Not a fan of sweets? Scientists link reduced sugar cravings to a gene defect

A new study published in the journal Gastroenterology suggests that genetic variation in our ability to digest dietary sucrose may influence our intake and preference for sucrose-rich foods. The research indicates that mutations in the sucrase-isomaltase (SI) gene, which plays a key role in breaking down sucrose (table sugar) and maltose (found in some cereals) into simple sugars for absorption by the small intestine, can make it difficult to digest these sugars, leading to a decreased preference for sugary foods.

An international team of researchers, including Dr. Peter Aldiss, now a group leader in the School of Medicine at the University of Nottingham, found that people in the UK with a defective, partially functional SI gene—almost 10 percent of the cohort—had a much lower preference for sugary foods than those with a functional SI gene. "Excess calories from sugar are an established contributor to obesity and type 2 diabetes," Dr. Aldiss said, according to Yahoo News.

The researchers conducted experiments on mice lacking the SI gene and observed that these rodents had a much lower preference for the intake of sucrose. According toYahoo News, they found that the mice developed a rapid reduction in sugar intake and preference. This led the scientists to explore whether similar genetic variations in humans could influence sugar consumption.

To test their theory, the researchers examined data from 6,000 people in Greenland and about 135,000 residents of the United Kingdom, using information stored in the UK BioBank. They found that Greenlanders who cannot digest sucrose at all consume far fewer sucrose-rich foods than those with a functional SI gene. Similarly, UK residents with a partially functional SI gene preferred sucrose-rich foods less.

"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," Dr. Aldiss said. People with irritable bowel syndrome (IBS) tend to have more defective SI gene variants than healthy people. About 10% to 15% of American adults suffer from IBS, which is characterized by abdominal cramps, bloating, a feeling of fullness or burning in the stomach, and is often accompanied by diarrhea or constipation.

"If you don’t like sweet foods, it is possible that you have reduced SI function, but it is more likely that other factors with larger effect sizes drive the reduced sweet liking," Dr. Mette Andersen, co-author of the study and assistant professor at the University of Copenhagen in Denmark, told BBC. 

Excessive sugar consumption is a big driver of obesity and type 2 diabetes rates. Large amounts of sugar can damage cells, causing chronic inflammation, which can lead to obesity, heart disease, diabetes, liver disease, and cancer. "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,” Dr. Aldiss noted referring to the UK. A recent poll found that Americans eat and drink an average of 99 grams of sugar daily, totaling 80 pounds a year.

The American Heart Association recommends no more than 9 teaspoons (36 grams or 150 calories) of added sugar per day for men and no more than 6 teaspoons (25 grams or 100 calories) per day for women. 

"Diabetes and obesity are heavily impacted by over intake of sugar-laden foods such as soda, juice, processed and fast foods," Dr. Rifka C. Schulman-Rosenbaum, director of inpatient diabetes at Long Island Jewish Medical Center, told the New York Post.

"Understanding mechanisms to potentially reduce desire for and intake of sugar is an exciting area of innovation and could have beneficial consequences in the future to reduce the burden of disease," Dr. Schulman-Rosenbaum, who was not involved with the new research, added.

Sources: The Independent, Yahoo News, New York Post, sciencefocus.com, Asharq Al-Awsat

This article was written in collaboration with generative AI company Alchemiq