Simple Sugars, There's More Than Science to Fueling Your Goals

Carbohydrates come in many forms; those include the simple and complex. In our previous carbohydrate article, Everything you Need to Know About Carb Cycling, there is a recommendation to use simple carbohydrates in a carb load. This current article aims at describing the basis for this recommendation as well as uncovering the differences that exist between the different types of simple sugars.

“Just before your training you want a small amount and it is best for this to come in simple carbs that are in an easy to digest form (fluid). After training you want a lot of carbohydrates in a mix of simple and complex.” This quote comes from our article on carb cycling. Reading it and using some context we can gather the reason for consuming a simple carb before and a complex after has something to do with digestion and fuel availability. Your priority when consuming food and drink around a training session is providing what your body needs at that time -- to optimize the results of training.

Before a session feeding is centered around providing fuel to perform the exercise, so it comes down to foods and fluids that provide fuel, fast, and that don’t upset the stomach. The problem with consuming complex carbs before an exercise session is the fiber content of those types of carbohydrates. Fiber can either put a brick in your gut or empty it very quickly, either of these cases is a negative outcome when you’re are about to train. To put in in context, eating a complex carb food heavy with fiber is like taking a fiber supplement right before a training session, it just doesn’t make sense. It is better to consume carbohydrate foods that contain simple sugars. These give your body access to the fuel quickly. Some examples include gummy bears, gummy worms, pixie sticks, honey, sugary drinks, etc.

You will take recognition that the foods listed may not paint the definition of “health”. What you need to understand is that health is continuum and not a fixed definition. The biggest thing you can take from this is that the people who allow themselves to stray from the fixed definition of health are often healthier than those that do not. Yes, there are people on both ends of the spectrum doing things that dietitians and mental health professionals want to classify as dysfunctional, but that doesn’t mean that you should limit your view of what is a healthy to a fixed construct.

The reason this is being called attention to is because clients will often stick to what they think of as healthy foods during a carb load. Or they will do the opposite and eat all processed foods and load more than just carbs. It is okay to eat a bunch of white, processed pasta or drink a soda to accomplish your goal, you may even enjoy it. For those that go off the deep end, you have to find balance in complex carbohydrates (whole foods) and processed while timing them correctly. It is important to know that you can find balance when loading calories or carbohydrates.

Second to this we need to dive a little bit into the idea of the glycemic index (GI). The GI is one of the most misinterpreted ideas that surrounds the carbohydrate food class, outside of the idea that carbs make you fat. Briefly, it is excess calories that that lead to unwanted excess body weight. You will likely hear people in the gym, or in any setting, talk about carbs in a polarizing manner. The GI will often come up as a way to qualify a carb source as healthy or unhealthy in one of these conversations. While the intent is good, this is a simple misunderstanding or, more often than not, improper interpretation of the data passed on from person to person. In reality the GI is an index that is relative to the body’s glycemic response to the carbohydrate food. That is, high GI foods have a high glycemic response and low GI foods have a low glycemic response (1).

To understand what this index means to your food selection we will go just a bit deeper. The glycemic response, or the magnitude of change in blood glucose, is relative to the body’s insulin response to that food, and insulin is the body’s signaling hormone that tells the body’s cells to take in glucose. High GI foods have low insulin responses while low GI foods have high insulin responses (2). Simply put, when you consume a low GI food your body will respond with the appropriate amount of insulin so that the body can properly regulate the new blood sugar, however, when you consume a high GI food the body doesn’t release the appropriate amount of insulin to regulate the new glucose.

This may sound like it could be bad but you have to remember that we fuel our body with different foods and these foods all have different purposes. Foods that contain simple sugars are often on the high end of the GI. But, insulin is not the only signaling mechanism the human body uses to tell its cells to take in blood glucose. The other primary mechanism is exercise, or mechanical and metabolic stress (3). So, you would want to consume a high GI food, that contains simple sugars, before or during a workout/competition. Additionally, there are numerous high-quality foods that are on the high end of the GI, for example brown rice and bananas.

