Traits

Trait: Bitter taste sensitivity

Dr Haran Sivapalan

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December 20, 2021

Are Brussels sprouts going to feature on your plate this Christmas? Perhaps surprisingly, the answer to this question may rely upon what genes you carry!

In this Christmas-themed Bitter Taste Sensitivity trait, we look at variants of the TAS2R38 gene, that strongly affect whether you’re overly sensitive to bitter compounds in broccoli, coffee, and that festive favourite (well, depending on your genes), the Brussels sprout.

Why do some foods taste bitter?

You may have noticed that foods such as broccoli, cabbage, grapefruit, and Brussels sprouts have a bitter edge to them. This is because all of these foods contain a class of related molecules known as thiourea compounds.

This class of compounds, which includes sinigrin in Brussels sprouts and broccoli, goitrin in cabbage, and naringin in grapefruit, all contain a thiourea (N-C=S) chemical group.

Source:Keller, K. L., & Adise, S. (2016). Variation in the ability to taste bitter thiourea compounds: implications for food acceptance, dietary intake, and obesity risk in children. Annual review of nutrition, 36.

When we eat these foods, the thiourea compounds activate specialised bitter taste receptors (TAS2Rs) on the surface of our tongue, giving rise to a bitter sensation. There are thought to be at least 25 different types of bitter taste receptors, with TAS2R38 (taste receptor 2 member 38) being particularly sensitive to thiourea compounds.

As we’ll discover in the following sections, however, people vary considerably in their ability to taste bitter thiourea compounds. Some people may find them extremely bitter, while others may be unable to taste them at all!

KEY POINTS

  • Cabbage, spinach, broccoli, Brussels sprouts, and grapefruit taste bitter because they contain thiourea compounds.
  • Bitter compounds in food activate bitter taste receptors on the surface of our tongue.
  • TAS2R38 is a bitter taste receptor that is activated by thiourea compounds.

How do people differ in their ability to taste bitter compounds?

It was a serendipitous event in 1931 which led to the discovery that people differ in their ability to taste bitter compounds.

A chemist by the name of Arthur Fox was trying to develop an artificial sweetener in his lab, when he accidentally blew crystals of PTC (phenylthiocarbamide), a thiourea compound, into the air. Some of these PTC crystals inadvertently landed on Fox's and his lab partner's mouths.

While his lab partner complained about the crystals' bitter taste, Fox could taste nothing at all. Intrigued by this, Fox got his family, friends, and colleagues to also taste PTC crystals impregnated on bits of paper. He found that it tasted extremely bitter to some individuals, but was completely tasteless to others.

In his studies, about 30% of subjects were “non-tasters” – unable to taste PTC, while the remaining 70% were “tasters” – able to taste PTC as bitter.

Subsequent studies using PROP (6-n-propylthiouracil), a less toxic alternative to PTC, have told a slightly more nuanced story. Rather than being a discrete binary division between non-tasters and tasters, it seems that people vary continuously in their sensitivity to PROP and other thiourea compounds.

Source: Duffy, V. B., Davidson, A. C., Kidd, J. R., Kidd, K. K., Speed, W. C., Pakstis, A. J., ... & Bartoshuk, L. M. (2004). Bitter receptor gene (TAS2R38), 6‐n‐propylthiouracil (PROP) bitterness and alcohol intake. Alcoholism: Clinical and Experimental Research, 28(11), 1629-1637.

While some “taste-blind” people cannot taste bitter compounds at a given concentration, other “non-tasters” can taste them, but only weakly. Furthermore, while some “tasters” are moderately-sensitive “medium tasters”, others, known as “supertasters” are extremely sensitive to bitter compounds, and may find foods such as raw broccoli, spinach, and the much-maligned Brussels sprout to be unbearably bitter.

The difference in bitter taste sensation between non-tasters, medium tasters, and supertasters across increasing PROP concentrations is shown in right-hand graph of the diagram above.

