Glazed, filled, dusted with powdered sugar—whichever doughnut you choose to celebrate National Doughnut Day with, there’s a good chance it’s going to be sweet. But why do we find sugary treats so tempting? The answer may be in our DNA.
Humans have been seeking out sugary foods for millions of years, long before the first doughnut was made. Part of the reason for this is that sugar has a lot of energy packed into its molecular makeup—energy that our bodies can use to keep us alive. Because sugar can be such a valuable nutrient, we evolved the ability to taste it, crave it, and extract energy from it. Put another way, we evolved a hunger for it. But too much sugar can have harmful effects on our health, so we also had to evolve a way to limit our cravings for it. One of the ways we do this is with help from the SLC2A2 gene.
Two 🍩 days!
There are two doughnut days (which is good, because doughnuts deserve to be celebrated twice). The first falls on the first Friday in June; the second is on November 5 each year.
After eating a meal, sugars are absorbed into the bloodstream and distributed throughout the body. Sugar levels in the blood are at their highest just after a meal, but as the sugar is absorbed and used by our organs, the amount of sugar in the blood drops. This change in blood sugar levels provides our body with a “craving gauge,” telling the body when it’s had enough sugar and when it needs more.
The SLC2A2 gene may be a key part of this. It has been called the “sweet tooth gene” because a research study in 2008 found that some people inherit a variant (a change in the DNA sequence) in this gene, and that those people were observed to consume roughly 30 grams more sugar per day on average than those without the variant—that’s as much as a chocolate bar1! 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 as efficiently. Slowed sugar intake by these cells may cause inaccurate sensing of blood sugar levels, which can cause us to continue seeking sugar when we otherwise wouldn’t1.
Find out more with the DNA Discovery Kit >
A similar variant has been found in the FGF21 gene. A change in the DNA coding for FGF21 has been shown in multiple independent studies to be correlated with increased sugar consumption2-5. People who inherit two copies of this variant may consume slightly more sugar on average (about one sweet snack serving more per week) when compared to people who don’t have the variant. It’s not clear why this change in the DNA is associated with a change in sugar cravings, but scientists suspect it has to do with regulation of FGF21 (a hypothesis that’s supported by some studies in mice)2-5.
This research is interesting, but it’s also important to see that genetics is not everything. In the instances where a genetic effect on a person’s sugar consumption has been observed, those effects appear to be small. This highlights the fact that our cravings, and the way our bodies process food, are complex traits that are influenced by a combination of genetics, a person’s environment, and their lifestyle.
Learn more about your DNA and how it may influence your body’s response to certain foods with DNAPassport by HumanCode >
1Eny, 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.
2Soberg, Susanna et al. “FGF21 Is a Sugar-Induced Hormone Associated with Sweet Intake and Preference in Humans”. Cell Metabolism 25, 1045-1053. (2017): 10.1016/j.cmet.2017.04.009. Web. 22 Dec. 2017
3Chu, Audrey Y. et al. “Novel Locus Including FGF21 Is Associated with Dietary Macronutrient Intake.” Human Molecular Genetics 22.9 (2013): 1895–1902. PMC. Web. 22 Dec. 2017.
4Von Holstein-Rathlou, Stephanie et al. “FGF21 Mediates Endocrine Control of Simple Sugar Intake and Sweet Taste Preference by the Liver.” Cell metabolism 23.2 (2016): 335–343. PMC. Web. 22 Dec. 2017.
5Sasaki, Tsutomu. “Neural and Molecular Mechanisms Involved in Controlling the Quality of Feeding Behavior: Diet Selection and Feeding Patterns.” Nutrients 9.10 (2017): 1151. PMC. Web. 22 Dec. 2017.