Insights
We want you to be totally informed before choosing to use our products.
JK Labs was founded on the belief that placing our customer’s health, safety and wellbeing should be at the heart of everything we do. And this ethos has been our core value in the pursuit of developing Dietary Enzyme Therapies that can make a difference to our lives today; so that instead of just surviving, you are thriving.
We invite you to join us on this remarkable journey towards optimal management of symptoms and freedom to enjoying food again.
What Is Fructose Malabsorption
Fructose is a simple sugar, known as a monosaccharide, that comes mostly from fruit and some vegetables. It’s also found in honey, agave nectar, and many processed foods that contain added sugars.
The consumption of fructose from high fructose corn syrup has increased over 1,000 percent just from 1970–1990. It’s possible that this rise in consumption has led to an increase in fructose malabsorption and intolerance.
Fructose exists in foods either as a monosaccharide (free fructose) or as a unit of a disaccharide (sucrose). Free fructose is absorbed directly by the intestine. When fructose is consumed in the form of sucrose, it is digested (broken down) and then absorbed as free fructose. As sucrose comes into contact with the membrane of the small intestine, the enzyme sucrase catalyzes the cleavage of sucrose to yield one glucose unit and one fructose unit, which are then each absorbed. After absorption, it enters the hepatic portal vein and is directed toward the liver.
The mechanism of fructose absorption in the small intestine is not completely understood. The majority of research supports the claim that fructose absorption occurs on the mucosal membrane via facilitated transport involving GLUT5 transport proteins. Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins. Fructose may be transported out of the enterocyte across the basolateral membrane by either GLUT2 or GLUT5, although the GLUT2 transporter has a greater capacity for transporting fructose.
Fructose Malabsorption
Fructose malabsorption is a digestive disorder in which the absorption of fructose in the small intestine is impaired. This leads to several abdominal symptoms like bloating, pain, nausea and cramps. For sometime, the public didn’t know of this disease and physicians often overlooked it. Today we know, that almost 40% of the population are suffering from some kind of fructose malabsorption, 30% of these people show the typical symptoms, such as nausea, bloating, gas, abdominal pain, diarrhea, vomiting, chronic fatigue and malabsorption of certain nutrients, such as iron.
Fructose malabsorption is sometimes called “fructose intolerance”. This term is misleading, as there is a disease called Hereditary Fructose Intolerance (HFI) which is even more serious. HFI is a genetic defect causes a deficiency in the fructose-1-phosphate aldolase B activity, and should NOT be confused with Fructose Malabsorption. This deficiency leads to the accumulation of fructose-1-phosphate, a derivative of fructose, within the liver. And this, in turn, causes severe toxic symptoms after fructose ingestion, such as serious hypoglycemia with tremors, vomiting and disorientation. In the worst case, it can lead to convulsion and coma. Dietary Enzyme Therapy is strongly NOT recommended for HFI sufferers.
If you have certain gut disorders such as IBS, Crohn’s disease, colitis, or celiac disease, you’re more likely to have dietary fructose malabsorption or intolerance.
However, whether one causes the other is unclear. In a study that involved 209 patients with IBS, about one-third had fructose malabsorption. Those who were compliant with restricting fructose saw improvement in symptoms. In addition, if you’re on a gluten-free diet but still having symptoms, you may be having trouble with fructose. It’s never a bad idea to get checked for fructose malabsorption if you have a major gut issue.
What happens in case of Fructose Malabsorption?
In the case of fructose malabsorption the protein GLUT5, which is involved in the absorption of fructose along the entire small intestine, is impaired. Meaning the absorption of fructose is reduced. The remaining fructose reaches the colon and is rapidly fermented by intestinal bacteria, as shown in the figure above. This bacterial fermentation results in the formation of hydrogen, carbon dioxide, methane and short-chain fatty acids (e.g. butyric and acetic), which causes abdominal symptoms like bloating, pain, and cramps.
Furthermore, untreated fructose malabsorption leads to a proliferation of intestinal bacteria and yeast, which metabolize the fructose. This worsens the symptoms over time. The amount of tolerated fructose varies greatly among FrucMals. Some people may be able to ingest modest amounts of fructose without experiencing any problems, while others show symptoms even after very small amounts.
