The Flavour Gamechanger You’ve Never Heard of: ATP
Walk into any distillery, winery, flavour lab, or sensory panel, and you’ll find people obsessing over esters, aldehydes, polyphenols, and pyrazines. But there’s one molecule that rarely gets a mention, despite being fundamental to everything we do. It’s not an aroma compound. It doesn’t smell or taste of anything. Yet without it, there would be no flavour perception whatsoever.
We’re talking about ATP (adenosine triphosphate): the molecular fuel that powers our cells. In the context of sensory science, ATP doesn’t get the airtime it deserves. It’s the backstage crew of flavour perception – unseen, uncelebrated, unnoticed, and yet absolutely vital.
While understanding personal odour and taste thresholds are important, it’s mitochondrial function and ATP production that may be behind them, including daily fluctuations and sensory dysfunction. So if you work in whisky, wine, chocolate, cheese, or perfumery, having at least a rudimentary awareness of ATP is essential.
Want a quick scan? Here are the key takeaways:
ATP is essential for flavour perception
It powers the taste, smell, and cognitive processes that let us experience flavour — yet it's often ignored in sensory science.Taste cells use ATP as a neurotransmitter
ATP doesn’t just fuel the process — it triggers taste signals by activating gustatory nerves.ATP sharpens your sense of smell
In the olfactory system, ATP modulates how clearly and accurately we detect and process odours.The brain needs ATP to interpret flavour
Neurons and astrocytes rely on ATP for attention, memory, and the multisensory integration that creates complex flavour experiences.Low ATP = duller senses and slower thinking
Fatigue, stress, poor sleep, and metabolic issues can all reduce ATP production — blunting sensory acuity and cognitive precision.Protect your mitochondria, protect your palate
Lifestyle, environment, drugs, diet, and ageing all impact ATP. Managing these can help maintain sensory sharpness and tasting accuracy.
What Is ATP, and Why Should Flavour Professionals Care?
ATP is produced by our mitochondria, the tiny energy generators within virtually every cell in our bodies. Known as the ‘energy currency’ of the cell, ATP provides readily releasable energy. Mitochondria produce this through multiple catabolic mechanisms including cellular respiration, beta-oxidation, and ketosis. It’s essential because..
ATP powers nearly all biological functions, from muscle movement to memory and even the neural activity required for tasting and smelling. This energy is essential for maintaining the sensitivity and performance of all systems, including our sensory systems, brain functions and olfactory neurons, which are metabolically demanding. When mitochondrial function is compromised, ATP production drops, leading to reduced sensory acuity, fatigue, and cognitive slowdown.
Every time a taste receptor fires, or an odour molecule is transduced into a neural signal, ATP is involved. And when the brain processes those signals, interpreting them as toasted coconut or ripe banana, it’s ATP doing the heavy lifting. Despite this, ATP remains absent from most flavour science conversations. Ask a room full of drinks industry professionals what lactones are, and you’ll get a robust discussion. Ask about ATP, and you'll get puzzled looks. But going beyond cellular energy, ATP plays a very specific role in how we taste.
ATP and Taste: More Than Just Receptors
In taste buds, ATP is more than a fuel source – it’s a neurotransmitter. When you taste something sweet, bitter, or umami, special cells in your taste buds respond by releasing ATP. But here, ATP isn’t used as fuel, it acts like a messenger, which is where it gets really interesting.
This ATP travels a tiny distance and binds to special receivers called purinergic receptors on nearby nerve endings. These nerve endings are part of the gustatory nerves, which send taste signals straight to your brain. So for those nerve signals to be released, ATP acts as the trigger.
Imagine each taste receptor cell is a firework, ready to launch a rocket (a nerve signal) to your brain. But it can’t do anything until it’s lit. That’s where ATP comes in. ATP acts like the fuse, once it’s released, it travels to nearby purinergic receptors, which then fire the signal to your brain.
So instead of the taste cell lighting up on its own, it releases ATP, which sets off the chain reaction – lighting the fuse, launching the firework, and creating the final experience of flavour in your brain. (Finger et al., 2005). But it’s important to understand this..
