Food Science and TechnologyVolume 35, Issue 3 p. 34-36 FeaturesFree Access Genetic preferences for food First published: 16 September 2021 https://doi.org/10.1002/fsat.3503_8.xAboutSectionsPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Dr Nicola Pirastu of the University of Edinburgh explains why the genetics of food liking is key to improving people's dietary choices. A woman enters a restaurant and sits at a table. A waiter approaches and asks ‘M'am would you like to try our special menu?’ The woman allows the waiter to scan her smart watch, downloading her genetic information so that the chef can add the optimum combination of different flavours to create a perfect match for the customer's genetic food preferences. Meanwhile across the street a man enters a dietitian's office, shares his genotype and the doctor provides a nutritional plan. The plan is not only healthier, but one that the customer will favour using products tailored to his taste profile. Finally in a lab outside the same city, many potential salt substitutes are tested in vitro, using cells engineered to express salt receptors on their surface, saving millions in product development costs. Although some of these scenarios are today relegated to science fiction books and might seem somewhat exaggerated, rapid advances in genetic techniques are making them increasingly plausible, for example human taste cell receptor assays are already in use for high-throughput screening in the flavour industry. Food preferences When people think of food preferences, a common belief is that they are mainly a cultural issue and that, in fact, you will like what you were raised to like. In this view of the world, differences in food preferences arise from either differences in parenting or personal experiences and people who do not like certain foods are considered to be ‘brought up differently’. This however does not coincide with what we know from studies of twins that have measured how food preferences are determined through familiar exposure, the environment and genetics. In these studies, differences in food preferences between identical twins are compared with differences between fraternal twins. Identical twins share 100% of the genome, while fraternal twins share only half. Having been born and raised the same way, the extent to which the preferences of the identical twins resemble each other compared to those of the fraternal twins will tell us how much they are determined through differences in the genetic code. This measure is referred to as ‘heritability’ and through the same model we can also measure the weight of the experiences the siblings share (i.e. the familiar environment) in comparison to those specific to each twin. A few years ago, we conducted a study on around 2,000 people from the Twins UK study to estimate how much these three components (genetics, familiar environment and personal experiences) weighed on differences in food preference1. We found that genetics accounted for between 35-60% of the variation in food liking, suggesting a much bigger role than was generally believed. The most surprising discovery was that the rest of the variation was due only to personal experiences (i.e. those not shared with brothers and sisters), whilst the familiar environment the siblings shared while growing up (i.e. the encouragement from parents or the foods they were exposed to within the household) did not have any measurable effect. Comparable studies conducted with children show similar results although the familiar environment does play a minor role (~20%). These results suggest that once people grow up, the familiar environment stops playing a role. This then brings into question the previous ‘multiple exposures will lead to liking’ model. Of course, to like or dislike something we need to be exposed to it (for example, I have personally never eaten Hákarl – the Icelandic rotten shark) and we do learn to enjoy and consume certain foods with an acquired taste (i.e. coffee or broccoli). There is, however, an underlying intrinsic ‘goodness’ in food, which is hard wired into our tongues, noses and brains. This will determine our first reaction to a food and if aversive, it will be hard to overcome without any accompanying positive stimuli. In this respect, looking at the inter-individual differences along with the biological hard-wiring will tell us how this mechanism works. This should enable us to tweak it to positively influence food consumption behaviour. So, the question becomes, can we use genetic studies to understand this extremely complex process? We certainly think so and in the last 10 years have conducted several studies to address these issues. Genetic studies One exemplary study looked at the relationship between bitter taste receptors (the receptors on our tongue responsible for perceiving bitter taste) and coffee liking2. In this study, data was collected from close to 5,000 people from Italy, the Netherlands and Central Asia. We looked for correlations between differences in coffee liking and differences in an individual's genetic code within the genes that encode for the bitter taste receptors. We found that a variant of a gene called TAS2R43, known to be responsible for triggering the bitterness perception of caffeine, was also associated with differences in coffee liking. Although this might have been expected, subsequent analyses revealed that contrary to our initial hypothesis, people who perceived caffeine to be more bitter also liked coffee more. This single study illustrates two important points. Firstly, the effect of caffeine is an important driver of coffee liking – confirming what is commonly believed although had not previously been demonstrated in a laboratory setting. Secondly, people can distinguish the specific bitterness of caffeine and assign it a different value in terms of liking compared to other bitter compounds. In fact, these people still do not like other bitter compounds but have unconsciously learnt to associate that specific bitterness with the beneficial psychoactive effects of caffeine. This means that although we generally refer to ‘bitterness’ as a unique sensation, it is possible that many different bitter sensations exist, although we may be unable to describe them at present. The previous example is a rather lucky one, where we