Researchers at Monash University in Australia developed dietary guidelines for managing fructose malabsorption, particularly for individuals with IBS.

According to the USDA database, 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. 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.

Sucrose intolerance can be caused by genetic mutations in which both parents must contain this gene for the child to carry the disease (so-called primary sucrose intolerance). Sucrose intolerance can also be caused by irritable bowel syndrome, aging, or small intestine disease (secondary sucrose intolerance). There are specific tests used to help determine if a person has sucrose intolerance. The most accurate test is the enzyme activity determination, which is done by biopsying the small intestine. This test is a diagnostic for GSID. Other tests which can aid in the diagnosis of GSID but which are not truly diagnostic for the disease are the sucrose breath test, and a genetic test which tests for the absence of certain genes which are thought to be responsible for GSID.

Sucrose (also termed "saccharose") is a disaccharide and is a two-sugar chain composed of glucose and fructose which are bonded together. A more familiar name is table, beet, or cane sugar. It was believed that most cases of sucrose intolerance were to do an autosomal recessive, genetic, metabolic disease. Based on new data patients with heterozygous and compound heterozygous genotypes can have symptom presentation as well. GSID involves deficiency in the enzyme sucrase-isomaltase, which breaks apart the glucose and fructose molecules. When disaccharides are consumed, they must be broken down into monosaccharides by enzymes in the intestines before they can be absorbed. Monosaccharides, or single sugar units, are absorbed directly into the blood.

A deficiency of sucrase may result in malabsorption of sugar, which can lead to potentially serious symptoms. Since sucrose-isomaltase is involved in the digestion of starches, some GSID patients may not be able to absorb starches as well. It is important for those with sucrose intolerance to minimize sucrose consumption as much as possible. Dietary supplements or medications may be taken as a substitute for the enzyme missing or to introduce healthy bacteria into the immune system.

Malabsorption is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition and a variety of anaemias.

Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency. A typical Western diet ingested by an adult includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the required sodium, potassium, chloride, calcium, vitamins, and other elements. Salivary, gastric, intestinal, hepatic, and pancreatic secretions add an additional 7–8 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents. This massive load is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1–2 g of nitrogen, and less than 20 mmol each of Na, K, Cl, HCO, Ca, or Mg.

If there is impairment of any of the many steps involved in the complex process of nutrient digestion and absorption, intestinal "malabsorption" may ensue. If the abnormality involves a single step in the absorptive process, as in primary lactase deficiency, or if the disease process is limited to the very proximal small intestine selective malabsorption of only a single nutrient may occur. However, generalized "malabsorption" of multiple dietary nutrients develops when the disease process is extensive, thus disturbing several digestive and absorptive processes, as occurs in coeliac disease with extensive involvement of the small intestine.

Orlistat (also known by trade names Xenical and Alli) is a diet pill that works by blocking the enzymes that digest fat. As a result, some fat cannot be absorbed from the gut and is excreted in the feces instead of being metabolically digested, sometimes causing oily anal leakage. Vytorin (ezetimibe/simvastatin) tablets can cause steatorrhea in some people.

There are anecdotal reports on the internet describing oily droplets in feces after eating large amounts of cashews or other whole nuts. They agree with studies showing that stool lipids are greatest when whole nuts are eaten, compared to their nut butters, oils or flour and that lipids from whole nuts are significantly less well absorbed.

The main purpose of the gastrointestinal tract is to digest and absorb nutrients (fat, carbohydrate, protein, micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the intestinal epithelial cells.

Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.

Intestinal malabsorption can be due to:

- Mucosal damage (enteropathy)

- Congenital or acquired reduction in absorptive surface

- Defects of specific hydrolysis

- Defects of ion transport

- Pancreatic insufficiency

- Impaired enterohepatic circulation

Bile acid malabsorption was first recognized in patients with ileal disease. When other causes were recognized, and an idiopathic, primary form described, a classification into three types was proposed:

- Type 1: Bile acid malabsorption, secondary to ileal resection, or ileal inflammation (e.g. in Crohn's disease)

- Type 2: Idiopathic bile acid malabsorption, Primary bile acid diarrhea

- Type 3: Secondary to various gastrointestinal diseases including cholecystectomy, vagotomy, small intestinal bacterial overgrowth, radiation enteropathy, celiac disease, chronic pancreatitis, etc.