Returning to the story of Arthur Fox, another question plagued him: what was causing some people to be tasters but others to be non-tasters?

After teaming up with the geneticist, Arthur Blakeslee, Fox tested and tracked families to see whether bitter taste sensitivity was inherited. They found that being unable to taste PTC was inherited in families in a Mendelian recessive pattern, meaning a non-taster would have to inherit the non-tasting trait from both parents.

Decades later, in 2003, with the advent of genotyping technology, a specific gene was identified as a major determinant of bitter taste sensitivity – the TAS2R38 gene.

As described in the previous section, the TAS2R38 receptor is a bitter taste receptor on the surface of our tongues that is activated by thiourea compounds. This receptor is encoded by the TAS2R38 gene, with some variants of this gene causing people to be “tasters”, while other variants causing people to be “non-tasters”. We’ll elaborate on this in the next section.

KEY POINTS

  • People vary in their ability to taste bitter compounds in food and synthetic bitter compounds such as PROP and PTC.
  • Non-tasters are unable to taste bitter compounds or taste them only weakly.
  • Tasters are able to taste bitter compounds.
  • Tasters includes medium tasters, who experience bitter compounds as moderately bitter, and supertasters, who experience such as compunds as extremely bitter.
  • Variants of the TAS2R38 gene, which encodes a bitter taste receptor, affect our ability to taste bitter compounds.

How do TAS2R38 gene variants affect our ability to taste bitter compounds?

It’s been shown that variation in the TAS2R38 gene, which encodes the TAS2R38 bitter taste receptor on the surface of our tongues, almost completely explains whether or not someone is able to taste PTC – the synthetic bitter compound used in Arthur Fox’s taste experiments described earlier.

Similar studies have also shown that the intensity of bitterness that people experience when tasting PROP is largely determined by what TAS2R38 gene variants they inherit.

To cut to the chase, those with one particular set of TAS2R38 gene variants, known as PAV, are considerably more likely to be “tasters”, whereas those with the AVI set of variants are more likely to be “non-tasters.”

In order to make sense of what PAV and AVI mean, we need to have a brief recap of genetics.

SNPs in the TAS2R38 gene

As you’ll know, genes are stretches of DNA that code for proteins. Proteins, which include enzymes, structural proteins, and receptors like the TAS2R38 bitter taste receptor, are made up of chains of individual amino acids linked together.

When we talk about DNA being the code for life, what we specifically mean is that the exact sequence of our DNA code determines what amino acids we make, which in turn determines the make-up, structure, function, and quantities of proteins that we produce.  

Looking more closely, our entire genome or DNA sequence is simply a very long string of four different nucleotide bases, denoted by the letters: A, C, G, and T. Units of three bases/ letters, called codons, correspond to specific amino acids. For example, the codon G, T, A in the DNA sequence of the TAS2R38 gene codes for the amino acid valine (V).

The exact sequence of letters/codons in a gene’s DNA code (i.e. the exact sequence of the letters A, C, G, T) therefore dictates the precise sequence of amino acids that make up a protein.

In the image below, for instance, we can see how the DNA sequence CACTGTTACGGT codes for the sequence of amino acids: histidine, cysteine, tyrosine, glycine.

Source: Source: Kasper, C. K., & Buzin, C. H. (2008). Genetics of Hemophilia A and B: An Introduction for Clinicians, 2009. Southland Publications.

Of course, identical twins excepted, our DNA sequences are different from one another. One of the most common types of genetic variations in people are SNPs (Single Nucleotide Polymorphisms) - single letter changes or mutations in the DNA sequence. For example, a SNP may cause a change in the DNA sequence from the nucleotide base / letter ‘T’ to the base / letter ‘A’.

As it’s the exact sequence of bases / letters that determine what amino acids we produce, SNPs, by causing single letter changes, can alter what amino acids make up a protein. For example, in the image above, a SNP causing a T --> A change in the DNA code (in the second from left codon) changes the amino acid from cysteine to serine.

