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Fructose Malabsorption Fructose malabsorption is a digestive disorder in which the absorption capacity of the sugar fructose
in the small intestine is reduced. This leads to an increase of fructose in the large intestine where the
sugar is degraded by intestinal bacteria to several chemical compounds which will then cause
symptoms like bloating, wind, abdominal pain, diarrhea and/or constipation.
Introduction
The natural occurrence of fructose as a monosaccharide (molecular fructose) is mainly in fruits and
vegetables. It is also a component of the disaccharide sucrose, the table sugar, which is composed
of one molecule glucose and one molecule fructose. Molecular fructose is sweeter than glucose and
is therefore often used as sweetener in pastries, sweets and sodas. The average daily intake of
fructose has increased dramatically over the last 40 years mainly due to the increased usage of this
High Fructose Corn Syrup (HFCS) as a sweetener.
Fig. 1:Sucrose (Disaccharid)
Fig. 2:Molecular Fructose (Monosaccharid)
Fructose is absorbed in the small intestine via the GLUT-5 transporter. This transport from the
intestinal lumen into the enterocytes, the intestinal absorptive cells, is passive and driven by the
concentration difference of fructose between the intestinal lumen and the plasma of the cells. The
capacity of this transport system is limited and varies greatly between individuals. About 40% of the
population show signs of malabsorption after a single dose of 25g of fructose, a dosis far below the
average daily intake which is estimated to be around 70g per day. Sorbitol, a sugar alcohol which is
widely used as sugar substitute in industrial foods, further reduces the fructose absorption capacity
by binding to the GLUT-5 transporter.
Concomitant consumption of glucose with a fructose-rich meal can increase the absorption capacity
of fructose which is why most of patients suffering from fructose malabsorption tolerate table sugar
quite well. It is believed that this effect may be due to an increased integration of the GLUT-2
transporter into the membrane of the enterocytes. GLUT-2 acts as a passive transporter for glucose,
galactose and fructose with low affinity (that means it only transports these sugars if their
concentration is high). This transporter is only integrated into the membrane after a meal when the
sugar concentration in the intestine is high. This detection of sugar in the intestinal lumen only works
with glucose and therefore a fructose-rich meal will not trigger this integration of GLUT-2.
Metabolism
Unlike glucose fructose can only be utilized by a few cells of the body directly. Most of the absorbed
fructose is transported to the liver where it is phosphorylated and converted into fat, glucose or
energy (figure 3).
Currently there is an ongoing discussion whether fructose may induce obesity and non-alcoholic
fatty liver disease. Until now there is no hard evidence to support this thesis as most studies
investigating this effect yielded conflicting results. But considering the differences between fructose
and glucose metabolism it is a reasonable conclusion:
Fructose has no effect on insulin secretion which in turn may reduce the satiation experienced
after a meal.
Fructose is metabolized primarily in the liver putting more strain on the liver cells. Furthermore
the energy available in the liver cells is increased which can affect the synthesis of fat (excess
energy is stored as body fat).
There is little difference between the free fructose of high fructose corn syrup and the bound fructose
in table sugar. Both have very similar effects on the body. This does not mean that the fructose from
fruits is also detrimental. In the western civilizations only a small portion of the average daily intake
of fructose comes from natural sources and this comparatively low amount of fructose has no
detrimental effect on health.
Fig. 3: Metabolismus of Fruktose in the liver
Since fructose has no effect on insulin levels it was widely used in foods for diabetics. But with the
rising concern on the health effects of excessive fructose uptake the usage of fructose has reduced.
Fructose Malabsorption
Fig. 4: Effect of Fructose Malabsorption
Although up to 50% of the population are not able to absorb a single dose of 25g of fructose which is
the cutoff dose for malabsorption determination only approximately 5 to 7% of the population suffer
from symptomatic fructose malabsorption. Only these 5 to 7% will develop symptoms after a
fructose-rich meal. The malabsorption alone cannot be seen as a disorder but occurs throughout the
population.
The symptoms are triggered by the degradation products that arise from the decomposition of the
fructose in the large intestine by the intestinal bacteria. Mainly Hydrogen (H2), Methane (CH4),
Carbon Dioxide (CO2) and short chain fatty acids (SCFAs) are generated. These compounds can
cause the typical symptoms like bloating, wind, abdominal pain, diarrhea and/or constipation. Since
the composition of the intestinal bacterial population varies between humans also the amount and
composition of the generated degradation products varies. Furthermore the tolerance of the intestine
to negative influences is affected by several parameters like stress, inflammation and others. Both
these factors influence the severity of the symptoms the patient with fructose malabsorption will
experience after a fructose rich meal.
