If you have been paying attention to the news, you may have noticed more and more emphasis being placed on sugar and its negative consequences. More and more studies are showing an association between excessive refined sugar consumption and:
- Weight gain and obesity
- Hypoglycemia and diabetes
- Inflammation and oxidative stress
- Depression and anxiety
- Non-alcoholic fatty liver disease
- Alzheimer’s disease and dementia
- and more
That’s a lot of negative consequences!
Sugar has become a predominant ingredient in our modern society and is added to so many packaged and processed foods. It’s literally everywhere! As I mentioned in my post about saturated fat, the amount of products containing sugar has risen substantially since the 1980s when nutritional guidelines changed in order to limit saturated fat intake.
Given the ubiquitousness of this ingredient, it is important to understand some details about sugar. The more you understand, the better positioned you can be to make optimal choices for you and your wellness.
This is a multi-part series, each post will explore a different aspect of sugar. In today’s post, I will talk about the two simple sugars glucose and fructose, and how they are metabolized in the body.
Today’s post is a little longer than usual; I didn’t expect to go on for so long on this topic but there you have it. It really is important to understand these details to truly understand WHY we choose what we eat and how much. There are some “sciencey” terms in this post, I try to explain things as simply as possible. If you are confused, please let me know!
So what is sugar?
Sugar is a carbohydrate, which is one of three macronutrients our body uses for energy. The other two macronutrients are fat and protein. There are 3 main forms of carbohydrates, namely monosaccharides (glucose, fructose), disaccharides (lactose, sucrose), and polysaccharides (starches and cellulose).
Monosaccharides consist of one (mono) molecule of sugar, which doesn’t need to be broken down in the intestine and is therefore quickly digested and absorbed into the bloodstream. Because these sugars do not need to be broken down into simpler forms, monosaccharides are referred to as "simple sugars".
Disaccharides consist of two monosaccharides joined together, and therefore require enzymes in the intestine to cut the bond between them before they can be absorbed.
Those with a lactose intolerance lack the enzyme lactase that is required to cut this bond. Therefore the lactose sugar will remain in the intestine. Intestinal bacteria love sugar and will feed on this disaccharide that has been left there. When these bacteria consume sugar, they produce methane gas, which is why someone with a lactose intolerance will develop smelly gas, bloating, and diarrhea.
Finally, polysaccharides contain multiple (poly) bonds. Therefore these forms of carbohydrates take a little longer to break down and get absorbed into the bloodstream as sugar.
Of the monosaccharides, glucose is regulated by the hormone insulin. The body is only able to tolerate 4 grams or 1 teaspoon of glucose in the bloodstream at one time. Any more hanging around for too long will cause complications, including blood vessel inflammation and eventual destruction.
Therefore, any more than that 4 grams circulating in the blood needs to be dealt with. This is where insulin comes in. This hormone is produced in the pancreas by cells called beta cells. Insulin is a storage hormone.
When it comes to blood sugar, one of the things insulin does is interact with and activate a transporter protein called GLUT4. This protein acts to shuttle glucose from the bloodstream into muscles and the liver for storage in the form of glycogen, to be used as fuel when those muscles contract. The glycogen stored in the liver is kept as a reserve in case blood sugar levels drop too low, for example, if you haven’t eaten for an extended period of time.
There are two main problems that can occur with glucose metabolism when glucose is consumed in too large quantities and too often.
First, If glucose is consumed in too large quantities, muscle and liver storage can’t keep up with the amount of glucose coming in. If the muscle isn’t burning the stored glucose faster than the glucose is entering the bloodstream, the body must do something with this glucose. It cannot remain circulating in the bloodstream. The liver can hold about 100 grams of glycogen, and the muscles about 500 grams, on average (1).
Glucose can also remain stuck in the bloodstream if the glucose transport proteins are no longer sensitive to insulin. This is what happens in type 2 diabetes. Insulin is produced, but the transporters it activates no longer respond to it. This is called insulin resistance.
As an aside, type 1 diabetes works in a completely different manner: it is an autoimmune condition where the beta cells of the pancreas are destroyed by the immune system, and hence the body is unable to produce its own insulin. Type 1 diabetes usually develops in childhood, whereas type 2 diabetes more commonly develops in adulthood, as a consequence of diet and lifestyle; namely overconsumption of sugar and inflammatory foods, and lack of exercise. It has been found that exercise can help keep those GLUT4 transport proteins more responsive or sensitive to insulin, which can help prevent or slow down the development of type 2 diabetes.
