Coca-Cola might be past its days of adding tiny amounts of cocaine to its sodas, but it can still induce addiction, and so are many other sodas. While caffeine, the active ingredient in coffee that stimulates our nerves, is added to Coca-Cola, it isn’t the sole addictive component in the famous soda. In fact, the difference between how our bodies respond to glucose and fructose creates a natural ‘sugar bias’, despite both sugars having the same number of calories.
A Tale of Two Sugars
Fructose and glucose are two common sugars found in many foods and drinks. Table sugar is a fifty-fifty mix of fructose and glucose. Unlike glucose, which is metabolized or ‘burned’ directly for energy, fructose must first be converted to glucose by the liver before it is used. As a result, fructose does not spike in the blood, like glucose, and has a lower glycemic index of just 19. But, dig deep enough, and the nerve pathways reveal darker secrets about both sugars than the numbers show.
Scientists at the Monell Chemical Senses Center discovered that fructose and glucose trigger different responses in the brain through separate gut-brain pathways. The study, published June 10 in the journal Neuron[1], identified a signaling route less effective than the one used by glucose, which allows fructose to communicate with the brain. The pathway for fructose is not as adept at reducing activity in neurons associated with hunger as glucose’s pathway. To investigate how the two sugars influence the brain, researchers observed neural activity in mice after exposing them to fructose and glucose.
What Separates Fructose and Glucose
The team found that fructose increased the levels of peptide YY (PYY), or peptide tyrosine tyrosine (Y is the one-letter abbreviation of the amino acid tyrosine). PYY signaled through the vagus nerve leads to a modest reduction in the activity of agouti-related protein (AgRP) neurons. AgRP neurons, once active, can induce intense food-seeking or foraging behavior until food is detected through visual cues or aroma– sometimes even suppressing fear or pain in the process.
When researchers disturbed the pathway, fructose could no longer affect those neurons. Glucose, however, produced a different response. Glucose strongly suppressed AgRP neuron activity without relying on the PYY-Y2 vagus nerve pathway, resulting in a much larger effect on the hunger-related brain signaling.
This independence might stem from the way glucose levels are maintained in our bodies. After a meal, our body has an increased amount of glucose in the bloodstream. The spike triggers insulin release. Insulin is a pancreatic hormone that triggers the uptake of glucose by cells to produce energy. A third player enters the play when glucose is metabolized inside fat-containing cells called adipocytes. This third player is a hormone called leptin, which signals fullness (satiety) and reduces hunger by lowering the AgRP neuron activity.
While fructose is heavily reliant on the PYY-Y2 vagus nerve pathway, glucose bypasses it altogether and has a more robust overall effect.
Sugar Type Can Influence Food Preferences
While fructose and glucose produced similar short-term effects on food consumption, the mice developed preferences that depended on the degree of AgRP neuron inhibition induced by each sugar. The researchers put high-fructose corn syrup (HFCS), specifically HFCS 55, which contains roughly 55% fructose and 42% glucose, to the test. HFCS is a widely used sweetener in sodas, such as Coca-Cola, and in other food products like cereals.
The mice showed a preference for HCFS, and the sweetener did a better job at suppressing AgRP neuron activity than fructose alone. Researchers believe that a stronger effect on hunger-related neurons may explain why foods and beverages that have HFCS are so appealing.
Not Another Calorie Tracker
The results challenge a long-held assumption that AgRP neurons primarily track calorie intake irrespective of where those calories are sourced from. Instead, the findings suggest that hunger-related neurons are controlled not only by quantity but also by quality. The neurons can distinguish between the separate pathways at work, and despite providing the same amount of energy, the mice’s brains sensed fructose and glucose differently.
“This work adds to our growing understanding of how modern diets, especially those high in fructose or high-fructose corn syrup, interact with the neural systems involved in appetite,” said senior author and Monell Member Amber Alhadeff, PhD. In fact, the study highlights how complex and fine-tuned our body is in nutrient sensing, where even simple sugars have distinct effects on the gut, brain, and behavior.
The Joys of Coca-Cola
One of the main concerns with Coca-Cola is its potentially addictive nature. While the company has written a piece addressing such concerns, we need to dive deeper— not into Coca-Cola’s secret recipe, but into HFCS.
HFCS offers a longer shelf life, enhanced sweetness, and is a cheaper option than cane sugar. Nearly all mainstream sodas and soft drinks use it, as it is safe and reliable. However, higher fructose content has been linked to addictive behavior like sugar-seeking in rats in a study conducted by the University of Guelph and the Rockefeller University, New York. On the other hand, glucose is preferred over pure fructose.
HFCS strikes the middle ground. We prefer glucose as an energy source, while fructose keeps us wanting more. HFCS is a win-win concoction that triggers dopamine release, largely reinforcing our dependence on foods or beverages containing the sweetener. The reward centers buzz, and we find it difficult to hold back our cravings.
In fact, it’s not too different for table sugar either. Equal parts of glucose and fructose make table sugar almost as rewarding as HFCS 55, and while cane sugar-based Cokes have been launched at the market recently, sugar on its own does more harm than good.
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