High-sugar fizzy drinks have been under fire from campaigners for contributing to obesity and type-2 diabetes, but this is the first study to suggest a link with ageing.
The researchers found that people who reported drinking a 350ml bottle of fizzy drink per day had DNA changes typical of cells 4.6 years older.
“Regular consumption of sugar-sweetened sodas might influence disease development, not only by straining the body’s metabolic control of sugars but also through accelerated cellular ageing of tissues,” said Prof Elissa Epel, of the University of California, San Francisco.
The study, published in the American Journal of Public Health, asked 5,309 healthy adults aged between 20 and 65 about their consumption of fizzy drinks and examined the DNA from each participant’s white blood cells.
The team found that telomeres – protective DNA caps on the end of chromosomes – were shorter in people who reported habitually drinking more fizzy drinks.
Telomeres are repetitive sections at the end of chromosomes that get shorter each time cells divide. They act as a kind of genetic ticking clock and in the past have been associated with human lifespan as well as the development of some forms of cancer, heart disease and diabetes. Other studies have suggested a link between telomere length and lifestyle factors such as smoking and psychological stress.
“It’s really been in the last four years or so that people have started asking if this is something that can start in early age,” said Epel. “This soda study really raises the question: if we’re seeing this apparent soda-induced telomere shortening in a diverse adult sample, what does that mean for our kids? It may be a large part of why we have such a vast epidemic of not only obesity as adults, but early disease onset. Soda may be one of the invisible culprits.”
She stressed that the study only showed an association and did not prove that sugary drink consumption caused cell ageing. If high soda consumption was to blame, it may be due to the huge rush of sugars into the blood after a drink, leading to oxidative stress and inflammation – “the perfect storm for degrading telomeres,” said Epel.
The study has its limitations. Since it looked at survey data from the now decade-old US National Health and Nutrition Examination Survey, it could only draw associations between DNA samples and what people self-reported about their diet at the time.
David Jacobs, a professor of public health and epidemiology at the University of Minnesota, who was not involved in the study, said: “It’s an interesting suggestion that, by taking these beverages that so emphasise a single molecule, there’s a fundamental relationship between excess sugar in the diet and telomeres. But disease is long-term, and these are small effects. You’re going to need long-term studies with follow-up to really see what happens.”
Epel said her research group planned to address these questions in further studies in which they might use a short-term diet high in sugar to see if they can induce effects associated with telomere shortening.