The process is energy-intensive. Mitochondria in taste cells work constantly to maintain the ATP supply needed to fire these signals. If mitochondrial function is compromised – due to ageing, illness, fatigue, or metabolic stress – ATP production drops, and taste perception dulls.
Several studies have shown that serotonin and noradrenaline, both modulated by ATP, play a key role in adjusting taste thresholds (Heath et al., 2006). In other words, your ability to taste bitterness or sweetness isn't just about the presence of receptors, but about having the cellular energy to use them. However, ATP goes far beyond taste.
ATP and Smell: The Invisible Modulator
In olfaction, ATP plays a different but equally crucial role. While it isn’t the main neurotransmitter in smell perception, it acts as a modulator within the olfactory epithelium and olfactory bulb.
Supporting cells in the nasal epithelium can release ATP in response to mechanical or chemical stimulation. This ATP then binds to purinergic receptors (remember those?) on olfactory sensory neurons (OSNs), affecting their excitability and amplifying or dampening their response to odours (Hegg et al., 2003).
The olfactory bulb is the brain's first stop for processing smell signals from your nose. It’s like the control tower where the brain starts figuring out what you're smelling. In this area, ATP plays a helpful role. It boosts the clarity of the smell signal by making it easier for the brain to detect important odours and ignore background noise or random static. (Vongtau et al., 2011). Think of it like adjusting the saturation in photo editing software - the important details stand out more clearly, making it easier to tell certain details apart.
And like in taste, OSNs rely heavily on mitochondrial ATP to maintain ion gradients, reset after depolarisation, and keep their cilia functional. Without ATP, even the most aromatic whisky will fall flat to a tired or metabolically stressed nose.
Just like in taste, your smell-sensing cells (OSNs) need a steady supply of ATP to do their job properly.
They use ATP to:
Keep their internal balance (ion gradients) stable
Reset after detecting a smell (like reloading after firing)
Keep the tiny hair-like structures (cilia) working – the part that actually detects odour molecules
If your body is low on energy, because you're tired, stressed, or run down, your nose won’t work at full power. Even the most aromatic whisky can seem dull when your brain and cells are too tired to notice it. Want to delve deeper? Here’s how ATP is central to cognitive function too.
ATP and the Brain: Cognition, Attention, and Flavour Integration
Flavour isn’t just about the nose and tongue. It’s a cognitive experience involving memory, attention, and multisensory integration, all of which are ATP-dependent. When you pick up a scent or try to describe a flavour – say, the smoky peat in a whisky or the subtle hint of citrus in a gin – your brain isn’t just passively receiving signals.
Instead, it’s actively assembling a rich sensory story by engaging multiple neural systems simultaneously. Think of it as a highly skilled orchestra, where different sections work together to create a complex, harmonious experience. At the core of this orchestra are neurons — the brain’s communication specialists.
These neurons send electrical signals to each other, passing on the sensory information about what you smell or taste. But neurons don’t work alone. Supporting them are astrocytes, the brain’s often-unsung heroes. These star-shaped glial cells do a heap of backstage work: they supply energy, regulate the chemical environment around neurons, recycle neurotransmitters, and maintain ion balance essential for the neurons’ electrical activity.
Now, all this intricate activity – neurons firing, neurotransmitters being recycled, ions shuffling back and forth – requires a steady supply of energy. That energy comes in the form of – you’ve guessed it – ATP. Without ATP, the neurons and astrocytes would falter, synaptic communication would break down, and your brain wouldn’t be able to make sense of those delightful aroma and flavour notes.
In essence: recognising and describing complex aromas isn’t just a simple sniff-and-think. It’s a symphony of brain cells working energetically and collaboratively, powered by ATP, to transform chemical signals into the rich sensory experiences you love, and sometimes struggle, to put into words.
When you identify an aroma or describe a complex flavour note, your brain draws on multiple neural systems. These processes are supported by astrocytes and neurons, both of which rely on ATP for synaptic activity, neurotransmitter recycling, and ion balance (Magistretti & Allaman, 2018).
Cognitive fatigue, low blood sugar, or mitochondrial inefficiency can lead to slower flavour identification, reduced attention to detail, and even distortions in perception. In a sensory panel or judging competition, this could be the difference between accuracy and error.
