Fructose malabsorption: Disorder or the new norm?

Paper: Gibson PR, Newnham E, Barrett JS, Shepherd SJ, Muir JG. Review article: fructose malabsorption and the bigger picture. Alimentary Pharmacology & Therapeutics. 2007 Feb 1;25(4):349–63.

Overview of paper: This review paper on fructose malabsorption was written by Dr. Peter Gibson and colleagues in 2007. It lays some of the groundwork for what would later be known as the low-FODMAP diet for irritable bowel syndrome (IBS) [1] by describing the effects of fructose, fructans (polymerized fructose), and sorbitol on digestion. Fructose malabsorption can lead to gas, bloating, and loose stools through multiple mechanisms.

The quotes:

When used as a sweetener in soft drinks such as in the US, fructose consumption can quickly approach levels at which malabsorption is seen in healthy adults. Evidence suggests that when solutions containing 25–50 g of fructose (equivalent to >500 mL HFCS[High Fructose Corn Syrup]-sweetened soft drink) are used in hydrogen breath testing, >50% of healthy subjects demonstrate malabsorption of fructose and consequently experience symptoms of abdominal pain, wind and loose bowels [2]. (p. 351)

The main difference between the symptomatic and asymptomatic populations has been the frequency of inducing symptoms…, suggesting that the sensitivity of the bowel to the change in luminal conditions induced by fructose malabsorption is the key difference rather than the malabsorption itself.

In other words, the vast majority of data indicate that fructose malabsorption is not abnormal, and its presence cannot be regarded as a ‘condition’ or ‘illness’. (p. 357)

Significance of quotes: Fructose malabsorption (sometimes called ‘dietary fructose intolerance’) occurs when fructose is not completely absorbed in the small intestine. Fructose piggy-backs on other molecules to pass through the intestinal wall and into the bloodstream, and when the amount of fructose exceeds the amount of available carriers, the excess gets left behind. When it reaches the large intestine, the remaining fructose pulls water into the colon; at the same time, it is rapidly fermented by intestinal bacteria to produce short chain fatty acids, carbon dioxide, hydrogen, and, in some people, methane.

Fructose malabsorption is most likely experienced by people who do not produce enough GLUT-5, the main fructose transporter molecule. For these people, even small amounts of dietary fructose (less than 25g) can produce symptoms. However, with fructose consumption at an all-time high, it is increasingly likely for normal GLUT-5 producers to experience fructose malabsorption – in fact, at least half of us, and possibly as high as 80% of us [3], will find ourselves in this situation from time to time. In these cases, the problem does not lie within us, but with what we choose to eat.


1. Shepherd SJ, Parker FC, Muir JG, Gibson PR. Dietary triggers of abdominal symptoms in patients with irritable bowel syndrome: randomized placebo-controlled evidence. Clin Gastroenterol Hepatol. 2008 Jul;6(7):765–71.

2. Beyer PL, Caviar EM, McCallum RW. Fructose Intake at Current Levels in the United States May Cause Gastrointestinal Distress in Normal Adults. Journal of the American Dietetic Association. 2005 Oct;105(10):1559–66.

3. Douard V, Ferraris RP. The role of fructose transporters in diseases linked to excessive fructose intake: GLUT5 and GLUT2 in fructose-associated diseases. The Journal of Physiology. 2013 Jan 15;591(2):401–14.