Diagnosis
A hydrogen breath test is a common test used to diagnose issues with digesting fructose. It’s a simple test that doesn’t involve a blood draw. You’re required to limit carbohydrates the night before and fast the morning of the test, this is very important as the consumption of carbohydrates can give false positives/negatives.
At a clinic, you’re given a high fructose solution to drink, and then every 20 to 30 minutes for several hours your breath is analyzed. The whole test lasts about three hours. When fructose is unabsorbed, it produces higher amounts of hydrogen in the intestines. This test measures how much hydrogen is on your breath from this malabsorption.
Eliminating fructose from your diet is another way to tell if you have fructose malabsorption. With the help of a registered dietitian, you can develop a plan to effectively remove any foods containing fructose and see if your symptoms resolve.
Different people have different tolerances for fructose. Some may be more severe than others. Keeping a food journal can help to track the foods you’ve eaten and any symptoms you have.
Tips on how to manage Fructose Malabsorption
If you suspect you may have a fructose malabsorption, you should consult with a gastroenterologist and/or dietitian. There is a couple of options to help address and manage your symptoms.
Enzyme therapy: Utilising a digestive enzyme called Xylose Isomerase, this enzyme specifically designed to break down fructose into glucose, (fructose is commonly found in many fruits and some vegetables). Reducing such symptoms as gas, bloating, indigestion, and diarrhea associated with fructose malabsorption. Just remember, everything in moderation is the key when taking digestive enzymes, its not a green light to eat your body weight in fructose rich foods.
Elimination Diet: A medical professional may design an exclusion diet in which you avoid food containing fructose for a limited period to see whether the symptoms go away. After the initial elimination of fructose, you should gradually add fructose-containing foods back into your diet one at a time to determine your individual intolerance. You should keep a diet and symptoms diary so that you can analyse the results obtained from eating different foods.
The low-FODMAP diet approach developed by Melbourne’s Monash University works in the same way. The idea is not to eliminate all FODMAPs from the diet forever, but ascertain the impact of each one and find a comfortable intake level as part of a balanced diet.
Before undertaking major changes to your diet, it is important to seek advice from your doctor and/or a dietitian to ensure that you are always eating a diet that is right for your nutritional needs.
2018 Clinical study of Intestinal Absorption of Fructose
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457363/
2024 Clinical study of Fructose/Fructan Malabsorption associated IBS
What Is Fructan Intolerance
Fructans and galactans are long carbohydrate chains of about 3 to 9 carbohydrate molecules. Fructans are also called fructooligosaccharides (FOS) and gallactans galactooligosaccharides (GOS).
Oligosaccharides belong to the non-digestible carbohydrates. These carbohydrates cannot be broken down in the small intestine and leave the body through the large intestine. In the colon, these undigested carbohydrates are fermented, releasing gas and attracting fluid, among other things.
No one can digest fructans and galactans properly, the difference is in the amount of symptoms you get as a result of the fermentation process. Our focus here is on fructan or galactan intolerance when someone suffers greatly from the fermentation process. It can differ from person to person whether someone only reacts to fructans or galactans, or to both types of oligosaccharides.
Note that fructan intolerance is not the same as fructose malabsorption or a fructose “allergy.” This is caused by a reaction to the units that make up fructans, which are a form of simple sugars known as fructose. Although they can cause similar symptoms, the main difference between fructan vs. fructose is that fructose is found primarily in fruits, fruit juices, agave nectar, honey, molasses, table sugar and high fructose corn syrup, while fructans are found in certain types of grains, vegetables and processed foods.
It’s also important to remember that a sensitivity to fructans is not the same as small bacterial overgrowth, or SIBO. This is a condition characterized by an excessive amount of bacteria in the small intestine, which can cause issues like diarrhea and malabsorption if left untreated. With a fructan intolerance, the main problem isn’t your gut bacteria, but the way that your body handles fructans.
Fructan Intolerance
The causes of fructan intolerance are not well understood. Some people seem to have less capacity than others to digest and absorb fructans into their bloodstream, and others experience stronger symptoms than others as a result of the fermenting of the unabsorbed sugars. A few of the most common high-fructan foods include: Barley, Rye, Wheat, Spelt, Cabbage, Fennel, Garlic, Leeks, Onions, Peas, Asparagus, Chickpeas, Lentils, Beans, and Soybeans.
