Qian Yang of the University of Nottingham and Joanne Hort of Massey University review the latest developments linking genetic variation with taste perception and food preference.
Introduction
Taste stimuli are detected by taste receptors located in taste buds throughout the oral cavity, including the tongue, palate and throat. If you stick your tongue out and look at it in a mirror, you can see small pink bumps on the tip of your tongue which are the fungiform papillae – one type of papillae that house taste buds.
Humans are able to recognise five basic tastes: sweet, bitter, sour, salty, and umami (savoury). Recently, fatty taste, named oleogustus, has been identified as a candidate for a sixth basic taste[1].
From an evolutionary perspective, each taste is believed to function as a detector for our nutritional or physiological needs or of potential hazards. Sweetness signals calorie-rich food, which is a great source of energy. Umami signals the presence of protein-rich food, which is essential for growth and repair of body cells. Salty signals the presence of sodium or other salts, which are essential for maintaining the body’s water balance and blood circulation. Bitter taste is innately aversive, and thought to be a warning for potentially poisonous food, as most toxic substances taste bitter to humans. Sour taste is believed to signal spoilage of foods. ‘Fat taste’ may have evolved to detect essential fatty acids that represent high energy food[2].
Many studies have published evidence that taste sensitivity varies greatly among individuals and is one of the potential factors affecting food preference and choice. Our body hormones and proteins are under genetic control, thus variations in our genes are believed to affect the efficiency of our taste receptors. Consequently understanding the link between genes, taste sensitivity, and food choice could provide insights into consumer segmentation and help to develop effective strategies to provide customised foods/ diets and promote healthy eating. In recent years, genome-wide association studies have become a popular tool to detect genetic variants that contribute to taste perception/preference and some diseases. Single nucleotide polymorphisms (SNPs) are representative of genetic variation among people, where the type of nucleotide (A-adenine, T-thymine, G-guanine, or C-cytosine) can differ between individuals. This article summarises current understanding concerning the link between individual variation in taste perception and genetics.
From an evolutionary perspective, each taste is believed to function as a detector for our nutritional or physiological needs or of potential hazards.
Sweet perception
Humans are innately predisposed to enjoy sweetness. However, excessive sugar consumption has been linked to a range of public health issues, such as diabetes and obesity. Recently, due to the alarming increase of these health problems in populations across the world, the World Health Organisation (WHO) urged global action to curtail consumption of sugary drinks to reduce obesity, type 2 diabetes and tooth decay[3]. Thus, understanding individuals’ genetic make-up, taste perception and their drive for sweetness could potentially help with interventions to tackle these health problems.
Individual preference to sweetness levels in food varies. Researchers have grouped individuals as sweet likers (SL), who prefer increasing sweetness levels, and sweet dislikers (SD), who prefer lower levels of sweetness and show increasing dislike as sweetness increases. This taste phenotype is referred to as an individual’s Sweet Liking Status (SLS)[4]. In a recent study conducted at the Sensory Science Centre at the University of Nottingham, overall liking for sugar solutions, orange juice and yoghurts varying in sweetness levels was collected from 58 participants. The study found that SL preferred the high sugar solution (36g/l sugar in water), whereas SD preferred the low to medium sugar solutions (3 to 12g/l sugar in water). Similar trends were observed for both orange juice and yoghurt, where SL did not have a clear preference over the 6 sweetness levels for both products, but SD preferred the low sweet orange juice and yoghurt over high sweet samples (see Figure 1).
T1R2 and T1R3 are G Protein- Coupled Receptors that function in combination to detect the sweetness of a wide variety of natural sugars and artificial sweeteners in the oral cavity. A genome-association study has examined variants at rs35874116 of TAS1R2 in 1037 diabetes-free individuals and 100 individuals with diabetes, as well as their dietary intakes. A significant association between rs35874116 and sugar consumption in BMI>25 diabetes-free individuals and diabetes individuals was observed, where the ‘Val’ genotype consumed less sugar than the Ile/Ile genotype [5]. Variants at rs307355 and rs35744813 of the TAS1R3 were also examined in a 144 mixed ethnicity cohort; CC genotype for both SNPs was significantly associated with increased sucrose sensitivity[6]. A recent study has examined the rs838133 of ‘Fibroblast growth factor 21’ (FGF21), a sugar-induced hormone that contributes to the metabolic regulation of energy balance, in 6514 Danes. The researchers reported that variants at rs838133 were associated with total intake of all types of sweet-tasting foods, with A alleles self-reported to have higher intake of sweet foods[7].
