Chapter 15: Taste & Flavor Perception
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Welcome back to the Deep Dive.
Today we are taking a stack of research that on the surface might seem like it belongs in a culinary school, but actually it belongs deep inside a neurobiology lab.
We are diving into chapter 15 of sensation and perception.
We are talking about taste.
And honestly, this is one of those topics where everyone sort of thinks they're an expert because well, everyone eats.
You do it three times a day, maybe more if you're lucky.
Right.
But the reality is the average person's understanding of what is actually happening in their mouth
is surprisingly backward.
We confuse the anatomy, we get the terminology all mixed up, and we definitely underestimate the sheer complexity of the machinery involved.
I have to admit, before I read this chapter, I was definitely in that camp.
I thought I knew what flavor was.
Turns out I didn't have a clue.
Most people don't.
It's one of the biggest misconceptions in all of sensory science.
So our mission today is to fix that.
We are going to provide a comprehensive summary of chapter 15.
We were going to look at the biological hardware, the tongue, the nerves, the brain, and then we were going to look at the psychology of why we eat what we eat.
But to kick this off, I want to start with a scene from a novel that the text uses.
It's from Nora Ephron's Heartburn.
Ah, the cookie dilemma.
I love this example.
Exactly.
So picture this.
You are in New York City.
It's late.
You are looking out the window at the lights, the people, the energy of the city.
Ephron writes that she looks out and looks for love and the world's greatest chocolate chip cookie.
And she describes her heart doing this little dance at the thought.
The text uses this to ask a really specific question.
Why do we love chocolate chip cookies so much?
It sounds like a philosophical question, almost poetic, but biologically it is a loaded one.
Really loaded.
Right.
Because when I eat a cookie, I just think this is delicious.
But the chapter immediately breaks that single experience down into all these different pieces.
Is it the smell?
Is it the sweet taste?
Is it the chocolate flavor?
Or is it the texture, the melting chocolate?
All of that.
And this is where we have to draw a hard line in the sand.
Right from the beginning.
The answer forces us to distinguish between what is innate,
what you were born with, and what is learned.
If you dissect that cookie experience, your love for the sweetness of the sugar, that is completely hardwired.
Meaning I came out of the womb loving that.
No learning required.
Yes.
A newborn baby, literally within hours of birth, will produce a smile if you put a drop of sugar water on their tongue.
That reaction is built into the brain stem.
It's survival mechanism.
Sweet means energy.
And energy means survival.
You don't need a single life experience to learn to like it.
Okay.
That makes sense.
But what about the chocolate part?
The actual chocolateness of it?
That is the trick.
The specific flavor of chocolate.
That is 100 % learned.
You were not born liking chocolate.
I find that incredibly hard to believe.
Chocolate feels like a fundamental truth of the universe.
It feels that way now.
But think about it.
If you strip away the sugar and fat, what is chocolate?
It's pure cocoa, which is a complex, slightly bitter, earthy flavor.
If you gave a little bit of pure cocoa to a baby, they would likely make a face and spit it out.
So why do I love it?
Because over the course of your life, your brain has paired that specific aromatic flavor with the massive hit of sugar and fat that always comes with it.
Your brain learns a very simple equation.
Oh, this specific smell, this smell predicts a huge calorie reward And so over time, you learn to love the flavor itself.
So the sweetness is the biological hook, and the chocolate flavor is the learned association that rides on top of it.
Exactly.
And that distinction between innate taste and learned flavor drives everything we're going to talk about today.
Taste is a gatekeeper.
Its primary evolutionary function is to help us swallow nutrients and spit out poisons.
It is a matter of life and death hidden inside a chocolate chip cookie.
That sets the stage perfectly.
So here's the roadmap for a deep dive today.
We are going to start by clearing up that biggest confusion of all,
the difference between taste and flavor.
Then we are going to do a deep dive into the anatomy.
And I promise you, we are going to debunk that tongue map you saw in your third grade textbook.
Oh, we have to.
It's a public service.
Then we will look at the basic tastes, the genetic lottery that makes some people super And finally, we will look at how our body regulates what we need to eat.
It is a full menu.
Let's get into it.
Let's start with the basics.
Taste versus flavor.
In casual conversation, I use these words interchangeably all the time.
The soup tastes good.
The soup has good flavor.
Same thing, right?
Not even close.
And the chapter calls this the anatomy of a misunderstanding for a reason.
This confusion goes back thousands of years.
Aristotle, the great philosopher, he got this completely wrong.
He categorized our senses by the action we perform, he thought.
If you are sniffing something, that is smell.
If you are touching something with your tongue, that is cased.
Which, to be fair to Aristotle, seems like pure common sense.
It's intuitive.
It is, but it completely ignores the internal plumbing of the head.
It wasn't until 1812 that a guy named William Prout, a student at Edinburgh University, actually paid close attention to what was happening inside his own head.
