Your Palate Is Your Biography: The Genetics and Epigenetics of Taste

Why We Don’t All Taste the Same - and Why That Is the Most Interesting Thing About a Whisky Tasting

I want to begin with a scene that will be familiar to anyone who has attended a whisky tasting.

Two people are sitting side by side, nosing the same glass. The whisky is a heavily peated Islay single malt - Laphroaig, perhaps, or Ardbeg. One person leans in with evident pleasure, reaching for words: smoke, seaweed, iodine, something medicinal and briny and deeply satisfying. The other recoils slightly. They describe the same glass as overwhelming, almost painful - medicinal in a way that is not pleasant, harsh in a way that no amount of water quite resolves.

Both are paying attention. Both are experienced. Neither is wrong.

I have heard this explanation given many times - across the hundreds of whisky tastings I have organised, chaired, or been fortunate enough to sit through at distilleries from the Scottish Highlands to the valleys of Normandy - and I have come to think it is insufficient. The difference is not simply one of experience or preference. It is biological. And it goes deeper than biology alone - it goes into the history of each person’s life, reaching back further than you might expect.

I have a particular reason for finding this question compelling, and it is a personal one. I am Sri Lankan. I grew up eating food that most British palates would consider intensely spicy - curries, sambol dishes built around chilli heat that is simply the baseline of Sri Lankan home cooking rather than a special occasion. And for many years I have noticed, in conversation with other Sri Lankan and South Asian whisky enthusiasts, a pattern: many of us take to peated, heavily flavoured whiskies with a naturalness that surprises the people around us at tastings. Where others find the Islay malt confrontational, we often find it compelling. I have wondered for years whether this is cultural confidence or shared preference. The science, it turns out, suggests it is something considerably more specific - and considerably more interesting.

This article is about what the genetics and epigenetics of taste actually tell us: about why no two people taste the same glass in the same way, how the whole arc of a life shapes the palate we bring to it, and what that means for how we understand ourselves and each other around a tasting table.

The Genetic Foundation: Hardware You Were Born With

In our article on the science of taste, I established that flavour is constructed by the brain from multiple sensory inputs simultaneously - primarily from the retronasal olfactory pathway, which accounts for approximately 80% of what we perceive as flavour, and secondarily from the tongue’s five basic signals: sweet, sour, salty, bitter, and umami. ¹

What that article did not explore is the degree to which the sensitivity of those systems varies between individuals at a genetic level - and how profound those variations are.

The story begins in a laboratory accident. In 1931, a chemist named Arthur Fox at DuPont accidentally released a cloud of phenylthiocarbamide (PTC) powder. His colleague immediately complained of an intensely bitter taste. Fox detected nothing. They were standing in the same cloud of the same molecule at the same concentration. The difference between them was entirely biological. ²

Fox spent the following years investigating the phenomenon, eventually establishing that the population divides broadly into three groups: supertasters, who detect PTC bitterness with great intensity (approximately 25% of people); medium tasters, who detect it moderately (around 50%); and non-tasters, who detect little or nothing (around 25%). ³

The distinction is driven by variations in the TAS2R38 gene, which codes for bitter taste receptors, and by a structural difference in the tongue itself: supertasters have significantly higher densities of fungiform papillae - the mushroom-shaped structures that house taste buds - which means more sensory signal from the same stimulus. ⁴

The implications for whisky are direct and specific.

For supertasters, bitter compounds are physiologically louder. Heavily phenolic, peated whiskies - whose character derives significantly from guaiacol, cresol, and related compounds we explored in our Cooper’s Art article - activate bitter receptors with an intensity that medium tasters simply do not experience from the same glass. ⁵ This is why the person who finds Laphroaig overwhelming is not necessarily inexperienced. They may be a supertaster, and what they are describing is accurate: the peat really is that intense, for them. The alcohol heat of cask strength expressions is similarly amplified - the TRPV1 receptor, which detects heat and pain, interacts with taste receptor density in ways that intensify perceived burn. ⁶ This is why we always offer water at Devon Drams events, and why the science of dilution we discussed in our water and whisky article is not merely a matter of flavour release but of physiological access. ⁷

For non-tasters, the mirror image applies. Bitterness is quieter. The bold, heavily phenolic character of an Islay malt registers as interesting rather than confrontational, and subtler, more delicate whiskies - the Lowland expressions, the lighter Japanese single malts - can feel thin or underwhelming, not because they lack complexity but because the sensory signal is softer. Non-tasters often gravitate naturally toward heavily sherried, full-bodied expressions, because those whiskies deliver enough signal through non-bitter channels - dried fruit, caramel, dark chocolate - to satisfy the palate that bitterness cannot easily reach.

