What does insulin do to the ageing process?

Chronically high insulin signalling accelerates ageing and increases the risk of age-related diseases. As you get older, your cells' sensitivity to insulin declines, the pancreas secretes insulin less efficiently, and insulin is broken down more slowly. This vicious pattern is strongly linked to type 2 diabetes, obesity, dementia and cardiovascular disease.

In animal research the reverse picture is equally compelling: less insulin signalling means a longer life. In roundworms and fruit flies, lifespan sometimes doubles when the insulin receptor is switched off. In mice the same principle applies: animals in which the insulin receptor was switched off only in fat tissue, or in which a specific substrate of the insulin receptor was absent, lived longer. This is one of the most consistent findings in ageing research.

The mechanism runs partly through a group of proteins called FOXO factors. These proteins promote stress resistance and cellular protection, but insulin suppresses their activity. Reduced insulin signalling allows these protective factors to be released. In humans, lower activity of these proteins is associated with a higher risk of cancer and diabetes.

Something else is also at play: as we age, cells read out genes faster, which produces more errors in protein production. Lower insulin signalling slows this acceleration, as does caloric restriction. This suggests that inhibiting insulin signalling helps preserve molecular precision in cells, although this has not yet been demonstrated directly in humans.

In practical terms the message is nuanced. Insulin is not the enemy: people who need insulin to survive, such as those with type 1 diabetes, literally depend on it. The issue is the pattern of chronically elevated insulin signalling caused by unhealthy diet, physical inactivity and fat gain. Ageing fat tissue worsens the insulin sensitivity of the entire body, setting in motion an upward spiral of metabolic decline.