As a result of this SNP, we can think of there being two different gene variants, versions, or ‘alleles’ – one that codes for cysteine at particular position, the other that codes for serine.

With this in mind, there are 3 major SNPs in the TAS2R38 gene that cause amino acid changes:

  • rs714598: which causes the 49th amino acid in the TAS2R38 gene to change from proline (P) to alanine (A).
  • rs1726866: which causes the 262nd amino acid to change from alanine (A) to valine (V).
  • rs10246939: which causes the 296th amino acid to change from valine (V) to isoleucine (I).

TAS2R38 haplotypes and bitter taste

Still with us? Interestingly, the three SNPs in the TAS2R38 gene mentioned above are often inherited together in a group called a haplotype.

If you were to inherit the TAS2R38 gene variant encoding alanine (A) at position 49 (rs714598), you are also highly likely to inherit the variants encoding valine (V) at position 262 (rs17126866) and isoleucine (I) at position 296.

We therefore have a set of variants or haplotype: AVI (Alanine, Valine, Isoleucine).

It is this AVI haplotype that is linked to “non-taster” status. People carrying the AVI haplotype are likely to be unable to taste bitter compounds in food or taste them only weakly. As shown in the table below, around 42.7% of the global population carry this TAS2R38 haplotype.

Source: Risso, D. S., Mezzavilla, M., Pagani, L., Robino, A., Morini, G., Tofanelli, S., ... & Drayna, D. (2016). Global diversity in the TAS2R38 bitter taste receptor: revisiting a classic evolutionary PROPosal. Scientific reports, 6(1), 1-9.

The other common haplotype is PAV (Proline, Alanine, Valine), carried by 50.76% of the global population.

This haplotype arises because inheriting the TAS2R38 gene variant encoding proline (P) at position 49 (rs714598), is linked to also inheriting the variants encoding alanine (A) at position 262 (rs17126866) and valine (V) at position 296.

The PAV haplotype is associated with being a “taster” i.e. being able to taste bitter thiourea compounds in foods such as broccoli, spinach, and Brussels sprouts.

Although the AVI and PAV haplotypes of the TAS2R38 gene are the most commonly seen across various populations (as illustrated in the diagram below), they are not the only combinations of TAS2R38 variants / amino acids possible.

Source: Risso, D. S., Mezzavilla, M., Pagani, L., Robino, A., Morini, G., Tofanelli, S., ... & Drayna, D. (2016). Global diversity in the TAS2R38 bitter taste receptor: revisiting a classic evolutionary PROPosal. Scientific reports, 6(1), 1-9.

For example, it is possible to inherit a set of TAS2R38 variants coding proline (P) at position 49, but valine (V) at position 262 and isoleucine (I) at position 296, giving rise to the PVI haplotype.

A quick of bit mental calculation and you can see that other possible haplotypes include: AAV, AVV, PAI, AAI, and PVV.

These non-AVI/PAV haplotypes are thought to be associated with intermediate bitter taste sensitivity.  

Generally speaking, as shown in the table above, these other (non-AVI / PAV) haplotypes are quite rare. The exception to this is AAI haplotype, which is seen in around 13% of African populations.

We won’t go into the complex evolutionary reasons for why there is ethnic variation in TAS2R38 haplotypes, but it is likely to be due to ancestral populations facing different selection pressures (more on this later) and differences in patterns of migration of ancient human populations.

KEY POINTS

  • Three co-inherited SNPs (haplotype) in the TAS2R38 gene affect bitter taste sensitivity.
  • The PAV haplotype is the "taster" haplotype associated with being able to taste bitter compounds.
  • The AVI haplotype is the "non-taster" haplotype associated with being unable to taste bitter compounds.
  • The PAV and AVI haplotypes are the most common in the global population.
  • There are other rare non-AVI/PAV haplotypes (e.g. AAV, PVV) that are linked to intermediate taste sensitivity.

How do TAS2R38 genotypes affect bitter taste sensitivity?

So far, we’ve established that the PAV and AVI haplotypes of the TAS2R38 gene are linked to being taster and non-taster, respectively.