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Figure 1 Overall liking of sucrose solution (a), orange juice (b), and yoghurt (c) between Sweet likers (SL) and Sweet dislikers (SD). Different letters indicate
significant difference at p≤0.05 |
Bitter taste perception
The ability to taste bitter compounds containing a thiourea (N-C=S) moiety, such as PTC and 6-n-propylthiouracil (PROP), varies greatly among individuals. This phenotype, called PROP Taster Status (PTS), has been studied widely since its discovery in 1932. Based on an individual’s ability to taste PTC/PROP, individuals can be grouped as ‘supertasters’ if they are supersensitive to PTC/ PROP and ‘nontasters’ if they are insensitive. Around 25% of caucasians are extremely sensitive to this compound and another 25% cannot taste it; this leaves about 50% of the population that perceive PTC/ PROP at a medium intensity.
Supertasters also have heightened taste sensitivity to other oral sensations, such as sweet, salty, fat and temperature sensations. PROP tasting has been associated with greater bitterness sensitivity to brassica vegetables and lower acceptance of cruciferous and some raw vegetables[8, 9], however, not all studies have found such trends. In addition, PTS did not only associate with bitter-food, but also with fat perception and preference of fat content in salad dressing[10], which is believed to be linked to the fact that, in general, supertasters have more fungiform papillae (see Figure 2).
So far, 43 human bitter receptors have been identified. The TAS2R38 receptor is the bitter receptor that affects ability to perceive PTC/PROP. The alleles in the TAS2R38 gene differ at three nucleotide positions resulting in amino acid changes in the protein (Proline48Alanine, Alanine262Valine, and Valine296Isoleucine), with amino acid combination proline-alanine-valine (PAV) identifying the taster variant, and alanine-valine-isoleucine (AVI) identifying the non-taster variant. However, variation in TAS2R38 cannot explain supertasters’ heightened responsiveness to other taste qualities. Some evidence has shown that gustin (rs2274333), which is a trophic factor for the growth and development of taste buds, may also be associated with PTS[11]. This was hypothesised to be the reason behind supertasters’ increased number of fungiform papillae and their super-sensitivity. However, a later study failed to replicate this finding[12].
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| Figure 2 Example of fungiform papillae density between supertaster and non-taster, and non-taster’s favourite food and supertaster least favourite food |
Salty taste receptors
There are at least two salt transduction pathways that have been proposed. The Amiloride-sensitive transduction pathway, is cation selective (Na+ and Li+) and is proposed to be mediated by ENaC, a member of the degenerin/ENaC superfamily of ion channels. An Amiloride-insensitive pathway is cation nonselective and can be activated by both sodium and nonsodium salts[13]. Transient Receptor Potential Vanilloid-1 (TRPV1) is a transducer of painful thermal stimuli and is also activated by capsaicin; it has been proposed to function as an amiloride-insensitive salt taste receptor in rodents[14]. A study has looked into the association between genetic variants in ENaC (SCNN1A, SCNN1B, SCNN1G and SCNN1D) and TRPV1 and salt sensitivity in 95 Canadians. Evidence showed that the SCNN1B gene was associated with salt sensitivity: those with homozygous A alleles for rs239345 and T alleles for rs3785368 perceived salt solution less intensely than T or C alleles respectively. For TRPV1 gene, T allele carriers of rs8065080 were significantly more sensitive to salt solutions than C allele carriers[15].
