You Are What You Eat

“You Are What You Eat”

“Dis-moi ce que tu manges, je te dirai ce que tu es” 

-Anthelme Brillat-Savarin, in Physiologie du Gout, ou Meditations de Gastronomie Transcendante, 1826

“You are what you eat.” This is sentiment—one that relates the food we consume to our state of mind and being—can be traced back further than Brillat-Savarin’s time. In fact, it’s been argued that cookery (the selection, preparation, and consumption of food) prior to early modernity (18th century) was based heavily on beliefs about food’s relationship to health (Leschziner et al. 2008)

More than just basic sustenance, or sensory pleasure, people in Europe ate food to maintain their “humoural balance.” This was the belief that humans had an ideal balance of both hot and moist qualities which eating certain foods could provide. People, then, who ate the foods with these qualities were considered healthy and those who did not were unhealthy. (See Theorizing Cuisine from Medieval to Modern Times: Cognitive Structures, the Biology of Taste, and Culinary Conventions). This “Old Dietetics”  philosophy and the philosophy of eating has evolved significantly, but the connection between how food affects what we are and what is going on inside us is still very relevant today.

This is the third and final blog post of my series examining the history and science of two amino acids—aspartate and glutamate—and what know about their wider functional roles in the body, specifically their potential neurotoxicity on human metabolism and metabolic pathways. Maybe you’re wondering what humours have to do with taste? The shift from “humoral balances” to “hedonic eating” was the result of several catalysts working together. As European society moved away from traditional scholastic medicine and toward new French cookery,  the importance of taste increased (Leschziner et al. 2008, 357-358). 

Taste, then, became a defining criterion for choosing what foods to eat. Moreover, Europe’s colonial expansion into tropical, sugar-centric countries allowed sugar to become much more accessible. Sweetness ceased being an “expensive luxury” and medicine, and became something people could get creative with. Soon after, sweet foods shifted into their own, distinct, end-of-the-meal category. Today in the United States, the strong distinction between sweet and non-sweet (i.e. savory) tastes remains.

However, similar to the “Old Dietetics” philosophy linking food to a humoural health, researchers continue to investigate possible consequences of consuming certain food “tastes” (including glutamate and aspartate!). 

Let’s first look at aspartame. Aspartame has become an sweet, low-calorie alternative to sugar (De la Peña 2010). The emergence of Dessert as a thing onto itself helped aspartame gain popularity; Americans could enjoy their coveted desserts with little caloric cost (which is assumed to mean, “health benefits”). However, aspartame has also received a lot of criticism as being a possible neurotoxin (poisons that act on the central nervous system). So, let’s break this down. Aspartame is made up of three components: aspartate, phenylalanine, and methanol. Research has shown that excessive amounts all of these molecular components can cause potential neurotoxicity, but let’s just stick with examining aspartate’s role. According to a study on the effects of aspartame metabolites on astrocytes and neurons, the aspartate metabolized from aspartame can act as a toxin that causes hyperexcitability, which leads to the degeneration of neurons in the brain (See blog 2). What’s more, the aspartate in aspartame has been linked to reduced dopamine and serotonin production in the brain, linking it to potential neurodegenerative effects like Alzheimer’s disease and Parkinson’s disease (See Neurobehavioral effects of aspartame consumption). Yet it is important to note there still remains a lot of unknowns and possible confounding variables. It is still difficult to tell exactly what is going on and how “toxic” aspartame and the aspartate in it are.

Glutamate has received similar “toxic” allegations. Let’s consider Monosodium Glutamate (MSG). MSG is the food additive for umami (savory) flavors. Even though the neurotoxicity of MSG has long been ruled out, according to a recent study, “excessive MSG intake may be associated with Metabolic syndrome (metS). metS is a “cluster of risk factors associated with cardiovascular dysfunction” including diabetes and high blood pressure (Day et al. 2015, 20). Yet how “causal” is this relationship? Does the glutamate in MSG directly lead to metS? According to the same study, there is a concern that glutamate consumption can cause overeating, which results in obesity and then metS. Yet can we (or should we) make the leap from glutamate consumption to metS without considering the other factors that go into overeating? Researchers repeatedly call for further study to pull these confounding variables apart.