Of course, we typically inherit two copies of every gene – one from our mother and one from our father – and our TAS2R38 gene is no exception. It is therefore perfectly possible to inherit both one copy of the PAV ‘taster’ haplotype and one copy of the ‘AVI’ non-taster’ haplotype.

Indeed, it is perfectly possible to inherit any combination of TAS2R38 haplotypes – so how do these pairs of gene combinations (known as genotypes) affect bitter taste sensitivity?

If we restrict our focus to the most common PAV and AVI haplotypes, studies suggest the following associations between genotype and bitter taste sensitivity:

  • PAV / PAV genotype – Supertasters: these people have two copies of the PAV ‘taster’ haplotype and are shown to be extremely sensitive to bitter compounds. Such “supertasters” may find compounds in raw spinach, broccoli, tonic water, and coffee to be unbearably bitter.
  • PAV / AVI genotype – Medium tasters: this group has one copy of the PAV ‘taster’ haplotype and one copy of the AVI ‘non-taster’ haplotype. Studies suggest this group, known as medium tasters, have intermediate sensitivity to bitter compounds, experiencing them as moderately bitter.
  • AVI / AVI haplotype – Non-tasters: this group has two copies of AVI ‘non-taster’ haplotype and shown to be insensitive to bitter compounds. They may be completely unable to taste bitter compounds in food (“taste-blind”) or only experience them as very weakly bitter.

These differences in intensity of bitter sensations across the three common genotypes are shown below. Subjects in this study were asked to taste PROP (6-n-propylthiouracil), a synthethic thiourea compound similar to those in cruciferous vegetables.

Source: Sollai, G., Melis, M., Pani, D., Cosseddu, P., Usai, I., Crnjar, R., ... & Barbarossa, I. T. (2017). First objective evaluation of taste sensitivity to 6-n-propylthiouracil (PROP), a paradigm gustatory stimulus in humans. Scientific reports, 7(1), 1-12.

Things get a bit less clear when we consider the rarer, non-AVI/PAV haplotypes (AAV, AVV, PAI, AAI, PVI, and PVV). Part of this lack of clarity results from the lower number of study subjects with these rare haplotypes. As mentioned in the previous section, existing studies have linked these haplotypes to an intermediate sensitivity to bitter compounds.

When it comes to genotypes, it appears that the PAV “taster” and AVI “non-taster” haplotypes exert significant influence on bitter taste sensitivity when paired with the rarer non-AVI/PAV haplotypes.

Therefore, the following associations between genotype and bitter taste sensitivity are seen:

  • PAV / rare haplotype (e.g. AAV, PVI etc) – Tasters: this group carries one copy of the PAV “taster” haplotype and one copy of a rare haplotype. They can taste bitter compounds and may have bitter taste sensitivity on the higher end of the spectrum, although aren’t necessarily more likely to be supertasters.
  • Rare haplotype / rare haplotype – Medium tasters: this group carries two copies of rare haplotypes, which are associated with intermediate bitter taste sensitivity.
  • AVI / rare haplotype ( e.g. AAV, PVI etc) – Non-tasters: this group carries one copy of the AVI “non-taster” haplotype and one copy of a rare haplotype. They are less likely to taste bitter compounds and may have bitter taste sensitivity on the lower end of the spectrum.

Bear in mind that the biological trait (or phenotype) of bitter taste sensitivity is a spectrum, ranging from inability to taste bitter compounds to being an extremely sensitive supertaster. Therefore, discrete genotype groups won’t necessarily neatly map onto having a particular bitter sensitivity level.

KEY POINTS

  • We inherit pairs of TAS2R38 gene variants / haplotypes - to form a genotype
  • The PAV/PAV genotype is linked to being a supertaster.
  • The PAV/AVI genotype is linked to being a medium taster.
  • The AVI/AVI genotype is linked to being a non-taster.
  • Genotypes involving rare non-AVI/PAV haplotypes vary in bitter taste sensitivity, depending on what haplotypes are inherited.