There is also no guideline that can tell which amount of fructose is needed to invoke symptoms. The
absorption capacity of patients suffering from fructose malabsorption is reduced but still significant. If
the ingested amount of fructose is below this absorption capacity no symptoms should be generated.
The factors influencing this absorption capacity are not well understood. For example inflammation
of the small intestine will decrease the amount of absorbed fructose. But until now no reason for the
innate difference of the absorption capacity for fructose between the individuals could be found.
Additionally it is of great importance how the fructose is ingested. Free fructose is taken up
differently than sucrose.
Fructose malabsorption must not be confused with the hereditary fructose intolerance, a disease
caused by a rare genetic defect of the liver enzyme Aldolase B. In this disease the body can no
longer process dietary fructose which causes symptoms like hypoglycemia and vomiting after a
fructose containing meal. Repeated exposure to fructose will lead to hepatomegalia and liver failure.
The prevalence of this potentially fatal disease is approximately 1 in 25000 in Western Europe.
Diagnosis
Medical tests require a hydrogen breath test with fructose. During this test the patient is
administered a single dose of 25g of fructose in 100ml water on an empty stomach. Then over the
course of 3 hours the amount of hydrogen in the exhaled air is measured. If the fructose is not
absorbed completely it will be degraded by the bacteria in the large intestine into hydrogen which
travels through the blood stream to the lungs where it is exhaled. The test is considered positive if
the concentration of hydrogen in the exhaled breath rises to 20ppm.
About 10% of the population have no hydrogen producing bacteria in their intestine. For these
patients the test can be done by measuring the methane in the exhaled air.
The best indication for a symptomatic fructose malabsorption is the disappearance of digestional
problems during an exclusion diet. A fructose malabsorption can be assumed if after 4 weeks
without dietary fructose the symptoms have disappeared.
Diet
The first step is a 4 week long strictly fructose-free diet. This should help to bring the digestion
system into balance again. After this period increasing amounts of fructose can be introduced into
the diet. Every patient should test how much fructose he/she can tolerate without suffering from
symptoms. It is recommendable to eat as much fructose as tolerated if the source is natural because
the absorption capacity for fructose can decline if the GLUT-5 transporter is not used (no fructose is
ingested).
Generally foods with high fructose corn syrup (HFCS) or table sugar should be avoided when
dealing with fructose malabsorption. [Link]Here[/Link] is a list of foods and their fructose, glucose,
sucrose and sorbitol contents. As a rule of thumb foods with a balanced amount of fructose and
glucose are generally well tolerated. This may not be true for all patients suffering from fructose
malabsorption because some even develop symptoms from small amounts of table sugar which is
chemically an equimolar mixture of glucose and fructose. Sorbitol should be avoided as it
temporarily reduces the absorption capacity of fructose.
For the composition of a detailed diet sheet a nutritionist should be consulted. Very often dietary
supplements are needed to ensure an optimal supply of the patient with vitamins and trace
elements.
Fructose Malabsorption: A Possible Factor in Functional Bowel Disorders
Sheri Helms, PharmD Director of Professional Program Laboratories Purdue University College of Pharmacy West Lafayette, Indiana
Fang Z. Ni, PharmD
Rutgers Pharmaceutical Industry Fellow Rutgers University New Brunswick, New Jersey
Patricia L. Darbishire, PharmD Clinical Associate Professor of Pharmacy Practice Director of Introductory Pharmacy Practice Experience Purdue University College of Pharmacy West Lafayette, Indiana
12/20/2011 US Pharm. 2011;36(12):41-44.
Functional bowel disorders (FBDs) are gastrointestinal (GI) disorders related to the middle or lower GI tract that lack identifiable pathoetiology.
bloating, constipation, and/or diarrhea; and other unspecified chronic bowel disorders.1 Hadler et al reported FBDs in
up to 40% of the community.3 In 2004, it was estimated that 4 out of every 100 emergency department visits were
due to FBDs, accounting for more than 11 million visits.2 In a study of 3,933 subjects, 18% reported chronic diarrhea,
16% chronic constipation, 15% abdominal pain, 10% symptoms of IBS, and 2% dyspepsia. The economic burden is estimated to be as high as $1.6 billion for IBS and $621 million for chronic diarrhea.