In fact, this same study authors claim it is “likely that MSG may alter an individual’s adiposity [fat content] and the risk of developing metS” (Day et al. 2015, 22) by identifying a possible pathway for how glutamate could be linked to diabetes II (a symptom of metS): glutamate consumption can cause increased plasma insulin. Insulin is a hormone that regulates glucose in the blood. So if you eat a lot of carbohydrates (glucose), your blood sugar levels rise, and your body produces insulin to help your body re-absorb the blood glucose. High plasma insulin can reveal insulin resistance which is an associated trait of diabetes. Yet even from this, the bridge between glutamate and metS is not entirely direct.

(See Re-Visiting Glutamate Toxicity: Implications of Monosodium Glutamate Consumption on Glutamate Metabolism and Metabolic Syndrome )

So, how “unhealthy” are aspartate and glutamate? Could they be interfering with our metabolic balance, so to speak? Should we stop eating these amino acids altogether, in their additive formsIt’s hard to say. First, much of the current research conclusions all point to, well, more research! There are still too many “unknowns” (about these amino acids, about metabolic pathways, about taste reception) to make a concrete, definitive answer. Second, like all foods, moderation is key. Cliché as it may sound, it’s sound advice. Overeating anything isn’t very good for you. (A 2007 study on aspartame dosage and cancer risk in rats revealed that “significant” dosage did cause cancer; however, in order to achieve these results, rats had to have constant food consumption of 20 g/day, which is simply unrealistic. If the aspartame consumption was modified, would the results be the same?). Third, there is a lot of “baggage” tied to both aspartate and glutamate. Aspartate’s connection to aspartame links it to all the fears about artificial sweeteners (e.g. THEY CAUSE CANCER?!! But of course, more research needs to be done). Glutamate still has a bad rep because MSG was historically racialized as the cause of “Chinese Restaurant Syndrome” (Mosby 2009). In short, people were complaining about bloating, headaches, and nausea after eating at Chinese Restaurants and blamed it on the use of MSG. It is fairly easy to recognize the racism behind this singular association of MSG with Chinese or Asian-American foods, but where does that leave us on the question of taste and health?

In other words, where do we go from here? For starters: research, research, research. Everything needs to have evidence to support claims. Online blogs (like this one!) can make claims but if there is nothing to back it up, then they are just empty words on a screen. I hope that just the small amount of interdisciplinary research reflected here shows how much we care, and how little we know, about sweetness and savoriness–even two centuries after Brillat-Savarin. My plan, at least, is to keep eating, and to keep reflecting on, all of life’s “sweetness” and “umami.”



Day, P. E., Matata, B., & Elahi, M. (2015). Re-Visiting Glutamate Toxicity: Implications of Monosodium Glutamate Consumption on Glutamate Metabolism and Metabolic Syndrome. Journal of Endocrinology and Diabetes Mellitus3(1), 20-31.

De la Peña, C. T. (2010). Empty pleasures: The story of artificial sweeteners from saccharin to Splenda. Univ of North Carolina Press.

Leschziner, V., & Dakin, A. (2008). Theorizing cuisine from medieval to modern times: cognitive structures, the biology of taste, and culinary conventions. In ideas (Vol. 31, pp. 59-105).

Lindseth, G. N., Coolahan, S. E., Petros, T. V., & Lindseth, P. D. (2014). Neurobehavioral effects of aspartame consumption. Research in nursing & health37(3), 185-193.

Mosby, I. (2009). ‘That Won-Ton Soup Headache’: The Chinese Restaurant Syndrome, MSG and the Making of American Food, 1968–1980. Social history of medicine22(1), 133-151.

Rycerz, K., & Jaworska-Adamu, J. E. (2013). Effects of aspartame metabolites on astrocytes and neurons. Folia neuropathologica51(1), 10-17.

Soffritti, M., Belpoggi, F., Tibaldi, E., Degli Esposti, D., & Lauriola, M. (2007). Life-span exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats. Environmental Health Perspectives115(9), 1293.

Similarly Different: Glutamate and Aspartate

The human body is as fascinating as it is complex to study. Examining what makes us, well us, takes us to the very molecular level of what we are. The makeup of the body goes something like this: the body is comprised of organ systems, organs are comprised of tissues, tissues are made up of cells, and cells communicate, signal and survive with the help of a bunch of other “little stuff” in the body. This “little stuff” consists of compounds like proteins and the amino acids that make them up which keep our bodies in homeostasis (a stable, “happy,” equilibrium state).

