In a new study, researchers found genes linked to aging that could help explain why some people age at different rates to others.
The finding suggests that maintaining healthy levels of iron in the blood could be a key to aging better and living longer.
It could accelerate the development of drugs to reduce age-related diseases, extend healthy years of life, and increase the chances of living to old age free of disease.
The research was conducted by scientists from the University of Edinburgh and the Max Planck Institute for Biology of Ageing in Germany.
In the study, the team focused on three measures linked to biological aging – lifespan, years of life lived free of disease (healthspan), and being extremely long-lived (longevity).
Biological aging – the rate at which our bodies decline over time – varies between people and drives the world’s most fatal diseases, including heart disease, dementia and cancers.
The researchers used information from three public datasets to enable analysis in unprecedented detail.
The combined dataset was equivalent to studying 1.75 million lifespans or more than 60,000 extremely long-lived people.
The team pinpointed ten regions of the genome linked to a long lifespan, healthspan, and longevity. They also found that gene sets linked to iron were overrepresented in their analysis of all three measures of aging.
They confirmed this using a statistical method – known as Mendelian randomization – that suggested that genes involved in metabolizing iron in the blood are partly responsible for a healthy long life.
Blood iron is affected by diet and abnormally high or low levels are linked to age-related conditions such as Parkinson’s disease, liver disease, and a decline in the body’s ability to fight infection in older age.
The researchers say that designing a drug that could mimic the influence of genetic variation on iron metabolism could be a future step to overcome some of the effects of aging, but caution that more work is required.
One author of the study is Dr. Paul Timmers from the Usher Institute at the University of Edinburgh.
The study is published in Nature Communications.
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