“Sugar” is a term we are all familiar with. When we say it everyone knows what we are talking about. Most of us probably picture white crystals; perhaps others picture cubes of sugar. Some of you may even think about fruit. Yet there are numerous different kinds of sugars and they are not all created equal despite their shared molecular formulas of C6H12O6. Each sugar has a different structure; and this makes all of the difference in the world of molecular biology. Glucose and Fructose are probably the most popular sugars. Despite the same molecular formula their metabolism inside the body is quite different. Glucose is the body’s main energy source and is derived from most of the carbohydrates we eat such as pastas or starches. A healthy amount of glucose in the diet is well tolerated and handled by the body; with insulin being the key player in regulating the blood sugar levels. People who overindulge in glucose will challenge their body’s insulin response and a constantly elevated blood sugar level can eventually lead to insulin resistance; which is the precursor to diabetes mellitus type 2. This simply means that the constant insulin overload eventually desensitizes insulin receptors and they no longer function properly. Ironically this clear-cut mechanism might not be the number one problem behind the obesity and diabetes epidemic going on in the western world. Fructose has a more insidious and complex way of damaging our bodies.
The problem with fructose is not the sugar itself. In fact some of you might know that fructose is the main sugar found in fruits. If you have heard that “an apple a day keeps the doctor away” all your life, then this may seem counterintuitive at first. No; you’re right. Fruits are indeed great for us, but not because of the fructose; their ample fiber and antioxidant content claim that honor. Fructose is basically an innocent bystander here. There is not enough of it in fruits to deal any damage to our bodies. The narrative changes with soft drinks such as Coke or Pepsi which contain large amounts. This is where the trouble with fructose (a major component of high fructose corn syrup) begins.
High fructose corn syrup is a very popular sweetener used in many soft drinks. Its content is essentially 55% fructose and 45% glucose. Lets compare soft drinks with fruits here to illustrate the point we are trying to make. A typical 20 oz soda contains about 240 calories and 65 g of sugar. If we take this 65 and multiply it by the percent of fructose (.55) we get 35.75 g.# Hence we have 35.75 g of fructose in 240 calories of soda. In order to get some perspective check out what a 20 oz soda is. Most soft drink enthusiasts can probably down one or two of these a day. Others may drink one with each meal. Now lets compare this to the amount of fructose found in 240 calories of bananas (or about 2 ¼ bananas). Bananas contain 16.4 g of fructose per 240 calories. In other words, you need FIVE bananas to get the same amount of fructose as in a 20 oz drink of soda. Now I have seen plenty of people in my life drink 20 oz bottles of soda, but not once have I seen anybody eat 5 bananas in one sitting. Therein lies the problem with comparing fruits to artificially sweetened drinks. The fructose is not the problem… its the amount per “normal” or “reasonable” serving. A few of you may drink two sodas a day, but i’m sure NONE of you eat 10 bananas a day. # Considering the growing body of evidence showing that over 50 g of fructose a day may be detrimental we more than meet that standard with just two 20 oz soft drinks a day.
The high fructose diet associated to the consumption of so many artificial sweeteners, and even breads that have high-fructose corn syrup these days, has likely played a major role in the obesity and diabetes epidemic. Although on average we consume about 15% of our calories a year from “added sugars”, about 50 million americans consume 25% or more of their calories from sugary beverages and other foods with “added sugars.”# In most cases this added sugar is fructose (particularly in the main culprit: Soft drinks). The epidemiology of the problem is quite concerning since many studies cited in Tappy and Le# have supported the view that eating a high fructose diet for more than a week increases VLDL cholesterol, triglycerides, and insulin resistance in both healthy and type 2 diabetic people. Although there are several mechanisms some of the best elucidated have had to do with the activation of transcription factors SREBP-1c and ChREBP.# Both of these transcription factors are lipogenic; meaning they increase fatty acid production. This then leads to dyslipidemia which in large part causes the insulin resistance associated to high-fructose diets. Interestingly high-fructose associated dyslipidemia has a tendency to increase visceral fat which is particularly important in determining diabetes type 2 risk (a low hip:waist ratio is one of the best indicators for this). Fructose seems to decrease this ratio in a way glucose does not.
A final point to here has to do with some more recent research involving the brain’s reaction to the two different sugars. Recent studies suggest that our brain may react differently to both sugars. Glucose was basically shown to “satisfy” the brain’s satiety centers in a more effective manner than fructose. The implication here is that fructose in some way fails to satiate the brain as effectively as glucose leading increased hunger and a desire to eat more in order to satisfy the brain’s glucose need. While more research is needed in this front it is still an interesting start in expanding our knowledge about the differences in sugar metabolism. We will examine other sweeteners in future posts.
Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric Sweetener Consumption and Dyslipidemia Among US Adults. JAMA. 2010;303(15):1490-1497. doi:10.1001/jama.2010.449.
Tappy, L and Le, K-A. Metabolic Effects of Fructose and the Worldwide Increase in Obesity. Physiology Review. January 1, 2010 vol. 90 no. 1 23-46.
McDevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM. De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutr 74: 737–746, 2001.
*All pictures obtained via google.com