Umami is the new kid on the block, but how does taste actually work?

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I still remember when I read that we had a new flavour. It was the early 2000s, maybe the late 1990s, but umami was finally being talked about in the West.

It seemed strange. How could we not notice an entire taste? It was like discovering an extra arm. It seemed a little careless. Maybe it was something we should have noticed.

The answer is that we’d always had umami, we’d just called it savoury. In the West we used savoury to describe a kind or richness or meaty quality, but we never really thought of it as a distinct taste.

In the East, the situation was different. What we now know as umami, was explicitly recognised as an important taste. Japanese cooking is famous for its use of umami sources like dashi, shitake mushrooms and kelp. In China it was called xian long before umami was discovered in the 20th century.

The west did have access to umami: meat, tomato, mushrooms, anchovies, cheese, cured meats, peas and corns, amongst many other sources, all add umami to a dish. But the lack of any umami bombs as potent as those found in the East maybe led the West to underestimate umami as a distinct taste.

But now we all know. We know that there are actually five tastes, not four. We have sweet, salty, sour and bitter, and now umami.

But it does raise an interesting question: could there be more tastes, like umami, that we haven’t cottoned onto yet?

To answer that question we can start with umami and how it was discovered.

The Discovery of Glutamate and the Invention of MSG

Umami was originally discovered in Japan. This is not that surprising. Japan is the spiritual home of umami.

In 1908 a Japanese chemist, Kikunae Ikeda, noticed that his wife’s kombu dashi, a stock made from a type of edible kelp or seaweed, had a flavour that he couldn’t really classify as sweet, salty, sour or bitter.

Being a chemist, he did what chemists do and boiled down 90 pounds of kelp. He then isolated molecules from the resulting sludge and tasted them. What he ended up with was a few grams of a brown crystalline substance that tasted of umami.

This substance was glutamate, also known as glutamic acid, a substance that we have seen before. It is an amino acid, one of the building blocks of proteins.

Kikunae developed a commercial version of glutamic acid and called it ‘Aji-no-moto’, or Essence of Flavour. The company he created, Ajinomoto, went on to become one of Asia’s bigger food companies.

It took a while for Kikunae’s work to get to the West but by the 1930’s and 40’s, with the rise in popularity of Chinese food, westerners started becoming aware of ‘Aji-no-moto’ although we gave it a much more prosaic name: monosodium glutamate, or MSG.

The MSG Panic

Something that contributed to the awareness of umami in the West was the “Chinese Restaurant Syndrome” panic that began in 1968. To this day some worry about the effects of MSG because of this panic.

The idea of a ‘Chinese restaurant syndrome’ stemmed from a single two paragraph letter to the New England Journal of Medicine in 1968.

The letter written by Dr. Robert Ho Man Kwok recounted his symptoms after eating at Chinese restaurants, including neck numbness, general weakness, and heart palpitations.

In it he questioned whether soy sauce, cooking wine, high sodium, or MSG could be the cause of his discomfort.

Showing that humans were more than capable of mass hysteria before social media, this simple letter, combined with some really bad science, wide spread apprehension about MSG.

The fact that MSG was an exotic new flavour enhancer from the mysterious East no doubt played into the fears of some.

The MSG panic has been covered in depth (see here, here and here for example) but current health advice is that MSG is perfectly safe for the general population.

How the Tongue Perceives Flavor: Taste Buds and Receptors

If umami is caused by a small molecule then how do we experience that small molecule in a way that causes a taste? Well, the answer is taste receptors.

A taste is caused by a molecule, like glutamic acid, interacting with a taste receptor that is able to stimulate a signal to our brain.

These taste receptors are on the surface of cells within structures known as taste buds, which are, in turn, grouped together within structures known as papillae.

Papillae are the little bumps you can feel on your tongue and they are also found on the cheeks, palate, throat and epiglottis.

When we eat, food molecules dissolve in our saliva and they enter the papillae via a ‘taste pore’.

In the papillae food molecules then come into contact with the receptors on the taste buds which triggers a cascade of intracellular events that, ultimately, results in nerve impulses that tells our brains what we are tasting.

What Makes a Taste Receptor?

We’ve come across cell receptors before. Chillies are hot because capsaicin binds to the TRPV1 heat receptors in our mouths.

But the TRPV1 receptor isn’t a taste receptor. What makes a receptor a taste receptor is that it is found in a taste bud.

Taste receptors can be found outside taste buds, for example, they can be found expressed on cells in the early parts of the GI tract, and some taste receptors have also been found in the lungs. But the rule is taste receptors are found in taste buds.

The Taste Map of the Tongue is Old Science

Previously it was thought that the tongue was divided up into a sweet zone, a bitter zone and so on.

You might have even seen diagrams of the tongue divided up into zones corresponding to the four different tastes but that is old science.

Each taste bud has all full complement of taste receptors though the number and ratios between each type of receptor may vary between taste buds.

The Genetics of Taste Receptors

If a taste is something that it is mediated by a taste receptor then we must have receptors for tastes other than umami. And that is exactly the case.

