The study, led by the University of Cambridge, is one of the first studies to show a direct link between food preference and specific genetic variants in humans. The research builds upon previous studies on mice, which highlighted that disruption of a particular pathway in the brain involving the melanocortin-4 reception (MC4R) can lead to mice eating a lot more fat. What was unusual was that these mice consumed a lot less sugar.
Chicken korma and an Eton mess
Recently published in the journal ‘Nature Communications’, Cambridge researchers have shown a similar correlation with humans who possess the MC4R gene. They gave participants to the study an all-you-can-eat buffet of chicken korma curry, one of the most popular dishes in the United Kingdom. They prepared three different options of korma, all manipulated to look and taste the same, but each with differing levels of fat content – one with 20 % (low), one with 40 % (medium) and finally one with 60 % (high) of the calories. The study tested lean people, obese people, and people who were obese because they have a defect in the MC4R gene (which affects approximately one in 100 obese people).
After taking a small taster of each meal, the participants were then allowed to eat freely from the three kormas. Importantly, they could not tell the difference between the foods and were unaware that the fat content varied in each dish. The research team discovered that although there was no overall difference in the amount of food eaten between the groups, individuals with the defective MC4R gene ate almost double the amount of high fat korma that lean individuals ate and 65 % more than obese individuals without the defect.
In a second experiment, the participants were served Eton mess, a traditional English dessert that includes strawberries, whipped cream and broken meringue. Again, there were three options to choose from, but this time it was the overall sugar content that differed between low, medium and high concentrations. The fat content though was fixed. Again, participants could choose which of the three desserts to eat.
Lean and obese individuals preferred the high sugar dessert more than the other two options. However, individuals with the MC4R defect were less enamoured with the high sugar option and actually ate significantly less of all three desserts compared to the other two groups. For obese individuals who do possess the defective MC4R gene, this makes them much more likely to put on weight. The research team believes that for these individuals, the fact that the MC4R pathway is not working may lead them to subconsciously prefer high fat food which then contributes to their weight problem.
A survival mechanism against starvation
‘Our work shows that even if you tightly control the appearance and taste of food, our brains can detect the nutrient content,’ commented Professor Sadaf Farooqi, who led the research at Cambridge. ‘Most of the time we eat foods that are both high in fat and high in sugar. 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.’
Prof. Farooqi and her colleagues believe that humans and animals may have evolved pathways in the brain that modulate the preference for high fat food in order to cope with 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 easily stored in our bodies,’ she explained. ‘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.’
The NEUROFAST project ended in March 2015, whilst the ERC-funded STILTS project will continue until December 2016.
For more information, please see:
STILTS project page on CORDIS
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