The Hidden Impacts of Environment, Lifestyle and Health
We’ve spoken a great deal about the crucial roles of ATP and how mitochondrial dysfunction can hamper one’s tasting credentials. So, the obvious question for any neuro-curious flavour explorer is: what impacts mitochondrial function and therefore ATP production?
While being robust little powerhouses, our mitochondria are sensitive to a range of factors. Understanding these is essential, not just for enabling sensory functions, but for health in general.
1. Reactive Oxygen Species (ROS)
Mitochondria naturally produce ROS as by-products of energy metabolism, but excess ROS can damage mitochondrial DNA (mtDNA), proteins, and lipids. This damage is particularly problematic because mtDNA has limited repair capacity, leading to long-term dysfunction. Hence, over-exercise or inadequate recovery from exercise, can exceed your body’s antioxidant defences leading to oxidative stress and mitochondrial damage.
2. Environmental Toxicants
Over the past 50 years, nearly 20,000 unique chemicals have been measured in the environment, according to a major bibliometric survey of scientific data. That’s 19,776 substances identified in environmental media such as air, soil, and water.
Yet astonishingly, this represents only a tiny fraction of the total number of chemicals in commercial use, with just 5% of measured substances appearing on industrial chemical inventories from the EU, US, or China. This means we are repeatedly testing the same known chemicals, while tens of thousands of others, many with unknown or toxic potential, remain unmonitored in our environment.
Numerous toxicants and drugs have been shown to damage mitochondrial membranes and impact the processes essential for making ATP. These include pesticides like rotenone, solvents, heavy metals, and air pollutants like PAHs.
Polycyclic Aromatic Hydrocarbons (PAHs) are a group of organic compounds made up of multiple fused benzene rings are commonly found in exhaust fumes, cigarette smoke, burnt or charred food, industrial emissions, plus coal and crude oil products.
Ajmani et al (2016), reviewed 18 studies, most comparing people living in highly polluted cities with those in less polluted areas. In nearly all cases, those in high-pollution environments had poorer olfactory function, especially in odour threshold and discrimination tasks (rather than identification). Young people were often more affected than older adults, who may already have age-related decline.
They highlighted how airborne pollutants can enter the olfactory epithelium, travel up the olfactory nerve, and reach the olfactory bulb and cortex. This process may cause inflammation, tissue damage, and mitochondrail stress – all of which have the potential to negatively impact ATP production.
3. Certain Pharmaceuticals
Some pharmaceuticals can negatively impact mitochondrial function, including AZT (an HIV/AIDS drug) that inhibits DNA polymerase gamma, crucial for mtDNA replication. Other drugs with mitochondrial liabilities include statins (antilipidemic), metformin (antidiabetic), antidepressants, beta-blockers, and NSAIDs. These drugs can impair mitochondrial respiration, reduce ATP production, or increase lactic acid.
4. Radiation
Ultraviolet (UV) radiation is a type of high-energy light from the sun (or artificial sources like tanning beds). UV rays can penetrate skin and cells, damaging DNA by creating pyrimidine dimers – mutations in the DNA structure. In mitochondria, which lack protective histones and have poor DNA repair mechanisms, UV exposure can lead to long-lasting mutations. This compromises the energy-producing machinery and increases ROS production.
5. Overeating / High-Calorie Diet
A high-calorie diet overwhelms your mitochondria, increasing oxidative stress and inflammation. This damages their ability to make energy and contributes to long-term health issues, even if you’re not visibly unhealthy.
6. Ageing
mtDNA mutations accumulate over time, reducing mitochondrial efficiency with age. Ageing also reduces cellular ability to respond to environmental stress and repair damage.
7. Stress
Chronic stress damages mitochondria by increasing oxidative stress, inflammation, and energy demand. The worse your mitochondria function, the harder it is to cope, and the duller your sensory world becomes.
When you're stressed, your body activates the HPA axis (hypothalamic-pituitary-adrenal). This floods your system with stress hormones like cortisol and adrenaline. These hormones increase energy demand, and your body shifts into survival mode. This means that your mitochondria must work harder to produce ATP under pressure, and that ramps up ROS production, which leads to sustained oxidative stress. It also activates pro-inflammatory pathways, which further damages mitochondrial function and structure.