So what happens to this excess glucose? It is converted into fat, in a process called de novo lipogenesis (meaning generation of fat from new), and occurs in both liver and adipose (fat) tissue, but mostly in fat tissue when lipogenesis occurs as a result of excess glucose (2,3). This is a complicated process that I’m not going to describe here, but it’s important to know that this occurs.
The other problem that happens when we consume glucose in high quantities is the problem of insulin itself. High concentrations of glucose rushing into the bloodstream triggers spikes and surges of insulin. There are so many detrimental effects of having ongoing insulin spikes.
As I already mentioned, type 2 diabetes means that the body is not sensitive to insulin as it once was. This disease develops because the body has been exposed to too high insulin levels over and over again, for far too long. But even before diabetes can develop, high levels of insulin will contribute to other problems; one of which is weight gain and obesity.
I described insulin as a storage hormone at the beginning of this section. It helps store glucose for storage, but it also keeps fat in storage, by preventing it from being metabolized. So if you have chronically high levels of insulin, you will have a difficult time trying to lose fat.
Chronically high levels of insulin will have a myriad of other negative side effects in the body as well, including inflammation, poor immune functioning, and negative effects on other hormones, including leptin. Leptin is a hormone that tells your body that you’re full and have had enough to eat.
Chronic insulin can mess with levels of leptin, and the body’s sensitivity to leptin. Just as you can become resistant to insulin from chronic exposure to too much glucose, you can become resistant to leptin from chronic exposure to too much insulin.
What happens when you are resistant to leptin? Your brain doesn’t get the message that you have had enough food to eat, and you feel constantly hungry! So not only is weight gain happening from the generation and storage of fat in the body as a result of the glucose and insulin, but then your brain thinks you are always hungry, and so you continue to eat more, and more, and more.
[ctt template="7" link="2RbDO" via="yes" ]Just as you can become resistant to insulin from chronic exposure to too much glucose, you can become resistant to leptin from chronic exposure to too much insulin.[/ctt]
Wow, what a mess! Funny, I didn’t expect to go on this long on this subject, but here you have it. I think it’s really important for you to understand this process if you didn’t know it already! I am sort of dumbing down the process a bit, but these are the most important take-home points to understand.
So now we have discussed what happens to glucose. What about fructose, the other monosaccharide?
Fructose is the other simple sugar and is found most commonly in combination with glucose in fruit, and to a lesser degree in vegetables (4). However, in recent years, the highest amounts of fructose are found in a highly refined product called high fructose corn syrup (HFCS). This is a highly concentrated, refined and processed form of fructose that is most commonly found in sweetened drinks, like soda pop.
Metabolism of fructose is not regulated by insulin, like its simple sugar counterpart, glucose. Therefore high levels of fructose do not spike insulin like glucose does. However, not much fructose ever actually makes it to the bloodstream.
Most absorbed fructose goes directly to the liver, and anywhere from 1/4 to 1/2 of the fructose will be converted into glucose within 2-6 hours, and eventually stored as glycogen, mostly in the liver. It appears that this conversion to glucose occurs to a lesser degree in women, as well as those with obesity and diabetes (4).
This fructose in the liver will be used in energy generation pathways, and excess will undergo lipogenesis (fat generation) within the liver. Remember I mentioned above that glucose can be fated for lipogenesis as well, but mostly in fat cells, whereas fructose lipogenesis occurs in the liver (4). Unfortunately, fat generation in the liver can contribute to non-alcoholic fatty liver disease (NAFLD), which can lead to cirrhosis or liver cancer (5). Excess fructose, especially from HFCS has been linked with the development of NAFLD (8,9,10).
Sadly, NAFLD has become the most prevalent form of chronic liver disease in children and teenagers, affecting 10%-20% of the pediatric population (7), and up to 30% of the adult population (9). More often than not, obesity and type 2 diabetes are observed in children and adults with NAFLD (7).
It may be of interest to note that type 2 diabetes used to be only observed in the elderly population. This disease is now being observed in younger and younger populations, including children. Large quantities of HFCS sweetened beverages may be playing a role in this trend.
Recent studies have observed that when small amounts of fructose are eaten, about 90% of it will be processed in the small intestine, with little of it actually reaching the liver, a scenario we would see with consumption of small to moderate amounts of whole fruits (5,6).
