My first two questions when my gastroenterologist told me I had fructose malabsorption were:
- What is fructose malabsorption?
- How did I get it?
I hardly ate sweets and did not drink soda or juices, I more often than not ate home cooked meals made from healthy and fresh ingredients, and when I purchased prepared or processed foods, I made sure they had no added sugar. I was confused why fructose absorption was the source of my problem when I hardly ate it.
The answer to my first question was pretty straightforward. Fructose is a simple sugar found in natural foods like fruits and honey and in processed foods in forms such as high fructose corn syrup and crystalline fructose. Once eaten, fructose moves to the small intestine where through the aid of protein transporters, it is absorbed into the bloodstream, ends up in the liver where it is metabolized and is then used by our organs. Fructose malabsorption, a digestive disorder that affects 30-40% of the population, occurs when fructose is unable to be absorbed in the small intestine and instead moves along to the large intestine. This can lead to the import of water into the intestinal lumen and the bacteria present in the intestine feeds off the fructose and may produce hydrogen, methane, carbon dioxide, and fatty acids. This can lead to diarrhea, bloating, and gas. Other symptoms may include cramping, nausea, joint pains, fatigue, brain fog, depression, and possible malnutrition.
The answer to my second question provided by my gastroenterologist was that the cause for fructose malabsorption is not known. So I started speculating. Was it due to the low-fat diet I was on during college and maybe I instead ate too many carbs, or did my digestive system stop processing sugars properly during graduate school when I was on the low carb diet, and did being vegetarian and eating soy based products which have vital wheat gluten (wheat has fructans = chains of fructose with a glucose at the end) do me in? In the end, I decided to look at the current research to try and gain a better understanding of what might be causing fructose malabsorption.
What is known:
- The GLUT5, protein transporter:
- Fructose is absorbed from the small intestine into the bloodstream mainly through a protein transporter called GLUT5. When scientists remove GLUT5 from mice, there is less fructose absorbed and the mice exhibit symptoms of fructose malabsorption including bloating and gas. However, no mutations in GLUT5 have been identified in patients with fructose malabsorption.
- GLUT5 production is low in infants. The theory is that throughout evolution, infants were not fed fruit until after they were weaned so GLUT5 was not needed until then. The amount of GLUT5 present in the small intestine increases with age, which correlates with the increase of fructose in our diets. One issue is that today, some infants are given fruit juice to drink and the high amounts of fructose without the presence of GLUT5 may result in infants having diarrhea and other related symptoms.
- Our inability to absorb unlimited amounts of fructose may be due to the fact that there is a ceiling to how much GLUT5 our intestines can produce. Studies have shown that 50% of the U.S. may have difficulty absorbing 25g of fructose in one sitting and 80% of the U.S. has trouble absorbing 50g of fructose at once. To provide a baseline, one 16 oz bottle of apple juice and a 22 oz bottle of soda may contain more than 30g of fructose. Today, the average consumption of fructose in the U.S. is 49g per day and 10% ingest 75g per day. An additional interesting fact and an indication of how we are currently eating is that the amount of fructose we are getting from fruit has decreased from 35% in 1978 to 16% today.
- The GLUT 2, protein transporter:
There is a second transporter, called GLUT2, which transports fructose with the assistance of glucose. Eating foods with equal amounts or more glucose in relation to fructose helps with the absorption of the fructose. However, if fructose is present at a higher rate than glucose then it may not be absorbed as well or at all. Fructose is used more than glucose in processed foods because it is sweeter so food manufacturers need less to sweeten their products, which results in cheaper manufacturing costs.
- Additional GLUTs:
GLUT7, GLUT8, and GLUT12 are also present and transport fructose but not to the same extent as GLUT5 or GLUT2. The multiple transporter proteins may compensate for each other since fructose is still tolerated even when GLUT2 is mutated.
- Other possible causes:
Inherited or acquired abnormalities of GLUT5, small intestinal bacterial overgrowth (SIBO), inflammation (found to reduce GLUT5 activity and production), stress (can affect GLUT2 production), celiac disease, bacterial variations or abnormalities in the gut, presence of sorbitol (a sugar alcohol), and chemotherapy.
- Other interesting facts:
Fructose malabsorption is more prevalent in women (a fact I suspected when there were only women present when I was going through my breath tests). Scientists speculate that this may be due to genetic or hormonal factors but other scientists have shown that fructose malabsorption does not seem to be due to genetics or related to ethnicity.
What to do?
Hopefully, the research will continue and we will gain more insight into how to better treat and possibly cure fructose malabsorption. In the meantime, the best way to prevent or limit the symptoms is by restricting fructose, fructans, other saccharides and polyols with the FODMAP (fermentable oligos- di- mono-saccharides, and polyols) diet. However, it is important to first discuss this with a nutritionist. There are many resources available including a shopping list of FODMAP friendly foods created by nutritionist, Kate Scarlata and two helpful apps; Low FODMAP diet by Monash Unversity and FODMAP swAPP by Dr. Kerith Duncanson.
Have you heard of other possible causes for fructose malabsorption?
- Beyer, PL, et. al. (2005) Fructose Intake at Current Levels in the United States May Cause Gastrointestinal Distress in Normal Adults. Journal of the American Diabetic Association 105(10), 1559-1566
- Biesiekierski, JR. (2014) Fructose-induced symptoms beyond malabsorption in FGID. United European Gastroenterology Journal 2(1), 10-13
- Douard, V. and Ferraris, RP. (2013) The role of fructose transporters in diseases linked to excessive fructose intake. The Journal of Physiology 591(Pt 2), 401-414
- Gracey, M, et al. (1971) Bacteria, bile salts, and intestinal monosaccharide malabsorption. Gut 12, 683-692
- Patel, C, et. al. (2015) Transport, metabolism, and endosomal trafficking-dependent regulation of intestinal fructose absorption. The FASEB Journal. 29, 1-13
- Schulzke, J, et al. (2009) Disorders of intestinal secretion and absorption. Best Practice & Research Clinical Gastroenterology 23, 395-406
- Jones, HF, et a. (2011) Intestinal fructose transport and malabsorption in humans. American Journal of Physiological – Gastrointestinal Liver and Physiology 300, G202-G206
- Szilagyi, A, et al. (2007) Fructose Malabsorption May Be Gender Dependent and Fails to Show Compensation by Colonic Adaptation. Digestive Diseases and Sciences 52, 2999-3004
- Wasserman, D. et. al. (1996) Molecular Analysis of the Fructose Transporter Gene (GLUT5) in Isolated Fructose Malabsorption. Journal of Clinical Investigations 98(10), 2398-2402
- Wilder-Smith, CH, et. al. (2014) Fructose transporters GLUT5 and GLUT2 expression in adult patients with fructose intolerance. United European Gastroenterology Journal 2(1), 14-21
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