What always boggles me is that there are only twenty amino acids and each one can play an extremely different role in the body depending on how they are aligned to make proteins, or even what functional groups they have. This is the second of three blog posts in which I continue to explore the history and science of two specific amino acids—aspartate and glutamate—and what we currently know about their wider functional roles in the body.

Let’s do a quick amino acid review. All amino acids have the same basic structure: a central alpha-carbon, which can attach to four other elements or compounds; an alpha amino group (NH3+); a carboxylic acid group (COO-); and, a “R-group” (some combination of different compounds) which distinguishes each amino acid from the others.

Something that makes glutamate and aspartate special: they are the only two amino acids that are acidic in a human body (this means they have an overall negative charge). They also have very similar R-groups: aspartate has a methylene (CH2) attached to a carboxylic acid (COO-), and glutamate has two methylene (CH2CH2) attached to a carboxylic acid (COO-). Pretty similar, right? That’s what I thought, too. In fact, when I first learned about these amino acids, I did little to distinguish them beyond the number of methlyenes. Yet, as discussed in my first post (link), little molecular differences can have enormous impacts on how the body perceives and uses compounds, and not just in the realm of taste. Here is my basic visual rendering of what’s going on:

Amino Acid Differences

But wait, if glutamate and aspartate are structurally so similar, couldn’t the body just rearrange a methylene and get glutamate from aspartate and vise versa? Well, not exactly, although that would be pretty cool. But in theory, this process actually happens. In a study study examining the citric acid cycle (a process in the body that eventually helps create ATP energy) in guinea-pig cerebral-cortex slices, scientists discovered that aspartate could be converted into glutamate via a modified citric acid cycle. How? An enzyme (another category of “little stuff” that helps catalyze, or bring about, various chemical reactions) called aspartate aminotransferase (AST) can help transfer an amino group (NH2) to another molecule (alpha-ketoglutarate), which in turn makes glutamate. (See drawing below and Role of aminotransferases in glutamate metabolism of human erythrocytes).

But wait, if the body can just make this transformation, why do we need both amino acids?

AST Enzyme

AST Enzyme

Well, even though these amino acids are so similar and even though we have the mechanisms to convert them between each other, they play a lot of different roles.

In my first post, I discussed how aspartate and glutamate were the amino acids associated with sweet and savory taste, respectively. Considering the major difference between sweet and savory tastes can help us better understand how different these little compounds actually are. Glutamate, for example, plays perhaps the biggest transmitter role in normal brain functioning. This amino acid is the primary fast excitatory synaptic neurotransmitter in the brain. This means a couple of things. First, glutamate is a neurotransmitter (a signaling mechanism that helps move nerve signals between each other). Second, glutamate is used by the majority of excitatory neurons (these help to increase the likelihood of producing an action potential, which is required to move nerve signals and do things such as muscle movements) in the central nervous system.

In plain English, glutamate is required to get information quickly from one place to the other. So would more glutamate present near the brain be good? Just the opposite actually. Glutamate, while extremely important in neurotransmission, has excitotoxic characteristics (the ability to destroy neurons by extending the excitatory state). Studies have shown that too much glutamate can lead to Alzheimer’s disease, Huntington disease, and Parkinson’s disease. (See Glutamate). A recent study  has even connected glutamate to Schizophrenia. With all these risks, why would we still want glutamate? Glutamate, as stated above, is the transmitter for brain function. It plays an extremely important role in cognition, memory and learning. So thinking about this blog right now, glutamate is helping your neurons fire so you don’t forget what you’ve read. This most important neurotransmitter is centrally involved in both healthy brain/body function and disease states.

So where does aspartate come in? Besides the (essential!, at least in my opinion) function of conferring sweet–and, much more weakly than glutamate, savory–taste, aspartate plays certain roles that no other amino acids can. For example, like glutamate, aspartate plays a central role in cognition and memory. The N-methyl-D-aspartate (NMDA) receptor, which is made of aspartate and other compounds stuck together, is used in conjunction with glutamate to increase excitatory synapses and thus memory and cognition. NMDA is used to open different ions channels and increase the synapses. Here we see how aspartate, and not glutamate is required to form heterodimer (structures that consisted of several different compounds) receptors for certain processes to take place. (See Is Aspartate an Excitatory Neurotransmitter?). However, like glutamate, excessive aspartate near the external brain can cause excitotoxicity, and damage neurons.