Why do TAS2R38 genotypes affect bitter taste sensitivity?

We know that our sensitivity to bitter compounds in food is strongly influenced by what TAS2R38 gene variants we inherit, but why is this the case?

Studies suggest that it is partly to do with our fungiform papillae – the small, nipple-like projections on the surface of our tongue that give it its rough texture. Fungiform papillae, in particular, are concentrated on the top (dorsum) and front tip of the tongue. These papillae contain taste buds, which in turn house taste receptors that, when stimulated, send electrical signals to the brain that give rise to taste sensations.

Researchers have found that supertasters and those with the PAV/PAV genotype have a significantly higher number and density of fungiform papillae on the surface of their tongue. This makes them much more sensitive to bitter taste compounds in food, with a given area of the tongue surface producing a stronger electrical signal in response to these bitter compounds.

Source: Sollai, G., Melis, M., Pani, D., Cosseddu, P., Usai, I., Crnjar, R., ... & Barbarossa, I. T. (2017). First objective evaluation of taste sensitivity to 6-n-propylthiouracil (PROP), a paradigm gustatory stimulus in humans. Scientific reports, 7(1), 1-12.

By contrast, non-tasters and those with the AVI/AVI genotype are shown to have a much lower number and density of fungiform papillae, making them less sensitive to bitter taste compounds. Stimulation of a given area of their tongue gives rise to a weaker electrical signal, resulting in a less intense bitter taste sensation.

For completion, as shown in the graph above, medium tasters and those with the PAV/AVI genotype have an intermediate number and density of fungiform papillae on their tongue surface.

KEY POINTS

  • TAS2R38 variants affect the number and density of fungiform papillae (nipple-like projections that house taste buds) on the surface of the the tongue.
  • Supertasters (PAV/PAV genotype) have a higher number and density of fungiform papillae on their tongue surface. This makes them more sensitive to bitter compounds in food.
  • Non-tasters (AVI/AVI genotype) have a lower number and density of fungiform papillae, making them less sensitive to bitter compounds.

Are there evolutionary reasons for differences in bitter taste sensitivity?

In the previous section, we essentially asked, “Why do people differ in their bitter taste sensitivity?”

The answer we provided was in terms of TAS2R38 gene variants and their effect on fungiform papillae density. In biology, we call this the “proximate cause” – it refers to the immediate mechanisms responsible for a behaviour, phenomenon, or outcome, in this case, differences in bitter sensitivity.

We might also be interested in the “ultimate cause” of bitter taste sensitivity – why did we evolve to be sensitive to bitter compounds in food in the first place. The answer to this question is seemingly straightforward – being able to detect and therefore avoid potentially toxic compounds in food would have enhanced our ancestors’ survival. Consequently, the genes that confer stronger bitter taste sensitivity (i.e. the PAV taster haplotype of the TAS2R38 gene) would have been positively selected for and spread in the population over generations.

In line with this, it has been hypothesised that “tasters” may have avoided certain bitter-tasting, cruciferous vegetables (e.g. cabbage), which contain compounds that limit our ability to absorb and use iodine, a nutrient required by our thyroid gland to make thyroid hormones.

This, however, raises some interesting follow-up questions: why are there still plenty of non-tasters and why is the “non-taster” AVI haplotype of the TAS2R38 gene in a sizeable chunk (approximately 43%) of the global population?

There are several theories that have been offered to explain this apparent conundrum. One theory is that the AVI haplotype encodes a TAS2R38 bitter taste receptor that is sensitive to another, as yet unidentified, bitter compound.

Another theory, based on the finding that we also express TAS2R38 receptors in our airways and gut, suggests that non-tasters may be better at clearing respiratory and gut infections. This gives rise to a case of what is known as balancing selection – whereby both the taster PAV haplotype and non-taster AVI haplotype are selected for and maintained in the gene pool.