If you experience such symptoms on a regular basis, it is a good idea to discuss them with a doctor. Diagnosis of fructan intolerance is still in its infancy, but, as with other intolerances of sugars such as fructose intolerance, breath tests can sometimes be used to measure the content of gases that are produced when fructans are fermented in the gut, but the results are no guarantee of a correct diagnosis.
Properly identifying your symptoms can also aid in diagnosis. An intolerance to fructans can cause many symptoms, which may include: Gas, Bloating, Stomach pain, Constipation, Diarrhea, Abdominal discomfort, Nausea and Cramps.
If you suffer from these symptoms, reducing your intake of fructans. Trying out a fructan elimination diet can also help determine if you may have a sensitivity to foods high in fructans.
What happens in case of Fructan Intolerance?
As all humans are unable to absorb fructans as part of the normal digestive process (which happens in the small intestine), these sugars will always arrive intact in the large intestine. However, your unique gut microbiome composition will determine how much fermentation will happen and what happens to the gas afterward. Some bacteria like to consume hydrogen and make other important products. A rapid build-up of gas can be quite debilitating for those with a sensitive gut.
Symptoms may appear several hours after meals and last for over 24 hours, generally the body can only absorb 5-15 percent of fructans and can often result in bloating, gas, and abdominal pain. It is important to identify your unique tolerance levels, as this can vary considerably from person to person.
Diagnosis
Diagnosis of fructan intolerance is still in its infancy, but, as with other intolerances of sugars such as fructose malabsorption, breath tests can sometimes be used to measure the content of gases that are produced when fructans are fermented in the gut, but the results are no guarantee of a correct diagnosis.
At a clinic, you’re given a high fructan solution to drink, and then every 20 to 30 minutes for several hours your breath is analyzed. The whole test lasts about three hours. When fructan is unabsorbed, it produces higher amounts of hydrogen in the intestines. You’re required to limit carbohydrates the night before and fast the morning of the test, this is very important as the consumption of carbohydrates can give false positives/negatives.
Eliminating fructan from your diet is another way to tell if you have fructan intolerance. With the help of a registered dietitian, you can develop a plan to effectively remove any foods containing fructose and see if your symptoms resolve. This type of elimination diet is call the FODMAP diet and is considered to be the gold standard when diagnosing dietary intolerances.
Tips on how to manage Fructan Intolerance
If you suspect you may have a fructan intolerance, you should consult with a gastroenterologist and/or dietitian. There is a couple of options to help address and manage your symptoms.
Enzyme therapy: utilising a digestive enzyme called Alpha Galactosidase, this enzyme aids in the digestion of complex carbohydrates found in grains, legumes, and cruciferous vegetables. Reducing such symptoms as gas, bloating, indigestion, and diarrhea associated with fructans and galactans intolerance. Just remember, everything in moderation is the key when taking digestive enzymes, its not a green light to eat your body weight in onions and garlic.
Elimination Diet: A medical professional may design an exclusion diet in which you avoid food containing fructans for a limited period to see whether the symptoms go away. After the initial elimination of fructans, you should gradually add fructan-containing foods back into your diet one at a time to determine your individual intolerance. You should keep a diet and symptoms diary so that you can analyse the results obtained from eating different foods.
The low-FODMAP diet approach developed by Melbourne’s Monash University works in the same way. The idea is not to eliminate all FODMAPs from the diet forever, but ascertain the impact of each one and find a comfortable intake level as part of a balanced diet.
Before undertaking major changes to your diet, it is important to seek advice from your doctor and/or a dietitian to ensure that you are always eating a diet that is right for your nutritional needs.
2014 clinical study of Dietary Fructan Intolerance
Xylose Isomerase, what is it?
Xylose Isomerase is an enzyme that promotes the conversion of fructose into easily absorbable glucose, in the small intestine.
