The holidays might be over, and all of the cookies might have already been devoured, but your body can feel the effects of all that extra sugar for a long time. Sugar can wreak havoc on your body’s natural processes, from your gut to your joints. Don't forget, our entire protein line and our supplements are no added sugar!
Carbohydrates occur naturally in many foods, and humans need them to produce cellular energy and survive. However, increased accessibility to sugary foods, and an increase in the amount of sugar in those foods has created health problems around the world. Particularly in the United States, added sugars from foods like sweetened beverages are contributing to a national health crisis. The introduction of high fructose corn syrup in the 1970s has played a role in this crisis, creating a much cheaper means of adding sweetness to food products(1).
The human body has natural ways of managing blood sugar levels. The pancreas is responsible for producing insulin, a powerful hormone that is involved in activating cellular glucose transporters. These transporters pull glucose from your blood and into cells, where it can be used or stored. However, long-term overexposure to high levels of blood glucose can interrupt this system, decreasing your body’s sensitivity to insulin and leading to the development of what is known as Type 2 diabetes. One review of current literature found consumption of 1-2 daily sugar sweetened beverages increased risk of developing Type 2 diabetes by 26%(2).
The understanding of the complex relationship between gut bacteria and overall health is constantly growing. As it does, it becomes more clear that excess sugar can disrupt the balance of this important microbiome, leading to a cascade of negative downstream effects. High sugar intake can shift the populations of the gut microbiome, killing off beneficial bacteria and producing a leaky intestinal lining, promoting insulin insensitivity (a precursor to Type 2 diabetes), and increased inflammation and fat deposition(3). In fact, a particular type of gut bacteria called proteobacteria, which thrives in a gut environment rich in simple sugars, carry molecules that trigger the release of interleukins. Interleukins are cells normally associated with immune system functioning that are key in general inflammatory processes(4). It is possible that this imbalance could create both increased systemic inflammation as well as dysregulation of the immune system.
Diets high in simple sugars also seem to impact your body’s natural fat-storing processes. Fructose is the main sugar found in most fruits and of course in products containing high fructose corn syrup. Modern research has revealed the cellular-level pathways that make fructose a powerful modulator of adiposity. The energy balance in the cell is immediately disrupted from processing fructose, and long term impacts may include dysregulation of the intracellular processing of fatty acids, and a system resistance to satiety hormones like leptin and an increase in fat deposition(1). Even more seriously, the adiposity-increasing nature of fructose seems to target the liver specifically, which can develop into non-alcoholic fatty liver disease and liver dysfunction(5).
It seems clear that consuming too much sugar has negative health impacts, but there’s also research supporting moving dietary choices in the opposite direction. One clinical study in obese children allowed the subjects to consume the same number of daily calories and simply replace any fructose and simple sugar sources with more complex carbohydrates, so that daily simple sugar intake decreased from 10% of total calories to around 4%. After just 10 days, common health parameters were measured. The study found, among other positive outcomes, a statistically significant decrease in BMI, as well as metabolic changes that implied increased fat breakdown and insulin sensitivity(6). Clinical studies investigating diet are often difficult to interpret because of the many possible confounding factors. However, this study creates evidence of both the causative nature between added sugar and multiple negative health outcomes, as well as the body’s ability to heal if it’s given the right nutrients.
Now that we’re all scared off of added sugar forever, it’s good to be reminded that very little of the damage these molecules can do is irreversible. And that indulging in sweets from time to time won’t ruin your healthy new year. Most of the studies discussed above touch on the results of chronic overexposure to added sugar. If you’re good about what you eat 90% of the time, that extra 10% where you’re more flexible can really be about enjoying yourself, instead of getting in your body’s way.
- Johnson, Richard J, et al. “Perspective: A Historical and Scientific Perspective of Sugar and Its Relation with Obesity and Diabetes.” Advances in Nutrition (Bethesda, Md.), vol. 8, no. 3, 2017, pp. 412–422, www.ncbi.nlm.nih.gov/pubmed/28507007, 10.3945/an.116.014654. Accessed 28 Nov. 2019.
- Hu, F. B. “Resolved: There Is Sufficient Scientific Evidence That Decreasing Sugar-Sweetened Beverage Consumption Will Reduce the Prevalence of Obesity and Obesity-Related Diseases.” Obesity Reviews, vol. 14, no. 8, 13 June 2013, pp. 606–619, 10.1111/obr.12040.
- Pushpanathan, Premalatha, et al. “Gut Microbiota and Its Mysteries.” Indian Journal of Medical Microbiology, vol. 37, no. 2, Apr. 2019, pp. 268–277, 10.4103/ijmm.ijmm_19_373. Accessed 10 Jan. 2021.
- Satokari, Reetta. “High Intake of Sugar and the Balance between Pro- and Anti-Inflammatory Gut Bacteria.” Nutrients, vol. 12, no. 5, 8 May 2020, p. 1348, 10.3390/nu12051348. Accessed 29 May 2020.
- Ter Horst, Kasper W, and Mireille J Serlie. “Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease.” Nutrients, vol. 9, no. 9, 6 Sept. 2017, p. 981, www.ncbi.nlm.nih.gov/pmc/articles/PMC5622741/figure/nutrients-09-00981-f001/, 10.3390/nu9090981.
- Lustig, Robert H, et al. “Isocaloric Fructose Restriction and Metabolic Improvement in Children with Obesity and Metabolic Syndrome.” Obesity (Silver Spring, Md.), vol. 24, no. 2, 2016, pp. 453–60, www.ncbi.nlm.nih.gov/pubmed/26499447, 10.1002/oby.21371. Accessed 9 Feb. 2020.