Receptors for sweet and bitter are the best characterised. There are three sweet receptors (encoded by the TAS1R genes) and a massive 25 bitter receptors (encoded by the TAS2R genes).

The receptors encoded for by these genes are all part of a very important receptor family called G-protein coupled receptors (GPCRs).

These receptors span the cell membrane and when a molecule, such as glutamic acid, binds to the receptor it begins a process in the cell that results in a nerve impulse being sent to the brain.

Give me the biology about GPCRs

G-protein coupled receptors are a very important class of cell receptors.

A GPCR spans the cell membrane and has a part of the protein outside the cell membrane and a part of the protein within the cell.

The internal part of the protein is able to interact and activate with a specialised protein, called a G-protein, when a molecule binds to the receptor on the outside part of the protein.

This triggers a pathway, often called a transduction pathway, that results in some cellular effect.

In the taste receptors it results in the release of neurotransmitters by the cell that trigger a nerve impulse that shoots off to the brain.

The GPCRs are the largest group of receptors in the human body and different ones are involved in mood, behavior, the immune system, nervous system transmission, and metabolic/endocrine functions.

They are also important for sensory perception. They are the receptors that mediate not only our sense of taste, but also smell and sight.

Sweet, Bitter and Umami Receptors

To get one sweet taste receptor you need two TAS1R proteins working in concert, specifically TAS1R2 and TAS1R3, and, together, they can bind a many different sugars and sugar substitutes. Giving us a sweet taste.

Taste	Receptor Type	Genes Involved	Primary Target Molecules
Umami	GPCR Dimer	TAS1R1 + TAS1R3	L-Glutamate, amino acids, purine nucleotides
Sweet	GPCR Dimer	TAS1R2 + TAS1R3	Sucrose, fructose, artificial sweeteners
Bitter	GPCR Monomer	TAS2R family (~25 genes)	Plant toxins, alkaloids, bitter compounds
Sour	Ion Channel	OTOP1	Hydrogen ions (H+ / acids)
Salty	Ion Channel	ENaC family	Sodium ions (Na+)

The umami receptor is also built out of sweet receptors, specifically TAS1R1 and TAS1R3. This complex of two receptors is able to bind amino acids, especially glutamic acid.

Bitter receptors can act on their own. They don’t need to form a complex to act as bitter receptors.

Evolution and Taste Receptors

As I pointed out above, we have an enormous amount of bitter receptor genes compared to our other taste receptors. We only have two sweetness receptor genes but 25 bitter ones.

The likely reason for this is that being able to detect bitterness was very important when our ancestors were walking around eating various leaves and berries.

Many poisons and toxins, especially plant toxins, are bitter. So as omnivores, who eat both meat and plants, being able to detect a wide range of bitterness is a good way to protect ourselves from harmful food stuffs.

Carnivores could be expected to have fewer TAS2R genes because they don’t eat plants and sure enough cats, for example, have only three full copies of the TAS2R genes (see here if you want to read more on the evolution of bitter taste receptors).

Cats also cannot taste sweetness. Once again, why would a carnivore need to taste carbohydrates? They only eat meat. So, over the course of evolution, they have lost the capacity to taste sweetness (see here for an easy read on the evolution of taste in various animals).

It is also interesting that our TAS2R bitter receptors are expressed throughout our airways and gut. Bacterial, and even parasitic molecules, can activate these receptors triggering an immune response.

Our immune system is often called our sixth sense because it is able to ‘sense’ pathogens in our environment and react accordingly. So, in a weird way, it makes sense that sensory receptors could also be used in this capacity, we ‘taste’ the bacteria that threaten our well-being.

Salty, Sour and Beyond?

The other tastes, sour and salty, also appear to be receptor mediated with a variety of ion channel receptors identified as actual receptors or potential receptors, though they are not as well characterised as the sweet/bitter/umami receptors.

Interestingly we may not be done with new flavours. A range of receptors have been identified that could provide us with new tastes.

These include a ‘fat’ receptor, called CD36, a carbonation receptor, an alkaline receptor (the opposite of sour) and an ammonia chloride receptor (think spoiled fish or meat).

You can read more on this here, but it appears that scientists aren’t done with our taste buds just yet.

Conclusion

The fact that we have taste system, called a gustatory system by scientists, and that we seem to be finding new taste receptors makes sense.

If we are going to eat, it is a good idea to have some idea what we are putting in our mouths. We not only want to avoid substances that may harm us but also to identify foods that are a good source of specific nutrients.

Our gustatory system has evolved to allow us to work out what is in food by it’s taste, carbohydrates are sweet, proteins are umami and bitter things are potentially toxic and so on.

What’s useful for survival can also end up being useful for enjoying dessert. Taste isn’t just a way of analysing what we put into our mouths, it’s the basis for our enjoyment of food.

But, anyone who has lost their sense of taste when they have a cold knows that the taste isn’t the only thing that is going on when we eat our favourite food.

When it comes to flavour, things are a little bit more complicated. Flavour is more than molecules interacting with taste buds. It’s also aroma, texture and even past experiences and preferences.

But that is a story for another post.