had enough knowledge about the function of the gene being studied to be able to make hypotheses about the causal mechanism. Moreover, the differences observed were large enough that they were detectable in a sample of 5000 people. In most genetic studies, the effect of each genetic variant on food liking is very small and very large numbers of people need to be tested to reliably detect differences. For this reason, in collaboration with UK biobank, we set up what is probably the largest study ever conducted on food preferences3. UK biobank is a very large cohort study, which included around half a million UK participants aged between 40-70 at the time of collection (between 2006 and 2010) for whom a set of information was available ranging from GP records to blood tests and genotypes. Many of the participants were sent a food and other behaviours preference questionnaire composed of roughly one hundred and fifty food, drink and health related behaviours (such as smoking or physical activity) to be rated from one to nine on a hedonic scale. The results of the questionnaire were then compared with more than 11m variations in the genomes of participants. This enabled identification of many genomic loci associated with preferences for a wide range of different foods. It was also possible to identify three main groups of foods: one which included all high rewarding (calorie dense) foods ranging from meat to desserts, another included all foods generally considered healthy, such as fruit and vegetables, and finally a third group composed of foods for which taste is acquired, such as alcohol, coffee and spices. Changing energy dense food consumption patterns cannot easily be achieved through simple ‘will power’ as it would be acting against a basic biological mechanism and thus other approaches need to be pursued. One of the most interesting findings was that the high rewarding food measure was completely unrelated to the other two, suggesting that biology in this respect travels in two different and parallel paths. The high rewarding foods in the questionnaire showed no associations with the taste receptor genes (not even the sweet or umami receptors). However, both taste and olfactory receptors were associated with the foods in the other two categories. This finding suggests that genetic variants that result in a lower liking for calorie dense foods are not, at least in terms of flavour, selected by evolution. This is extremely important as otherwise our ability to acquire the necessary energy to survive would be reduced. It also means that changing energy dense food consumption patterns cannot easily be achieved through simple ‘will power’ as it would be acting against a basic biological mechanism and thus other approaches need to be pursued. Influencing food choices Designing medications to shift food choices toward less energy dense options thus improving overall quality of diet remains a possibility. We have shown that a genetic variation in the GIPR (Gastric Inhibitory Polypeptide Receptor) gene is responsible for higher liking of low-calorie foods combined with lower liking of fatty foods, such as cheese or cream3. GIPR is the receptor of a hormone called GIP that together with another hormone (GLP-1) is responsible for many of the metabolic effects induced by eating a meal, including for example, an increase in insulin. Medications that mimic the effect of GLP-1 have been shown to lead to weight loss of about 3kg in 28 weeks without any dietary interventions. However, when a drug that also targeted GIPR was used, the weight loss increased to 11kg over the same period. Unfortunately, it is not known whether this effect was due to a change in food choices, but certainly there is enough data to indicate that this is a possibility and that this could be a potential mechanism to facilitate weight loss. Conclusions Despite all the results from studies carried out so far, we have still only scratched the surface of what can be accomplished. There is a growing realisation that for dietary interventions to work, we need to understand how to help people comply with them because the ‘will power’ approach is rarely successful. In this respect understanding how food preferences work from a biological point of view may be the key to improving people's food choices through pleasure rather than guilt or judgement. In the future it may be possible to develop new recipes, products, additives and, for the most serious cases, medications aimed at improving the quality of what people eat without having to reduce their enjoyment. Understanding the biology behind these processes would allow such research to be more informed rather than proceeding by trial-and-error. This would ultimately save billions in terms of development costs while being more rapid and successful. This approach is already being implemented within the pharma sector, where companies, such as Regeneron, GSK and Pfizer, are investing in similar studies focused on diseases, because genetic studies have finally reached a point where the results are directly transferable to applied research. The food industry and the public sector could similarly benefit from research into the biology of food preference informed by genetics, leading eventually to new successful healthier products and thus improvements in public health. Dr Nicola Pirastu, Chancellor's Fellow, Usher Institute, The University of Edinburgh Email nicola.pirastu@ed.ac.uk To find out more come along to Dr Pirastu's webinar on the 18th November 2021 Using genetics to understand the factors influencing food liking and their role in food choices hosted by IFSTs Sensory Science Group. References 1Pallister, T. et al. Food Preference Patterns in a UK Twin Cohort. Twin Res. Hum. Genet. 18, 793– 805 (2015). Google Scholar 2Pirastu, N. et al. Association analysis of bitter receptor genes in five isolated populations identifies a significant correlation between TAS2R43 variants and coffee liking. PLoS One 9, e92065 (2014). Google Scholar 3May-Wilson, S. et al. Large-scale genome-wide association study of food liking reveals genetic determinants and genetic correlations with distinct neurophysiological traits. bioRxiv (2021) doi:https://doi.org/10.1101/2021.07.28.454120. Google Scholar Volume35, Issue3September 2021Pages 34-36 ReferencesRelatedInformation