He noticed that when he ate nutmeg, it had this rich, spicy, woody character.
But then he did a simple experiment.
He held his nose shut while eating it, and it was gone.
Gone, like completely.
Vanished.
He realized that the nutmegdus, the character of it, wasn't happening on the tongue at all, it was happening in the nose.
But because the food was in his mouth, his brain was telling him the sensation was in his mouth.
He was confused.
So Prout figured out that we smell our food while we eat it.
Yes, but we need to be very precise here.
The text uses figure 15 .1 to explain this, and it distinguishes between two types of smelling.
There's orthonasal olfaction and retronasal olfaction.
Okay, orthonasal.
That sounds like orthodontist.
What does that mean?
Ortho just means straight or correct.
Orthonasal olfaction is what you think of as normal smelling.
It's what happens when you sniff a flour or a carton of milk to see if it's gone bad.
You inhale through the nostrils, the air goes up, hits the olfactory epithelium at the top of your nasal cavity.
That is smelling.
Simple enough.
So what is retronasal?
Retro means backwards.
This is the game changer.
When you chew food and swallow, you are physically mashing it up, warming it, mixing it with saliva.
This releases volatile molecules, tiny aromatic gases, essentially.
Because your throat and your nose are connected by an opening at the back,
those volatiles don't go out your mouth.
They travel from the back of the mouth up into the nasal cavity through this rear entrance.
They hit the very same olfactory epithelium, but from the other side.
This is retronasal olfaction.
And that is what we call flavor.
Exactly.
What you call flavor, the strawberry -ness of a strawberry, the coffee -ness of coffee, the vanilla, the smoke, is almost entirely the smell of the food rising up from your throat into your nose.
I feel like this is the Matrix moment of the episode, The Spoon Isn't Real.
Because when I eat a strawberry,
I swear on my life that the strawberry sensation is happening on my tongue.
I feel it right there in my mouth.
Are you telling me that is a hallucination?
It is a sensory illusion.
The textbook calls it taste flavor, mislocalization.
Mislocalization.
That is a very polite way of saying, my brain is lying to me about where a sensation is coming from.
Well, it's not lying so much as it's binding.
Think about it.
When you eat, you have all these sensations happening at once.
You have tactile sensations in your mouth, the texture of the berry, the temperature, the feeling of chewing.
You have the true taste, the sweetness and the sourness happening on the tongue.
And then you have this cloud of strawberry scent hitting the nose from the back.
The brain, in its infinite wisdom, says all the chewing and touching and true taste is happening in the mouth, so this smell must be coming from there too.
It integrates all those signals and creates a single unified experience that it localizes to the mouth.
Why would evolution do that?
Why not just let us know it's a smell?
It seems less confusing.
The leading theory is that it ensures we swallow.
If you perceive the deliciousness of food just as smell, you might be content to just snick it.
By localizing the entire flavor package to the mouth, the brain strongly encourages ingestion, which is what you need to do to get the calories.
That makes a strange kind of sense.
Now the text mentions a demonstration, the strawberry candy experiment.
I actually tried this before we started recording and it is freaky.
It's the best way to prove this to yourself.
You take a strawberry candy or a jelly bean works great too.
You pinch your nose shut completely really tight, you pop the candy in your mouth and start to chew.
And when I did that, it was just
sweet.
It was a generic, sweet, slightly sour lump.
There was no red flavor.
It was just a vague sweetness.
It could have been anything.
Exactly.
Because with your nose plugged, you stop the airflow from your mouth to your nasal cavity.
No airflow means no retronasal olfaction.
You are only getting the taste signal from your tongue, sweet and sour.
That's it.
And then while still chewing, I let go of my nose.
It was like a color explosion in my head.
Suddenly strawberry just flooded my perception.
It was instantaneous and overwhelming.
That whoosh is the air rushing from your mouth up to your nose carrying all those strawberry volatiles with it.
That single moment proves that the nuance, the character, the identity of food, the chocolate, the vanilla, the strawberry, the smoke is all smell.
It's flavor.
This has to have huge implications for the food industry, doesn't it?
If flavor is just smell, can't they just manipulate it to hack our brains?
Oh, they are trying.
The text details a fascinating study from the University of Florida on tomatoes.
They call it volatile enhanced taste.
Right.
This is the heirloom tomato thing.
Yes.
Everyone knows that the typical supermarket tomato tastes like, well, wet cardboard.
A sad watery sphere.
Exactly.
But a good heirloom tomato tastes amazing.
So the researchers wanted to know why.
The obvious assumption was that heirlooms must just have more sugar.
That seems like a reasonable assumption.
More sugar equals better taste.
Right?
That's what they thought.
But when they actually analyzed the chemistry of hundreds of varieties, they found something really weird.
Some of the best tasting heirloom tomatoes actually had less sugar than the bland supermarket ones.
Wait, how is that possible?
