Taste impacts food selection, and food intake impacts nutritional status. The taste of food is a major factor in determining food selection. From infancy, we derive pleasure from sweet foods and have an innate dislike for bitter-tasting foods [1]. Taste directs food preferences and plays a role in forming dietary patterns that impact health. Diet impacts risk for many chronic diseases, including cancer, cardiovascular disease (CVD), hypertension, type 2 diabetes mellitus, and obesity. Decades of research suggest that these chronic conditions result in major morbidity and mortality and consume significant health care resources in the United States [210]. Collectively, these studies also suggest that a majority of chronic diseases could be prevented or mitigated by the adoption of healthier eating habits. Here, we review the role of taste in modulating nutrient intake as well as what is currently understood with respect to genetic variation in genes involved in chemoreception and their impact on food intake and risk of chronic disease. (Table 1)

Table 1 Genetic variants associated with taste, food preference, and intake

Sensory systems, particularly taste and olfaction, strongly influence food selection and intake. Chemosensory, thermosensory, and mechanosensory signals arising from specialized receptors positioned in both the oral-pharyngeal and nasal cavities and gastrointestinal tract are transmitted to the central nervous system (CNS), imparting information related to macronutrient composition, caloric density, osmolarity, and potential toxicity of food [1114]. Chief among these neural signals are those provided by the gustatory system, which is the final guardian of the alimentary tract. It is widely believed that these orosensory inputs, especially taste, integrate with other neural and endocrine signals related to energy, fluid, and electrolyte status and ultimately influence central neural circuits controlling food and fluid intake.

Before we review what is currently known about variation in taste perception, its genetic underpinnings, and how this variation may impact upon nutrient ingestion, we provide a brief primer on the organization of the taste system, with a particular focus on the peripheral gustatory system [1517].

Functional Organization of the Peripheral Gustatory System

Taste stimuli elicit perceptions that can be categorized into five qualities—sweet, bitter, salty, sour, and umami—each of which is associated with a biologically relevant class of compounds [15, 18]. The detection of these stimuli occurs in taste cells. Taste cells on the tongue are grouped into buds, which in turn are clustered within papillae. Within each taste bud, taste cells fall into three morphological subtypes, types 1, 2, and 3, which seem to correspond to functional classes. Type 2 cells express receptors for sweet, bitter, and umami taste, as well as associated downstream signaling components. These taste cells do not form traditional synapses with afferent nerve fibers but appear to form purinergic connections with nerve fibers and neighboring cells [1921]. Type 3 cells, by contrast, do form traditional synapses with ascending nerves and are identified by the presence of serotonin and synaptic machinery such as SNAP-25 and NCAM [22, 23]. It appears that at least some type 3 cells are sensors for sour stimuli [24, 25]. Type 1 cells are thought to play more of a supporting, glial-like role, though these cells have recently been implicated in salty taste (Fig. 1) [2628]. Little is currently known about cell-to-cell communication and its affect on the neural output of the taste bud; therefore, more research is needed to further elucidate details of these mechanisms.

Fig. 1
figure 1

Schematic description of taste bud with morphologic cell types. TRC taste receptor cell

Three genes from the TAS1R gene family encode three G-protein-coupled receptors (GPCRs), T1R1, T1R2, and T1R3, which are responsible for mediating perceptions of sweet and amino acid tastes. T1R2 and T1R3 combine to from a heteromeric receptor that binds with sugars and a variety of other structurally diverse compounds that give rise to a sweet taste perception [16, 29, 30], while T1R3 in complex with T1R1 forms a heterodimer that responds to L-amino acids. In humans, this receptor is narrowly tuned to the amino acid glutamate [31], the detection of which results in a “savory” perception referred to as umami. The TAS2R genes encode bitter taste receptors. It is said that there are about 25 members of this family in humans, which encode broadly tuned GPCRs, allowing for the detection of a large number of structurally diverse bitter compounds [32, 33].

While perceptions of sweet, bitter, and umami tastes are mediated by G-protein-signaling cascades, salty and sour taste detection is mediated via ion channels [34]. Epithelial sodium channels allow for the entrance of Na+ ions into the cells, leading to a salty taste perception [28]. A subset of type 3 cells appears to be specialized for detecting hydrogen ions released by acidic taste stimuli, leading to a sour perception [24, 25]. Recent work suggests that one pathway in which H+ ions enter and transduce taste cells is by passing through a specialized proton channel that expresses the polycystic kidney disease 2-like 1 ion channel [24].

