The prevalence of overweight and obesity in Canada has been growing at an alarming rate, and children are not exempt from this epidemic growth. According to the World Health Organization, 31.5% of children and adolescents aged 5–17 years old—an estimated 1.6 million Canadians—were classified as overweight (19.8%) or obese (11.7%) from 2009 to 2011 [1
]. The accessibility of palatable, processed foods high in fats and sugars has increased in modern society. Chronic diseases such as obesity, cardiovascular disease (CVD), type 2 diabetes (T2D), and metabolic syndrome (MetS) have been partially attributed to poor eating habits in those compelled by the hedonic qualities of food [2
]. The taste of food is a particularly important factor for parents when selecting foods for themselves and their children [3
]. Through the individual selection of unhealthy foods, taste perception may therefore be an important determinant of chronic disease risk.
Research on the genetic predisposition to selecting specific foods based on taste perception may be significant in advancing our fundamental knowledge of genetic factors influencing habitual dietary intake and the development of chronic disease. Genetic variation in taste perception can be characterized in terms of single nucleotide polymorphisms (SNPs) in taste receptor genes. Taste receptor function for sweet, fat, and bitter tastes forms much of the basis for the known inter-individual differences in taste perception [4
]. The fat taste receptor cluster determinant 36 (CD36), the sweet taste receptor type 1 member 2 (T1R2) and sweet taste receptor type 1 member 3 (T1R3), and the bitter taste receptor T2R38 contain common polymorphisms that may alter taste perception, food preference, and consequently food selection [2
Research related to fat taste perception has focused on the fatty acid translocase CD36
gene. Decreases in fatty acid taste sensitivity have been associated with the AA genotype of the rs1761667 SNP in the CD36
]. A lower oral sensitivity to fatty acids has been found to associate with a higher preference and consumption of dietary fat [7
]. However, little is known about the effect of this SNP on dietary intake in children.
The heterodimer T1R2 and T1R3 allows humans to taste a variety of sweet substances [8
], and genetic variations in TAS1R2
may pertain to changes in taste sensitivity to sugar [10
]. Specifically, the TT genotype of the rs35874116 SNP in the TAS1R2
gene has been linked to habitual sugar consumption in overweight and obese adults [20
] and children [21
]. In children, dental caries risk is a concern associated with the consumption of sugar [22
]. The prevalence of dental caries was observed to be associated with the rs35874116 SNP [23
]. Research to date has yet to show a relationship between the rs35874116 SNP and sugar consumption in children.
The perceptions of bitter and sweet tastes interact in such a way to affect eating habits, especially in children [4
]. Consuming bitter compounds generally results in food rejection, an evolutionary adaptation to avoid toxic substances such as rancid fat, hydrolyzed protein and plant alkaloids [24
]. Sensitivity to bitterness may lead to the avoidance of Brassica vegetables rich in fiber, thereby potentially being replaced with the consumption of energy-dense foods rich in sugar [26
]. These eating habits have the potential to increase the risk of obesity, CVD, and cancer [28
]. Kim et al. (2003) showed that the bitter receptor T2R38 mediated the sensitivity to PTC, a thiol compound chemically related to those found in green, leafy vegetables (Brassica vegetables) [29
]. Three common SNPs in the TAS2R38
gene result in amino acid substitutions at residues P49A (rs713598), A262V (rs1726866) and V296I (rs10246939). The C allele of the rs713598 SNP is associated with the PAV haplotype while the G allele is associated with the AVI haplotype. Individuals carrying two copies of the PAV haplotype typically have a strong aversion to the bitterness of PTC. Those who seldom taste PTC carry two copies of the AVI haplotype while heterozygotes (PAV/AVI) typically have an intermediate taste phenotype [30
The prevalence of snacking, or the consumption of foods and/or beverages between meals, is increasing in children as 98% of U.S. children snacked daily in 2006 compared to 74% in 1977 [31
]. Young children are especially inclined to snacking and typically consume small meals throughout the day rather than larger meals [32
]. These snacks are frequently energy-dense and nutrient-poor choices such as desserts, salty snacks, and sugary drinks which lead to excess energy consumption [32
]. While existing evidence identifies snacking as a substantial source of calories in preschoolers’ diets, there is limited knowledge about the factors that drive snacking patterns, including snacking frequency and the quantity and quality of snacks consumed. The genetics of taste is one factor that may help better understand snacking patterns of children. Studies examining the relationship between the genetics of taste and snacking in children are limited despite existing evidence that taste receptor SNPs may impact taste perception, and therefore food selection [2
]. Examining snacking patterns among children may provide important insight into the contribution of genetic variation in taste receptors to food selection.
The putative fat taste receptor CD36, the sweet taste receptor T1R2, and the bitter taste receptor T2R38 contain common polymorphisms which may alter taste perception, food preferences, and consequently snacking patterns. Thus, the present study aimed to determine the relationship between SNPs in CD36, TAS1R2, and TAS2R38 taste receptor genes and snacking patterns measured in children aged 1.5–5 years in the Guelph Family Health Study pilot.