A related theory here, is that it was pathogens (e.g. bacteria) and not humans that were the real targets of natural selection, with such pathogens benefitting from having non-taster human hosts.

KEY POINTS

  • The taster PAV haplotype may have helped our ancestors detect and avoid potentially toxic compounds in food.
  • The non-taster AVI haplotype may have helped detection of another (hypothetical) bitter compound or enhanced clearance of pathogens.
  • Both the taster and non-taster TAS2R38 haplotypes are common in the population, suggesting both carried evolutionary advantages.

How does bitter taste sensitivity affect dietary choices?

Unsurprisingly, “tasters” and especially “supertasters” are less likely to consume and enjoy the taste of bitter vegetables such as raw broccoli, raw spinach, and bitter gourd.

For example, one study of preschool children found that compared to “non-tasters”, “tasters” (as assessed by sensitivity to PROP) consumed significantly fewer servings of bitter vegetables, including raw broccoli, black olives, and cucumber, but not non-bitter vegetables such as red peppers and carrots.

This is illustrated in the graph below, with tasters and non-tasters represented by the grey and solid black bars, respectively.

Source: Bell, K. I., & Tepper, B. J. (2006). Short-term vegetable intake by young children classified by 6-n-propylthoiuracil bitter-taste phenotype. The American journal of clinical nutrition, 84(1), 245-251.

Similarly, tasters gave broccoli significantly lower liking ratings than non-tasters. Before you use this as an excuse to eschew broccoli for the rest of your life, however, it’s worth noting that another study found that offering “tasters” a regular or light dipping sauce increased their intake of raw broccoli. If you’re a taster or supertaster, you’ll also find that cooking broccoli and other bitter vegetables can degrade their bitter thiourea compounds, making them more palatable.

Coffee

Ask a connoisseur why coffee tastes bitter and they’ll run off a list of factors such as brewing time, water temperature, mismatched grinds, and oversteeping. Ask a geneticist, and they’ll tell you it’s because TAS2R38 gene variants make people more sensitive to bitter-tasting chlorogenic acid lactones and phenylindanes in coffee.  

On this note, a large study using the UK Biobank database found that people with the ‘A’ taster allele (rs1726866) consumed less coffee than those with the non-taster ‘V’ allele. It’s worth bearing in mind that only a small effect was observed. A 1-standard deviation increase in sensitivity to PROP (a bitter-tasting thiourea compound) was associated with 0.021 fewer cups of coffee per day.

The same study found PROP tasters also consumed less alcohol per month. Presumably they were avoiding coffee liqueurs!

Fatty foods

Differences in TAS2R38 genotype and bitter taste sensitivity not only affect our intake of bitter thiourea compounds in vegetables, but are also shown to alter our perception of fat and sugar.

Compared to “tasters”, “non-tasters” are shown to be less sensitive to the taste and texture (e.g. creaminess) of fat in foods. For example, in one study, “non-tasters” were unable to distinguish between high-fat and low-fat versions of Italian salad dressings. By contrast, “tasters” are able to detect small amounts of a fatty acid (linoleic acid) infused into ice cream, which they may experience as unpleasant and pungent, while “non-tasters” remain blissfully impervious to them.

These differences in fat taste sensitivity likely result from the differences in the number and density of fungiform papillae on the surface of the tongue, described earlier. By virtue of having a greater density of papillae, the nipple-like projections on the tongue surface that contain taste-buds, “tasters” are more sensitive to not only bitter thiourea compounds, but fats and fatty acids too.

Interestingly, as described in the Fat taste sensitivity (CD36) trait, people with reduced fat taste perception tend to compensate by eating higher amounts of fatty foods. On this note, some studies have found “non-tasters” to consume greater amounts of fat in their diet, including from foods such as fatty meats, eggs, and nut butters.  

Sweet foods

Being sensitive to bitter compounds in food may also be linked to having a sweet tooth.

Although findings are mixed, and some studies are complicated by the fact that their subjects are children (who, on the whole, tend to love sweets), it has been reported that “tasters” have a greater preference for sugar.