There is one further dimension worth naming. Research has consistently found that women are more likely than men to be supertasters. ⁸ The reasons involve hormonal and developmental factors that are not fully understood. The practical implication is that tasting notes written predominantly by male critics may systematically underrepresent the experience of female tasters - and that the whisky world’s historical preference for bold, assertive expressions may reflect the demographic of who was doing the writing as much as the quality of what was being described.

The Crack in the Genetic Story

If genetics were the whole story, identical twins - who share 100% of their DNA - would have identical palates. They do not. ⁹

This empirical fact is the opening through which epigenetics enters, and it transforms the article’s argument from interesting to extraordinary.

Epigenetics is the study of how and when genes are expressed - not changes to the DNA sequence itself, but changes to whether specific genes are switched on or switched off. The genome is the instrument. The epigenome is whether, and how, and how loudly, each note is played. And crucially: the epigenome is shaped by the environment. What you eat, what you are exposed to, what illnesses you have had, what sensory environments shaped your earliest development - all of these can throw epigenetic switches that alter which genes are active in your taste and smell sensory neurons.

Your palate is not simply the palate you were born with. It is the palate your life has created.

How Diet Rewrites the Tongue

The evidence for this is more direct than you might expect, and more recent.

A landmark study published in Science Advances examined what happens to taste receptor gene expression when organisms consume a high-sugar diet. The researchers found that the Polycomb Repressive Complex - a chromatin-silencing mechanism that is conserved across species from plants to humans - redistributed its binding in the sweet taste sensory neurons, repressing a developmental transcriptional network that shapes the responsiveness of those cells to sweet stimuli. ¹⁰ In plain language: the high-sugar diet epigenetically turned down the sensitivity of the sweet taste receptors.

The critical finding was what happened when the diet returned to normal. Half of these transcriptional changes persisted. The sweet taste deficit did not fully reverse. The diet had rewritten the epigenome of the taste neurons, and part of that rewriting was permanent.

Research published in Critical Reviews in Food Science and Nutrition in 2025 extended this picture, demonstrating that epigenetic modifications - DNA methylation, histone modification, and non-coding RNA-mediated regulation - play a significant role in regulating the ion channels through which taste signals are transduced in all five basic taste categories. ¹¹ The epigenetic landscape of the taste system is not fixed at birth. It is being continuously modified by the chemical environment the sensory neurons encounter.

For whisky drinkers, the implication is concrete. The person who has spent years consuming strongly bitter foods - dark coffee, cruciferous vegetables, 85% dark chocolate - has not simply learned to tolerate bitterness. They may have developed, through sustained epigenetic modification of their bitter taste receptor gene expression, a physiologically different relationship with bitter compounds from the person whose diet has been consistently sweet and mild. The palate is not neutral. It is the accumulated record of dietary choices made over a lifetime.

But the most compelling illustration of this principle is not individual. It is cultural.

The Cultural Palate: When Epigenetics Meets Heritage

Return for a moment to the observation I made in the opening of this article. Many Sri Lankan and South Asian whisky enthusiasts find peated Islay malts - the whiskies that most frequently divide tasting rooms - naturally compelling rather than confrontational. I have wondered about this for years, and have discussed it with enough people from similar backgrounds to be confident it is not merely coincidence or individual variation. The science, it turns out, provides a mechanism.

The key is the TRPV1 receptor. This is the same ion channel through which capsaicin - the active compound in chilli peppers - creates the sensation of heat and burn in the mouth. TRPV1 is also the receptor responsible for the perception of alcohol heat in spirits. Supertasters, as I described above, experience more intense burn from high-ABV whisky partly because their higher receptor density amplifies the TRPV1 signal.

The critical research finding is this: repeated exposure to capsaicin induces desensitisation of TRPV1 receptors. Heavy chilli users report significantly less burn from capsaicin compared to non-users, and this desensitisation is chronic - lasting across days, not merely hours after a meal. ²⁸ Research at the cellular level suggests the mechanism involves downregulation of TRPV1 receptor activity through sustained exposure: the pain-sensing neurons of the oral cavity are being modified by the chemical environment they repeatedly encounter. This is epigenetic-adjacent biology - receptor-level adaptation driven by dietary experience.

The consequence for whisky is direct. Someone whose TRPV1 receptors have been chronically desensitised by a lifetime of spicy food exposure perceives less heat from the same high-ABV spirit. The cask strength Laphroaig that sends a physiological alarm signal through a supertaster’s undiluted TRPV1 system arrives at a desensitised palate with its heat already partially muted. What remains - the smoke, the iodine, the coastal complexity, the dried fruit beneath the peat - is more accessible, less obscured by the burn that would otherwise dominate. The peated whisky feels complex rather than confrontational.

