Taste is one of our most intimate senses. The foods we love, the foods we hate, and the flavors we crave are deeply personal. But while our preferences feel uniquely our own, growing scientific evidence suggests genetics influence our tastes more than we might expect.
What is taste?
Taste, also known as gustation, is the sense through which we detect flavors. Our taste buds contain receptor cells that identify five primary tastes: sweet, sour, salty, bitter, and umami (savory). While the distinctive flavors we experience eating foods are shaped by smell and texture, it is our taste receptors that detect basic tastes.
When we put food in our mouths, chemicals from the food interact with taste receptors, sending signals to the brain that translate into specific tastes. For instance, sugar molecules bind with sweet receptors, acidic molecules like vinegar bind with sour receptors, and so on. The combination of tastes produces an overall flavor that is unique to the food.
How does taste vary between people?
While the basic mechanisms of taste are similar across humans, we do not all experience tastes in the same way. Within a cultural context, people vary substantially in their taste preferences and sensitivities. Some people have a sweet tooth while others prefer salty snacks. Some love spicy foods that make others’ mouths burn. Some vegetable-haters are strongly sensitive to bitter flavors.
On a biological level, much of this variation is genetic. Over the past two decades, scientists have uncovered key genes that account for differences in our taste abilities. Understanding the genetics behind taste provides insight into food preferences, diet, and health.
The Genetics of Bitter Taste
Of all taste perceptions, bitter is perhaps the most variable and genetically determined. Bitterness evolved as an adaptive trait to detect toxins in plants. However, sensitivity ranges widely across people, dictated largely by versions of the TAS2R gene family.
The TAS2R genes
Human genomes contain around 25 different TAS2R genes, which encode protein receptors responsible for detecting bitterness. Each TAS2R gene contains instructions for making a receptor attuned to a specific array of bitter chemicals. Collectively, the TAS2R receptor repertoire allows us to sense thousands of bitter compounds.
However, people inherit different numbers and versions of TAS2R genes. Having more functional TAS2R genes leads to greater bitter sensitivity. Genetic mutations also alter receptor function. Individual receptors may be hypersensitive, hyposensitive, or completely unable to detect specific bitter chemicals as a result of inherited sequence differences.
Bitter taste across populations
On a population level, patterns of TAS2R gene diversity correspond to differences in bitter perception. For instance, the average person of European descent possesses around 15 normal TAS2R genes. In contrast, most indigenous peoples of Africa and Latin America carry far fewer normal TAS2R genes. On average, they experience bitterness less intensely due to mutations that impair receptor function.
Impacts on diet and health
Variable bitter sensitivity shapes food preferences across cultures. Populations with fewer functional TAS2R genes tolerate bitter plant compounds, enabling unique culinary traditions rich in bitter greens, roots, herbs and spices. Meanwhile, strong bitter perceivers tend to avoid these foods, negatively impacting vegetable intake.
Nutritionally, bitter greens like broccoli, Brussels sprouts and kale are rich in beneficial compounds but unpalatable to picky eaters. Bitter deficiency takes a toll, associated with higher risks of cancer, heart disease and diabetes. Understanding personal taste genetics may help overcome inborn aversions, opening avenues to better nutrition.
Sweet Taste Genetics
Along with bitter, genetic differences affect sweet perception – influencing the foods we love, how much sugar we eat, and even alcoholism risk.
The TAS1R genes
Two genes, TAS1R2 and TAS1R3, encode the subunit proteins that combine to form sweet receptors. TAS1R3 acts as the primary sweet detector, binding sugars like glucose and sucrose. However, it only functions when paired with TAS1R2.
Inherited mutations often disrupt sweet receptor activity. Variants in either TAS1R2 or TAS1R3 can hamper subunit binding, muting sweet perception. Other mutations over-sensitize the receptor, amplifying sweet signals.
Sugar sensitivity and intake
TAS1R gene variants that decrease sweet sensitivity associate with heightened sugar consumption. In less sensitive individuals, weaker sweet signals likely prompt sugar cravings as the brain seeks greater sensory intensity.
In particular, a non-tasting TAS1R2 mutation prevalent among the Finnish boosts daily sugar intake by around 2 teaspoons. Obese individuals also exhibit slightly reduced sweet sensitivity, contributing to excessive consumption.
Alcoholism and sweet genes
Altered sweet perception additionally relates to alcohol abuse. A hypersensitive TAS1R3 variant occurs more frequently among alcoholics, linked to sweeter tasting drinks. Those with sweet-insensitive TAS1R2 variants show lower alcoholism rates, potentially finding alcoholic beverages unpleasantly bitter.
Umami Genetics
Umami flavor, produced by glutamate salts and certain nucleotides, makes savory foods like meat and mushrooms so satisfying. Genetic variations in umami receptor genes influence flavor perception, acceptance of umami-rich foods, and appetite regulation.
The TAS1R1 gene
Located alongside the sweet taste genes, TAS1R1 encodes half of the umami receptor. When combined with TAS1R3, it forms a functional umami sensor. Mutations can diminish glutamate binding, limiting umami intensity. Total loss of TAS1R1 function eliminates all umami taste.
Population differences
A disabling TAS1R1 mutation present in up to 23% of Europeans eliminates umami sensitivity in homozygous carriers. Likely originating as a random mutation, the non-functional variant became common by genetic drift rather than selective advantage.
Its absence among Asians and Indigenous Americans supports this, as their ancestral populations separated before the mutation appeared. Lacking the variant, their cuisines integrated ingredients naturally high in umami.
Effects on taste and health
By blunting umami, this common variant likely drives overuse of salt, soy sauce and MSG to amplify flavor. Compared to umami-sensitive individuals, insensitive homozygotes show greater acceptance of processed foods along with elevated BMI. Enhancing umami naturally through mushrooms and tomatoes may improve their nutrition.