If sweetness is the main driver of liking a fruit, how can the less sugary one taste better and sweeter?
Because of the volatiles.
The heirloom tomatoes were packed with specific scent molecules.
The researchers found, and they use a statistical technique called regression analysis to prove this, that certain volatile smells actually enhance our perceived intensity of sweetness.
So you're saying if I smell the right smell, my brain literally hallucinates more sugar than is actually there?
Effectively, yes.
The scent primes the sweet receptor pathway in your brain.
The scent and the taste work together, and the whole is greater than the sum of its parts.
The implication of this is massive.
For food companies.
Absolutely.
If you are a soda company and you are under public pressure to reduce sugar, normally that means your soda tastes worse.
But if you can identify these specific sweetness enhancing volatiles and add them to the recipe, you could potentially cut the sugar by half, but the consumer would perceive the exact same level of sweetness.
That is a cheat code.
That is literally hacking the human sensory system.
It is.
But there is a catch.
The text is careful to mention the blueberry exception.
I love that this has a name.
It sounds like a spy movie.
The blueberry exception.
It's a great name.
And what it means is that with blueberries, there are no volatiles that seem to enhance sweetness.
The sweetness of a blueberry comes 100 % from its sugar content.
That's it.
So this hack works for tomatoes, it works for strawberries, but it doesn't work for everything.
Nature has different rules for different fruits.
Okay.
So we have established that flavor is mostly smell.
It's retronasal.
Now let's talk about the hardware in the mouth.
The actual taste part.
The text calls the tongue the retina of the mouth.
It is a beautiful analogy.
The retina detects photons, waves of light.
The tongue detects chemical molecules dissolved in saliva.
But the structure is where people get confused.
If you look at your tongue in the mirror, you see all those little bumps.
The taste buds?
I walked right into that one.
I knew it as I was saying it.
You did.
But it's the most common mistake.
Those bumps are not taste buds.
Those bumps are called papillae.
The taste buds are microscopic structures buried inside the papillae.
Kind of like clothes in an orange.
You absolutely cannot see a taste bud with the naked eye.
Okay.
So the bump is the house and the taste buds are the tiny residents living inside the house.
Perfect.
And not all of these houses are created equal.
We really need to break down the four types of papillae because one of them is basically an imposter.
An imposter?
I'm intrigued.
The filiform papillae.
These are the most numerous bumps on your tongue.
They're small, cone -shaped, and they cover the entire front two -thirds of your tongue, giving it that rough texture.
But here is the kicker.
They have absolutely no taste function.
Zero taste buds.
Wait a minute.
The stuff covering most of my tongue can't taste anything at all?
Then what on earth are they for?
Mechanics.
Purely for friction and movement.
Think about a cat's tongue.
You know how it feels incredibly rough, like sandpaper?
Yeah, it's scratchy.
That is because cats have giant backward -facing filiform papillae shaped like hooks.
They use them to groom their fur and to rasp meat off of bones.
Humans have them too.
They're just much smaller and less hook -like.
But their job is the same.
To create friction.
They help grip the food and move it around your mouth so you can chew it properly.
But they're completely blind to taste.
That is wild.
I always assumed the rough part of my tongue was the tasting part.
So if it's not them, where is the actual tasting happening?
For that, you have to look for the fungiform papillae.
Fungi, like fungus, or mushroom.
These are mushroom -shaped bumps.
And they're located mostly on the tip and sides of the tongue.
Are these the little red dots I can sometimes see if I look really closely?
Yes, exactly.
They're larger than the filiforms, and they have a good blood supply, which makes them look pinkish or reddish.
On average, you might have about six taste buds buried in the surface of each one of these fungiform papillae.
And the text mentions a really cool way to see these clearly using blue food coloring.
It's a classic demonstration.
If you swab your tongue with blue food dye, the filiform papillae, the rough, non -tasting ones,
stain a deep blue.
But the fungiform papillae don't stain as easily, so they stand out like little pink polka dots against this blue background.
It makes them incredibly easy to count.
And we will definitely come back to counting them later when we talk about supertasters.
So that's the front.
What about the back of the tongue?
On the sides of the tongue, you have foliate papillae, which look like little vertical folds or gills.
And then way at the back, you have the circumvallae papillae.
These are the heavyweights.
They form an inverted V -shape pointing down your throat.
They look like little islands surrounded by a moat.
A moat?
It's literally a trench.
The papilla is the mound in the middle, and it's surrounded by a deep groove.
The taste buds aren't on top.
They're buried in the walls of that trench, protected.
It sounds medieval, like a fortress.
It's a bit like that.
But here is a fact that usually surprises people.
Taste buds aren't just on the tongue.
You have them in other places, too.
Where else?
On the roof of your mouth.
Specifically at the junction where the hard palate meets the soft palate.
You have them in your throat, on your epiglottis.
That explains why, if I burn the roof of my mouth on a hot piece of pizza, food tastes weird for a day or two.