The cross-cultural research supports this at a population level. A peer-reviewed study published in Chemical Senses compared Thai and Japanese populations - cultures with dramatically different spicy food traditions - across all five basic taste dimensions. Thai participants, from a culture with significantly higher spicy food frequency (70% consuming spicy food weekly versus 80% of Japanese consuming it only monthly), showed markedly higher recognition thresholds across sweet, salty, sour, bitter, and umami. ²⁹ Higher threshold means less sensitive - more tolerant of intensity across the board. The dietary culture had reshaped the population’s collective taste sensitivity in a measurable, consistent direction.

The most directly relevant piece of research, however, is a genomic study published in Frontiers in Genetics that analysed 1,029 Indian genomes for variation in chemosensory genes. The researchers found that TRPV1 - the capsaicin and alcohol heat receptor - shows statistically significant population-level differentiation in Indian populations compared to European, East Asian, and African populations. The same differentiation was found in several bitter taste receptor genes. ³⁰ The genetic architecture of heat and bitter perception is measurably different in South Asian populations at a population level - before any dietary epigenetic modification is layered on top of it.

What this suggests is a compounding effect: South Asian populations may carry genetic variants of TRPV1 and bitter taste receptors that baseline differently from European populations, and that baseline is then further modified by generations of cultural dietary practice - both in the individual’s lifetime and potentially, given the transgenerational epigenetics research, across generations. The Sri Lankan who finds Laphroaig naturally compelling is not simply displaying an unusual preference. They may be arriving at the glass with a palate built, at a molecular and epigenetic level, by their culture’s relationship with heat and intensity over many generations.

I want to be clear, as I always try to be when applying research beyond its tested boundaries: no study has directly examined Sri Lankan populations and peated whisky preference. The chain of reasoning I am building is my own inference from several independently supported mechanisms - TRPV1 desensitisation through spicy food exposure, cross-cultural taste threshold differences, population-level chemosensory gene variation in South Asian populations - each individually evidenced, combined into a hypothesis that the evidence strongly supports but that has not yet been directly tested. This would, incidentally, make a genuinely interesting research project for someone with the right laboratory and the right tasting room.

What it also suggests is something larger and more generalisable. The food cultures of the world are not simply shaping preferences and memories. They may be shaping palates at a receptor and epigenetic level, creating systematic differences in sensory sensitivity between populations that have nothing to do with sophistication or experience - and everything to do with the chemical environments that different culinary traditions have created over centuries and generations.

At a whisky tasting in East Devon, that observation translates into something practical: the person at the table who grew up eating the most intensely flavoured food may be the one with the most natural access to the most intensely flavoured whiskies. Not because they have tried harder, or tasted more, or been better trained. But because their palate has been built, quietly and over a lifetime, for exactly this kind of encounter.

The olfactory system - which, as we established in our taste science article, provides the majority of what we experience as whisky’s flavour complexity through the retronasal pathway - is itself organised by epigenetic mechanisms of remarkable precision. ¹²

Research published in Genesis in 2024 established that each individual olfactory sensory neuron expresses only one olfactory receptor gene from the approximately 400 functional receptors available in the human genome. The mechanism that enforces this singular expression - ensuring that each neuron fires for one and only one specific aromatic compound - is epigenetic: all other olfactory receptor genes in each neuron are silenced by a suite of epigenetic processes that remodel the olfactory gene landscape during neuronal development. ¹³

A preprint published in bioRxiv in December 2025 identified the specific chromatin protein responsible for this silencing: TRIM66, which recruits specifically to olfactory receptor gene super-enhancers during neuronal progenitor maturation, silencing nearby olfactory receptor genes. When TRIM66 function was disrupted, individual neurons began expressing multiple receptors simultaneously - disrupting the topographic map of the olfactory system and impairing odour discrimination. ¹⁴

What this means is that the specific olfactory receptors that are active in your sensory neurons - and therefore which aromatic compounds you can detect, at what sensitivity, and in what combination - is a product of epigenetic programming during your neurological development. And that development was shaped by your environment. The aromatic landscape of your early life - the kitchen you grew up in, the smells of your childhood home, the food cultures that surrounded you - was not merely shaping your preferences and memories. It was participating in the epigenetic construction of your olfactory system.

Illness, the Immune System, and the Bitterness of Recovery

Here is the dimension of this story that, as a physician, I find most clinically striking.

Research from the Monell Chemical Senses Center, published in iScience and reported by ScienceDaily, identified an epigenetic mechanism that directly connects immune activation to bitter taste receptor gene expression. When organisms are exposed to bacterial lipopolysaccharide - the immune system’s signal for bacterial presence - the accessibility of bitter taste receptor genes (the Tas2r family) is markedly increased through an epigenetic opening mechanism. ¹⁵ The bitterness distortion of illness - why food tastes wrong during a fever, why flavours are flattened or distorted during infection - is driven by epigenetic remodelling of taste receptor accessibility in response to immune challenge.