In humans, the most common causes of EPI are chronic pancreatitis and cystic fibrosis, the former a longstanding inflammation of the pancreas altering the organ's normal structure and function that can arise as a result of malnutrition, heredity, or (in the western world especially), behaviour (alcohol use, smoking), and the latter a recessive hereditary disease most common in Europeans and Ashkenazi Jews where the molecular culprit is an altered, "CFTR"-encoded chloride channel. In children, another common cause is Shwachman-Bodian-Diamond syndrome, a rare autosomal recessive genetic disorder resulting from mutation in the SBDS gene.

EPI is often treated with pancreatic enzyme replacement products (PERPs) such as pancrelipase, that are used to break down fats (via a lipase), proteins (via a protease), and carbohydrates (via amylase) into units that can be digested by those with EPI. Pancrelipase is typically porcine derived and requires large doses. A novel treatment called Sollpura (Liprotamase) is under trial that uses biotechnology derived enzymes to help treat EPI.

Because of the ease of therapy (dietary exclusion of fructose), HFI can be effectively managed if properly diagnosed. In HFI, the diagnosis of homozygotes is difficult, requiring a genomic DNA screening with allele specific probes or an enzyme assay from a liver biopsy. Once identified, parents of infants who carry mutant aldolase B alleles leading to HFI, or older individuals who have clinical histories compatible with HFI can be identified and counselled with regard to preventive therapy: dietary exclusion of foods containing fructose, sucrose, or sorbitol. If possible, individuals who suspect they might have HFI, should avoid testing via fructose challenge as the results are non-conclusive for individuals with HFI and even if the diagnostic administration fructose is properly controlled, profound hypoglycemia and its sequelae can threaten the patient's well-being.

Sucrose intolerance, also called sucrase-isomaltase deficiency, congenital sucrase-isomaltase deficiency (CSID), or genetic sucrase-isomaltase deficiency (GSID), is the condition in which sucrase-isomaltase, an enzyme needed for proper metabolism of sucrose (sugar) and starch (i.e., grains and rice), is not produced or the enzyme produced is either partially functional or non-functional in the small intestine. All GSID patients lack fully functional sucrase, while the isomaltase activity can vary from minimal functionality to almost normal activity. The presence of residual isomaltase activity may explain why some GSID patients are better able to tolerate starch in their diet than others with GSID.

The highest prevalence rates are seen in the Inuit populations of Greenland (5–10%), Alaska (3–7%) and Canada (about 3%). European descent prevalence ranges from 0.2% to 0.05%. There is a lower prevalence reported in African Americans and Hispanics compared to Caucasians.

Treatment of HFI depends on the stage of the disease, and the severity of the symptoms. Stable patients without acute intoxication events are treated by careful dietary planning that avoids fructose and its metabolic precursors. Fructose is replaced in the diet by glucose, maltose or other sugars. Management of patients with HFI often involves dietitians who have a thorough knowledge of what foods are acceptable.

Glucose-galactose malabsorption is a rare condition in which the cells lining the intestine cannot take in the sugars glucose and galactose, which prevents proper digestion of these molecules and larger molecules made from them.

Glucose and galactose are called simple sugars, or monosaccharides. Sucrose and lactose are called disaccharides because they are made from two simple sugars, and are broken down into these simple sugars during digestion. Sucrose is broken down into glucose and another simple sugar called fructose, and lactose is broken down into glucose and galactose. As a result, lactose, sucrose and other compounds made from carbohydrates cannot be digested by individuals with glucose-galactose malabsorption.

Bile acid malabsorption, known also as bile acid diarrhea, is a cause of several gut-related problems, the main one being chronic diarrhea. It has also been called bile acid-induced diarrhea, cholerheic or choleretic enteropathy and bile salt malabsorption. It can result from malabsorption secondary to gastrointestinal disease, or be a primary disorder, associated with excessive bile acid production. Treatment with bile acid sequestrants is often effective.

GSE can result in high risk pregnancies and infertility. Some infertile women have GSE and iron deficiency anemia others have zinc deficiency and birth defects may be attributed to folic acid deficiencies.

It has also been found to be a rare cause of amenorrhea.

Folate is found in leafy green vegetables. Multi-vitamins also tend to include Folate as well as many other B vitamins. B vitamins, such as Folate, are water-soluble and excess is excreted in the urine.

