Does someone with diabetes age faster biologically?
Yes, diabetes noticeably accelerates biological ageing: the risk of cardiovascular disease, dementia, and premature death increases, and keeping blood sugar well under control is the most direct way to slow that process.
Diabetes and biological ageing reinforce each other. People with diabetes have more so-called senescent cells in their tissues: cells that have stopped dividing but continue to secrete harmful substances. Those same cells promote insulin resistance, completing the circle. This pattern closely resembles what happens during normal ageing, only faster and more intensely.
Large population studies show how strong the link is. In a study of more than 376,000 people, biologically older participants had a 77% greater chance of developing type 2 diabetes than biologically younger people of the same chronological age. Conversely, people with diabetes and accelerated biological ageing lost more than two years of life expectancy, and their risk of a heart attack or stroke was 23 to 62% higher. The relationship therefore runs in both directions: diabetes accelerates your biological clock, and an aged biological profile makes diabetes worse.
The damage is not limited to the heart. Diabetes also increases the risk of cognitive decline and dementia, through the same mechanisms involved in ordinary brain ageing: chronically high blood sugar produces harmful glycation end-products and disrupts insulin signalling in the brain. In diabetic eye disease, immune cells in the retina enter a senescent state and sustain damaging inflammation.
There is a striking finding regarding metformin, the most widely prescribed diabetes medication. Diabetes patients who used metformin had an even slightly lower mortality rate than people without diabetes who were on no medication at all. Whether this is because metformin also inhibits ageing processes, or because healthier patients were more likely to be prescribed metformin, cannot be proven with observational research. Ongoing trials need to settle this question.
Finally, in pregnant women with poorly controlled diabetes, high blood sugar levels in the embryo can trigger cellular senescence and cause congenital abnormalities. This has been demonstrated primarily in mouse models that mimic the human situation, but it underlines how early the biological effects of diabetes can begin.
Based on a large prospective study (n=376,083), a British cohort (n=341,159), multiple observational studies, and mechanistic/animal research. Causality is plausible but difficult to establish definitively; the bidirectional relationship complicates this further.