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Carbohydrate Intolerance and Celiac Disease

Prepared by Jean E. Guest, PhD, RD, LMNT

It is rare to read a health or diet article without seeing something about high carbohydrate, low carbohydrate, or specific carbohydrate diets. Common advice is to avoid foods containing certain carbohydrates. The suggestion is that these carbohydrates are unhealthy or “bad”. Carbohydrates are an essential source of nutrition for humans. There are no “bad” carbohydrates just ones that cannot be absorbed and used properly due to specific medical conditions such as celiac disease. In celiac disease gastrointestinal dysfunction causes carbohydrates to be incompletely digested leading to malabsorption and intolerance. Since symptoms of carbohydrate malabsorption mimic those of gluten exposure it is important for individuals with celiac disease to be aware of carbohydrate malabsorption and intolerance.

Carbohydrates

Carbohydrates are an important part of a healthy diet. They provide about half of the daily energy intake for most individuals. Carbohydrate is just another word for sugar including a Greek word, saccharide. Saccaride is the term used to describe chemical configurations of carbohydrates. For instance monosaccharide indicates a single sugar molecule, disaccharide describes two sugar molecules and polysaccharides are multiple sugar molecules bonded together. (Table 1) Traditionally monosaccharides are called simple sugars while disaccharides and polysaccharides are known as complex carbohydrates.

The chemical structure of carbohydrates indicates how they are absorbed. At a cellular level humans use the monosaccharide glucose for fuel. This mean disaccharides and polysaccharides must be hydrolyzed (broken down) into single sugar molecules to be utilized. Most carbohydrates need enzymes for hydrolysis. These enzymes are located on villi in the brush border of the small intestine. (Table 2) A decrease or absence of enzymes results in carbohydrate intolerance. The most common type of carbohydrate intolerance associated with celiac disease is lactose although fructose and other types of carbohydrate malapsorption have been documented.

 

 

Lactose Intolerance

Lactose is a carbohydrate (sugar) found in milk, milk products, and other items. (Table 3) Prior to digestion lactose must be hydrolyzed by the enzyme lactase. Lactase is located on the tip of small intestinal villi. If for any reason lactase levels are decreased or deficient lactose intolerance occurs. There are different types of lactose intolerance including primary, secondary acquired, and congenital.

Primary lactose intolerance is inherited (genetic). In this type of lactase deficiency lactose is usually tolerated during infancy and childhood. With increasing age the ability to produce lactase decreases leading to lactose intolerance. Primary lactose intolerance affects some ethnic groups more than others. In the United States anywhere from 20% to 80% of adult African Americans, American Indians, Ashkenazi Jews, American Asians and American Mexicans have some degree of primary lactose intolerance. Adult Americans of European decent are less likely to be lactose intolerant with a rate of about 5 to 12%. Individuals with celiac disease may have primary lactose intolerance, but the secondary or acquired type is more usual.

Acquired lactose intolerance is the consequence of a decrease or deficiency of lactase due to damage of villi located in the small intestine. The villi damage linked to celiac disease is frequently caused by an inflammatory immune-response to gluten. However, villi damage may also be the result of illness, injury, surgery, or gastroenteritis. Acquired lactose intolerance can be transient (lasting only a short time) or permanent. Children with celiac disease are more likely to have transient lactose intolerance. One reason is children tend to be diagnosed and treated sooner than adults. This allows faster healing of the villi and therefore regeneration of lactase.

Congenital lactase deficiency is rare and not associated with celiac disease. The cause of congenital lactase deficiency is a mutation in the gene responsible for making lactase. Infants with congenital lactase deficiency cannot tolerate lactose containing formulas or breast milk and are fed a lactose-free formula. These infants need to be on a strict lactose free diet for life.

Symptoms of lactose intolerance include gas, bloating, nausea, abdominal cramping, foul smelling stools, and diarrhea. Symptoms vary from individual to individual. Some barely notice symptoms while others know right away when they have been exposed to lactose. Since the symptoms of lactose intolerance are similar to those seen with gluten exposure it is recommended to see a physician to be diagnosed.

Lactose intolerance can be diagnosed in two ways. One is a breath hydrogen test and the other is a stool acidity test. The stool acidity test is used for infants and young children. Since lactose intolerance is uncommon in children under 2 years of age the test should be conducted after consultation with a pediatric gastroenterologist. In older children and adults the presence of hydrogen in the breath indicates lactose malabsorption. Some foods, medications, and cigarettes can interfere with the accuracy of breath hydrogen tests. Before having a breath hydrogen test check with a medical professional for a list of restricted items.