Fat Taste Genetics
Along with the five basic tastes, growing evidence supports the existence of a sixth taste for fats. Sensing dietary fats likely evolved important for energy and essential fat intake. Intriguingly, genetics impact fat detection, preferences for high-fat foods, and susceptibility to obesity.
CD36 and GPR120
At least two receptor proteins contribute to oral fat perception. CD36, encoded by the CD36 gene, gets activated by fatty acids, including those in oils and dairy. GPR120, from the GPR120 gene, also responds to fat breakdown products. Together, they send signals perceived as a fat taste.
Fatty acid sensitivity
A common CD36 mutation diminishes receptor activity, reducing fatty acid taste sensitivity, especially to shorter chain fats. Having one or two copies of the variant associates with high-fat food cravings yet lower BMI, implying importance for fat intake regulation.
GPR120 mutations also occur, but links to fat taste are unknown. CD36 likely plays the primary role in generating fat taste sensations for dietary regulation.
Fat taste and obesity
Though requiring more research, CD36 status may relate to obesity susceptibility. Mice lacking CD36 consume more fat overall, overeat when fed high-fat diets, and develop obesity. If similarly disrupted fat taste contributes to human obesity is an important question.
Genetic Differences in Taste Beyond the Tongue
Though we detect tastes in the mouth, growing evidence reveals taste receptors throughout the digestive system also influence food choices, appetite, and metabolism. Intriguingly, genetic variation shapes their functions and disease risks.
Taste receptors in the gut
Taste-sensing cells line the intestinal tract, chemically sampling digested food. Sweet, bitter and umami receptors detect sugars, toxins, protein, and more, sending signals that optimize absorption while regulating appetite and glycemic responses. Genetic mutations perturb this sensing, altering digestion-related signals to the body and brain.
Sweet and diabetes
Gut taste may be especially important for sugar metabolism. Intestinal sweet receptors sense arriving glucose from digestion, stimulating insulin release to control blood sugar spikes. Loss of gut sweet perception associates with poor glycemic regulation and increased type 2 diabetes risk in animal models. Whether TAS1R2 gene variants similarly predispose humans remains unknown.
Bitter and immunity
Bitter receptors also populate the airways and respiratory system, detecting inhaled toxins. Though not fully proven, taste genetics may relate to lung infections and chronic inflammatory diseases. Given the central role the gut-lung axis plays in immunity, bitter receptors likely provide key surveillance.
Genetics Versus Environment in Food Preferences
While taste genetics clearly influence eating behaviors, cultural and environmental factors remain equally important in shaping food choices. Familiarity develops preference, overcoming unlearned aversions. Moreover, ecological factors dictate food availability.
Learned food preferences
Despite inborn sensory differences, cultural practices teach flavor appreciation. Through regular exposure, children form lasting preferences for initially unpalatable or unfamiliar foods. Parental and peer behaviors also powerfully mold children’s tastes and food choices.
Genetics and experience likely interact. Taste genes define initial responses on which environment and learning act. Together, nature and nurture contribute to the cuisine each person favors.
Environmental food access
Beyond culture, food availability limits choice. Food deserts provide few fresh ingredients to select populations, forcing reliance on processed options. Agricultural practices also steer preferences, as through centuries of breeding fruits and vegetables for sweetness and mildness.
Though tastes vary genetically, access determines actualized diet. Changing food geography and practices may enable healthier eating patterns.
The Future of Taste Genetics
Advances in nutrigenetics and taste pharmacology offer avenues to override genetic differences, enhancing wellbeing. Genotyping for taste genes could guide personalized nutrition, while modifier compounds target receptors to align sensory responses with health needs.
Nutritional genomics
Knowing one’s taste genetics can reveal inherent flavor affinities and aversions. For example, the high vegetable bitterness associated with poor TAS2R function may justify using bitter masking supplements to improve intake.
Genotype-guided bitter blocking or sweet enhancing could reshape progenitor receptor profiles, facilitating acceptance of personalized healthy diets.
Designer taste modifier drugs
Researchers pursue compounds targeting taste receptors to intentionally alter sensory responses. Sweetness blockers might aid weight loss by reducing appeal of sugary foods. Enhancing bitter receptors could boost avoidance of toxins or inhalant irritants.
Future designer drugs may adjust taste phenotypes, augmenting nutrition while preventing overconsumption of salt, sugar and fat independent of genotype. They may also help smokers quit by conferring bitter perception of nicotine.
Conclusion
Taste genetics research is unveiling that our unique flavor perceptions result from variations in receptor genes. Sweet, bitter, umami and fat taste sensitivities differ based on TAS1R and TAS2R genes. These influence nutrition-related behaviors like sugar and vegetable intake in measurable ways. Further, extra-oral taste receptors in the gut importantly regulate digestion, metabolism and immunity.
While our taste world is intrinsically sensory and personal, decoding the genes that shape it will yield profound insights into diet, disease risks and human flavor diversity. Genomics-based nutrition and designer taste drugs may someday circumvent consumer genotype, allowing tailored food experiences to empower healthier living.
| Taste | Primary Receptor(s) | Key Gene(s) | Effects of Variants |
|---|---|---|---|
| Bitter | T2R proteins | TAS2R gene family | Decrease or increase bitter sensitivity |
| Sweet | T1R2 + T1R3 | TAS1R2, TAS1R3 | Decrease or increase sweet sensitivity |
| Umami | T1R1 + T1R3 | TAS1R1 | Reduce or eliminate umami perception |
| Fat | CD36, GPR120 | CD36, GPR120 | Decrease oral fat sensitivity |