Every clinician recognises this. Patients frequently describe food as tasting different during and after serious illness. We have typically explained this as a combination of appetite suppression and mucosal changes. The molecular mechanism, it now appears, is epigenetic: the illness is throwing switches in the taste receptor gene landscape.

The further implication - and this is where I would urge some epistemic caution, because the research is ongoing - is that a serious illness in your past may have left an epigenetic mark on your bitter receptor gene accessibility that has not fully reversed. The conditioned taste aversion research supports this possibility: research from the University of Michigan has shown that food aversions created by association with nausea or illness are consolidated epigenetically in the insular cortex through histone modification mechanisms, and that while these memories can in principle be modified, they are remarkably persistent. ¹⁶ The whisky drinker who finds certain compounds genuinely aversive despite every effort to approach them with curiosity may be experiencing not mere preference but an epigenetically consolidated memory of a past negative sensory event.

This is not a counsel of despair. The insular cortex research also showed that histone deacetylation - the epigenetic mechanism that consolidates aversive taste memories - can be interrupted, and that memory strength is malleable for a period after learning. ¹⁷ The palate is not permanently fixed by past experience. But it is genuinely shaped by it in ways that go deeper than conscious preference.

The Long Shadow: What Your Parents Ate

The most extraordinary dimension of the epigenetic story is how far back the shaping reaches.

Nutritional epigenetics has established - through decades of research, beginning with the agouti mouse experiments and extending through human population studies - that diet in prenatal and early postnatal life shapes the epigenome in ways that persist for a lifetime. ¹⁸ The mechanism is primarily methylation: nutrients that donate methyl groups - folate, B vitamins, S-adenosylmethionine - regulate the attachment of methyl tags to gene promoters, turning specific genes on or off. The maternal diet during pregnancy is, in effect, programming the offspring’s gene expression landscape before the child has tasted anything at all.

Research into early flavour experience and epigenetics, published in Nutrients in 2021, found that the period of complementary feeding - when infants first encounter solid food - is a window of particular epigenetic sensitivity. ¹⁹ The flavour environments encountered during this period appear to shape taste receptor gene expression and neural pathway development in ways that influence food preference and sensory sensitivity throughout life. The child who is introduced to a diverse, complex, varied flavour environment in early development may be building a differently calibrated sensory system from the child whose early diet is narrow and mild.

And the Swedish harvest records study - one of the most striking pieces of transgenerational epigenetics research - found that food availability for paternal grandfathers between the ages of nine and twelve correlated with the lifespan of their grandchildren. ²⁰ The grandfather’s nutritional environment during a critical developmental window was leaving an epigenetic mark that transmitted across two generations.

I want to state this carefully, because the transgenerational evidence in humans is suggestive rather than conclusive. But the direction it points is genuinely humbling: the palate you bring to a tasting table may carry the dietary history not just of your own life but of the lives that preceded it.

What This Means for Your Relationship With Whisky

Pulling these threads together, here is what I believe the science is telling us.

Your palate is a biography. It begins with the genetic architecture you were born with - your supertaster or non-taster status, your specific constellation of functional olfactory receptors, your baseline sensitivity thresholds across the five basic tastes. But that architecture has been continuously modified by:

-The diet your mother ate during pregnancy, which shaped your earliest epigenetic programming

-The flavour environments of your childhood, which participated in the epigenetic construction of your olfactory system and taste receptor expression

-Every dietary habit that has been reshaping your taste receptor gene accessibility ever since

-Illnesses that threw epigenetic switches in your bitter receptor genes

-Conditioned taste aversions that were consolidated epigenetically in your insular cortex

This is both humbling and - I think - liberating. Humbling because it means that your tasting notes carry more personal history than you realise. They are not objective reports from a neutral instrument. They are readings from an instrument shaped by the entirety of a life’s biological and sensory experience. This is why the same whisky can produce genuinely different experiences in different people, and why those differences deserve respect rather than correction.

Liberating because it means the palate is not fixed. Epigenetic mechanisms are, in principle, dynamic. Sustained exposure to a flavour environment has genuine molecular effects. The whisky enthusiast who has spent five years tasting attentively is not merely more practised than the person who started last month. They may be genuinely, molecularly different - their taste receptor gene expression subtly reshaped by years of deliberate flavour encounter. This is what is actually happening when someone develops a taste for heavily peated whisky after years of finding it confrontational. It may not be simply habituation. It may be epigenetic reprogramming.

As I explored in our article on temperature and the dram, whisky rewards patience - the patience to let the glass warm, to wait for the aromatics to open, to give the retronasal pathway time to do its work. ²¹ The epigenetic story suggests that the same patience operates at a longer timescale too. The palate develops not just within a tasting but across a life.

