Scientists are narrowing in on why many of us find certain foods so irresistible. In a new study, researchers in the United Kingdom found that people with a particular gene mutation have a much stronger preference for fatty foods than those without the mutation.
These same people who preferred the fatty food also showed far less desire for sweet foods compared with other study participants, the researchers found. Although the mutation is rare, affecting less than 1 percent of the population, the findings suggest that all kinds of food preferences may be hard-wired into our brain circuitry, and defined by our genetics, the researchers said.
Understanding these genetic underpinnings of food preference may lead to better appetite-suppressing drugs that could help people avoid overeating, the researchers wrote in a study published Oct. 4 in the journal Nature Communications.
Most people find high-fat foods appetizing. This craving likely had evolutionary advantages because fat has twice as many calories per gram as protein and carbohydrates, and securing a sufficient number of calories was crucial for survival, according to Sadaf Farooqi of the Wellcome Trust–Medical Research Council Institute of Metabolic Science at the University of Cambridge, who led the new study.
"When there is not much food around, we need energy that can be stored and accessed when needed," Farooqi said. "As such, having a pathway that tells you to eat more fat at the expense of sugar [a carbohydrate], which we can only store to a limited extent in the body, would be a very useful way of defending against starvation."
A craving for fat
Previous studies in mice have shown that disruption of a particular neural pathway in the brain involving the melanocortin-4 receptor (MC4R) can lead to mice eating a lot more fat and a lot less sugar. This led researchers to speculate that the MC4R gene may be involved in appetite control.
Farooqi's group wanted to see how this mutation might affect the foods that people choose to eat. So, they devised a straightforward study involving some people with a rare mutation of the MC4R gene, and others without that mutation. Some of the people with the mutation were obese.
In a study, the researchers offered study participants an all-you-can-eat buffet of three different versions of chicken korma, a creamy curry dish. The three options in the buffet were manipulated to look and taste the same, but in fact the fat content was very different, containing either 20 percent (low), 40 percent (medium) and 60 percent (high) of the total calories.
Study participants fell into three categories: lean people, obese people and people who were obese because of the defective MC4R gene. After tasting a small sample of each dish, the participants were allowed to eat freely, unaware of the fat-content difference.
Although each group ate the same total amount of food, those with the defective MC4R gene ate about twice as much of the highest-fat option compared with the lean people. They ate about 1.5 times as much as the obese participants who did not have this gene mutation.
Then, in part two of this study, subjects were offered a dessert called Eton mess, a sweet mixture of strawberries, sugar, meringue and whipped cream. This time, the three options varied in their amount of sugar, but all had the same amount of fat.
In a caloric turnabout, the lean participants and the obese participants without the gene mutation went for the option with the highest sugar, while those with the mutation seemed to dislike that option and ate significantly less of all three desserts, compared with the other two groups, the study found.
A way to target hunger
With no perceptible difference in the look, smell and texture of the foods, the difference in preferences could only be explained by a genetic underpinning, not learned behavior, which may make it hard for some people to control their eating habits, the researchers concluded.
But manipulating this neural pathway that controls appetite in humans is proving to be difficult, according to Dr. Bradford Lowell, a professor of medicine at Beth Israel Deaconess Medical Center and Harvard Medical School, who led earlier research on the melanocortin-4 receptor in mice.
"The MC4R is indeed a potential drug target for treating obesity," Lowell told Live Science. "However, its activation, in addition to causing decreased hunger, also causes adverse cardiovascular effects. This is a problem made worse by the fact that individuals with obesity often are at increased risk for cardiovascular disease."
Lowell said his research team is continuing to investigate in mice the specific neural pathways that mediate the hunger-versus-cardiovascular effects of MC4Rs with the goal of activating only the appetite-control aspect of this neural pathway.
Farooqi told Live Science that there are "many other genes to explore, several of which seem to modulate the same pathways" and that she hopes to study them in the future.