DNA-based aging linked to kidney disease in type 1 diabetes
An observational study using 10 DNA-based aging measures in two cohorts of people with type 1 diabetes linked several measures to kidney disease and its progression.
Limit: DNA-based clock estimates served as proxies for biological aging
Edited by Boris Djordjevic · AgingResearch.News
In people with type 1 diabetes from two cohorts, an observational study compared 10 epigenetic clocks—measures that estimate age from chemical marks on DNA. The researchers assessed whether these estimates were older than expected for a person’s actual age, known as epigenetic age acceleration.
Greater acceleration on the clock called phenotypic age and shorter DNA-based estimates of telomere length—the length of protective chromosome ends—were associated with diabetic kidney disease. Progression from normal to severely increased levels of albumin, a blood protein, in urine was associated with greater age acceleration. Actual age, DNA-based age and age acceleration were also associated with progression to end-stage kidney disease.
Why it matters
The results support developing DNA-based aging markers to help predict the onset and progression of diabetic kidney disease.
Caveats
The observational findings cannot show that faster epigenetic aging causes kidney disease. The study concerned people with type 1 diabetes; the abstract does not report their numbers, ages or follow-up duration.