A Note on Cigars, Smoke, and the Epigenetics of Tobacco

Before I describe the Devon Drams tasting format, I want to address something that sits at the edges of this article’s argument - and that I would not feel honest ignoring, given the scientific territory we have been exploring.

I must be unequivocal about the health position first. Smoking causes cancer. The evidence is incontrovertible and the risk is serious across all tobacco products, including cigars. The NHS estimates that around 75% of lung cancer cases in the UK are caused by smoking, and cigar smoke contains the same carcinogens as cigarette smoke - often at higher concentrations per smoke session due to longer burn times and greater volume. ²⁵ Devon Drams does not recommend smoking, does not advocate for the use of any tobacco product, and this section is written as an honest scientific observation about a pairing that exists in the world, not as an endorsement of it.

With that stated clearly and without equivocation: the pairing of fine cigars and whisky is one of the oldest flavour relationships in the history of either product, and it has a chemistry that connects directly to what this article has been exploring.

The chemistry of why they interact

The reason cigars and whisky have been paired for centuries is not merely cultural or ceremonial - it is molecular. Not all tobacco aromas are released in the mouth because they do not dissolve in water (saliva), but they do dissolve in alcohol - hence a sip of whisky adds new flavours and enhances the bouquet of the cigar by distributing volatile aroma compounds throughout the mouth and supporting their transport to internal receptors. The alcohol in whisky acts as a solvent, stripping the fat-soluble flavour compounds from cigar smoke and carrying them to parts of the palate that the smoke alone would not reach. The whisky and the cigar are, at a molecular level, releasing each other’s flavour.

The principle of weight-matching is the governing rule: a full-bodied, high-ligero cigar delivering substantial earth, dark leather, espresso, and roasted nut will overpower a delicate single malt matured in light oak - the whisky disappears beneath the smoke. Conversely, a light Connecticut-wrapped cigar whose character is subtle, creamy, and restrained will be obscured by a cask-strength Pedro Ximénez release of dense texture and concentrated dark fruit. The weight of the cigar and the weight of the whisky must occupy similar registers, or one silences the other.

There is also an intensity-curve dynamic that experienced pairing enthusiasts note. The intensity curve of alcohol increases quickly initially and then decreases slowly, while the intensity of a cigar gradually increases during smoking - because the aroma compounds of the drink tend to be on the surface, while in a cigar they are located inside. Accordingly, tobacco aromas are only released more intensively as you draw deeper into the smoke. This means the pairing is not a static experience but a dynamic one: the whisky is at its most expressive when it is first poured; the cigar reaches its peak intensity in the second and third quarter of its burn. A pairing that begins in apparent imbalance may resolve beautifully as both objects move through their respective intensity curves.

Both tobacco leaves and aged spirits contain tannins and phenols acquired during fermentation and ageing - and when you sip a smoky Islay Scotch, the alcohol acts as a solvent, stripping away the oils from the cigar smoke on your palate. This is precisely the chemistry we explored in the Cooper’s Art article: the phenols and lignin-derived compounds that cask ageing produces in whisky are chemically similar to those produced by the fermentation and curing of tobacco leaf. When a peated Islay malt - whose guaiacol content we discussed in our science of taste article - is paired with a full-bodied cigar, the shared phenolic register is not coincidence. They are drawing from overlapping chemical vocabularies.

The epigenetics connection

Here is where this section connects most directly to the article’s central argument.

Tobacco smoke is one of the most potent environmental modifiers of gene expression we know of - and some of its epigenetic effects are specifically in the taste and olfactory system. Research has found that chronic tobacco exposure alters the methylation patterns of taste receptor genes, and that these alterations affect both bitter taste sensitivity and olfactory acuity. ²⁶ Long-term smokers often report that their palate becomes more tolerant of bold, bitter, heavily flavoured foods and drinks - and the science suggests this is not merely adaptation but genuine epigenetic modification of taste receptor gene expression over time.

This has a direct implication for cigar and whisky pairing. The experienced cigar enthusiast who finds the heavily peated Islay malt a natural companion is not simply habituated to smoke. Their taste receptor epigenome may have been modified by years of tobacco phenol exposure in a way that makes the phenolic register of a peated whisky feel familiar rather than confrontational. The pairing works partly because the palate has been shaped, at a molecular level, by the same class of compounds.

This is an observation, not a recommendation. The epigenetic modification of taste receptors by tobacco smoke is accompanied by the far more consequential carcinogenic modification of lung and airway tissue - and no flavour pairing justifies that risk.

If you are interested in the flavour territory without the tobacco, the good news is that the specific flavour profile of the cigar-and-whisky pairing - the earthiness, the roasted depth, the shared phenolic register - is accessible through food pairings that carry none of tobacco’s health burden. Dark chocolate with high cocoa content shares phenolic compounds with both cigar smoke and peated whisky, creating a similar trilateral chemical conversation. Strong espresso alongside a sherried, full-bodied Speyside occupies a comparable weight register. Smoked charcuterie - particularly heavily smoked products like lardo or smoked duck - brings that same smoke-and-fat combination that makes the cigar pairing work, without any of its risks.

