Trick or treat! That’s right: it’s the season for werewolves, vampires, and zombies, and these creepy creatures have more in common than you might think. Sure, they’re all scary, and they all make great Halloween costumes—but they also share an insatiable craving for forbidden food.
Us mortal humans are motivated by cravings for specific tastes, too—many of us have a sweet tooth. We’ve already talked a little bit about how sugar, blood, and DNA interact, but did you know that our cravings for sugar are a whole-body experience?
We are born with an array of biological tools that enable us to find and detect food sources. Among these tools, taste has proven to be a critical part of our survival by providing immediate information about a food’s molecular makeup. At its most basic level, taste is simply our body figuring out what nutritional value a food type has. Bitter and sour flavors communicate that a food might be poisonous. Similarly, sweetness means sugars, and sugars mean energy.
Sugars are carbohydrates (“carbs”), and they are essential because they can provide energy for our cells. Once in the body, carbs are broken down to a basic unit of sugar, glucose, which is then transported throughout the body. Each cell uses glucose to generate energy that it needs for normal cell function—activities like building proteins, communicating with other cells, and building DNA precursors. Because sugar is so important, our body is programmed to recognize it and seek it out within food sources.
Plants can be rich in carbs (think of fruit, rice, and other grains). Initially you might not group grains and fruits into the same taste category, but both types of food are enzymatically broken down into basic sugars which stimulate sweet receptors. These taste receptors are specialized proteins that are found on the surface of some cell types and function through physical interaction with molecules outside of the cell. In the case of sweet taste receptors, carbs in our food (glucose, sucrose, lactose, maltose, and so on) bind to the receptor proteins, which triggers a signaling back through the body to indicate that we have found a source of energy.
The receptors responsible for tasting sweetness are called TAS1R2 and TAS1R3. These two proteins link to one another, forming a unique complex capable of detecting sugars in food. Believe it or not, you don’t just taste sweetness on your tongue—sweet taste receptors are expressed throughout the body1-5 in organs that contribute to sugar metabolism. In the small intestines, for example, sweet taste receptors help regulate sugar absorption and hunger-associated hormone release in response to sugar intake. Other body locations where sweet taste receptors have been found include the liver (where sugar is stored), the pancreas (where insulin is produced), and in the hypothalamus, a region of the brain that regulates sugar metabolism.
Variations in all of our taste receptors (those that detect bitter, sour, salty, sweet, and umami flavors) can alter how we perceive flavor. At the extreme end of this, cats have accumulated numerous changes in their TAS1R2 gene which prevent them from being able to taste sweet flavors6. This is believed to explain why domestic cats, tigers, and even cheetahs seem ambivalent towards sugary foods, whereas dogs and humans are drawn to them. More commonly, some people experience changes in taste receptors that affect their ability to sense bitter and sweet compounds6. These changes may serve as a basis for taste preference variability among individuals.
Our bodies need sugar, as long as we don’t overdo it
There are other genetic factors that can affect our body’s desire for sugar. An association between increased sugar consumptions and a single DNA variant in the SLC2A2 gene was reported in 20087. Since that time, this variation has been referred to as the “sweet tooth gene” because individuals who inherited this variant were observed to consume roughly 30 grams more sugar (about one chocolate bar) per day on average than those without the variant7. The SLC2A2 gene codes for a protein that moves sugar from the blood into cells. The researchers behind this study believe this DNA variant prevents brain cells from taking in sugar from the blood efficiently. Slowed sugar intake by these cells may cause inaccurate sensing of blood sugar levels, which can cause our us to continue seeking sugar when we otherwise wouldn’t.
But don’t worry, trick-or-treaters: our bodies need sugar, as long as we don’t overdo it. The development of specialized taste receptors enables us to enjoy the sweetness of fruits and candy, detect the sugar within them, and initiate a whole body response to ensure proper regulation of blood sugar levels. Once an adaptive advantage, sweet cravings can be harder to manage in a modern world of ice cream and candy bars—so the next time you’re foraging at a vending machine or enticed in the checkout lane, remember that this instinct is best indulged in moderation.
1Ren, Xueying et al. “Sweet Taste Signaling Functions as a Hypothalamic Glucose Sensor.” Frontiers in Integrative Neuroscience 3 (2009): 12. PMC. Web. 27 Oct. 2017.
2Young, Richard L. “Sensing via Intestinal Sweet Taste Pathways.” Frontiers in Neuroscience 5 (2011): 23. PMC. Web. 27 Oct. 2017.
3Fournel, Audren et al. “Glucosensing in the Gastrointestinal Tract: Impact on Glucose Metabolism.” American Journal of Physiology – Gastrointestinal and Liver Physiology 310.9 (2016): G645–G658. PMC. Web. 27 Oct. 2017.
4Roper, Stephen D., and Nirupa Chaudhari. “Taste buds: cells, signals and synapses.” Nature Reviews Neuroscience, vol. 18, no. 8, 2017, pp. 485–497., doi:10.1038/nrn.2017.68. Web. 27 Oct. 2017
5Kojima, Itaru et al. “Sweet Taste-Sensing Receptors Expressed in Pancreatic Β-Cells: Sweet Molecules Act as Biased Agonists.” Endocrinology and Metabolism 29.1 (2014): 12–19. PMC. Web. 27 Oct. 2017.
6Li, Xia et al. “Cats Lack a Sweet Taste Receptor.” The Journal of nutrition 136.7 Suppl (2006): 1932S–1934S. Print.
7Eny, K. M., et al. “Genetic variant in the glucose transporter type 2 is associated with higher intakes of sugars in two distinct populations.” Physiological Genomics, vol. 33, no. 3, 2008, pp. 355–360., doi:10.1152/physiolgenomics.00148.2007.