NMDA Receptor

NMDA Receptor

So wait, are you telling me that if I keep eating MSG (containing glutamate) or the artificial sweetener aspartame (containing aspartate), I’ll experience excitotoxicity and my brain cells will all die?

Well, not really. A ton of research has gone into establishing a basic consensus among scientists that excitotoxicity does not just happen because you consume foods with these amino acids; there are, thankfully, a lot of other mechanisms playing roles to try to maintain homeostasis, like the Blood Brain Barrier (BBB). In plain English, the BBB is a form of protection between the brain and the rest of the body; so only certain “little stuff” can get through the capillaries (little vein-like structures that carry blood to the brain), but neither glutamate or aspartate is one of them. Therefore, these amino acids would have to be converted into other compounds or cross the barrier by correct receptors on the BBB. (See Monosodium glutamate neurotoxicity, hyperosmolarity, and blood-brain barrier dysfunction)

Blood Brain Barrier

So maybe glutamate and aspartate aren’t that different after all? Perhaps structurally and near the brain. But as I explored in my first post, these two little compounds that have similarly different functions in foundational bodily processes also help to create what we understand culturally as completely different tastes: sweetness and savoriness. And thanks to both aspartate and glutamate, I can remember how tasty each one is.


References to check out:

Ellinger, J. J., Lewis, I. A., & Markley, J. L. (2011). Role of aminotransferases in glutamate metabolism of human erythrocytes. Journal of biomolecular NMR49(3-4), 221-229.

Herring, B. E., Silm, K., Edwards, R. H., & Nicoll, R. A. (2015). Is aspartate an excitatory neurotransmitter?. Journal of Neuroscience35(28), 10168-10171.

McCall, A., Glaeser, B. S., Millington, W., & Wurtman, R. J. (1979). Monosodium glutamate neurotoxicity, hyperosmolarity, and blood-brain barrier dysfunction. Neurobehavioral toxicology1(4), 279-283.

Purves, D., Augustine, G. J., Fitzpatrick, D., Katz, L. C., LaMantia, A. S., McNamara, J. O., & Williams, S. M. (2008). Glutamate receptors. Augustine GJFD, Hall WC, LaMantia A, McNamara JO, et al. Neuroscience. Massachusetts, USA: Publishers Sunderland, 126-133.

Simon, G., Drori, J. B., & Cohen, M. M. (1967). Mechanism of conversion of aspartate into glutamate in cerebral-cortex slices. Biochemical Journal102(1), 153.



Taste Technologies: Sweetness versus Savoriness

Adlai Nelson

If you were asked to distinguish between cheese and chocolate, I doubt there would be much difficulty—if someone replaced your Hershey’s square on a s’more with a slice of Gouda, you would notice right away.

While the distinction between sweet and savory may seem quite obvious, the science is surprisingly similar—and yet complicated. Right now, researchers see the divide between these tastes as thinly balanced between two amino acids in particular: glutamate and aspartate. This post is the first of a three-part series, I which I explore the history and science of these two seemingly “opposite” taste experiences—savory (umami) and sweet—and their relationship to the two amino acids listed above. I’m curious about what the history of two common food additives, monosodium glutamate (MSG) and aspartame, can teach us about how small variations between structure can affect the taste perception of sweet and savory.

Before I get to the subtle (yet important) differences between sweet and savory tastes, let’s establish how our bodies are currently understood to taste at all. Let’s consider this scenario: you’re smelling your grandma’s freshly baked chocolate cookies. “Taste” proper does not actually begin with mastication (chewing), but rather in the combination of the olfactory and gustatory cortexes. In everyday English, that means what you smell now can affect what you taste later. That sweet, homey aroma flooding your nose and making you drool is part of the complex chemosensory relationship between taste and smell (see Taste perception, associated hormonal modulation, and nutrient intake). Olfactory nerves, stimulated by this sugary bouquet, flood your brain with “signals” that in turn relay information to the gustatory (taste) cortex. So before you even begin indulging grandma’s secret recipe, your body is already preparing for what’s to come based on smell alone (See Food-Related Odors Activate Dopaminergic Brain Areas). When you finally satisfy your cravings, gustatory cells clustered on your taste buds send information to your brain once again (See Taste perception, associated hormonal modulation, and nutrient intake) and you perceive sweetness.

