Supercharged mitochondria spark aging-related blood disorders (MitoQ and Metformin help)

Medical Xpress / Jackson Laboratory / Nature Communications / Nature ^ | April 16, 2025 | Kira A. Young et al / Steven Chan et al

[ConservativeMind]

As we age, blood stem cells, the essential source of new blood cells in the body, can accumulate genetic mutations. Now, scientists have not only discovered the mechanism that fuels their unchecked growth but have also found a way to stop it.

The study reveals that a common aging-associated mutation in the gene Dnmt3a boosts the power-generating function of mitochondria in blood stem cells.

This mutation allows the cells to make copies of themselves more readily than normal and creates fertile ground for the development of clonal hematopoiesis, a condition that dramatically increases the risk of heart disease, blood cancers, and other illnesses.

Clonal hematopoiesis develops silently with age—more than half of all 80-year-olds are estimated to be affected by the condition.

In this new study, the team discovered that in middle-aged mice, the mutated stem cells had double the energy-producing capacity of normal cells. The mutated stem cells also contained turbocharged mitochondria, which gave the cells a strong competitive growth advantage.

In isolated stem cells and mice with Dnmt3a mutations, the team tested the effect of MitoQ and d-TPP—molecules, which disrupt the normal function of mitochondria and prevent them from producing energy.

In a separate paper, Trowbridge and co-authors report that metformin—a first-line treatment for type 2 diabetes—also diminishes the competitive advantage of stem cells carrying the Dnmt3a mutation.

In mice with Dnmt3a mutations and clonal hematopoiesis, the mitochondria-targeting drugs had drastic effects. Within a few days of treatment, about half of all mutant cells died and among the remaining mutant cells, their energy production dropped to normal levels. Normal cells—which don't rely as heavily on the same metabolic pathway—were not impacted.

The mitochondrial drugs worked not only in mice with clonal hematopoiesis, but in human blood stem cells engineered to have the DNMT3A gene mutation.

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TOPICS: Health/Medicine
KEYWORDS: aging; blood; disorders; mitochondria

[ConservativeMind]

MitoQ, an over-the-counter supplement I’ve posted threads on in the past and metformin both appear capable of blocking clonal hematopoiesis, which over half of everyone over 80 will have acquired.

This could help reduce heart disease and blood cancers.

I used to take MitoQ, but found a similar product, Urolithin A, that appears an even better choice for mitochondria, but this study did not check Urolithin A for this benefit, so take the MitoQ, if needed.

[ConservativeMind]

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[C210N]

I prefer over metformin, non-pharma berberine.

[Rockingham]

My guess is that magnesium deficiency is a key part of the problem. Magnesium is essential to mitophagy, the process by which defective mitochondria are eliminated. Although magnesium deficiency is known to be common, it is rarely identified because it is hard to detect in the body through blood tests since blood magnesium levels are tightly regulated.