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.”

 

References!

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.

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