Exactly.
You have scorched some of your sensors.
Now, speaking of myths,
we have to address the big one.
We have to kill the tongue map.
You know the one I'm talking about.
The diagram from every health class that shows sweet is on the tip, sour is on the sides, bitter is in the back.
I hate that map.
It is the zombie of sensory science.
No matter how many times you kill it, it just keeps coming back.
Why is it so wrong?
Where'd it come from?
It's an incredible story of bad science communication.
It is based on a translation error from a German paper published in 1901.
A scientist named D .P.
Hanig was studying taste thresholds.
He found that the tip of the tongue was slightly more sensitive to sweet and the back was slightly more sensitive to bitter.
We are talking minute, microscopic differences in the threshold of detection.
Okay, so there's a tiny kernel of truth in there.
A tiny one.
But years later, the famous Harvard psychologist Edwin Boring was writing a textbook and he decided to include Hanig's data.
He created a graph to illustrate it.
But, and this is a classic data visualization fail, he didn't label the y -axis clearly.
The graph made these tiny differences in sensitivity look like massive all or nothing differences.
It looked like the tip had 100 % sensitivity to sweet and the back had zero.
So a graphical typo basically became scientific law for the next 70 years.
Pretty much.
It got into textbooks and once it's in a textbook, it's treated as gospel.
The reality is you can taste sweet, sour, salty, and bitter on all parts of the tongue that have taste buds.
If you put a grain of salt on the very back of your tongue, you'll taste salt.
The map is a myth.
I feel like I need to call my third grade teacher and set the record straight.
Okay, let's zoom in even further.
We are inside the papilla.
We are looking at a single taste bud as shown in figure 15 .6.
What does it look like?
It looks like a cluster of garlic cloves or the segments of an orange.
It's a bundle of about 50 to 100 long, skinny cells.
And there are three main types of cells you need to know about.
Type I, type II, and type III.
Very imaginative names.
Scientists are very literal people.
Type I cells are the housekeeping cells.
They're glial -like support cells.
They keep the electrolytes balanced, clear out waste products.
They are the support staff that makes everything else possible.
Okay, what about type II?
These are the fascinating ones.
Type II cells are the receptor cells for sweet and bitter and also umami.
But here's the really weird thing about them.
They don't have traditional synapses.
Wait, if they don't have synapses, the little wires that connect neurons, how on earth do they talk to the brain?
They use what is essentially a wireless signal.
Instead of a direct wire connection to a nerve fiber, they secrete a chemical called ATP.
Normally ATP is just the energy fuel for cells.
But here, the type II cell shouts by releasing a puff of ATP into the fluid outside the cell.
That ATP floats over and excites the nearby nerve fibers.
So it's a wireless router in a world that's otherwise hardwired.
That is a perfect analogy.
And you can contrast that directly with type III cells.
These are the cells that mediate sour taste.
They do have traditional synapses.
They are hardwired directly to the nerve.
Why the difference?
Why is sour, hardwired, and sweet is wireless?
Is there a reason?
We don't fully know.
But it suggests they might have different evolutionary origins or that the system needs to process them in different ways.
It's one of the active areas of research, figuring out why you'd have these two different signaling systems in the same taste bud.
And these cells, they don't live very long, do they?
No, not at all.
Yeah.
Being a taste receptor is a dangerous, high turnover job.
You're exposed to boiling hot coffee, abrasive toast, spicy chili peppers, bacteria, acids.
A taste cell only lives for a few days, maybe 10 days, at the absolute maximum.
Then it dies and is replaced by a new one growing from the base.
That is an incredibly fast regeneration cycle.
It has to be.
If they didn't regenerate, you would lose your sense of taste permanently the first time you drank tea that was too hot.
This constant renewal is why taste is so robust.
Even in very elderly people, while vision and hearing might fade significantly, taste often remains pretty strong because the hardware is constantly being replaced.
It's brand new every week or two.
So the signal leaves the taste bud.
It travels along the cranial nerves on its way to the brain.
Specifically, three of them.
There's the corda tympani nerve, which is a branch of the facial nerve, and it serves the front two -thirds of the tongue.
Then there's the glossopharyngeal nerve for the back of the tongue.
And finally, the vagus nerve, which handles the very back, the throat region.
The corda tympani has a really weird path, doesn't it?
The text mentions this.
It takes a bizarre detour.
On its way from the tongue to the brain stem, it passes right through the middle ear.
Through the ear.
Yes, right past the bones that you use for hearing.
This is why, if you damage that nerve, maybe during ear surgery or from a very bad ear infection, it can seriously affect your taste.
But it can also do something even stranger.
It can create phantom tastes.
Ooh, spooky.
What is a phantom taste?
Normally, these different taste nerves inhibit each other.
It's a system of checks and balances to keep the signals clear.
The corda tympani inhibits the glossopharyngeal and vice versa.
