'Don’t you have any taste?'
It is an interesting, if potentially rude, question that encompasses a broad church of possible topics. Are you about to be criticised for your taste in art? Theatre? Books? Clothes or music perhaps? And of course, let us not forget food.
A large proportion of food tastes are acquired. Take the different types of starchy carbohydrates, which make up more than 50 per cent of calories consumed throughout the world. My wife, who is of white Northern European ancestry, loves it in the form of bread.
I am of Chinese ancestry and can take or leave bread. Rice and noodles, however, I can easily eat every single day. The love of carbs is largely universal, but the ‘tastes’ for its different forms are culturally embedded from an early age.
What is less well known is that there are genes that influence our ‘taste’ for certain types of food.
In my lab, we study the genetics of bodyweight, which we now know to be powerfully influenced by how our brain controls our feeding behaviour. One of the key genes that play a role in the control of food intake is the melanocortin 4 receptor or MC4R, which forms part of the circuit in our brain that senses how much fat we are carrying.
This is important because how much fat we have onboard is directly related to how long we would survive without food. We have shown that around 0.3 per cent of the UK population, potentially up to 200,000 people in the country, carry mutations in the MC4R, making them, at 18 years of age, on average 18kg heavier than someone without an MC4R mutation. Of that 18 kg, 15 kg is fat.
Why? Because people with mutations in MC4R have brains that are less sensitive to the amount of fat in their bodies; their brains think they are carrying less fat than they actually are. As a result, they eat more, and end up heavier.
But the MC4R doesn’t only influence how much we eat, but also what we eat. A colleague of mine here in Cambridge, Professor Sadaf Farooqi, devised two different experiments, to try to understand the role that MC4R plays in influencing food choice. She tested lean individuals, and individuals with obesity with and without MC4R mutations.
In the first experiment, she gave participants an all-you-can-eat buffet with three options of chicken korma (a mild, sweet, almond-based curry). The three curries were the same, in look, smell and taste, but differed in fat content, which was manipulated to provide a ‘Goldilock’s-selection’ of 20 per cent (low), 40 per cent (medium) and 60 per cent (high) of the calories from fat.
What happened was those carrying a mutation in MC4R ate almost twice the amount of high-fat curry than the lean individuals ate, and 65 per cent more than individuals with non-MC4R obesity.
In the second experiment, the same three groups were given Eton mess, which is, in effect, what happens when someone drops a Pavlova made of strawberries, whipped cream and meringue on the floor, and scoops it back in a bowl.
Again, there were three options from which to choose, this time differing in the amount of sugar present in the meringue and cream, providing 8 per cent (low), 26 per cent (medium) and 54 per cent (high) of calorific content.
Paradoxically, in contrast to the fat choice experiment, individuals with a mutation in MC4R liked the high sugar dessert less than their lean and obese counterparts and in fact, ate significantly less of all three desserts compared to the other two groups. It turns out that people with a defective MC4R preferred higher fat food but had a decreased preference for sugary foods.
How about the taste or distaste for specific types of food? Brussels sprouts for instance?
I once did a talk at the Royal Institution in London about the genetics of feeding behaviour and performed a demonstration with 12 people from the audience. Everyone got a little blank bit of paper and were told to put it on their tongue (I did it too, to reassure that I wasn’t trying to poison anyone).
Half of the volunteers (including me) encountered an acutely bitter taste, while the other half tasted nothing, and were looking around, puzzled by the difference in reaction. What was going on?
Well, all the pieces of paper were infused with a little drop of phenylthiocarbamide, the chemical responsible for the bitter taste found in brassicas, plants in the cabbage and mustard family, which include the aforementioned Brussels sprouts.
However, only around 50 per cent of people, known as ‘supertasters’, carry a variation of the gene TAS2R38, that allows them to detect the bitterness. The ability to taste this bitterness doesn’t automatically mean you hate sprouts, but it certainly influences the taste sensation you get from eating them and other related vegetables.
Then there is the Marmite reaction of different people to the herb coriander (or cilantro, depending on where in the world you hail from), which many people consider tasty (me), but some, famously, the chef Julia Child, find disgusting. This dislike may, of course, simply reflect preference. However, for those coriander-phobes amongst you, for whom the herb has a strong soapy taste, it is indeed genetic.
Some people have a genetic variation in the olfactory-receptor gene OR6A2, allowing them to strongly perceive the aldehydes in coriander leaves, which are the source of the soapy-flavour. Interestingly, the prevalence of this genetic variation varies geographically, with regions where coriander is more popular, such as Central America and India, having fewer people carrying this ‘soapy’ variation.
So next time a dinner companion expresses a like or dislike for a specific food, it could be for cultural reasons, but it could indeed also have a genetic basis. Whatever the reason, it is probably best not to.
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