As I explored in our food pairing article, the principle of shared volatile compounds creating flavour harmony applies regardless of the source of those compounds. ²⁷ The chemistry of satisfaction is the same. The health arithmetic is not.

The Devon Drams Genetics and Biography Tasting Evening

This is where the science becomes an event format - and I should be honest about where this idea currently stands.

At the Athenaeum, where I chair the Whisky Interest Group, I have been leaving out an aroma kit on the table before tastings begin - a collection of individual aromatic compounds, each sealed in a small vial, that participants can nose independently before the whisky is poured. I have done this for some time, but if I am being candid, most people don’t use it. It sits there. People arrive, they find their seats, they fall into conversation, and the vials are largely ignored until someone more curious than the rest picks one up and asks what it is.

Writing this article has made me think about that differently.

What I have been offering is the right tool, but without the context that would make people want to use it. The aroma kit is interesting as a curiosity. It becomes genuinely revelatory once you understand that the people around the table are not simply bringing different levels of experience to the same glass - they are bringing different biological and epigenetic architectures, shaped by genetics they were born with and by the entire dietary and sensory history of their lives. With that context established, the vials are not a novelty. They are an instrument for understanding something real about yourself and the people beside you.

What I am now thinking about - and intend to develop into a proper event format, first at the Athenaeum and then at Devon Drams and the other tastings I run - is something more deliberately structured around the science in this article.

The evening begins with a PTC taste-strip for each participant - a small paper strip impregnated with phenylthiocarbamide, inexpensive and widely available online. Each person tastes it before anything else. The response is immediate: either strong bitterness, indicating supertaster or medium taster tendency, or very little, indicating non-taster tendency. Results are shared voluntarily. This single act changes the room before the evening has properly begun. The people around the table are no longer simply whisky enthusiasts with varying experience. They are people with measurably different sensory hardware, about to compare what that hardware delivers from the same flight of glasses.

The aroma kit follows - but this time with purpose built into the introduction. A small selection of isolated aromatic compounds chosen specifically to correspond to aromas that will reappear in the whiskies being tasted: vanillin, guaiacol, perhaps a peaty phenol marker, a fruity ester. Each person noses each vial and notes what they detect, how vividly, and whether it reminds them of anything. The variation in response across the table - the compound that one person finds overwhelming and another barely registers - is the first live demonstration of the evening’s central argument. It happens before anyone has touched a glass of whisky, and it sets up everything that follows.

Before the tasting begins, each participant shares one sentence about their flavour biography: where they grew up, what food culture shaped them, one strong taste memory from earlier in their life. Not as a prediction of what they will taste, but as an acknowledgement - made openly and together - that what each person brings to the glass is the product of more than this evening. The person who grew up in a household where food was intensely seasoned brings a different epigenetic history from the person whose early diet was mild and largely unchanged. Both are valid. Both are worth naming.

Then the flight.

Glass One: A delicate Lowland or triple-distilled Irish single malt - Chosen to be maximally accessible to supertasters and maximally challenging to non-tasters. The question for the group: who finds this revelatory, and who finds it thin? The divergence in response is the first illustration of the evening’s central argument. Discussion point: is subtlety a quality of the whisky or a function of the receptor?

Glass Two: A lightly peated Highland or Island expression - Highland Park 12, or Kilchoman Machir Bay - The middle ground. Most participants will find something here. The question: where does the smoke register for supertasters versus non-tasters? Does the peat feel warming or confrontational? Discussion point: the Cooper’s Art article’s exploration of phenolic compounds in cask chemistry - what the distillery put in the glass at the production stage, and what each palate is able to retrieve from it.

Glass Three: A rich, heavily sherried expression - GlenDronach 18, or Aberlour A’bunadh - Tests bitterness sensitivity through a different channel: tannins from the sherry cask rather than phenols from peat. Supertasters will often find the tannin grip more pronounced here. Discussion point: how cask choice interacts with individual sensitivity - from our Wood Series Part One, the Jerez Secret. ²²

Glass Four: A full Islay peat bomb at standard strength - Laphroaig 10 or Lagavulin 16 - The supertaster challenge. The question is not whether this is a good whisky (it is) but what each person actually detects. The aim is to destigmatise divergent response entirely. And - if anyone in the room grew up with spicy food as a cultural staple - does this glass feel different from what the group might have expected? The cultural palate dimension of the evening lives here most vividly. Discussion point: is this whisky’s intensity a fact about the bottle, or a biological relationship between the bottle and the person holding it?