If you damage the corda tympani nerve, you release that inhibition.
The other nerves are no longer being held back, so they start shouting louder.
So it's like taking the brakes off the system.
Exactly.
Patients will report tasting intense, bitter or metallic things when there is absolutely nothing in their mouth.
Or they might feel burning sensations.
This is actually a leading theory for a very painful condition called burning mouth syndrome, which is often seen in post -menopausal women.
It might not be a pain problem at all.
It might actually be a taste nerve issue where the taste signal that usually dampens pain is gone.
So the pain signal runs wild.
That is mind -blowing.
The idea that taste actively inhibits pain helps explain why we eat when we are stressed, maybe.
That oral comfort is a real thing.
It's very possible.
Oral stimulation is a powerful analgesic.
Okay, so the signal gets to the brainstem, then the thalamus, and then to the cortex.
The primary taste cortex is in the insular cortex.
And then it projects to the orbital frontal cortex, which is where taste gets integrated with smell and touch and even vision to create that multimodal experience of flavor.
But a crucial detail here.
The projections are ipsilateral.
Meaning they stay on the same side of the body, unlike vision, which crosses over.
Alright, taste from the left side of your tongue goes to the left side of your brain.
Okay, let's get to the stars of the show.
The basic tastes.
Salty, sour, bitter, and sweet.
And the key here is that basic means hardwired, right?
Yes.
A basic taste is one that has a dedicated receptor on the tongue and a hardwired behavioral response.
You either innately like it or innately hate it.
No learning required.
Let's start with salty.
Salt is life.
Literally.
Your entire nervous system runs on electricity, and that electricity is generated by sodium ions, Na +, moving across cell membranes.
If you run out of sodium, your nerves stop firing, your muscles stop working, and you die.
It is absolutely essential.
So we are built to find it.
We are built to crave it, especially when we are deficient.
The mechanism is elegantly simple.
The receptor for salt isn't a complex lock and key protein.
It's just an ion channel, a gate.
When you eat salt, the sodium ions from the salt just flow directly into the cell through this specific channel.
Boom, signal sent.
It's the most direct mechanism possible.
And our liking for it is really flexible, right?
Highly flexible.
The text discusses how if you decide to go on a low -salt diet, after a few weeks, your body adapts.
Your saliva actually becomes less salty, which makes your salt receptors more sensitive.
Suddenly, food that used to taste bland now tastes salty enough.
And the reverse is also true.
Absolutely.
If you go for a long run and sweat a ton, you lose a lot of sodium.
Your body flips a switch in your brain that makes salt suddenly taste incredibly delicious, far more pleasurable than usual.
It's the wisdom of the body in action.
Next up, sour.
Sour is the taste of acid.
It's the taste of hydrogen ions, H+.
The mechanism is a bit more complex than salt.
It seems to involve hydrogen ions passing through channels and also undissociated acid molecules interacting with the cell.
And why do we need to taste acid?
What's its purpose?
Two main reasons.
One, to detect fermentation, which can be good, like in yogurt or sourdough bread, or it can be bad, like in rotting fruit.
It's a sign of bacterial action.
Two, it's a warning for tissue damage.
Strong acids burn tissue.
So our innate reaction to a strong sour taste is rejection.
It's a warning shot.
Careful, this might burn you.
But we like it in sour candy.
We seek it out.
We like it in low concentrations, usually when it's balanced with a lot of sugar.
It's that thrill of the almost dangerous, like a roller coaster.
It provides a pleasant satinizing, but at high concentrations, it's universally aversive.
Okay, now for the most complex one, bitter.
Bitter is the body's dedicated poison detection system.
In the natural world, a huge number of plant toxins are alkaloids, and alkaloids taste bitter.
Things like strychnine, cyanide, arsenic.
We have a lot of different ways to detect them.
This is the security team analogy.
For a nutrient like sugar, you only need one guy at the door because sugar is sugar.
But for poison,
there are thousands and thousands of different potential poisons in nature, so you can't inherit just one receptor.
Our genome has a family of genes called TALUS2R that encodes about 25 different bitter receptors.
That is a massive security detail compared to the one receptor for sweet.
It has to be.
We prioritize defense.
Some of those 25 receptors are generalists.
They'll bind to a wide range of bitter compounds.
They arrest anyone who looks suspicious.
Others are specialists.
They are tuned to detect very specific, very common toxins.
But interestingly, even though we have 25 receptors, we don't distinguish between different bitter tastes.
No, we don't.
Your brain doesn't care if it's cyanide or strychnine.
All 25 receptor types, when activated, funnel down to the same signal.
The signal is just bitter.
And the command is always the same.
Spit it out.
Do not swallow.
You don't need to know the chemical name of the poison to survive it.
The text mentions a fascinating connection to pregnancy here.
Yes.
It's been shown that pregnant women, especially in the first trimester, become hypersensitive to bitter tastes.