---

Now that we have laid out the basis of our simple carbohydrate recommendation, we can explore these sugars on a deeper level. There are many types of compounds that provide a sugary or sweet taste but they are all designed around or similar to glucose. First of all, glucose is the cell’s preferred way to create energy. Your body can and does take chemicals from other molecules to make more glucose when it desires to, through a process called gluconeogenesis. If this term seems a bit too chemistry for you break it into its parts and its meaning will reveal itself. Gluco-neo-genesis becomes glucose-new-make (or make new glucose), so it simply means that the body makes new glucose when it needs it, if it has what it needs to. This is a very significant process that the body performs on a regular basis to maintain life (4). There are specific places in the body that have predetermined amounts of glucose and are highly monitored. The most common of these is blood glucose, think about your body monitoring this like it does your temperature, when your temperature goes down your body does things that create heat, like shivering. When your blood glucose thermometer recognizes lower levels it corrects this drop, often by gluconeogenesis.

All carbohydrates can be broken down into their parts, like a house has bricks. Glucose is one of these parts, and while there are other simple sugars out there, there are only a couple that stack up to build the larger molecules. Those include the infamous glucose as well as two others, fructose and galactose. These three are also known as the monosaccharides. When you break carbohydrates down, they all come down to different combinations of the monosaccharides.

Even more interestingly the monosaccharides are made of the same three chemicals in the same amounts. That is six carbons, twelve hydrogens, and six oxygen. With this on the table we need to revisit the aim of this article, uncovering of the differences that exist between simple sugars, specifically these monosaccharides. Based on the chemical make-up of these molecules not much could be different. How these molecules differ is in their chemical structure and biological behavior rather than the numbers. The below figure is representative of the structural difference.

Fructose should stand out with its 5 points versus 6 in glucose and galactose. One of the primary differences is that fructose does not get transformed into glucose, like galactose. It remains fructose when we consume it. To understand this in its full breadth we need to first explore the commonly referenced high-fructose corn syrup. First, the prefix “high” tells the consumer that the corn syrup is high in fructose without any context. In reality high-fructose corn syrup only has 5% more fructose than (low-fructose) corn syrup. High-fructose corn syrup contains 55% percent fructose and 45% glucose where corn syrup and table sugar contain 50% fructose and 50% glucose.

That prefix is misleading and makes the consumer think that it is exponentially higher, when in reality it’s not. To add to that there is a body of research that would have you believe that high-fructose corn syrup is one of the major contributors to the obesity epidemic (5). However, this is a skewed view of the science behind this sugar derivative. In fact, any amount of fructose could be interpreted as bad, depending on your world view and what you think makes someone fat. Because any fructose has the same effect on physiology and there is no metabolic difference between table sugar, fructose, and high-fructose corn syrup (6).

---

Before we dive into that it is important to recognize that corn syrups are modified in a way that could potentially make them more addictive, if you don’t have self-control. That is, they are processed with enzymes (7). This could lead to fructose and glucose tasting sweeter. Enzymes are crucial players in metabolic processes, in this context they assist in the chemical breakdown of these sugars before they get to you. When sugars are broken down in this way, the sweetness is enhanced. In fact, your body releases an enzyme called salivary amylase in your mouth to begin the chemical breakdown of carbohydrates. If you, instead of swallowing something made of sugars immediately, were to hold it in your mouth it would actually get sweeter and sweeter as time progressed.

Corn syrups (high-fructose or not) come two-fold with potential mechanisms for people to blame their health status on, the addition of enzymes to increase the sweetness and fructose. Fructose is not processed by your body like glucose or galactose is, and recall galactose becomes glucose in the body. This is just one was that fructose behaves differently.

Before going into the other differences, we first need to identify how the body responds to the primary monosaccharide, glucose. When your body recognizes the increase in blood glucose it responds by releasing insulin to assist in glucose uptake (8). The food type will depict how much insulin is released (9). Because glucose is such a large and polar molecule it must travel through a transporter (Glucose Transporter or GLUT). For our purposes we are discussing consuming sugar to fuel skeletal muscle. Skeletal muscle contains GLUT-2 and GLUT-4 and glucose is able to pass into the muscle cell (fiber) for normal carbohydrate metabolism via these (10). Consumption of glucose will also cause a suppression in ghrelin (11) and release of leptin (12), where insulin and these two are directly related in the normal physiological response (13, 14, 15). Ghrelin and leptin are the two primary hormones related to hunger and energy intake control (16). Ghrelin is associated with increases in hunger (17) and leptin stimulates the feeling of fullness or satiation (15). These are the normal physiological responses to glucose.

