Seems like a vastly overhyped finding… but I hope it develops into something.
According to Cancer Research UK, formaldehyde causes DNA damage to blood stem cells, which can accelerate their ageing and increase the likelihood of blood cancers.
The research, published in the journal Cell Metabolism, identified a common link between DNA damage in blood cancer and ageing.
More information:
Damage and ageing
New research from the Weatherall Institute of Molecular Medicine at the University of Oxford, and the Wellcome-MRC Cambridge Stem Cell Institute at the University of Cambridge has shown that a molecule called formaldehyde causes DNA damage to blood stem cells, which can accelerate their ageing and increase the likelihood of blood cancers.
Most importantly, this research now identifies a common link between DNA damage in blood cancer and ageing.
Previous research, led by our chief scientist Professor KJ Patel, had identified aldehydes, the group of molecules to which formaldehyde belongs, as a source of DNA damage that causes mutations in blood stem cells and increases blood cancers.
Now, this latest research shows that the DNA damage arising from formaldehyde can also age the blood stem cells.
Therefore, if we can find ways to limit formaldehyde production in our bodies, we may be able to slow, or even fully stop, this DNA damage occurring. Doing that could slow the ageing process of these cells and could be a step toward preventing certain blood cancers.
Full Paper:
Genotoxic aldehyde stress prematurely ages hematopoietic stem cells in a p53-driven manner
Summary
Aged hematopoietic stem cells (HSCs) display diminished self-renewal and a myeloid differentiation bias. However, the drivers and mechanisms that underpin this fundamental switch are not understood. HSCs produce genotoxic formaldehyde that requires protection by the detoxification enzymes ALDH2 and ADH5 and the Fanconi anemia (FA) DNA repair pathway. We find that the HSCs in young Aldh2 −/− Fancd2 −/− mice harbor a transcriptomic signature equivalent to aged wild-type HSCs, along with increased epigenetic age, telomere attrition, and myeloid-biased differentiation quantified by single HSC transplantation. In addition, the p53 response is vigorously activated in Aldh2 −/− Fancd2 −/− HSCs, while p53 deletion rescued this aged HSC phenotype. To further define the origins of the myeloid differentiation bias, we use a GFP genetic reporter to find a striking enrichment of Vwf+ myeloid and megakaryocyte-lineage-biased HSCs. These results indicate that metabolism-derived formaldehyde-DNA damage stimulates the p53 response in HSCs to drive accelerated aging.
Open Source Paper:
https://www.cell.com/molecular-cell/fulltext/S1097-2765(23)00419-7
The first paragraph explains what the headline hypes.
Scientists may have identified a major reason why individuals age, which could lead to therapy to slow down the process as well as reduce the risk of blood cancer.