However larger amounts seem to overwhelm the small intestine and can no longer keep up with the process. Researcher Joshua D. Rabinowitz says that the small intestine probably starts to get overwhelmed halfway through a can of soda or a large glass of orange juice (5). This is when fructose will start to spill over into the liver, increasing the likelihood of consequent liver fat production, and possible development of NAFLD.
Interestingly, the study also showed that the fructose was more likely to be processed in the small intestine if eaten as part of a meal. Meaning, in a fasted state (i.e. first thing in the morning, or between meals), more of that fructose was absorbed and sent to the liver. The take-home message being fructose-containing items are best consumed in small, moderate quantities, and not on an empty stomach (5).
Given this last finding, I wonder what the repercussions are on people eating a fruit-based breakfast. I often encounter people consuming large quantities of high-sugar tropical fruits as their first meal of the day, with a side of fruit juice, thinking they are doing their body a favour. I will discuss optimal breakfast choices in an upcoming post, but for a few reasons, it might be best to stray away from a fruit-based breakfast if that is what you tend towards.
Joshua Rabinowitz’s advice? “Limit sweets to moderate quantities after meals, and do not have sweets or sweet drinks away from meal time” (5).
[ctt template="7" link="wLGst" via="yes" ]The small intestine probably starts to get overwhelmed halfway through a can of soda or a large glass of orange juice. This is when fructose will start to spill over into the liver, increasing the likelihood of consequent liver fat production, and possible development of NAFL[/ctt]
Wrapping up part 1
Have I overwhelmed you with science yet? I hope not!
Today I discussed the physiology of sugar metabolism, particularly of glucose and fructose, and their different mechanisms. The main takeaways here:
- Glucose requires insulin for its metabolism, and too much glucose can create a number of imbalances in terms of insulin regulation, and fat production and storage. Too much insulin causes a whole host of other problems in the body as well, which impact immune function, levels of inflammation, and regulation of other hormones.
- Fructose does not require insulin for its metabolism. Small quantities are processed in the small intestine, larger amounts are absorbed and handled almost exclusively in the liver, where excess is converted into fat. Excess liver fat can lead to various liver diseases, which are becoming more common in our society.
Whew! What a topic! What did you learn from this? Is there anything that surprised you? Will you make any adjustments to your diet as a result? Comment below and let me know!
Stay tuned for future posts where I discuss other aspects of sugar, and what you can do to prevent consuming too much.
Think you might benefit from reducing your sugar intake?
Check out this free resource below, it just may help!
- Vann K. How is excess glucose stored? 2017. https://www.livestrong.com/article/264767-how-is-excess-glucose-stored/
- Kersten, S. Mechanisms of nutritional and hormonal regulation of lipogensis. EMBO reports. 2001; 2(4):282-286. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1083868/
- Tsiloulis T, Watt M. Molecular and cellular regulation of adaptation to exercise. Prog in molec biol and translational sci. 2015; 135:175-201. https://www.sciencedirect.com/science/article/pii/S1877117315001301
- Sun S, Empi M. Fructose metabolism in humans - what isotopic tracer studies tell us. 2012; 9:89. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533803/
- Cell Press. Mouse study reveals what happens in the gut after too much fructose. 2018, Feb. https://www.eurekalert.org/pub_releases/2018-02/cp-msr013118.php
- Jang C, Hui S, Lu W, et al. The small intestine converts dietary fructose into glucose and organic acids. Cell metab. 2018; 27(2):351-361. http://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30729-5
- Temple J, Cordero P, Li J, et al. A guide to. Non-alcoholic fatty liver disease in childhood and adolescence. 2016; 17(6): 947. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926480/
- Harvard Health Letter. Abundance of fructose not good for the liver, heart. 2011. https://www.health.harvard.edu/heart-health/abundance-of-fructose-not-good-for-the-liver-heart
- Basaranoglu M, Basarangolu G, Bugianesi E. Carbohydrate intake and nonalcoholic fatty liver disease fructose as a weapon of mass destruction. Hepatobiliary Surg Nutr. 2015; 4(2): 109-116. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405421/
- Rapaport L. Fructose tied to advanced liver disease in children and teens. 2017. https://www.reuters.com/article/us-health-fructose-fattyliver-kids/fructose-tied-to-advanced-liver-disease-in-children-and-teens-idUSKBN1602AG