Glass Five: A cask strength expression - served first neat, then with a few drops of water - The final illustration. Each person adds water until the heat resolves for them. The amount of water required will vary significantly between supertasters and non-tasters - a visible, immediate demonstration of individual physiological difference. For anyone whose TRPV1 receptors have been shaped by a lifetime of spicy food: notice how much water you need compared to your neighbour. The difference is not preference. It is biology. Discussion point: the water and whisky article’s explanation of guaiacol release through dilution, and the temperature article’s explanation of how warmth and dilution interact. ²³ ²⁴

After the fifth glass, the conversation opens. What did you find that surprised you? What did you find that confirmed what you already knew about your palate? Did anything in your flavour biography - the sentence you shared before the tasting - appear to be legible in what you detected? Was the person who grew up with the spiciest food the one who found the Islay malt most accessible? Did the person from a milder culinary tradition find the delicate Lowland most revelatory?

The evening does not produce consensus. It produces something richer: a group of people who understand, more concretely than they did when they sat down, that they are each tasting from a unique biological and biographical position - shaped by genetics, by diet, by illness, by the kitchens they grew up in, and by the food cultures their families carried long before they were born. That understanding makes the shared experience not less interesting but considerably more so. The whisky in the glass is the same for everyone. The world it opens into is different for each person at the table.

I am not presenting this as something Devon Drams has already delivered. It is something I intend to develop - here and at the other groups and institutions where I host tastings - informed directly by the research that went into writing this article. The science changed how I think about the aroma kit that has been sitting on the table for months. I hope it changes how you think about the glass in front of you.

If this is an evening you would like to be part of when it arrives, let us know.

A Note on the Limits of the Science

Before closing, intellectual honesty requires me to say clearly where the evidence is robust and where it is speculative.

The genetics of taste perception - supertaster status, TAS2R38 variants, olfactory receptor gene diversity - is well-established and well-replicated science. The epigenetic regulation of olfactory receptor gene expression during neuronal development is established peer-reviewed research, published in leading journals. The epigenetic modification of bitter and sweet taste receptor gene accessibility by diet and immune challenge is emerging but well-founded research, with the key studies published in Science Advances and iScience.

The application of these mechanisms specifically to whisky tasting is my own inference, grounded in the science but not directly tested in a whisky laboratory. The cultural palate hypothesis - that Sri Lankan and South Asian populations may find peated whisky more naturally accessible due to a combination of genetic TRPV1 variation and lifelong dietary desensitisation through spicy food - is similarly my own synthesis from independently evidenced mechanisms rather than a directly tested finding. And the transgenerational epigenetics story - the suggestion that your grandparents’ dietary history may be legible in your palate - is the most speculative thread in this article, based on suggestive human population data and robust animal model evidence, but not yet settled science in the way the direct dietary epigenetics is.

I have tried to signal these distinctions through the language I have used throughout. I am a physician trained to read evidence carefully and present uncertainty honestly. The science here is genuinely exciting, genuinely relevant, and genuinely incomplete. That is not a reason to dismiss it. It is a reason to hold it with the same calibrated curiosity we bring to every glass.

At Devon Drams, the most important thing we can do is create the conditions for honest, curious engagement - with what is in the glass and with each other. The science in this article suggests that those two things are more connected than we might have thought.

Your palate is your biography. And a tasting table is, in the most literal molecular sense, a gathering of different biographies - all attending to the same glass and finding different worlds.

Come and find us at our next event.

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Devon Drams articles referenced in this piece

What Are You Actually Tasting? The Science Behind Every Dram - on retronasal olfaction, the brain’s construction of flavour, and why context shapes perception ¹ ¹²

The Cooper’s Art: Why the Barrel Maker May Matter More Than the Distiller - on phenolic compounds, cask chemistry, and how the wood shapes the bitter and sweet compounds in the glass ⁵

Water and Whisky: What Happens Inside You When You Drink - on the physiology of dilution and the science of adding water to whisky ⁷ ²³

Does Temperature Matter? The Science of a Warm Dram - on aromatic release, volatility, and how warmth shapes what you can detect ²¹ ²⁴

The Wood Series, Part One: The Jerez Secret - on sherry cask sourcing, tannin contribution, and what the cask adds to the glass ²²

Whisky and Wellbeing: What the Science Says - on alcohol physiology and responsible consumption

Sources

1. Devon Drams. What Are You Actually Tasting? The Science Behind Every Dram. devondrams.com/news (Accessed: June 2026)

2. Fox, A.L. (1931). ‘Six in ten “tasteblind” to bitter chemical’. Science News-Letter, 9 September 1931. [General reference to the PTC discovery]

3. Bartoshuk, L.M., Duffy, V.B. and Miller, I.J. (1994). ‘PTC/PROP tasting: anatomy, psychophysics, and sex effects’, Physiology & Behavior, 56(6), pp. 1165–1171.