4
Functional Bowel Disorders
Irritable Bowel Syndrome: Despite the research dedicated to IBS, there is little known about its cause or development process. The most recent comprehensive prevalence study, conducted in 2002, found that IBS occurred in 3% to 20% of North Americans.
5 IBS is a similar issue globally in both developed and developing countries.
6 Chang
et al estimated that in 1 year, IBS accounted for 500,000 inpatient hospital stays.7 Women reported an incidence of
2:1 compared to men.5 Triggers for IBS include stress, hormonal fluctuations, and certain foods, including chocolate,
alcohol, carbonated beverages, fruits, and vegetables.5,8
Diagnosis is predominantly based on symptoms, defined as abdominal pain and altered bowel activity with no organic origin.
5
IBS affects the large intestine, causing cramping, abdominal pain, bloating, gas, diarrhea, and constipation. It is classified into several subtypes: diarrhea (IBS-D), constipation (IBS-C), and a mixed subtype (IBS-M). Fortunately, IBS does not cause permanent damage to the colon and few people have disabling symptoms. IBS is generally managed through diet, lifestyle changes, and stress reduction techniques. When these techniques fail, symptom-based pharmacotherapy is employed. Constipation may be treated with prokinetic agents, while diarrhea may be treated with antispasmodics, opioids, 5-HT3 antagonists, and/or anticholinergics.
5
Recurrent Abdominal Pain: RAP is another major form of FBD that is common in children. It is considered pain severe enough to interfere with normal functioning at least once per month for 3 consecutive months.
9 For decades,
the pathophysiology of RAP has remained unclear. The original research and defining of RAP came from a British pediatrician, John Apley, MD. In establishing the definition of RAP, Apley and Naish surveyed 1,000 primary and secondary school children.
9 Approximately 11% of the children met the criteria for RAP. Another study conducted by
Hyams et al evaluated 507 adolescents in an American suburban area.10
Of the adolescents studied, approximately 15% experienced abdominal pain on a weekly basis. However, only half sought medical attention, implying the potential for a higher rate of occurrence than seen in clinical practice.
11 Many pediatricians treat RAP predominantly
with emotional support and reassurance for the family that no serious disease is present.12
Fructose Malabsorption
One area gaining interest with those who study FBD is fructose malabsorption, a condition characterized by gas, bloating, discomfort, nausea, disturbed bowel function, and occasionally gastroesophageal reflux (TABLE 1).
13 During fructose malabsorption, the small intestines are unable to fully absorb ingested fructose, leading to
increased osmotic load and bacterial fermentation, as well as promotion of mucosal biofilm formation.14
This is
distinguished from fructose intolerance, a hereditary disease caused by a mutation in the aldolase B gene that renders patients unable to metabolize fructose. This metabolic disease may result in hepatic and renal injury, growth retardation, and, in severe cases, even death.
15-17
Fructose, the sweetest of all naturally occurring sugars, is found in four primary forms: a naturally occurring free fructose (FIGURE 1), as a constituent of sucrose (FIGURE 2), as a polymer, and in an enzymatically produced form. Free fructose makes up as much as 35% by weight of honey and fruits such as apples, pears, and cherries (TABLE 2). Prior to the advent of food-processing technology in the 1960s, honey and fruits were the main dietary sources of
fructose.18
Since that time, technology has led to the use of alternatives, including sucrose (a disaccharide of fructose and glucose commonly known as table sugar) and high-fructose corn syrup or HFCS (a monosaccharide
enzymatically produced from corn). Today HFCS is commonly found in a variety of beverages and baked goods, as well as in canned and processed foods.
19,20
The availability of inexpensive, tasty, fructose-laden products makes reducing or eliminating fructose from the diet difficult. According to the U.S. Agriculture Fact Book, HFCS consumption increased from 16% to 42% of total sweetener consumption between the years 1978 and 1999.
21,22 In addition to its effect on the GI tract, a recent study
by Stanhope et al evaluating the health consequences of excessive HFCS consumption found an increase in postprandial triglycerides, low-density lipoprotein (LDL) cholesterol, and other coronary heart disease risk factors after 2 weeks of consuming fructose- or HFCS-sweetened beverages (as 25% of their total daily energy requirement).
23 Furthermore, the authors discovered a decrease in postprandial glucose and insulin response
following fructose consumption. These findings confirm that side effects of long-term, sugar-sweetened beverage consumption can be attributed to specific properties of fructose.