That said, these physiological responses are not seen with fructose. With fructose consumption the body does not release insulin to get it into the cell (18). Also, since fructose is not transformed into glucose it is reliant on a different transporter, GLUT-5, and GLUT-5 receptors are mostly found in central organ tissue (10); most significantly the liver (18). Once fructose makes it into the liver cell it goes through a different version carbohydrate metabolism which creates a different set of byproducts, which are more likely to become fat (18, 19, 20).

---

There are some pretty serious public health concerns that present themselves when we translate these findings to the general public. The mechanism that is subject of finger pointing and the reason you are told to never touch high-fructose corn syrup is the limited leptin response (6). Leptin resistance is thought to have a significant relationship with obesity and its dynamic pathology (21). The problem is high fructose corn syrup is not independent in the potentially negative effects. As consuming any form of fructose results in a dysregulated hormonal response where the normal ghrelin suppression and release of leptin are diminished compared to glucose (6). Recall, table sugar is the same percent fructose as corn syrup but without the added enzymes.

You could take this evidence to support an anti-sugar opinion, but healthy behaviors come down to more than a physiological response. In reality there is evidence to support that it still requires excess energy consumption to accumulate unwanted bodyweight, whether you consume fructose or not. A review of the scientific literature on this topic discusses this, “This finding strongly suggested that energy balance is a major determinant of the potential for dietary sugars to influence measures of body fatness… the data suggests that the change in body fatness that occurs from modifying intake of sugars results from in alteration in energy balance rather than physiologic or metabolic consequence of monosaccharides or disaccharides.”, and finds that weight gain is dependent on energy balance, not whether or not sugars are a part of the diet (22).

In closing, yes there are differences in simple and complex carbohydrates, especially when looking at fructose. But as long as you are eating the number of calories you need to meet your goals then you are going to be where you need to be. It is always important to consider that losing or gaining weight is a long-term goal, not short. How you get there can be become very specific and in this we can utilize simple and easy to digest carbs to facilitate quality training and recovery.

Take-aways:

1) Simple, easy to digest carbohydrates should be consumed before a training session or competition (or during if it is long and fatiguing)

a. Examples included (but are not limited to) gummy bears, gummy worms, pixie sticks, honey, and sugary drinks

2) Complex carbohydrates contain fiber (soluble or insoluble) so eating a fiber heavy food can be like taking a fiber supplement

3) The Glycemic Index is not a measure of a food’s healthiness, it is only relative to the insulin response that food causes – many high quality, whole foods are rated high

4) There are 3 monosaccharides (single sugar molecules) – glucose, galactose, and fructose

a) All carbohydrates are made of varying combinations of these 3

i) Glucose (and galactose):

1) 6 carbon ring molecule

2) Insulin released

3) Leptin released

4) Ghrelin suppressed

5) Enters skeletal muscle via GLUT-2 and 4 receptors

6) Normal carbohydrate metabolism

i. Fructose:

1) 5 carbon ring molecule

2) Insulin NOT released

3) Leptin NOT released

4) Ghrelin NOT suppressed

5) Enters liver via GLUT-5 receptor

6) Dysregulated carbohydrate metabolism that can lead to fat synthesis

5) Even though there are differences between the simple sugars, total energy intake still determines whether you will maintain, lose, or gain body weight/fat

References

1. Schenk, S., et al. (2003). "Different glycemic indexes of breakfast cereals are not due to glucose entry into blood but to glucose removal by tissue." Am J Clin Nutr 78(4): 742-748.

2. Eelderink, C., et al. (2012). "Slowly and Rapidly Digestible Starchy Foods Can Elicit a Similar Glycemic Response Because Of Differential Tissue Glucose Uptake in Healthy Men." Am J Clin Nutr 96(5): 1017-1024.