Things they used to tolerate suddenly taste awful.
The evolutionary theory is that this is to protect the developing fetus.
During that early stage of organ development, the fetus is incredibly vulnerable to toxins.
So the mother system ramps up the gain on the poison detector to ensure she doesn't eat anything even slightly risky.
That makes morning sickness, and all those common food aversions make so much more sense.
It's a feature, not a bug.
It's the body protecting the next generation.
Finally, let's talk about SWEET.
SWEET is the all -clear signal.
It's the go -for -it taste.
It detects biologically useful high -calorie sugars,
primarily glucose, fructose, and sucrose.
And the mechanism here is different from salt and sour.
Very different.
It's a heterodimer receptor, which is shown in figure 15 .1010.
That means two different proteins, one called TAS1R2 and another called TAS1R3, have to join hands to form a single functional receptor.
It acts like a very specific lock.
Only a molecule with the right shape can fit into the keyhole and turn it.
And this brings us to the diet soda paradox.
Artificial sweeteners fit that lock, right?
They do.
Molecules like aspartame, sucralose, saccharin, they have a shape that is just right to fit into that lock and trigger the SWEET signal.
But they aren't sugar.
So you get the perception of sweetness without the calories.
Which sounds great on paper.
All the taste, none of the guilt.
But the text warns about this.
It's a very controversial area.
But there is data, like the study mentioned, with rats showing a paradoxical effect.
Rats that were fed artificial sweeteners actually ended up gaining more weight than rats fed regular sugar.
Wait, how does a zero -calorie drink make you gain weight?
That sounds impossible.
The theory is metabolic confusion or uncoupling.
Normally, for millions of years of evolution, when you taste sweet, your body preps for an influx of energy.
It releases hormones, it revs up the metabolism to deal with the incoming sugar.
But with diet soda, the taste comes.
But the energy never arrives.
The body feels tricked.
After this happens repeatedly, the system might get disrupted.
The body might learn, OK, that SWEET signal is unreliable.
I'm going to stop ramping up my metabolism when I taste it.
Or it might make you hungrier later to make up for the calories it was expecting but didn't get.
You uncouple the sensory signal from the metabolic reward and the whole regulatory system can break down.
That is terrifying.
We are basically confusing our ancient hardwired hardware with very modern software.
And the long -term consequences are still being debated.
Now, what about the idea that there are more than four tastes?
The text looks at two main candidates.
What about umami and fat?
The candidates?
Let's look at umami first.
It was discovered by Japanese chemists, and it's the savory taste of the amino acid glutamate, most famously found in MSG.
That savory, brothy, meaty flavor.
Right.
And there is no question that we have receptors for it on the tongue.
But the text is skeptical about calling it a basic taste.
And the same league is the big four.
Why the skepticism?
A few reasons.
First, the affect, the innate emotional response, isn't as clear.
You put sugar on a baby's tongue, they smile.
You put MSG.
They're kind of indifferent.
The liking for MSG seems to be learned and conditioned, not innate.
The problem is that glutamate is also a medial neurotransmitter in the brain.
Receptors for it are everywhere in the body.
Also, it signals protein, but proteins are huge molecules.
We mostly detect them in the gut after digestion, not on the tongue.
So umami might be more of a signal to the gut that protein is coming, rather than a true hardwired taste for immediate decision making like poison or energy.
And what about fat?
Same story, but even more so.
Fat molecules, triglycerides, are way too big to stimulate a taste receptor.
They are absolutely massive.
They can't be tasted.
So how do we taste fat?
When I eat ice cream, I perceive fat.
You feel it.
It's a somatosensory sensation.
It's tactile.
You feel the oiliness, the viscosity, the creaminess on your tongue.
The text argues that our powerful love for fat is a conditioned preference.
Our gut has receptors for fatty acids.
The gut detects the massive calorie payload, tells the brain that was high energy, and the brain learns to love that slimy, creamy, viscous texture in the mouth.
But it's not a taste in the strict technical sense.
Got it.
So for the purposes of this chapter, we are sticking to the Big Four as the only true hardwired basic tastes.
For now, that seems to be the scientific consensus.
Let's shift gears to genetics, because it turns out we do not all live in the same sensory world.
I love the origin story of this discovery with Arthur Fox.
It's a fantastic story.
It's 1931 at the DuPont Chemical Company.
A chemist named Arthur Fox is synthesizing a compound called BTC phenylthiocarbamide.
It's a fine white powder.
And being a 1930s chemist, I'm guessing safety protocols were a little loose.
Very loose.
He accidentally puffs some of the powder into the air.
His colleague, who's standing nearby, starts gagging and complaining that the dust tastes incredibly bitter and disgusting.
And Fox.
Fox tastes absolutely nothing.
He's standing in the same cloud of dust and perceives nothing.
He thinks his colleague is hallucinating or playing a prank.
