Genetic flaw might be key to stopping people craving sugary treats – study

Scientists have identified a genetic mutation which may be the key to stopping people from craving sugary treats.
The findings open up the possibility of developing treatments to target the gene in order to help curb population-wide sugar intake.
According to the study, people who lacked a specific gene, called sucrase-isomaltase (SI), ate fewer sugary foods, while those who had a partially functional SI gene liked sucrose-rich foods less.
The researchers found that changes in the ability to digest dietary sucrose (sugar) can influence someone’s intake, and preference, for sucrose-rich foods.
Dr Peter Aldiss, now a group leader in the School of Medicine at the University of Nottingham, said: “Excess calories from sugar are an established contributor to obesity and type 2 diabetes.
“In the UK, we consume 9-12% of our dietary intake from free sugars, such as sucrose, with 79% of the population consuming up to three sugary snacks a day.
“At the same time, genetic defects in sucrose digestion have been associated with irritable bowel syndrome, a common functional disorder affecting up to 10% of the population.
“Now, our study suggests that genetic variation in our ability to digest dietary sucrose may impact not only how much sucrose we eat, but how much we like sugary foods.”
The team of experts began by investigating dietary behaviour in mice lacking the SI gene.
They found that the animals developed a rapid reduction in sugar intake, and preference.
This was confirmed in two large population-based studies involving 6,000 people in Greenland and 134,766 in the UK BioBank.
They found that people with a complete inability to digest dietary sucrose in Greenland consumed significantly less sucrose-rich foods, while those with a defective, partially functional SI gene in the UK liked sucrose-rich foods less.
Dr Aldiss added: “These findings suggest that genetic variation in our ability to digest dietary sucrose can influence our intake, and preference, for sucrose-rich foods whilst opening up the possibility of targeting SI to selectively reduce sucrose intake at the population level.
“In the future, understanding how defects in the SI gene act to reduce the intake, and preference, of dietary sucrose will facilitate the development of novel therapeutics to help curb population-wide sucrose intake to improve digestive and metabolic health.”
The study, led by Dr Aldiss, alongside Assistant Professor Mette K Andersen, at the Novo Nordisk Foundation Centre for Basic Metabolic Research in Copenhagen and Professor Mauro D’Amato at CIC bioGUNE in Spain and LUM University in Italy, is published in the Gastroenterology journal.