A scientific double bind study conducted in 2012 by Sciotec Diagnostic Technologies, Austria, found that orally administered dose of 43.12mg Xylose Isomerase significantly improved symptoms (Nausea and abdominal pain) in 84% of patients that ingested 25g fructose.
An abstract from the 2012 study
BACKGROUND: Incomplete resorption of fructose results in increased colonic hydrogen production and is a frequent cause of abdominal symptoms. It has been suggested that healthy subjects have the capacity to absorb up to 25 g of fructose, whereas many have incomplete absorption and intolerance with intake of 50 g of fructose. Ingestion of food that contains fructose in excess of glucose may result in symptoms such as abdominal bloating or diarrhoea and also may provoke symptoms in patients with irritable bowel syndrome (IBS). It has been suggested that as little as 3 g of fructose may induce symptoms in functional bowel disorders.
Incompletely absorbed fructose reaches the colon, where bacterial carbohydrate metabolism results in production of short chain fatty acids and gases like hydrogen. This may cause symptoms like abdominal pain, bloating, discomfort and diarrhoea. These symptoms are not specific for fructose malabsorption but also occur with other incompletely absorbed carbohydrates, like dietary fibres, sorbitol, lactose in case of lactase deficiency or carbohydrate malabsorption in severe restriction of pancreatic digestive or intestinal absorptive capacity. Recently the term FODMAP, describing fermentable oligo-, di- and monosaccharides and polyols has been used to characterise short chain carbohydrates which potentially may trigger abdominal symptoms and for which dietary restriction has been suggested to be efficacious. Continued ingestion of high amounts of fructose has been suggested to result in a variety of other impairments. Since 1975 it has been discussed that enhanced dietary fructose could induce obesity, accelerated ageing, insulin resistance and non-alcoholic fatty liver disease. In addition, some types of depression could be related to long time consumption of high fructose diet.
AIM: To study whether orally administered xylose isomerase (XI), an enzyme that catalyses the reversible isomerisation fructose, can decrease breath hydrogen excretion in patients with fructose malabsorption. We hypothesised that orally administered XI is able to catalyse the conversion of poorly absorbable fructose into well-absorbable glucose in the human intestine in vivo and thereby reduce breath hydrogen excretion after ingestion of fructose in patients with incomplete fructose absorption. To assess this hypothesis, we performed a double-blind randomised crossover study in patients with previously established fructose malabsorption. Breath hydrogen excretion was assessed in patients who received either XI or placebo with an oral watery fructose load. A secondary endpoint was the assessment of the effect of XI on symptoms using a visual analogue scale (VAS).
METHODS: The study was performed in patients who were referred for a fructose hydrogen breath test for the evaluation of abdominal symptoms, and in whom fructose malabsorption was confirmed within the preceding 12 months. Tests were performed in the departments of gastroenterology or dermatology of our university. Fructose malabsorption was confirmed if there was an increase in end expiratory breath hydrogen concentration of at least 20 ppm over baseline after 25 or 30 g of fructose; 30 g was used at the department of gastroenterology and 25 g was used at the department of dermatology. Exclusion criteria were pregnancy, breast feeding, diabetes mellitus and gastrointestinal surgery, endoscopy or antibiotic treatment within the preceding 4 weeks.
Patients received 25g fructose in 100mL water together with either placebo or XI capsules. Primary endpoint was the reduction in breath hydrogen excretion, as assessed by the area under the breath hydrogen curve over 4 h (AUC). A secondary endpoint was the reduction in abdominal pain, bloating and nausea assessed on a visual analogue scale (VAS, range: 0-10). A P value <0.05 was considered statistically significant.
Two tests were performed at an interval between 4 days and 21 days. One day prior to each visit, subjects were asked to consume a lactose- and fructose-restricted diet. All the subjects fasted overnight and were not allowed to smoke 12 h before the test. The fasting end expiratory breath H2 concentration (termed 0 min) was measured using a Gastro+ Gastrolyser (Bedfont Scientific Ltd, Rochester, England) which has a sealed electrochemical sensor specific for H2. Immediately thereafter subjects had to take three capsules ‘X’ or ‘Y’ and then to ingest 25 g of fructose freshly dissolved in 100 mL of mineral water taken from one single production batch which was added to the plastic bottles which contained the fructose. Subjects were advised to drink the solution within 5 min. Thereafter, end expiratory breath H2 concentration was recorded every 30 min for the first 2 h, then every 60 min for the next 2 h (for a total of 240 min) by a study physician (M. A.-M.). The second test was performed identically with the remaining capsules (‘Y’ or ‘X’).