For example, people with two copies of the “taster” PAV haplotype are shown to prefer sweeter sucrose solutions and higher sugar-content cereals compared to those with “non-taster” alleles.

The reason for this may be that “tasters” simply experience greater intensity sweetness when consuming sugar.

KEY POINTS

  • Tasters and supertasters are shown to consume fewer portions of bitter vegetables (e.g. raw broccoli), less coffee, but more sugar.
  • Non-tasters may be less sensitive to fat content in food and compensate for this by consuming greater amounts of fatty foods.

How does bitter taste sensitivity affect BMI?

There may be a link between being a “non-taster” and having a higher body mass index (BMI).

For example, a study of middle-aged women found that non-tasters had significantly higher BMI, body fat percentage, and triceps skinfold measurements (a measure of fat mass) compared to tasters.

When it came to BMI, non-tasters had an average BMI that was 6.2 kg/m2 higher than tasters. Furthermore, as shown in the graph below, there was an inverse correlation between bitter taste sensitivity (as measured by ability to taste PROP) and BMI, body fat percentage and triceps skinfold measurements.

Source: Goldstein, G. L., Daun, H., & Tepper, B. J. (2005). Adiposity in middle‐aged women is associated with genetic taste blindness to 6‐n‐propylthiouracil. Obesity research, 13(6), 1017-1023.

The reasons behind this relationship are not clear. As mentioned in the previous section, we know that “non-tasters,” in addition to being insensitive to bitter compounds, also have reduced fat taste sensitivity. To compensate for this, they may consume more fatty foods, which, in turn, can contribute to increased BMI and body fat content.

Another related reason, which we discussed in the Fat taste sensitivity (CD36) trait, is that the non-taster TAS2R38 variant affects the function of TAS2R38 receptors in the gut, which may regulate satiety and food intake.

An alternative explanation is that, rather than causing higher BMI and body fat percentage per se, being a non-taster is simply a marker of some other trait that increases bodyweight and risk of obesity.

KEY POINTS

  • Non-tasters are shown to have a higher BMI and body fat percentage than tasters.
  • The reasons behind this association are unclear, but may be due to differences in fat taste sensitivity and gut satiety mechanisms that control food intake.

Your Bitter taste sensitivity trait

Your Bitter taste sensitivity trait looks at well-studied variants (haplotypes) of your TAS2R38 gene that explain differences in ability to taste bitter compounds in food.

Depending on your DNA results, you will be classified into one for the following groups:

  • Supertaster (PAV / PAV) – you have two copies of the PAV “taster” haplotype are more likely to find foods such as raw broccoli extremely bitter.
  • Taster (PAV / rare haplotype) – you have one copy of the PAV “taster” haplotype are likely to taste bitter compounds in food.
  • Medium taster (PAV / AVI) – you have one copy each of the PAV “taster” and AVI “non-taster” haplotypes. You are likely to taste bitter compounds in food, experiencing them as moderately bitter.
  • Medium taster (rare haplotype / rare haplotype) – you have two copies of rare haplotypes associated with intermediate bitter taste sensitivity. You are likely to taste bitter compounds in food, experiencing them as moderately bitter.
  • Non-taster (AVI/AVI or AVI/rare haplotype) – you have one or two copies of the AVI haplotype and are likely to be a non-taster. You may be unable to taste bitter compounds in food (more so with the AVI/AVI genotype) or can only weakly taste them.

To find out your result and decide whether you want Brussels sprouts this Xmas, please login to truefeed.

From everyone at FitnessGenes, we wish you a Merry Christmas and a Happy New Year!

Dr Haran Sivapalan

A qualified doctor having attained full GMC registration in 2013, Haran also holds a first-class degree in Experimental Psychology (MA (Cantab)) from the University of Cambridge and an MSc in the philosophy of cognitive science from the University of Edinburgh. Haran is a keen runner and has successfully completed a sub-3-hour marathon during his time at FitnessGenes.

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