So like any good scientist, he decides to test it.
He makes the colleague taste the pure chemical again.
Intensely bitter.
Fox tastes it.
Still nothing.
So it wasn't the chemical.
It was the person's tongue.
Exactly.
They had stumbled upon a fundamental genetic difference in the ability to taste.
They went on to test friends and family and discovered that you are either a taster of PTC or a non -taster.
And today we know the specific gene responsible for this, right?
It's TAS2R38.
That's the one.
It's one of those 25 bitter receptor genes.
But the story gets even deeper.
In the 1970s, researcher Linda Bartoszak realized that among the tasters, there was a distinct subgroup.
People who didn't just taste the compound, which is actually PRP, a safer chemical cousin of PTC as bitter, but experienced a violent, overwhelming, burning reaction.
She called them supertasters.
Supertasters.
It sounds like a superhero, but from the description, it sounds more like a curse.
It can be.
A supertaster's world is a lot more intense.
If you look at a supertaster's tongue, and you can do this with that blue dye test we talked about, which is shown in figure 15 .4, it is just jam -packed with fungiform papillae.
They have a much higher density of them.
So they just have more hardware.
Way more hardware.
More taste buds, which means more touch receptors, more pain fibers.
So everything is louder for them.
Sweet is sweeter.
Salt is saltier.
The burn of chili is more painful.
And the texture of fats can be unpleasantly greasy.
The text mentions cross -modality matching as a way to measure this.
How does that work?
It's a clever way to quantify a subjective experience.
You ask a person to rate the intensity of bitterness of PROP, but instead of using a number scale, you ask them to match it to the intensity of something else, like a sound or a light.
A non -taster might match the bitterness to the sound of a whisper.
A regular taster might match it to the sound of a normal conversation.
A supertaster might match it to the brightness of the sun or the pain of a severe headache.
It shows you they are living in a totally different sensory reality.
And this has real -world effects on their diet and health.
Grastically.
Supertasters find many vegetables, especially bitter ones from the brassica family, like broccoli, kale, brussel sprouts, to be incredibly unpleasantly bitter.
So statistically, they tend to eat fewer of these vegetables.
Which, as the text points out, raises their risk for certain things, like colon cancer, because those vegetables have protective compounds.
Correct.
But on the flip side, they also find high -fat foods to be cloying and overwhelming.
The fatty texture is just too intense.
So they tend to eat less fat, have lower VMIs, and have a lower risk for cardiovascular disease.
So supertasters get colon cancer, and non -tasters get heart attacks.
That is a very dark way to put it.
But statistically, there are different risk profiles.
It also affects other behaviors.
Tasters and supertasters find the bitterness of alcohol and the harsh irritation of cigarette smoke to be much more aversive.
So they are less likely to become alcoholics or heavy smokers.
This teaches us that picky eating isn't just someone being difficult or childish.
It's not a moral failing.
If you are a supertaster, that broccoli literally tastes different and more intensely awful to you than it does to me.
It's a huge lesson in sensory empathy.
This brings us to the final big question.
How do we know what to eat?
The book calls this the omnivore's dilemma.
We are generalists.
We can eat almost anything.
That is a huge evolutionary advantage, but it's also a curse.
Because anything includes things that are nutritious and things that will kill you.
So we need systems to regulate what nutrients we seek out.
We already talked about the hardwired affect, the baby smiling at sugar.
This was studied by Jacob Steiner in figure 15 .12, showing these reactions in newborns, even in encephalic infants without a cortex.
Right.
Proving it's a brain stem reflex.
Sweet equals a smile and sucking motions.
Sour causes a pucker.
And bitter causes a gaping mouth, spitting, and disgust.
It's innate.
But what about when your body is missing something specific?
This leads to the specific hunger theory.
This was the old intuitive idea.
If your body is deficient in, say, vitamin B, you will suddenly develop a powerful craving for vitamin B rich foods.
Your body just knows.
And there is a tragic story from the 1930s that seemed to support this.
The story of the boy, DW.
The boy with the salt craving.
This is a heartbreaking case.
DW was a three -year -old boy who was absolutely obsessed with salt.
He would scream for the salt shaker at meals.
His first word was practically salt.
And his parents, trying to be good parents and follow medical advice at the time, tried to stop him.
They did.
They hid the salt.
But he would sneak into the kitchen and find ways to eat it by the spoonful.
It turned out he had a tumor on his adrenal gland that made it impossible for his body to retain sodium.
He was constantly urinating it all out.
He needed massive amounts of salt just to keep his nerves and muscles functioning.
But the doctors at the time didn't know that.
No.
He was eventually hospitalized for his strange behavior.
The doctors put him on a standard low -sodium hospital diet to cure him of his unusual craving.
He died within days.
His body just crashed without the sodium.
That is just devastating.
It is.
But it proved, tragically, that for salt specifically, we do have a hardwired hunger.