The present study showed that genetic variation in taste receptors are associated with potentially unhealthy snacking patterns in children. Three SNPs were investigated within taste receptor genes for fat (CD36
; rs1761667), sweet (TAS1R2
; rs35874116), and bitter taste (TAS2R38
; rs713598). The prevalence of snacking in this cohort is similar to the prevalence of snacking in American children, and the calories from snacks are similar as well [31
]. In addition, in a Brazilian study, the prevalence of snacking in children can be divided into children who are light-snackers and heavy-snackers. The prevalence of snacking and the calories from snacks are similar between heavy-snackers in Brazil and children from North American cohorts. However, the light-snackers in Brazil consume less snacks which also comprise a smaller portion of calories than North American children [35
Adults with the A/A genotype of the rs1761667 variant have been shown to have lower oral sensitivity to fat and higher preference for fat [6
]. In the present study, no relationship was observed between carrying the AA genotype and snack quantity, frequency, or calories from fat; however, children carrying the AA genotype consumed higher energy density of snacks than children carrying the G allele at this locus. While studies have shown differences in sensory outcomes based on this CD36
SNP, an effect on dietary intake has never been observed. The present finding suggests that a fat taste receptor SNP genotype may influence the intake of energy-dense snacks. This finding is potentially due to the decreased sensitivity to fat taste and subsequent higher preference for fatty foods; however, measures of taste sensitivity were not determined in this study. Although the relationship between fat taste sensitivity and energy density of snacks in this study is consistent with the energy density of fat as a macronutrient, no difference was found between the calories from fat in snacks for this genotype. This apparent contradiction may be due to the challenges of measuring the contribution of fat in a complex diet which contains foods simultaneously high in fat and carbohydrates. Future research studies would benefit from performing hedonic tests for fat taste with children in more controlled settings in addition to tracking food records. A genetic predisposition to prefer fatty foods due to lower taste sensitivity may be of concern for children in the long term as high fat diets may lead to metabolic complications such as obesity, MetS, and CVD [37
Carriers of the TT genotype at the rs35874116 locus (Ile191Val) in the TAS1R2
sweet taste receptor gene have been shown to prefer sweet foods [20
]. Children in the GFHS cohort carrying the TT genotype were found to consume snacks with significantly more calories from sugar than children carrying the C allele. While the percent of calories from sugar was different, it is not clear why the energy density of snacks was not significantly different based on rs35874116 SNP genotype. As snacks contain a complex combination of different macronutrients, it is difficult to discern which macronutrients contribute a higher proportion of energy density. While consistent with previous research linking the Ile191Val variant with habitual sugar consumption in overweight/obese adults and dental caries in children [20
], the present finding demonstrates that taste preferences and dietary intake may also be related in children. Upon further analysis, it was found that sugary snacks were most frequently consumed in the evening by children with the TT genotype. If the evening is a time of day when children with a “sweet tooth” potentially consume more sugary snacks, this finding warrants future studies to assess the availability and accessibility of sugary foods in the home environment as a means to address the role of parents in the intake of sugary foods by young children during the evening. Future studies may also benefit from including genetic variants in the TAS1R3
sweet taste receptor gene to examine determinants of sweet food intake [21
]. Chronic overconsumption of sugar is a well-known risk factor for MetS and T2D [39
]. With the advancement of research pertaining to this variant, there may be reason to use genotype at this locus as a risk factor for overconsumption of sugar in children. Adapting the Ile191Val SNP genotype into a clinical biomarker of dietary intake patterns in children may be helpful to mitigate the risk of developing obesity, MetS, and T2D.
The bitterness of green leafy vegetables (Brassica vegetables), related to the taste of thiol compounds, may be stronger in those homozygous for the C allele at the rs713598 locus in the TAS2R38
taste receptor gene. Those who do not carry the C allele may not taste PTC, and this may then influence the perceived bitterness of Brassica vegetables [30
]. We hypothesized that carriers of the CC genotype in our study would be more likely to consume energy-dense snacks due to their potential avoidance of bitter vegetables [4
]. In support of this hypothesis, CC genotype carriers and CG genotype carriers had higher total energy density of snacks compared to GG genotype carriers. No relationships were observed between rs713598 genotype and snack quantity, frequency, or calorie composition, in line with previous research [41
]. This finding contributes to a growing, controversial body of literature about this genetic locus, showing that this genotype may adversely affect quality of dietary intake [43
]. Similar to the other variants investigated in the present study, this SNP may serve as a biomarker for at-risk eating patterns with the potential of developing into adverse metabolic and health outcomes.
The prevalence of combinations of the taste receptor SNP genotypes associated with snacking patterns are important to consider. Participants can be classified by the proportion of “at-risk” genotypes they carry based on the three SNPs included in the present analysis. The “at-risk” genotypes were AA for the CD36 SNP (fat preference), TT for the TAS1R2 SNP (sweet preference), and CC for the TAS2R38 SNP. None of the children in this study had all three “at-risk” genotypes, 13/47 (28%) of the children had two “at-risk” genotypes, 24/47 (51%) of the children had one “at-risk” genotype, and 10/47 (21%) of the children had no “at-risk” genotypes. Therefore, the prevalence of carrying at least one “at-risk” genotype was almost 80% within this cohort. This observation is an indicator that these genotypes are sufficiently common and warrant parents’ awareness of the potential influence on habitual dietary intake in young children. It is not known whether the potential disadvantage of carrying “at-risk” genotypes is additive when a combination of these genotypes is present. Moreover, it is difficult to assess whether one “at-risk” genotype can be cancelled out by a “healthy” genotype at a different locus within the same taste receptor gene. Analysis of the relative influences that each SNP has on habitual dietary intake requires a greater understanding of the individual effect on habitual dietary intake as well as a much larger study cohort.
This study’s limitations should be considered when interpreting the results. These data were obtained in a pilot phase of the GFHS, and the probability of type 2 error is higher with a small sample size. Due to the exploratory nature of this study, multiple testing was not accounted for and there is a possibility of false discovery in the findings. Furthermore, there is uncertainty that the quantity, quality, frequency, or composition of snacks consumed reflect the taste preferences of the children rather than parental feeding styles and practices. While it is probable that taste preferences are strong indicators of food selection in this study, the parents’ influence on food availability and accessibility need to be considered in future investigations.