After plotting the breath H2 concentrations (in ppm) vs. time for the 4 h observation period the area under the curve (AUC) was calculated for each subject for both tests and expressed as ppm/240 min. Fasting breath H2 concentration at 0 min was used as the baseline for AUC determination. For example, if basal breath hydrogen concentration was 5 ppm, the AUC was calculated from the area under the curve exceeding this baseline of 5 ppm.
The symptoms bloating, nausea and abdominal pain were assessed individually before ingestion of the test solutions and at each time of breath hydrogen measurement by visual analogue scale covering a range of 0 (none) to 10 (most severe).
RESULTS: Sixty-five patients in whom fructose malabsorption had been diagnosed by positive breath hydrogen test within the previous year, were included in the study [15 males, 50 females; mean age 43.3 (s.d. = 14.4), range: 21-73 years]. The median AUC was 885 ppm/240 min in the XI group compared to 2071 ppm/240 min in the placebo group (P = 0.00). Median scores for abdominal pain (0.7 vs. 1.3) and nausea (0.2 vs. 0.6), but not for bloating (P = 0.053), were significantly improved after XI (P = 0.009 and P = 0.005) as compared with placebo.
CONCLUSIONS: In this study, oral supplementation of XI revealed a statistically significant decrease in breath hydrogen excretion over a 4 h period after ingestion of fructose, as compared with placebo. Decrease in the area under the breath hydrogen curve after XI suggests that XI catalysed the isomerisation of fructose which resulted in a lower amount of fructose reaching the colon. It is reasonable to end the measurement period at 4 h since breath hydrogen excretion after ingestion of poorly absorbable carbohydrates reaches its peak before that time.
As XI is able to convert poorly absorbable fructose to well-absorbable glucose in vitro, this enzyme could be used for conversion of excess fructose to glucose in the human small intestine in vivo. Oral administration of xylose isomerase significantly decreased breath hydrogen excretion after ingestion of a watery fructose solution. Nausea and abdominal pain were significantly improved by xylose isomerase.
A surprising finding in our study was, that, although patients had presented in the preceding year for evaluation of abdominal symptoms, indicating that they were bothered by their symptoms enough to warrant diagnostic evaluation at a tertiary care centre, only few patients had high scores on the VAS assessment of symptom severity during this study. This may indicate a large intra-individual variability in the severity of symptom scores presumably associated with incomplete fructose absorption.
You can read the full clinical study here:
Alpha-Galactosidase, what is it?
Alpha-galactosidase is used in the treatment of indigestion. Alpha-galactosidase is a digestive enzyme that breaks down complex carbohydrates such as Fructan, found in certain food like legumes, grains, and cruciferous vegetables to make them easier to digest. Thus, it prevents flatus and other gastrointestinal symptoms resulting from Fructan Intolerance. Of note: Poorly digested, fermentable carbohydrates may also induce symptoms of irritable bowel syndrome (IBS) and Fructan Intolerance may be one of the leading causes of IBS.
A scientific double bind study conducted in 2007 by The University of Pavia, Italy, found that the administration of 1200 GalU of alpha-galactosidase induced a significant reduction of both breath hydrogen excretion, bloating and severity of flatulence.
An abstract from the 2007 study
BACKGROUND: Bloating, abdominal distention, and flatulence represent very frequent complaints in functional fructan disorders: the prevalence of functional abdominal bloating, for example, reaches 15% of community-based populations, with a female predominance. However, the mechanism responsible for their onset and the best treatment for their management are still largely not well defined. Patients very frequently associate the occurrence of these symptoms with an excessive amount of intestinal gas, though a clear interrelationship between them has been demonstrated only for flatulence. It has, however, been shown that a subgroup of bloating patients is characterized by an increased production of gas, thus suggesting that this mechanism may also have a role in the pathophysiology of this very frequent symptom. The reduction of intestinal gas production may therefore represent an effective therapeutic strategy for the management of functional symptoms when their onset depends, at least in part, on gas hyperproduction. Current therapeutic approaches are based on the administration of simethicone, activated charcoal, a low-carbohydrate diet, and probiotics, but contradictory results are obtained. On the contrary, the use of antibiotics has produced encouraging results but the need for repeated treatment cycles requires a milder approach with less impact on the quality-quantity composition of intestinal bacterial flora. In this framework, the breaking down of nonabsorbable oligosaccharides contained in legumes, fruit, and vegetables.