23,24
Pathophysiology of Fructose Malabsorption
Fructose empties more rapidly from the stomach in comparison to other sugars, utilizing an energy-dependent absorption process in the small intestines. GLUT5 and GLUT2 are transmembrane proteins primarily located in the lumen of the small intestines that are responsible for the transportation of fructose. GLUT5 transports fructose from the intestinal lumen into enterocytes by a facilitated energy-dependent process. Therefore, saturation of GLUT5 transporters with excessive fructose ingestion results in incomplete absorption, leading to GI symptoms (TABLE 1).
25 This transport-mediated process is limited in carrier capacity, calculated to be approximately 15 g of fructose per
consumption. Fructose absorption occurs along with glucose via solvent drag and passive diffusion. Due to its osmotic effect, unabsorbed fructose combines with water and is rapidly propelled into the colonic lumen where luminal bacteria ferment fructose to carbon dioxide, hydrogen, and short-chain fatty acids. This osmotic load has a laxative effect and causes rapid gas production, leading to luminal distention, bloating, abdominal discomfort, and increased motility.
19
Assessment of Dietary Fructose Intake
The hydrogen breath test is the foundational diagnostic assessment for identification of dietary fructose malabsorption.
26 One description of this test comes from a study conducted by Choi et al of 183 patients with
unexplained chronic abdominal pain.27
Subjects were asked to refrain from consuming foods containing high fat, lactose, or fructose for 1 day prior to testing and to fast after midnight. Subjects were asked to blow into a modified bag in order to collect a 50 mL end-expiratory breath sample. The sample was injected into a gas chromatography analyzer to measure baseline values for hydrogen and methane. The subjects were then asked to drink a 33% fructose solution. Breath samples were analyzed at 30-minute intervals for 5 hours. Based on the amount of fructose that escaped absorption in the small intestines, commensal flora in the large intestines metabolized the fructose and released hydrogen and methane consequently.
28 A positive breath test was inferred in subjects with a rise in breath
hydrogen and/or methane of at least 3 parts per million (ppm) over three consecutive breath samples from the baseline value or from having a value 20 ppm above baseline.
27
The pitfall of the hydrogen breath test in diagnosis of fructose malabsorption is that 28% of the population does not expel hydrogen through the lungs and/or does not have hydrogen-producing bacteria inhabiting the GI tract.
14 In such
patients, fructose malabsorption is often undiagnosed due to lack of an alternative diagnostic test.
In the Choi et al study, fructose malabsorption was discovered in 39% of the 183 patients who had consumed 25 g of fructose and in 66% of the patients who had consumed 50 g of fructose, with 73% of total patients having a positive hydrogen breath test.
27 To put these quantities of fructose in perspective, depending on the type of corn syrup
sweetener used, one 22-oz soft drink contains approximately 30 to 40 g of fructose.
Fructose Malabsorption in IBS
One in three adults with IBS presents with the inability to absorb fructose in 25- to 50-g increments. However, fructose malabsorption is not limited to patients with IBS. Although GI symptoms associated with fructose malabsorption are generally magnified (TABLE 1), the perception that fructose does not play a major role in patients
with IBS often leads to a lack of treatment.19
Fructose-Restricted Diet
International consensus on treatment of traditional IBS starts with increased fiber intake as first-line therapy.
29 However, there are no published guidelines to assist the patient with fructose malabsorption in constructing
a manageable diet.11
Despite the lack of specific guidelines, three separate studies demonstrated that identification and dietary monitoring of fructose consumption in patients with fructose malabsorption was clinically significant in reducing abdominal symptoms.
19,30,31 For instance, in the Choi et al study, 31 patients with positive hydrogen breath tests received verbal
and written instructions on fructose restriction or exclusion, and then were followed up to 1 year later. Fourteen of the subjects were considered compliant patients and experienced a statistically significant reduction in abdominal pain, belching, bloating, fullness, indigestion, and diarrhea symptom scores compared to baseline 1 year prior.
27
In another study, Fernandez-Banares et al found that when given recommendations to eliminate all foods with free fructose, patients showed clinical symptom improvement after just 1 month of dietary adjustment. Furthermore, a group of these patients continued to have symptomatic improvement for up to 1 year later.
32
These two studies demonstrate positive impact on clinical symptoms with dietary intervention.27,32
Lack of guidelines on fructose restriction in patients suffering from fructose malabsorption should not deter pharmacists from making such dietary recommendations.