Sour taste receptors
Many ion channels have been proposed to mediate sour taste. It has been suggested that a broad range of receptors and mechanisms might be responsible for sour taste perception[13]. PKD2L1 and PKD1L3 are popular candidates for sour taste receptors that have been identified through animal studies, however, none has been definitely proven[13]. Little is known about individual variation in sour taste perception and how such variation may be linked to genetic variation. The sour taste receptor is only just beginning to be explored and a lot more research is needed to understand its complexity.
Genetic variation in taste perception and food preference has only just started to be explored; more research is now needed to understand this link.
Fat perception
The perception of fat involves many sensory modalities, such as somatosensory, olfactory and potentially gustatory systems. Recent evidence has suggested fatty taste could be another basic taste with evidence that fatty acids are detectable by humans[1]. Although the transduction mechanism of fat taste is not fully understood, CD36, a fatty acid translocase that is involved in fat detection and preference in animal studies, has been suggested as an orosensory receptor for long chain fatty acids.
A number of genome-wide association studies have investigated the relationship between CD36 SNPs and fat sensitivity. The most studied SNP is rs1761667 CD36. AA genotype of rs1761667 was found to be associated with greater perceived creaminess that was independent of fat concentration in salad dressings when tested in 317 African American adults[16]. But in another study tested in 64 Italian adults, AA genotype was associated with lower sensitivity to oleic acid[17], which conflicts with Keller’s findings. A significantly higher A-allele frequency was observed in young obese Algerian children (n=57) than lean children (n=59)[18]. Although studies to date are limited and some findings are conflicting, it is important to characterise genetic variations to understand the role of genetic variation in fat perception/ diet in order to understand the development of diet-related health problems.
Temperature perception
The temperature of food and beverages is very important for their acceptance; it can affect how food is perceived. It does not only affect the physical properties of the products, it also affects human temperature perception.
Interestingly, part of the population (between 20 to 50%) has an ability to perceive a taste sensation from warming or cooling their tongue and these people are called Thermal tasters (TT)[19]. Sweetness was commonly reported during warming (15 to 40°C) and bitterness was commonly reported during cooling (35 to 5°C). In addition, metallic is also often reported[20]. This means that some people might find a glass of hot water has a hint of sweet taste or a glass of cold water is a little bit metallic and bitter.
TRPM5 is a highly temperature sensitive ion channel. Evidence has shown that increasing temperature from 15 to 35°C markedly enhances the gustatory nerve responses to sweet compounds in mice, which has been suggested to be one of the possible mechanisms behind TTS[21]. However, to date no genetic link to this phenomenon has been found.
Studies conducted at the Sensory Science Centre at the University of Nottingham have found that individuals who can perceive a taste from either warming or cooling, also have heightened taste sensitivity and disliked strawberry drinks at extreme temperatures (e.g. warm or frozen) more than individuals who can only experience temperature changes but perceive no taste (Figure 3).
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Figure 3 Overall liking of strawberry drink at four different temperature between hermal tasters (TT) and thermal non-tasters (TnT). * indicate significant difference
at p≤0.05. |
Summary
The sensory properties of food are critical factors in determining the type of foods we choose to eat. Other factors, such as physiological, nutritional, environmental, and sociocultural factors, also contribute to our food choice and enjoyment.
Polymorphisms of genes that code for taste receptors partially account for variation in taste sensitivity, food preference and dietary habits. Genetic variation in taste perception and food preference has only just started to be explored; more research is now needed to understand this link. By investigating the link between genes, taste, food choice and health status, our understanding of consumer segmentations would be advanced such that food manufacturers can develop customised food products that are tailored to sub-populations’ needs, especially for a genetically diverse global market. This could facilitate more food enjoyment and effective dietary interventions to improve population health (Figure 4).
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| Figure 4 Factors that affect food selection and enjoyment and its ultimate the link to personalised food/diet |
Dr Qian Yang
Sensory Science Centre Manager
Division of Food Science, University of Nottingham, Sutton Bonington Campus, LE12 5RD
Email:Qian.Yang@nottingham.ac.uk
Professor Joanne Hort
Fonterra Riddet Chair in Consumer and Sensory Science
Riddet Institute, Massey University, Palmerston North, New Zealand
Email:J.Hort@massey.ac.nz
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