It is here on the taste buds where “flavor” begins. Umami and sweetness are perceived by Type II G-proteins coupled cells in the gustatory complex of the mouth. On these cells, families of taste receptors (TAS1Rs) perceive different sensations. There are three types of these heterodimer TAS1Rs: TAS1R1, TAS1R2, and TAS1R3. Savory (umami) tastes are sensed by both TAS1R1 and TAS1R3, while sweetness is perceived by TAS1R2 and TAS1R3. In a study dealing with mice that lack TAS1R3 (the taste receptor for both umami and sweetness), signs of  perception for both umami and sweetness existed, hinting that the separate taste receptors (TAS1R2 and TAS1R1) were specific for umami and sweetness (See The endocrinology of taste receptors). A recent study on rats without the required transient taste receptors and calcium modulators for sweetness and umami also revealed the importance of ATP in both umami and sweetness perception. Type II cells communicate taste to the gustatory cortex via ATP release, which helps increase enteroendocrine (in this case that means taste receptors inside the gut) hormone release that can cause changes in appetite and satiety. What is interesting to note here is that the perception of and response to sweet and savory tastes are almost identical.

So why are umami and sweetness so different? What is it about the glutamate in MSG and the aspartic acid in aspartame make them taste so different? The beginning of this answer is found in the TAS1R1 and TAS1R2 receptors. If we examine the structure of aspartate (a component of aspartame) and glutamate (a component of MSG), we would find the difference between these two acidic compounds is as small as an extra methylene on glutamate. No big deal, right? In fact, in the molecular world, a carbon and two hydrogen can greatly affect orientational binding in corresponding receptors—a small difference in structure makes a big difference in how a molecule affects the body. As found in the study above, TAS1R1 is responsible for the umami taste. The TAS1R1 and TAS1R3 receptors in a heterodimeric formation (this means these two receptors combine and work together in a one collective unit) can bind specifically to L-glutamine, which is the foundational amino acid in MSG and umami-tasting foods (See Glutamine Triggers and Potentiates Glucagon-Like Peptide-1 Secretion by Raising Cytosolic Ca2+ and cAMP).

In a recent study on Old World Monkey, researchers demonstrated that TAS1R2 coupled with TAS1R3 was the heterodimer required to perceive sweetness in both natural and artificial sweeteners. The same study demonstrated that aspartame specifically interacted with the “Venus Flytrap Module” (insert plain English translation) of TAS1R2 receptors. This complex binding is still being researched, yet it appears to act in the same way as a fly landing on a Venus Flytrap. Aspartate can interact with TAS1R2, which then binds and “closes,” sending “sweetness” signals to the brain. Both TAS1R1 and TAS1R2, however, remain a puzzle to researchers.

Venus Fly Trap Receptor

Venus Fly Trap Receptor

Sending sweetness to the brain!

So I’m not the only one with questions left about savoriness, sweetness, and taste perception in general. How exactly taste receptors coordinate to the brain continues to be researched. Yet what has been found is that small differences in molecular structure have a big impact on taste. Glutamate and aspartate are practically the same amino acid, but each one relays a different taste perception to the brain. For now, it is clear that in food there is much more that meets the eye (and the tongue for that matter!).

References to check out!

Calvo, S. S. C., & Egan, J. M. (2015). The endocrinology of taste receptors. Nature Reviews Endocrinology11(4), 213.

Loper, H. B., La Sala, M., Dotson, C., & Steinle, N. (2015). Taste perception, associated hormonal modulation, and nutrient intake. Nutrition reviews73(2), 83-91.

Sorokowska, A., Schoen, K., Hummel, C., Han, P., Warr, J., & Hummel, T. (2017). Food-related odors activate dopaminergic brain areas. Frontiers in human neuroscience11, 625.

Tolhurst, G., Zheng, Y., Parker, H. E., Habib, A. M., Reimann, F., & Gribble, F. M. (2011). Glutamine triggers and potentiates glucagon-like peptide-1 secretion by raising cytosolic Ca2+ and cAMP. Endocrinology152(2), 405-413.


