Scientists reveal how particular brain pathways can influence food choices through a study of individuals that carry defects in a gene that is associated with obesity. The study – led by the University of Cambridge in the United Kingdom – provides insight into what guides our preference for certain foods and identifies a direct link between food selection and specific gene variants.
People with the MC4R gene defect ate nearly twice the amount of high-fat korma, compared with the other groups.
Understanding the science behind food choice may increase knowledge of obesity and consequently assist with strategies to decrease the global obesity burden that affects more than 600 million people worldwide.
The development of food preferences begins early in humans, even before birth, and what people like and dislike changes into adulthood. Many determinants affect food choice. While hunger is a key element, what individuals choose to eat is not determined just by physiological and nutritional needs.
Factors that may influence food choice include aspects that tantalize the senses, such as taste, appearance, smell, and texture, as well as more subtle economic, physical, social, and psychological elements. New research published in the journal Nature Communications indicates that biology may also play a role.
Previous research has shown that a defect in the melanocortin 4 receptor (MC4R) gene causes obesity. Research suggests that 1 in 100 obese people have the defect, which makes them more likely to gain weight. In mouse studies, the MC4R gene variant has been shown to induce obesity as a result of disrupting a particular pathway in the brain that leads to mice eating considerably more fat.
While the mice with the gene defect were found to eat more fat, they ate significantly less sugar. The University of Cambridge study adds to these findings by revealing the relevance of this high-fat, low-sugar eating behavior.
Assessing how MC4R gene variant affects food preferences
The new research observed people’s preference for high-fat and high-sugar foods by providing participants with an all-you-can-eat buffet of chicken korma curry with a dessert of Eton mess (a mixture of strawberries, whipped cream, and crushed meringue).
Three korma curry options were provided that were manipulated to look and taste the same; however, the fat content in each varied. Fat content across the choices provided 20 percent (low), 40 percent (medium), and 60 percent (high) of the calories.
Participants were divided into groups of lean people, obese people, and people who were obese as a result of having the MC4R gene variant.
All groups were tested on their food preferences by initially having a taste from each of the three curries – unaware that there was a difference between the kormas or that the fat content varied – and they were then asked to eat freely from any of the three.
Gene defect increased high-fat, but not high-sugar food preference
Prof. Sadaf Farooqi, from the Wellcome Trust-Medical Research Council Institute of Metabolic Science at the University of Cambridge, and team found that while there was no difference overall in the amount of food eaten between the groups, people with the defective MC4R gene ate nearly twice the amount of high-fat korma, compared with lean individuals, and 65 percent more than the obese group.
To test the sugar section of the study, the three groups were given three options of Eton mess dessert to freely choose from with sugar content providing 8 percent (low), 26 percent (medium), or 54 percent (high) of calorie content, but with a fixed fat content across the three.
In contrast to the results from the fat content experiment, people in the lean and obese groups both preferred the high-sugar Eton mess to the other two desserts. Individuals with defective MC4R liked the high-sugar Eton mess much less than the other two groups and ate significantly less of all three desserts overall than the lean and obese divisions of the study.
Prof. Farooqi and colleagues indicated that individuals with the MC4R gene defects might unknowingly prefer high-fat foods because of the MC4R brain pathway not functioning, which contributes to them gaining weight.
“Our work shows that even if you tightly control the appearance and taste of food, our brains can detect the nutrient content. Most of the time we eat foods that are both high in fat and high in sugar,” says Prof. Farooqi, leader of the study. “By carefully testing these nutrients separately in this study, and by testing a relatively rare group of people with the defective MC4R gene, we were able to show that specific brain pathways can modulate food preference,” she adds.
The researchers hypothesize that brain pathways in both humans and animals may have evolved to modulate the preference for high-fat foods to survive in times of famine.
“When there is not much food around, we need energy that can be stored and accessed when needed: fat delivers twice as many calories per gram as carbohydrates or protein and can be readily stored in our bodies,” Prof. Farooqi explains.
“As such, having a pathway that tells you to eat more fat at the expense of sugar, which we can only store to a limited extent in the body, would be a very useful way of defending against starvation.”
Prof. Sadaf Farooqi
Future work may focus on the many other genes that increase the risk of obesity that could be studied in combination with eating behavior.
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