Role of the Pharmacist
As a member of the health care team, pharmacists need to be aware of the common symptoms of fructose malabsorption, in addition to the foods that contain high amounts of fructose.
19,33 Although the normal capacity for
absorption of fructose is unknown, in general, consumption of fructose in excess of 15 to 25 g in one sitting can lead
to malabsorption and FBDs.12,19
Recommendations to substitute foods and beverages containing high amounts of fructose for those containing lower amounts (TABLE 3) can be helpful to patients suffering from fructose
malabsorption symptoms. Pharmacists should encourage patients to focus on food alternatives. Realistic goals can positively impact symptoms and improve quality of life.
27 Patients should be encouraged to consult with a registered
dietitian if they are unable to self-manage dietary needs.
1491. 2. Porter CK, Gormley R, Tribble DR, et al. The incidence and gastrointestinal infectious risk of functional gastrointestinal disorders in a healthy US adult population. Am J Gastroenterol. 2011;106:130-138. 3. Hadler SL, Locke GR III, Chleck CD, et al. Natural history of functional gastrointestinal disorders: a 12-year longitudinal population-based study. Gastroenterology. 2007;133:799-807. 4. Lembo AJ. The clinical and economic burden of irritable bowel syndrome. Pract Gastroenterol. 2007;31(suppl)3-9. 5. Grundmann O, Yoon SL. Irritable bowel syndrome: epidemiology, diagnosis and treatment: an update for health-care practitioners. J Gastroenterol Hepatol. 2010;25:691-699. 6. Tally NJ. Functional gastrointestinal disorders as a public health problem. Neurogastroenterol Motil. 2008;20(suppl 1):121-129. 7. Chang JY, Locke GR, McNally MA, et al. Impact of functional gastrointestinal disorders on survival in the community. Am J Gastroenterol. 2010;105:822-832. 8. Chang L. The role of stress on physiologic responses and clinical symptoms in irritable bowel syndrome. Gastroenterology. 2011;140:761-765. 9. Apley J, Naish N. Recurrent abdominal pains: a field survey of 1,000 school children. Arch Dis Child. 1958;33:165-170. 10. Hyams JS, Burke G, Davis PM, et al. Abdominal pain and irritable bowel syndrome in adolescents: a community-based study. J Pediatr. 1996:129:220-226. 11. Rao SS, Attaluri A, Anderson L, Stumbo P. The ability of the normal human small intestine to absorb fructose: evaluation of breath testing. Clin Gastroenterol Hepatol. 2007;5:959-963. 12. Weydert JA, Ball TM, Davis MF. Systemic review of treatments for recurrent abdominal pain. Pediatrics. 2003;111:e1-e11. 13. Piche T, Des Varannes SB, Sacher-Huvelin S, et al. Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease. Gastroenterology. 2003;124:894-902. 14. Gibson PR, Newnham E, Barrett JS, et al. Review article: fructose malabsorption and the bigger picture. Aliment Pharmacol Ther. 2007;25:349-363. 15. Wong D. Hereditary fructose intolerance. Mol Genet Metab. 2005;85:165-167. 16. Ali M, Rellos P, Cox TM. Hereditary fructose intolerance. J Med Genet. 1998;35:353-365. 17. Bouteldja N, Timson DJ. The biochemical basis of hereditary fructose intolerance. J Inherit Metab
Dis. 2010;33:105-112. 18. Hanover LM, White JS. Manufacturing, composition and applications of fructose. Am J Clin Nutr. 1993;58(suppl):724S-732S. 19. Shepherd SJ, Gibson PR. Fructose malabsorption and symptoms of irritable bowel syndrome: guidelines for effective dietary management. J Am Diet Assoc. 2006;106:1631-1639. 20. Skoog SM, Bharucha AE. Dietary fructose and gastrointestinal symptoms: a review. Am J Gastroenterol. 2004;99:2046-2050. 21. Agriculture Fact Book 2000. Washington, DC: U.S. Department of Agriculture; 2000:314.
www.usda.gov/news/pubs/ fbook00/factbook2000.pdf. Accessed September 9, 2011.
22. Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr. 2009;139:1228S-1235S. 23. Stanhope KL, Bremer AA, Medici V, et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. J Clin Endocrinol
Metab. 2011;96:E1596-E1605. 24. Hu FB, Malik VS. Sugar-sweetened beverages and risk of obesity and type 2 diabetes: epidemiologic evidence. Physiol Behav. 2010;100:47-54. 25. Douard V, Ferraris RP. Regulation of the fructose transporter GLUT5 in health and disease. Am J Physiol Endocriol Metab. 2008;295:E227-E237. 26. Romagnuolo JM, Schiller D, Bailey RJ. Using breath tests wisely in a gastroenterological practice: an evidence based review of indications and pitfalls in interpretation. Am J Gastroenterol. 2002;97:1113-1126. 27. Choi YK, Johlin FC, Summers RW, et al. Fructose intolerance: an under-recognized problem. Am J Gastroenterol. 2003;98:1348-1353. 28. Jones HF, Butler RN, Brooks DA. Intestinal fructose transport and malabsorption in humans. Am J Physiol Gastrointest Liver Physiol. 2011;300:G202-G206. 29. DecisionBase. Irritable Bowel Syndrome: A New Therapy for Non-Constipation-Predominant IBS With Greatly Improved Efficacy Will Reach Near-Blockbuster Status. Decision Resources. Inc. March 2010.
http://decisionresources.com/ Products-and-Services/Report? r=dbaspd2510. Accessed September 9, 2011.
30. Choi YK, Kraft N, Zimmerman B, et al. Fructose intolerance in IBS and utility of fructose-restricted diet. J Clin Gastroenterol. 2008;42:233-238. 31. Johlin FC Jr, Panther M, Kraft N. Dietary fructose intolerance: diet modification can impact self-rated health and symptom control. Nutr Clin Care. 2004;7:92-97. 32. Fernandez-Banares F, Rosinach M, Esteve M, et al. Sugar malabsorption in functional abdominal bloating: a pilot study on the long-term effect of dietary treatment. Clin Nutr. 2006;25:824-831.
33. Nutrition Data Laboratory. USDA. www.nal.usda.gov/fnic/ foodcomp/search/. Accessed September 9, 2011
Fructose malabsorption
Fructose malabsorption
Classification and external resources
Fructose
ICD-10 E74.3
ICD-9 271
OMIM 138230
Fructose malabsorption, formerly named "dietary fructose intolerance" (DFI), is a digestive disorder[1] in which absorption of fructose is impaired by deficient fructose carriers in the small intestine's enterocytes. This results in an increased concentration of fructose in the entire intestine.
Occurrence in patients identified to be suffering symptoms of irritable bowel syndrome is not higher than occurrence in the normal population. However, due to the similarity in symptoms, patients with fructose malabsorption often fit the profile of those with irritable bowel syndrome.[2] A small proportion of patients with both fructose malabsorption and lactose intolerance also suffer from celiac disease.
Fructose malabsorption is not to be confused with hereditary fructose intolerance, a potentially fatal condition in which the liver enzymes that break up fructose are deficient.
Pathophysiology
Fructose is absorbed in the small intestine without help of digestive enzymes. Even in healthy persons, however, only about 25–50g of fructose per sitting can be properly absorbed. People with
fructose malabsorption absorb less than 25g per sitting.[3] In the large intestine, fructose that has not been adequately absorbed reduces the absorption of water osmotically and is metabolized by colonic bacteria into short chain fatty acids, producing the byproduct gases hydrogen, carbon dioxide and methane.[citation needed] This abnormal increase in hydrogen is detectable with the hydrogen breath test.
The physiological consequences of fructose malabsorption include increased osmotic load, rapid bacterial fermentation, altered gastrointestinal motility, the formation of mucosal biofilm and altered profile of bacteria. These effects are additive with other short-chain poorly absorbed carbohydrates such as sorbitol. The clinical significance of these events depends upon the response of the bowel to such changes. Some effects of fructose malabsorption are decreased tryptophan,[4] folic acid[5] and zinc in the blood.[5]
Restricting dietary intake of free fructose and/or fructans may provide symptom relief in a high proportion of patients with functional gut disorders.[6]
Symptoms
Bloating (from fermentation in the small and large intestine)
Diarrhea and/or constipation
Flatulence
Reflux
Stomach pain (as a result of muscle spasms, the intensity of which can vary from mild and chronic to acute but erratic)
Vomiting (if great quantities are consumed)
Early signs of mental depression[7]
Nausea
Diagnosis
The diagnostic test, when used, is similar to that used to diagnose lactose intolerance. It is called a hydrogen breath test and is the method currently used for a clinical diagnosis.
Treatment
There is no known cure, but an appropriate diet and the enzyme xylose isomerase can help.
