses revealed that VC remodels intercellular signaling, nominating a VC-responsive, progranulin (GRN)-linked candidate pathway.

As the core of the hematopoietic system, bone marrow sustains lifelong production of all blood lineages, making it a central determinant of immunity and systemic homeostasis. With advancing age, however, bone marrow function declines markedly. This deterioration is characterized by diminished regenerative capacity of HSPCs, myeloid-biased differentiation, and impaired lymphoid potential. Complexity of bone marrow aging is further amplified by its anatomical heterogeneity.

We conducted a 40-month longitudinal study (roughly equivalent to 10 human years). Aged female cynomolgus monkeys (12–16 years old, equivalent to approximately 40–53 human years) were randomized into two groups: one receiving daily oral VC (30 mg/kg) and a control group receiving water.

We combined a prolonged oral VC regimen in non-human primates with deep single-cell transcriptomic mapping of anatomically distinct bone marrow compartments to investigate aging-related molecular adaptations. We observed that VC supplementation was characterized by a partial mitigation of aging-associated compositional dysregulation, including higher observed CLP frequencies, and correlated with lowered biological age predictions at both transcriptomic and epigenetic levels.

This study provides a valuable resource and a benchmark dataset for dissecting modifiable components of primate bone marrow aging, establishing a programmatic framework to guide future functional interrogation of VC-responsive candidate pathways.”

https://www.sciencedirect.com/science/article/abs/pii/S193459092600233X “Vitamin C attenuates primate bone marrow aging at the molecular and progenitor level” (not freely available)

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These researchers didn’t confirm, but this study’s intervention group may have been the same as “Vitamin C conveys geroprotection on primate ovaries” mentioned in 2026 diet and supplement changes.

It was encouraging that vitamin C partially reverses bone marrow cells’ age-associated myeloid skewing and lymphoid depletion. It may be too intrusive to directly assess HSPCs in human trials.

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