Neurophysiologic studies in several mammalian species have shown that four major branches of three cranial nerves innervate taste buds in the oral cavity. These nerves carry gustatory neural signals from the oral cavity to the solitary nucleus in the brainstem. These signals are then propagated up through the gustatory neuroaxis. The chorda tympani branch of the facial nerve innervates taste buds on the anterior two thirds of the tongue. The greater superficial petrosal branch of the facial nerve innervates the taste buds of the soft palate. The lingual–tonsilar branch of the glossopharyngeal nerve innervates taste buds of the posterior third of the tongue. The superior laryngeal branch of the vagus nerve innervates a small number of taste buds located on the laryngeal epithelium.

Genetic Variation Known to Influence Taste Preference

Bitter Taste

The most well-characterized human taste phenotype is the relative sensitivity of individuals to the bitter taste evoked by any variety of compounds containing an N–C = S (thiourea) moiety, such as phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) [35, 36]. As early as the 1930s, investigators found that not everyone can perceive the taste of the bitter compound PTC [37]; the earliest studies of the genetics of taste perception utilized PTC (decades later PROP, another bitter compound to which many people are taste blind, became more widely used when it was found to be less toxic). Early studies on PTC and PROP focused on tasters versus non-tasters. More recently, three categories of tasting ability have emerged: non-tasters, medium tasters, and tasters of PROP. Non-tasters cannot distinguish the taste of solutions containing PROP from that of pure water, whereas tasters characterize PROP as having a distinctively bitter taste [38]. PROP-tasting ability is a heritable trait. Non-tasters were thought to be homozygous for the recessive allele of the PROP-tasting gene, medium tasters heterozygous, and tasters homozygous dominant [38].

It was discovered in 2003 that the chief determinant of an individual’s responsiveness to PROP/PTC was the inheritance of haplotypes of the gene TAS2R38 [39, 40]. TAS2R38 has been extensively characterized in vitro, in vivo, and in human populations, and is responsive to a variety of the bitter-tasting stimuli, all of which contain the N−C = S (thiourea) moiety (eg, PTC and PROP). TAS2R38 haplotype predicts the majority (55–85 %) of phenotypic variance in PROP sensitivity [39]. Two common haplotypes have been shown to influence perception of these compounds: among individuals of Northern European decent, the nontaster haplotype and taster haplotype represent 47 % and 49 % of all haplotypes, respectively, and 30 % and 70 %, respectively, among individuals of East Asian decent. [39]. Although also studied with respect to bitter taste in general, PROP taster status is not a specific marker for sensitivity to the bitterness of other bitter compounds [41].

As mentioned above, three categories of PROP-tasting ability have been identified: non-tasters, medium tasters, and tasters. However, a subset of tasters are able to perceive the bitterness of PROP at significantly lower concentrations than do typical tasters [38]. These individuals have been dubbed supertasters. Interestingly, supertasters not only do have a heighten sensitivity to PROP but also respond more robustly to a variety of taste compounds, and perceive more burn from oral irritants (alcohol and capsaicin). It was postulated that the supertaster phenotype was due to increased neural “gain” in signals emanating from the oral cavity. This assertion was supported by the fact that the density of taste buds on the anterior tongue was correlated with supertaster status [38]. Additionally, it was recently demonstrated that genetic variation in the taste bud trophic factor gene GUSTIN (CA6) is also strongly associated with PROP sensitivity [42, 43, 44••].

Although the vast majority of research on the genetic determinants of bitter taste perception has focus, almost exclusively, on the PROP taste sensitivity phenotype, a handful of other studies have attempted to uncover genetic factors associated with taste sensitivity to other prototypical bitter-tasting compounds. Reed et al. [45•] performed a genome-wide association study attempting to discover variants associated with the perceived taste intensity of quinine HCl (QHCl), caffeine, and sucrose octaacetate (SOA). For caffeine and SOA, no single nucleotide polymorphism (SNP) association reached the genome-wide statistical significance criterion. For quinine, however, a peak association was centered in a region that contains the bitter taste receptor TAS2R19. It should be noted, however, that the SNP in TAS2R19 was in tight LD with other bitter receptors, as well as with salivary proline-rich protein genes, which have also been associated with bitter taste responsiveness. In another study, Hayes et al. [46] found, using a candidate gene approach, that a haploblock across TAS2R3, TAS2R4, and TAS2R5 was associated with variability in the bitterness of espresso coffee [46]. They also found that variation in TAS2R19 was associated with the perceived bitterness of grapefruit juice.