When cooking, use of steaming, a food steamer, or a microwave oven can help keep more folate content in the cooked foods, thus helping to prevent folate deficiency.

Folate deficiency during human pregnancy has been associated with an increased risk of infant neural tube defects. Such deficiency during the first four weeks of gestation can result in structural and developmental problems. NIH guidelines recommend oral B vitamin supplements to decrease these risks near the time of conception and during the first month of pregnancy.

Some situations that increase the need for folate include the following:

- hemorrhage

- kidney dialysis

- liver disease

- malabsorption, including celiac disease and fructose malabsorption

- pregnancy and lactation (breastfeeding)

- tobacco smoking

- alcohol consumption

Glucose-galactose malabsorption generally becomes apparent in the first few weeks of a baby's life. Affected infants experience severe diarrhea resulting in life-threatening dehydration, increased acidity of the blood and tissues (acidosis), and weight loss when fed breast milk or regular infant formulas. However, they are able to digest fructose-based formulas that do not contain glucose or galactose. Some affected children are better able to tolerate glucose and galactose as they get older.

Small amounts of glucose in the urine (mild glucosuria) may occur intermittently in this disorder. Affected individuals may also develop kidney stones or more widespread deposits of calcium within the kidneys.

Glucose-galactose malabsorption is a rare disorder; only a few hundred cases have been identified worldwide. However, as many as 10 percent of the population may have a somewhat reduced capacity for glucose absorption without associated health problems. This condition may be a milder variation of glucose-galactose malabsorption.

The prognosis of children diagnosed with intolerance to milk is good: patients respond to diet which excludes cow's milk protein and the majority of patients succeed in forming tolerance. Children with non-IgE-mediated cows milk intolerance have a good prognosis, whereas children with IgE-mediated cows milk allergy in early childhood have a significantly increased risk for persistent allergy, development of other food allergies, asthma and rhinoconjunctivitis.

A study has demonstrated that identifying and appropriately addressing food sensitivity in IBS patients not previously responding to standard therapy results in a sustained clinical improvement and increased overall well being and quality of life.

Some studies reported up to 80% of patients with irritable bowel syndrome (IBS) have SIBO (using the hydrogen breath test). Subsequent studies demonstrated statistically significant reduction in IBS symptoms following therapy for SIBO.

There is a lack of consensus however, regarding the suggested link between IBS and SIBO. Other authors concluded that the abnormal breath results so common in IBS patients do not suggest SIBO, and state that "abnormal fermentation timing and dynamics of the breath test findings support a role for abnormal intestinal bacterial distribution in IBS." There is general consensus that breath tests are abnormal in IBS; however, the disagreement lies in whether this is representative of SIBO. More research is needed to clarifiy this possible link.

While GI disease is one of the major symptoms of GSE that are characterized by increased levels of IgA/IgG to food proteins, many conditions like chronic constipation and irritable bowel disease persist after GF diet. Some of this may be due to persistent undetected food allergies, increased sensitivity of the damaged gut, or problems masked by GSE itself.

Inborn errors of carbohydrate metabolism are inborn error of metabolism that affect the catabolism and anabolism of carbohydrates.

An example is lactose intolerance.

Carbohydrates account for a major portion of the human diet. These carbohydrates are composed of three principal monosaccharides: glucose, fructose and galactose; in addition glycogen is the storage form of carbohydrates in humans. The failure to effectively use these molecules accounts for the majority of the inborn errors of human carbohydrates metabolism.

To treat people with a deficiency of this enzyme, they must avoid needing gluconeogenesis to make glucose. This can be accomplished by not fasting for long periods, and eating high-carbohydrate food. They should avoid fructose containing foods (as well as sucrose which breaks down to fructose).

As with all single-gene metabolic disorders, there is always hope for genetic therapy, inserting a healthy copy of the gene into existing liver cells.

Fibromyalgia is a poorly understood pain condition. Lactulose breath testing has shown that patients with fibromyalgia have a more pronounced degree of abnormal results compared to both IBS patients and the general population. This study also demonstrated positive correlation between the amount of pain and the degree of abnormality on the breath test. A subsequent study also demonstrated increased prevalence of intestinal hyperpermeability, which some believe occurs commonly with SIBO.