Does excess weight accelerate ageing?

Prolonged excess weight from childhood already leaves clear marks at a young adult age. People aged 28-31 who had lived with obesity since childhood had significantly higher levels of inflammatory markers (with large effect sizes), an accelerated epigenetic clock and shorter telomeres compared with peers of a healthy weight.

Telomeres are the protective 'caps' at the ends of chromosomes. Excess weight causes oxidative stress -- harmful oxygen compounds in cells -- that shorten these caps and damage DNA. The body repairs that damage less effectively than normal. This also applies to adipose tissue itself: in obesity, senescent fat cells accumulate, promoting chronic inflammation, insulin resistance and type 2 diabetes, and that damage then spreads to other organs.

The consequences for the heart and blood vessels have also been measured and demonstrated. For each additional year of biological age acceleration, the risk of stroke rose by 68%, and the risk of heart disease by 35%. Biological age acceleration explained 10 to 25% of the association between obesity and cardiovascular disease. The effect was strongest in people between the ages of 45 and 65.

Importantly, not every extra kilogram automatically leads to this accelerated ageing process. People with excess weight but a healthy metabolic profile -- meaning normal blood sugar, blood pressure and blood lipids -- showed no accelerated increase in vulnerability. Only the combination of excess weight with a disrupted metabolic profile proved harmful. This makes metabolic health at least as relevant as the number on the scale.

Losing weight and exercising help. The combination of fewer calories and more physical activity slows the molecular damage associated with obesity, including telomere shortening and oxidative stress. Time-restricted eating and the Mediterranean diet are also mentioned in this context, but the evidence in humans is still too limited to draw firm conclusions from.