It is well-known that a variety of artificial sweeteners possess bitter aftertaste (eg, saccharin). It was discovered that activation of bitter taste receptors mediate this perception [47] and that genetic variation in specific TAS2R genes (particularly TAS2R31) strongly influenced the perceived bitterness of the artificial sweeteners saccharin and acesulfame K [47].

Sweet and Umami Taste

Although less well-studied than bitter taste, evidence exists suggesting that genetic variation also impacts upon sweet and umami taste perception. For example, Fushan et al. [48] found two SNPs located upstream of the TAS1R3 coding sequence that were strongly associated with human taste sensitivity to sucrose. This same group also tested if variation in other genes encoding taste-signaling molecules can influence sweet taste perception [49]. Their association analyses revealed a significant correlation between sucrose responsiveness and genetic variation occurring in the GNAT3 gene. GNAT3 encodes the taste-specific Gα subunit α-gustducin, a G protein subunit involved in taste cell signal transduction. Raliou et al. [50, 51] showed that variation in monosodium glutamate detection thresholds was also associated with polymorphisms in the TAS1R1 and TAS1R3 genes.

Very few studies have attempted to identify whether genetic variation in genes other than those already know to impact the functioning of the peripheral gustatory system can influence sweet and/or umami taste responsiveness. To the best of our knowledge, only one genome-wide study designed to identify genetic factors associated with sweet taste functioning has been published [52]. Keskitalo et al. [52] found a significant association with genetic variation on chromosome 16 and sweet taste preference. It should be noted that these investigators only tested 146 subjects and conducted a genome-wide analysis with only 450 markers. As such, the possibility of type II error was likely high.

Salty and Sour Taste

Although no genetic variants have been identified that impact upon variation in human salty and sour taste sensitivity, heritability studies suggest that genetic factors do play a part in variation sour taste responsiveness [53]. An investigation by Wise et al. [53] found that sour taste sensitivity displays heritability on par with that of sensitivity to the bitter compounds PROP, strongly suggesting that genetic factors play a large role in variation in this phenotype [54]. Data from a recent study on acid taste sensitivity in humans suggest the involvement of PKD-like receptors as well as other receptors in the mediation of sour taste. Huque et al. [55] measured the expression level of gene transcripts in taste receptor cells between subjects ageusic to sour tasting stimuli and those with normal sour taste sensitivity. Various ASIC isoforms as well as the channels PKD1L3 and PKD2L1 were readily detectable in subjects with normal taste sensitivity. However, none of these transcripts were detectable in subjects with sour taste ageusia [55]. In the Wise et al. [53] study detailed above, it was also reported that salty taste sensitivity did not show significant genetic heritability. Much more research needs to be conducted on variation in sweet and sour taste perception before it can be ascertained if genetic variation influences taste responsiveness toward these stimuli.

Variation in Taste Responsiveness and its Association with Food Preference and Intake

Although all taste modalities impact upon food selection, the influence of bitter taste perception on food preference has been the most extensively studied [56]. A large body of research indicates that individuals who possess enhanced perception of bitter taste avoid certain foods, including specific fruits and vegetables [5765]. For example, the perceived bitterness evoked by tasting various types of vegetables (eg, brussels sprouts, kale, asparagus) was shown to predict the preference for those vegetables as well as self-reported measures of vegetable intake [58]. Indeed, bitter taste perception is thought to have evolved to detect toxins in plants, vegetables, and foods and to modulate the ingestion of them [66, 67]. It has been postulated that plants evolved to protect themselves from being eaten by animals by synthesizing phytochemicals such as phenols, flavonoids, isoflavones, terpenes, and glucosinolates, which are almost always bitter, acrid, or astringent [66, 67]. Paradoxically, some of these bitter-tasting phytochemicals, including many flavonoids and polyphenols, have been associated with positive health benefits [68].