Alpha-galactosidase transform non absorbable oligosaccharides in the intestinal tract to prevent them fr0m being fermented by intestinal bacterial flora (a gas producing process); in reducing intestinal gas production, visceral distention is decreased and therefore, symptoms like distention, abdominal pain and flatulence decrease as well. Alpha-galactosidase hydrolyses three complex carbohydrates: raffinose, stacyose and verbascose to transform them into monosaccharide: glucose, galactose and into the disaccharide; sucrose (whose hydrolysis is instantaneous during normal digestion). Alpha-galactosidase is not normally produced by human beings, for which reason raffinose, stachyose and verbascose arrive intact at the colon, where they are fermented by bacterial flora in a chemical reaction that produce hydrogen and methane (gas). Supplementation of Alpha-galactosidase with foods is believed to breaks up these three oligosaccharides before they arrive in the colon, preventing fermentation and gas production.
AIM: Bloating, abdominal distention, and flatulence represent very frequent complaints in functional disorders but their pathophysiology and treatment are largely unknown. Patients frequently associate these symptoms with excessive intestinal gas and the reduction of gas production may represent an effective strategy. The aim was to evaluate the effect of alpha-galactosidase administration, in a randomized double-blind placebo-controlled protocol, on intestinal gas production and gas-related symptoms after a challenge tests in healthy volunteers.
METHODS: Exclusion criteria were: 1) any suspected episodes of hypersensitivity/allergy; 2) any chronic organic disorders, as assessed by full clinical history and examination, and supported by normal results of initial limited laboratory investigation including complete blood cell count, erythrocyte sedimentation rate, C-reactive protein, blood glucose, amylase and lipase, tissue transglutaminase antibodies with total serum IgA; 3) inability of the parent to comprehend the full nature and purpose of the study and unwillingness to co-operate with the Investigator; 4) patients who have used any drug affecting GI motility or intestinal microbiota during the previous 4 weeks.
Healthy volunteers ingested 300 or 1200 GalU of alpha-galactosidase or placebo during a test meals containing 420 g of fructan rich cooked beans, to stimulate fructan intolerance symptoms. Breath hydrogen excretion and occurrence of bloating, abdominal pain, discomfort, flatulence, and diarrhea were measured for 8 hr, giving true comparative markers with the placebo group.
RESULTS: The mean hydrogen excretion decreased more in the alpha-galactosidase than placebo group; the difference between the hydrogen excretion score change in the two groups was statistically significant. The hydrogen excretion score improved more in the alpha-galactosidase group, with higher rates of improvement (71%) than placebo (33%). The significant decrease of hydrogen excretion score and the marginal change in the placebo group provides evidence of the efficacy of alpha-galactosidase. The significant effect on hydrogen excretion and bloating was also confirmed in the following days with repeated decreases of scores.
CONCLUSIONS: Bloating and distension together with belching, aerophagia and flatulence, have been attributed to excessive intestinal gas accumulation, impaired handling of gas in the small intestine, impaired clearance from the proximal colon, psychological factors, altered gut microflora, incomplete digestion and malabsorption of carbohydrates. This study his provided evidence that the administration of 1200 GalU of alpha-galactosidase induced a significant reduction of both breath hydrogen excretion and severity of flatulence. A reduction in severity was apparent for all considered symptoms, but both 300 and 1200 GalU induced a significant reduction in the total symptom score. Alpha-galactosidase reduced gas production following a meal rich in fermentable carbohydrates and may be helpful in patients with gas-related symptoms.
2007 clinical study in Adults
https://pubmed.ncbi.nlm.nih.gov/17151807/
2013 clinical study in Children