It’s a vicious circle too because mitochondria regulate the body’s response to stress, including how intensely you feel it. They interact with stress signalling pathways and can even amplify or buffer psychological stress, depending on their condition. When mitochondria are already dysfunctional, stress feels worse, and you become more fatigued, anxious, and cognitively foggy.
8. Sleep Deprivation
Sleep is when your mitochondria recharge, repair, and reset. Deprive yourself of sleep, and you risk lower ATP, higher oxidative stress, brain fog, and blunted flavour perception. Studies show that sleep-deprived brains produce more ROS, especially in the prefrontal cortex (linked to focus, memory, and sensory judgement). At the same time, ATP levels drop, leaving cells with less energy to function. This leads to cognitive fatigue, poor memory, and dull sensory processing.
So What Can We Do About It?
Raise Awareness: Start talking about ATP in sensory training. Make it part of the conversation, just like you would with olfactory receptors or flavour wheels.
Promote Mitochondrial Health: Encourage good nutrition, hydration, sleep, and stress management in sensory professionals, plus consider the environment and air quality. Consider wellness as part of sensory accuracy.
Time Tastings Wisely: Schedule important tastings when panellists are well-rested and well-fed. Avoid late afternoons or post-lunch slumps.
Monitor Performance: Track individual panellist performance over time. Variations may signal more than preference, they may indicate physiological fluctuations affecting ATP.
Bridge Disciplines: Collaborate with neuroscientists and nutritionists to better understand how metabolic health affects sensory work.
Conclusion: It's Time to Talk About ATP
ATP may not smell of anything, but it underpins everything we do in flavour. It fuels taste receptor firing, olfactory signalling, and the brain’s ability to interpret and articulate what we experience. Yet it remains woefully overlooked in flavour science.
As the sensory world moves towards deeper, more interdisciplinary understanding, ATP deserves a place at the table. It might not be the molecule you nose for in a dram of Islay single malt, but it's the reason you can nose it at all.
Once we begin to look at the causes of mitochondrial dysfunction and reduced ATP production, it becomes clear that cellular health is at the heart of many illnesses and all bodily functions. The interesting perspective for flavour professionals is understanding how essential ATP is for sensory perception, and in which ways its production can be impacted.
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References:
Finger, T. E., et al. (2005). ATP signaling is crucial for communication from taste buds to gustatory nerves. Science.
Heath, T. P., et al. (2006). Human taste thresholds are modulated by serotonin and noradrenaline. Journal of Neuroscience.
Hegg, C. C., et al. (2003). ATP modulation of olfactory signal transduction in sustentacular cells of the mouse olfactory epithelium. Journal of Physiology, 552(Pt 3), 731-741.
Vongtau, H. O., et al. (2011). Purinergic modulation of mitral cell activity in the olfactory bulb. Neuroscience.
Magistretti, P. J., & Allaman, I. (2018). A cellular perspective on brain energy metabolism and functional imaging. Neuron.
Hiroshi Kobayashi, Shogo Imanaka. (2024). Mitochondrial DNA Damage and Its Repair Mechanisms in Aging Oocytes. International Journal of Molecular Sciences.
Sahlin, K., Shabalina, I.G., Mattsson, C.M., Bakkman, L., Fernström, M,. Rozhdestvenskaya, Z., Enqvist, J.K., Nedergaard, J., Ekblom, B., Tonkonogi, M. (2010). Ultraendurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle. Journal of Applied Physiology.
Tanskanen, M., Atalay, M., Uusitalo, A. (2019). Altered oxidative stress in overtrained athletes. Journal of Sport Sciences.
Ajmani, G. S., Suh, H. H., & Pinto, J. M. (2016). Effects of ambient air pollution exposure on olfaction: A review. Environmental Health Perspectives.
Ramanathan, L., Gulyani, S., Nienhuis, R., & Siegel, J. M. (2002). Sleep deprivation decreases superoxide dismutase activity in rat hippocampus and brainstem. NeuroReport.