Interestingly, as mentioned above, many plants and vegetables synthesize glucosinolates, a class of compounds that also contain the thiourea moiety [69]. It has been proposed by many [58, 70, 71] that taste sensitivity to PROP can be used as a marker for individual differences in taste perception that influence food preferences and intake. For example, it has been demonstrated by multiple laboratories that children identified as insensitive to PROP consumed more vegetables than did the “taster” children during a free-choice intake test [72, 73]. These children also expressed greater “liking” for raw broccoli relative to taster children in a hedonic test [72]. Additionally, in female subjects, sensitivity to the bitterness of PROP was shown to be associated with lower acceptance of cruciferous and selected green and raw vegetables [5961]. Similarly, female PTC non-tasters reported greater use of cooked turnip and raw watercress than did PTC tasters [64]. Colon cancer patients who tasted PROP as more bitter also reported less vegetable intake [74]. PROP and PTC tasters have also been reported to regard sodium benzoate (a common food preservative) and potassium chloride (a dietary salt substitute) as more bitter than non-tasters [75].

Based on the associations detailed above, one would predict that TAS2R38 haploypes would also influence the ingestion of certain foods. Indeed, individuals who posses at least one copy of the PROP-sensitive allele of TAS2R38 eat fewer cruciferous vegetables than do adults who are homozygous for the PROP-insensitive allele [76]. Colares-Bento et al. [77] also reported a similar finding in a cohort of older Brazilian women. Feeney et al. [78] reported that vegetable intake in both men and women was influenced by TAS2R38 genotype, but in women, the insensitive allele of the TAS2R38 was also associated with a macro- and micronutrient nutrient intake pattern indicative of healthy eating. Collectively, these data suggest that individuals with a strong sensitivity to bitter taste, along with a concomitant altered perceived taste sensation evoked by certain foods, such as vegetables, reduced their intake of these foods. Intake of fruits and vegetables has been negatively correlated with risk of cancer [79]. Consistent with this observation, bitter taste sensitivity/responsiveness has also been associated with body mass index (BMI), adiposity, and risk factors for CVD [78, 8084] in adults, as well as with BMI in children [73]. However, there are studies that suggest no links exist [85, 86].

Although less well-studied, variation in sweet taste responsiveness also impacts food preference and intake. Eny et al. [87] found that genetic variation in TAS1R2 was associated with consumption of sugars, specifically in overweight participants. Moreover, as with the perceived bitterness of certain foods, perceived sweetness was shown to predict the preference for sampled vegetables as well as vegetable intake in adults [58, 60]. In addition, evidence suggests that sweet-tasting substances induce cephalic phase hormonal response reflexes [8890], providing another route through which sweet taste responsiveness can impact upon health. Indeed, recent evidence suggests that sweet taste receptors in the tongue and palate may be important in initiating preabsorptive metabolic responses to ingested nutrients [91]. However, at least in humans, it appears that sweet taste must be coupled with additional sensory modalities (eg, touch and smell) in order to produce preabsorptive hormone secretions [92, 93]. Be that as it may, it seems clear that variation in sweet taste responsiveness can lead to variation in food intake, as well as in the body’s postprandial hormone response to the ingestion of those nutrients, which could potentially impact upon metabolic health. In support of this contention, multiple investigators have shown that the perceived sweetness of foods is correlated with BMI [9496]. It has also been demonstrated that a higher preference for sucrose solutions was associated with increased preferences for sweet desserts [60]. These data are particularly compelling considering the recent finding that revealed a positive association between the consumption of sugar-sweetened beverages and blood pressure [97] and with risk of metabolic syndrome and type 2 diabetes mellitus [98].


The ability to detect and discriminate taste stimuli is essential for health and survival and can drive ingestive behaviors. The gustatory system critically influences food preference and food intake. A large body of research clearly suggests a strong link between taste functioning, in particular bitter and sweet taste sensitivity, and food preference and intake. Moreover, a number of genes previously known to influence taste perception have been shown to also impact upon food preference and intake.

However, despite the fact that many other factors in addition to taste receptor biophysiology contribute to the functioning of the gustatory system, genetic association studies of taste functioning have largely been limited to the evaluation of genetic variation in and around taste receptor genes. However, a significant portion of variation in taste preferences likely depends on genes that are not involved in peripheral taste processing [99]. For example, genes involved in central mechanisms of taste processing and reward or motivation are also likely to strongly influence taste perception and food intake [100]. Thus, it is necessary for researchers in chemosensory genetics to expand the breadth and depth of genomic analysis beyond the evaluation of candidate genes to fully understand and explain the greatest proportion of variation in taste perception and its impact of nutritional intake. Indeed, understanding the role of genetics and how genetic variation influences taste functioning and food intake has significant implications for public health. Early ascertainment of heritable risk may facilitate timely implementation of preventive eating strategies that may decrease associated morbidity and mortality.