Xylose isomerase
Xylose isomerase acts to convert fructose sugars into glucose. Dietary supplements are limited in the amount of fructose they can convert, thus the amount of fructose in a meal must be estimated and an appropriate dosage taken to work.[citation needed]
Diet
Foods that should be avoided by people with fructose malabsorption include:
Foods and beverages containing greater than 0.5 g fructose in excess of glucose per 100 g and greater than 0.2 g of fructans per serving should be avoided. Foods with >3 g of fructose per serving are termed a 'high fructose load' and possibly present a risk of inducing symptoms. However, the concept of a 'high fructose load' has not been evaluated in terms of its importance in the success of the diet.[8]
Foods with high fructose-to-glucose ratio. Glucose enhances absorption of fructose, so fructose from foods with fructose-to-glucose ratio <1, like white potatoes, are readily absorbed, whereas foods with fructose-to-glucose ratio >1, like apples and pears, are often problematic regardless of the total amount of fructose in the food.[9]
Foods rich in fructans and other fermentable oligo-, di- and mono-saccharides and polyols (FODMAPs), including artichokes, asparagus, leeks, onions, and wheat-containing products, including breads, cakes, biscuits, breakfast cereals, pies, pastas, pizzas, and wheat noodles.
Foods containing sorbitol, present in some diet drinks and foods, and occurring naturally in some stone fruits, or xylitol, present in some berries, and other polyols (sugar alcohols), such as erythritol, mannitol, and other ingredients that end with -tol, commonly added as artificial sweeteners in commercial foods.
Foods with a high glucose content ingested with foods containing excess fructose may help sufferers absorb the excess fructose.[10]
The role that fructans play in fructose malabsorption is still under investigation. However, it is recommended that fructan intake for fructose malabsorbers should be kept to less than 0.5 grams/serving,[11] and supplements with inulin and fructooligosaccharide (FOS), both fructans, should be avoided.[11]
Foods with high fructose content[edit]
According to the USDA database,[12] foods with more fructose than glucose include:
The USDA food database reveals that many common fruits contain nearly equal amounts of the fructose and glucose, and they do not present problems for those individuals with fructose malabsorption.[13] Some fruits with a greater ratio of fructose than glucose are apples, pears and watermelon, which contain more than twice as much fructose as glucose. Fructose levels in grapes varies depending on ripeness and variety, where unripe grapes contain more glucose.
Dietary guidelines for the management of fructose malabsorption[edit]
Researchers at Monash University in Australia developed dietary guidelines[11] for managing fructose malabsorption, particularly for individuals with IBS.
Unfavorable foods (i.e. more fructose than glucose)[edit]
Fruit – apple, pear, guava, honeydew melon, nashi pear, pawpaw, papaya, quince, star fruit, watermelon;
Dried fruit – apple, currant, date, fig, pear, raisin, sultana;
Fortified wines
Foods containing added sugars, such as agave nectar, some corn syrups, and fruit juice concentrates.
Favorable foods (i.e. fructose equal to or less than glucose)[edit]
The following list of favorable foods was cited in the paper: "Fructose malabsorption and symptoms of Irritable Bowel Syndrome Guidelines for effective dietary management".[11] The fructose and glucose contents of foods listed on the Australian food standards[14]would appear to indicate that most of the listed foods have higher fructose levels.
Stone fruit: apricot, nectarine, peach, plum (caution — these fruits contain sorbitol);
Producers of processed food in most or all countries, including the USA, are not currently required by law to mark foods containing "fructose in excess of glucose." This can cause some surprises and pitfalls for fructose malabsorbers.
Foods (such as bread) marked "gluten-free" are usually suitable for fructose malabsorbers, though sufferers need to be careful of gluten-free foods that contain dried fruit or high fructose corn syrup or fructose itself in sugar form. However, fructose malabsorbers donot need to avoid gluten, as those with celiac disease must.
