What do mitochondrial mutations mean for how quickly you age?

Mitochondria are the powerhouses of your cells, but they also contain their own DNA. That mitochondrial DNA is more vulnerable than the DNA in the cell nucleus: it sits close to where energy is produced, and therefore close to the harmful byproducts of that process. Damage to this DNA, to the proteins that mitochondria import, or to the metabolic enzymes involved, leads to accelerated ageing and a broad range of diseases.

One complication is that a cell can contain thousands of copies of mitochondrial DNA, and those copies do not all have to be identical. Sometimes a cell carries both normal and mutated copies. As long as the mutated copies are rare, you will notice little effect. However, less severe mutations escape natural selection in the female germline more easily and can then accumulate in the body as you grow older. In this way they contribute, later in life, to the risk of conditions such as neurodegeneration.

Poor mitochondrial function is also measurably associated with faster biological ageing in humans and with greater susceptibility to multiple diseases simultaneously. The association has been demonstrated, but causality has not been firmly established in all cases: it is partly an interplay in which damage and dysfunction reinforce each other.

From an evolutionary perspective, ageing is not a programmed process but the result of accumulating damage because our bodies never maintain themselves perfectly. Mitochondrial damage is an important part of that broader accumulation of damage, alongside telomere shortening, genomic instability, and loss of protein quality. Mitochondrial activity itself can promote ageing, while processes such as cellular recycling (autophagy) and DNA repair work against it.