His body knew exactly what it needed, and it drove his behavior powerfully to get it.
So the specific hunger's theory is true, then?
For salt and sugar, yes.
But for things like vitamins, no.
It falls apart.
This is the rat experiment.
Right.
Researchers deprived rats of vitamin B.
The rats got sick.
Then they offered them a choice of different diets.
The rats reliably switched to the diet that contained vitamin B.
It looked like a perfect example of a specific hunger.
Well, it was a trick.
It was.
The researcher Paul Rosin does a clever control experiment.
He offered the sick rats a choice between the bad diet that made them sick and a new diet that was also vitamin B deficient.
And the rats still switched to the new bad diet.
They still switched.
They weren't seeking vitamin B because they can't taste vitamins.
They were just running away from the food that made them feel sick.
It is called condition diversion.
So it's not a positive, I need vitamin B.
It's a negative.
That last meal made me feel like garbage.
Let's try literally anything else.
Exactly.
It's trial and error.
We learn to avoid diets that make us sick, and we learn to prefer diets that make us healthy, but we can't do it for nutrients we can't taste.
Which brings us right back to the beginning, to the cookie.
We love the chocolate flavor because of evaluative conditioning.
Yes.
We pair the neutral flavor of chocolate with the positive consequence of calories from sugar and fat.
And so we learn to value and love the flavor itself.
Before we wrap up, I want to touch on two last things.
First, how does the brain know what it's tasting?
The coding debate.
Pattern coding versus labeled lines.
Is taste coded like vision, where the overall pattern of activity across all receptors defines a color?
Or is it like hearing, where specific neurons are labeled for specific pitches?
And for taste, the evidence points to?
Labeled lines.
The reasoning is pretty straightforward.
You need to identify bitter, poison, instantly and unambiguously.
In a complex mixture like a soup, if it were pattern coding, the combination of salty, sweet and umami might create a totally new pattern the brain wouldn't recognize.
With labeled lines, the bitter neuron fires.
And you know there's poison, no matter what else is in there.
That makes sense for survival.
And what about the very last topic in the chapter?
The chili pepper, capsaicin.
The great human anomaly.
Why is it an anomaly?
Because capsaicin, the active molecule in chili peppers, does not trigger any of the five taste receptors.
It triggers pain receptors.
Specifically, it activates the trigeminal nerve, which handles touch, temperature and pain in the face.
It is not a taste, it is a thermal burn.
So why on earth do we eat it?
Are we all just masochists?
Biologically, maybe.
We are the only species that voluntarily enjoys it.
You cannot get a rat to eat chili unless you force it.
But for humans, it's likely a combination of social learning and desensitization.
We see our parents and family eating it, we associate it with safety and social bonding.
And the more you eat, the less it burns?
Correct.
The receptors get desensitized.
But there is a brilliant medical application for this, mentioned in the context of figure 15 .14.
Right, the candy for cancer patients?
Yes.
Patients undergoing chemotherapy can get terrible painful mouth sores.
Doctors found that if they gave these patients a candy laced with capsaicin - Wouldn't it hurt like hell?
That seems cruel.
At first, yes, it burns.
But if they keep sucking on it, the pain receptors in the mouth become completely desensitized.
They shut down.
And in doing so, it numbs the mouth to the pathological pain of the sores.
It can give them relief for hours, allowing them to finally eat and drink.
It's using the hair of the dog to hack the pain system for a therapeutic benefit.
That is sensory science literally saving lives.
It is.
It's a fantastic example.
So we have covered the anatomy, the physics of flavor, the genetics, and the psychology of regulation.
What is the big final takeaway here?
For me, it's that we have to trust our bodies, but we also have to verify.
We are running on this ancient, hardwired system that was perfectly designed for survival on the African savanna.
Seek sugar, seek salt, avoid bitters at all costs.
It is a brilliant system for an environment of scarcity and natural poisons.
But we don't live on the savanna.
We live in a supermarket filled with engineered foods.
Exactly.
In our modern world of processed food,
that wisdom of the body can become a liability.
The innate drive for sugar leads to obesity and diabetes.
The innate drive for salt leads to hypertension.
As the blueberry exception shows us, food companies are getting better and better at tricking our flavor systems into perceiving sweetness that isn't really there.
So we have to use our brains, our prefrontal cortex, to override the ancient instincts of our tongue.
We do.
And we need to have empathy.
Empathy for the fact that we're all experiencing a different sensory reality.
If your friend hates broccoli, don't judge them.
Their TAS2R38 gene might just be shouting poison at them with an intensity you can't even imagine.
I will never look at a chocolate chip cookie or my own tongue the same way again.
That is the goal.
Your next meal should be an experiment.
Pay attention.
Is this taste or is this flavor?
Thank you for listening to this deep dive into sensation and perception.
And a big thank you from the entire Last Minute Lecture Team.
Keep learning.
See you next time.
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