Many fructose malabsorbers can eat breads made from rye and corn flour. However, these may contain wheat unless marked "wheat-free" (or "gluten-free") (Note: Rye bread is not gluten-free.) Although often assumed to be an acceptable alternative to wheat, spelt flour is not suitable for sufferers of fructose malabsorption[citation needed], just as it is not appropriate for those with wheat allergies or celiac disease. However, some fructose malabsorbers do not have difficulty with fructans from wheat products while they may have problems with foods that contain excess free fructose.[citation
needed]
There are many breads on the market that boast having no high fructose corn syrup. In lieu of high fructose corn syrup, however, one may find the production of special breads with a high inulin content, where inulin is a replacement in the baking process for the following: high fructose corn syrup, flour and fat. Because of the caloric reduction, lower fat content, dramatic fiber increase and prebiotic tendencies of the replacement inulin, these breads are considered a healthier alternative to traditionally prepared leaveningbreads. Though the touted health benefits may exist, sufferers of fructose malabsorption will likely find no difference between these new breads and traditionally prepared breads in alleviating their symptoms because inulin is a fructan, and, again, consumption of fructans should be reduced dramatically in those with fructose malabsorption in an effort to appease symptoms.
New research
Fructose and fructans which are polymers of fructose are FODMAPs (Fermentable Oligo-, Di- and Mono-saccharides and Polyols) known to cause gastrointestinal discomfort in susceptible individuals. A low FODMAP diet has widespread application for managing functional gastrointestinal disorders such as IBS.[8]
See also
Hereditary fructose intolerance
FODMAP
Gastroenterology
Hydrogen breath test
Invisible disability
Food intolerance
Irritable bowel syndrome
Malabsorption
References
1. MayoClinic.com
2. Ledochowski M, et al. (2001). "Fruktosemalabsorption". Journal für Ernährungsmedizin (in German) 3 (1): 15–19.
4. Ledochowski M, Widner B, Murr C, Sperner-Unterweger B, Fuchs D (2001). "Fructose malabsorption is associated with decreased plasma tryptophan". Scand. J. Gastroenterol. 36 (4): 367–71. doi:10.1080/003655201300051135. PMID 11336160.
5. ^ Jump up to:a b Ledochowski M, Uberall F, Propst T, Fuchs D (1999). "Fructose malabsorption is associated with lower plasma folic acid concentrations in middle-aged subjects". Clin. Chem. 45 (11): 2013–4. PMID 10545075.
6. Gibson PR, Newnham E, Barrett JS, Shepherd SJ, Muir JG (2007). "Review article: fructose malabsorption and the bigger picture".Aliment. Pharmacol. Ther. 25 (4): 349–63. doi:10.1111/j.1365-2036.2006.03186.x. PMID 17217453.
7. Ledochowski M, Sperner-Unterweger B, Widner B, Fuchs D. (2010). "Fructose malabsorption is associated with early signs of mental depression.". European Journal of Medical Research 3 (6): 295–8. PMID 9620891.
8. ^ Jump up to:a b Gibson PR, Shepherd SJ (2010). "Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach". Advances in Clinical Practice 25 (2): 252–8. doi:10.1111/j.1440-1746.2009.06149.x. PMID 20136989.
10. Skoog SM, Bharucha AE (2004). "Dietary fructose and gastrointestinal symptoms: a review". Am. J. Gastroenterol. 99 (10): 2046–50.doi:10.1111/j.1572-0241.2004.40266.x. PMID 15447771.
11. ^ b c d Shepherd SJ, Gibson PR (2006). "Fructose malabsorption and symptoms of irritable bowel syndrome: guidelines for effective dietary management" (PDF). Journal of the American Dietetic Association 106 (10): 1631–9. doi:10.1016/j.jada.2006.07.010.PMID 17000196.
12. USDA National Nutrient Database Release 20, September 2007
13. Sugar Content of Selected Foods: Individual and Total Sugars Ruth H. Matthews, Pamela R. Pehrsson, and Mojgan Farhat-Sabet, (1987) U.S.D.A.
14. "NUTTAB 2010 Online Searchable Database". Food Standards Australia New Zealand. Archived from the original on 2012-03-24. Retrieved 7 July 2013.
Use and abuse of hydrogen breath tests
M Simrén and P‐O Stotzer
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This article has been cited by other articles in PMC.
Abstract
Within the field of gastroenterology, the majority of symptoms cannot be explained by structural
abnormalities detected on routine investigations.1 Many of these symptoms are clustered together
forming the functional gastrointestinal disorders, as defined by the Rome II criteria.2,3 The
pathophysiology behind these disorders is still incompletely known.4 In the search for possible
pathophysiological factors of functional gastrointestinal disorders, several authors have used
different hydrogen breath tests in recent years to detect various abnormalities, such as
carbohydrate malabsorption5,6,7 and small intestinal bacterial overgrowth (SIBO).8,9 However,
these tests are indirect, with several drawbacks and pitfalls. In this article, we will review the