3. Röhling, M., et al. (2016). Influence of Acute and Chronic Exercise on Glucose Uptake. Journal of diabetes research, 2016, 2868652.

4. El Bacha, T., Luz, M. & Da Poian, A. (2010) Dynamic Adaptation of Nutrient Utilization in Humans. Nature Education 3(9):8

5. Bray, G. A., Nielsen, S. J., & Popkin, B. M. (2004). Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. The American journal of clinical nutrition, 79(4), 537–543.

6. Rippe, J. M., & Angelopoulos, T. J. (2013). Sucrose, high-fructose corn syrup, and fructose, their metabolism and potential health effects: what do we really know?. Advances in nutrition (Bethesda, Md.), 4(2), 236–245.

7. Clarke, M.A., (2003). Encyclopedia of Food Sciences and Nutrition (Second Edition), Pages 5711-5717.

8. Tseng, C. C., Kieffer, T. J., Jarboe, L. A., Usdin, T. B., & Wolfe, M. M. (1996). Postprandial stimulation of insulin release by glucose-dependent insulinotropic polypeptide (GIP). Effect of a specific glucose-dependent insulinotropic polypeptide receptor antagonist in the rat. The Journal of clinical investigation, 98(11), 2440–2445.

9. Schäfer, G., Schenk, U., Ritzel, U., Ramadori, G., & Leonhardt, U. (2003). Comparison of the effects of dried peas with those of potatoes in mixed meals on postprandial glucose and insulin concentrations in patients with type 2 diabetes. The American journal of clinical nutrition, 78(1), 99–103.

10. Navale, A. M., & Paranjape, A. N. (2016). Glucose transporters: physiological and pathological roles. Biophysical reviews, 8(1), 5–9.

11. Caixás, A., Bashore, C., Nash, W., Pi-Sunyer, F., & Laferrère, B. (2002). Insulin, unlike food intake, does not suppress ghrelin in human subjects. The Journal of clinical endocrinology and metabolism, 87(4), 1902.

12. Wellhoener, P., Fruehwald-Schultes, B., Kern, W., Dantz, D., Kerner, W., Born, J., Fehm, H. L., & Peters, A. (2000). Glucose metabolism rather than insulin is a main determinant of leptin secretion in humans. The Journal of clinical endocrinology and metabolism, 85(3), 1267–1271.

13. Granata, R., Baragli, A., Settanni, F., Scarlatti, F., & Ghigo, E. (2010). Unraveling the role of the ghrelin gene peptides in the endocrine pancreas. Journal of molecular endocrinology, 45(3), 107–118.

14. Yada, T., Dezaki, K., Sone, H., Koizumi, M., Damdindorj, B., Nakata, M., & Kakei, M. (2008). Ghrelin regulates insulin release and glycemia: physiological role and therapeutic potential. Current diabetes reviews, 4(1), 18–23.

15. Sahu A. (2003). Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Frontiers in neuroendocrinology, 24(4), 225–253.

16. Klok, M. D., Jakobsdottir, S., & Drent, M. L. (2007). The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obesity reviews : an official journal of the International Association for the Study of Obesity, 8(1), 21–34.

17. Cummings D. E. (2006). Ghrelin and the short- and long-term regulation of appetite and body weight. Physiology & behavior, 89(1), 71–84.

18. Havel P. J. (2005). Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutrition reviews, 63(5), 133–157.

19. Tappy, L., & Lê, K. A. (2010). Metabolic effects of fructose and the worldwide increase in obesity. Physiological reviews, 90(1), 23–46.

20. Parks, E. J., Skokan, L. E., Timlin, M. T., & Dingfelder, C. S. (2008). Dietary sugars stimulate fatty acid synthesis in adults. The Journal of nutrition, 138(6), 1039–1046.

21. Sáinz, N., Barrenetxe, J., Moreno-Aliaga, M. J., & Martínez, J. A. (2015). Leptin resistance and diet-induced obesity: central and peripheral actions of leptin. Metabolism: clinical and experimental, 64(1), 35–46.

22. Te Morenga, L., Mallard, S., & Mann, J. (2012). Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ (Clinical research ed.), 346, e7492.

---

Need help with your nutrition? This article was authored by MPS Coach Joe. Contact him.

---