This DNA may prove to be a useful predictor of overall risk of frailty and death from any cause 10 to 15 years before symptoms appear, according to new research from The Johns Hopkins University.
"We don't know enough yet to say whether the relationship is one of correlation or causation," said Dan Arking, associate professor of genetic medicine.
"But either way, mitochondrial DNA could be a very useful biomarker in the field of ageing," Arking said.
Previous research from Arking's laboratory linked genetic differences in mtDNA to increased frailty and reduced muscle strength in older individuals.
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Frailty refers to a well-recognised collection of ageing symptoms that include weakness, decreased energy, lower activity levels and weight loss.
To further test this link, Arking's team analysed the amount of mtDNA in blood samples collected for two large, human studies that began in the late 1980s and tracked individuals' health outcomes for 10 to 20 years.
And, when grouped by amount of mtDNA, white participants in the bottom one-fifth of the study population were 31 per cent more likely to be frail than participants in the top one-fifth.
"It makes intuitive sense that decreased mtDNA is associated with bad health outcomes. As we age, our energy reserves decrease, and we become more susceptible to all kinds of health problems and disease," said Arking.
The researchers also analysed the age at which participants died. In one of the studies, high levels of mtDNA corresponded to a median of 2.1 extra years of life compared to those with the lowest levels of mtDNA.
They also found that women had an average of 21 per cent more mtDNA than men. According to Arking, this could play a small role in why women live two to four years longer than men on average.
Researchers also found that averaged over the population, an increase of 10 years in age corresponded to 2.5 per cent less mtDNA.