Umami the new secret to in-flight menu success


Photograph by Ruth Fremson for The New York Times

In March, major news outlets covered airline management buzz around umami having a unique taste property: for some reason, it still works right at 35,000 feet.

According to the New York Times piece, “At high altitudes, only umami — the pleasant, savory “fifth” taste beloved by Japanese chefs — is enhanced for reasons that are not entirely clear. So Bloody Marys, which contain the umami-rich tomato and Worcestershire sauce, taste far better in the sky than on the ground. It’s the most consumed cocktail on passenger flights, airlines say.”

Charles Spence is an expert in how different sensory mechanisms interact with one another. He speculates that the noise on the plane, even at 80-85 decibels (“quieter than in a New York restaurant”), stresses out our inner cave(wo)man:

“When faced with predators or during stressful situations, our ancestors may have turned to umami, which prompts dollops of saliva, ‘in order to get the energy to fight or flight.'”

Combine that with humidity lower than most deserts, and low atmospheric pressure, and our smell mechanisms (which make up a big part of ‘flavor’ – or what most of us call ‘taste’) just don’t respond the way they do on the ground, according to taste expert Peter Barham of the University of Bristol…

Read the full article here: Airlines Aim to Trick Your Taste Buds at 30,000 Feet

(Article originally published March 1, 2017 on

Additional links:

LA Times – Palate pleasers at 30,000 feet

National Post – From opulence to budget, why is airline food so universally terrible and consistently disappointing?

The Boston Globe – Experts share their recipes for good food — and wine — at altitude

The Economist – What to drink at 30,000 feet – It’s all about umami for these airline specialty beverages




“The Hippies Have Won”


Photograph by Cole Wilson for the New York Times.

“Consider granola: The word used to be a derogatory term. Now it’s a supermarket category worth nearly $2 billion a year. Kombucha was something your art teacher might have made in her basement. The company GT’s Kombucha brews more than a million bottles annually and sells many of them at Walmart and Safeway. And almond milk? You can add it to your drink at 15,000 Starbucks locations for 60 cents.”

In her recent piece for the New York Times, Christine Muhlke walked us through the quirky, healthy, and undeniably hipster food trends that have flooded Instagram feeds and modish restaurant scenes across the country. The idea that these trends stem from advances in nutrition science (e.g. newfound understanding of the human microbiome informing the popularity of fermented foods) fits in with our hypothesis that the molecularization of taste has validated the acceptance of “umami-rich flavors” as a dietary staple.

Read the full article here: “The Hippies Have Won”

(Article originally published April 4th, 2017 on

Penguins Can’t Taste Umami. Eat Fish Anyway.


Image ID: corp2417, NOAA Corps Collection, Photographer: Giuseppe Zibordi, Credit: Michael Van Woert, NOAA NESDIS, ORA [Public domain], via Wikimedia Commons

Who doesn’t love reading about penguins?

In the seemingly random fashion of the internet, this study out of the University of Michigan was recently picked up by another blog (, where the above image featured. We think it’s interesting.

Original U Michigan coverage of the study findings are excerpted here:

“ANN ARBOR—A University of Michigan-led study of penguin genetics has concluded that the flightless aquatic birds lost three of the five basic vertebrate tastes—sweet, bitter and the savory, meaty taste known as umami—more than 20 million years ago and never regained them.

Because penguins are fish eaters, the loss of the umami taste is especially perplexing, said study leader Jianzhi “George” Zhang, a professor in the U-M Department of Ecology and Evolutionary Biology.

“Penguins eat fish, so you would guess that they need the umami receptor genes, but for some reason they don’t have them…”

Read the whole article here: “Sweet, bitter, savory: penguins lack three of the five basic tastes”

Breaking down Ramen noodles, literally


(Image from YouTube video made by Stefani Bardin)

USA Today College

By LaTonya Darrisaw

“After a long day of classes, Macon State College senior Kristina Whitaker does not always have time to prepare a big, healthy meal. For at least two or three nights a week, her go-to food is Ramen noodles.

‘As a full-time college student, money and time are major issues that you have to deal with and buying packages of noodles are cheap,” Whitaker said. “They fill you up and are great when you are constantly on the go and have deadlines to meet…'”

Read the rest of the story: Breaking down Ramen noodles, literally