4. EBSCO Research Starters. Taste Bud. Available at: https://www.ebsco.com/research-starters/health-and-medicine/taste-bud (Accessed: June 2026)

5. Devon Drams. The Cooper’s Art: Why the Barrel Maker May Matter More Than the Distiller. devondrams.com/news (Accessed: June 2026)

6. ScienceDirect. Epigenetic Regulation of Ion Channels in the Sense of Taste. Critical Reviews in Food Science and Nutrition (2025). Available at: https://www.sciencedirect.com/science/article/abs/pii/S1043661821003443 (Accessed: June 2026)

7. Devon Drams. Water and Whisky: What Happens Inside You When You Drink. devondrams.com/news (Accessed: June 2026)

8. Bartoshuk, L.M. et al. (1994). Ibid.

9. General reference to twin studies on taste concordance and epigenetic divergence.

10. Jiao, Y. et al. (2021). ‘Persistent epigenetic reprogramming of sweet taste by diet’, Science Advances, 7(6), eabc8492. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC7673743/ (Accessed: June 2026)

11. ScienceDirect. Epigenetic Regulation of Ion Channels in the Sense of Taste. Ibid.

12. Devon Drams. What Are You Actually Tasting? The Science Behind Every Dram. Ibid.

13. Yusuf, I.O. et al. (2024). ‘Epigenetic programming of stochastic olfactory receptor choice’, Genesis, 62(2), e23593. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC11003729/ (Accessed: June 2026)

14. bioRxiv. The transcription of a single olfactory receptor per neuron is enforced by epigenetic silencing of their enhancers. Preprint, December 2025. Available at: https://www.biorxiv.org/content/10.64898/2025.12.22.695993v1 (Accessed: June 2026)

15. Wang, H. et al. (2023). ‘Epigenetic mechanism that causes bitter taste distortion discovered’, Monell Chemical Senses Center / iScience. Reported in ScienceDaily, August 2023. Available at: https://www.sciencedaily.com/releases/2023/08/230824120153.htm (Accessed: June 2026)

16. Rodriguez-Blanco, L.A. et al. (2019). ‘Epigenetic mechanisms in conditioned taste aversion’. Reported in: Neuroepic, University of Michigan. Déjà Food: The Epigenetics of Taste Aversions. Available at: https://courses.lsa.umich.edu/neuroepic/deja-food-the-epigenetics-of-taste-aversions/ (Accessed: June 2026)

17. Ibid.

18. Learn Genetics, University of Utah. Nutrition and the Epigenome. Available at: https://learn.genetics.utah.edu/content/epigenetics/nutrition/ (Accessed: June 2026)

19. Parisi, F. et al. (2021). ‘Epigenetics and Modulations of Early Flavor Experiences: Can Metabolomics Contribute to Prevention during Weaning?’ Nutrients, 13(11), 3768. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC8539480/ (Accessed: June 2026)

20. Learn Genetics, University of Utah. Nutrition and the Epigenome. Ibid. [Swedish harvest records, transgenerational epigenetics]

21. Devon Drams. Does Temperature Matter? The Science of a Warm Dram. devondrams.com/news (Accessed: June 2026)

22. Devon Drams. The Wood Series, Part One: The Jerez Secret. devondrams.com/news (Accessed: June 2026)

23. Devon Drams. Water and Whisky: What Happens Inside You When You Drink. Ibid.

24. Devon Drams. Does Temperature Matter? The Science of a Warm Dram. Ibid.

25. NHS. Lung Cancer: Causes. Available at: https://www.nhs.uk/conditions/lung-cancer/causes/ (Accessed: June 2026)

26. General reference to tobacco smoke epigenetic modification of taste and olfactory receptor gene methylation. See: Monell Chemical Senses Center research on taste receptor epigenetics; ScienceDaily (2023). Available at: https://www.sciencedaily.com/releases/2023/08/230824120153.htm (Accessed: June 2026)

27. Devon Drams. The Art and Science of Pairing. devondrams.com/news (Accessed: June 2026)

28. Nolden, A.A. et al. (2024). ‘Inducible desensitization to capsaicin with repeated low-dose exposure in human volunteers’, PMC10842799. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC10842799/ (Accessed: June 2026)

29. Trachootham, D. et al. (2018). ‘Differences in Taste Perception and Spicy Preference: A Thai–Japanese Cross-cultural Study’, Chemical Senses, 43(1), pp. 65–72. Available at: https://academic.oup.com/chemse/article/43/1/65/4609710 (Accessed: June 2026)

30. Ganapathy, A. et al. (2022). ‘Landscape of Variability in Chemosensory Genes Associated With Dietary Preferences in Indian Population: Analysis of 1029 Indian Genomes’, Frontiers in Genetics. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC9315315/ (Accessed: June 2026)