Treatment for lactose intolerance depends on lactase activity. Some individuals are able to drink a little milk while others cannot have a drop. Lactose tolerance can be influenced by when and how much is consumed. Taking small amounts of lactose several times a day are better tolerated than large amounts eaten at one time. Other ways to improve lactose tolerance are to use oral lactase enzymes and to use milk treated with Lactaid or acidopholus (a bacteria culture).

Milk and milk products are the primary source of calcium in the American diet. In lactose intolerance soy, rice, and nut based milks may be used as a milk substitute in older children and adults. Nutrient content and proportions in milk substitutes are not the same as breast or cow’s milk so they are not appropriate for infants and small children. Even with the use of milk substitutes, yogurt, and low lactose foods it may be difficult to obtain adequate calcium intake. So a daily calcium and vitamin D supplement is recommended.

Milk and milk products obviously contain lactose, but other sources of lactose are not as easy to detect. (Table 3) When reading labels look for the words milk, milk solids, dry milk solids, whole or skim milk dry powder, and whey. Non-dairy products made from milk derivatives contain lactose as do many medications. Check with a pharmacist for lactose content in medications.

Fructose Intolerance

There are two types of fructose intolerance. One is “ hereditary” and the other is “acquired”. Hereditary fructose intolerance is a rare genetic disorder where the liver lacks a certain enzyme needed to metabolize fructose. Acquired fructose intolerance is a functional problem in the small intestine where the ability to absorb fructose is decreased. Individuals with celiac disease usually have acquired fructose intolerance although a few cases of heredity fructose intolerance have been reported.

Symptoms of fructose intolerance are similar to those of lactose intolerance and gluten exposure. Symptoms include gas, bloating, belching, nausea, abdominal cramping, and diarrhea. Symptoms vary individually ranging from mild to severe. Individuals on a strict gluten-free and lactose free diet whose symptoms do not improve may consider consulting their physician about screening for fructose intolerance.

Fructose intolerance is diagnosed with a breath hydrogen test. A beverage containing fructose is consumed before the test. An increased level of breath hydrogen indicates fructose malabsorption resulting in a diagnosis of fructose intolerance. Fructose malabsorption is not well understood. Fructose is absorbed by facilitated diffusion through the use of transporters known as GLUT 5 and GLUT 2. When these transporters are decreased or overloaded unabsorbed fructose passes directly into the colon where it is fermented and produces short-chain fatty acids and gases.

In the United States high fructose corn syrup added to the food supply has led some to believe that fructose intake has increased. According to the United States Department of Agriculture (USDA) Food Availability Tables fructose intake has not changed significantly since 1909. Even so fructose malabsorption has been reported in a number of studies in the general population. One study in 2005 at the University of Kansas tested fructose tolerance in 15 healthy free-living adults. In this study breath hydrogen testing was done with fructose doses commonly consumed by free-living adults. The results in the study showed significant symptoms of fructose malabsorption in up to two-thirds of the volunteers. These researchers concluded the study demonstrated that fructose malabsorption happens in healthy individuals.

In addition to high fructose corn syrup, fructose can be found in honey, fruits, vegetables, wheat, sucrose, and sucrose containing foods and beverages. (Table 4) A common misconception in the general public is that the only sugar in fruit is fructose. Actually some fruits and vegetables naturally contain as much sucrose as fructose. Fructose found in vegetables and wheat is often in the form of oligosaccharides (complex carbohydrates) known as fructans and galactans.

Treatment of fructose intolerance includes limiting or eliminating fructose and sucrose from the diet. Remember sucrose becomes fructose (and glucose) during digestion. Fructose tolerance dictates how strict the diet needs to be. One way to figure out individual tolerance is to try an elimination diet. In other words eliminate fructose containing foods and beverages until symptoms improve. Then slowly reintroduce one food or beverage at a time waiting to see if symptoms reappear. Before beginning a fructose elimination diet consult with a registered dietitian.

Individuals following a fructose restricted diet should avoid sugar substitutes such as sorbitol, mannitol, xylitol,malitol, and isomalt (also known as polyols and alcohol sugars). These sugar substitutes are not absorbed in the small intestine and pass directly into the colon (large intestine). Small amounts of sugar substitutes are usually well tolerated, but large amounts may have a laxative effect. Watch for these sugar substitutes in sugar-free foods, beverages, gums and some medications. Other sugar substitutes like sucrolose (Splenda), aspartame (Equal, Nutrasweet), and saccharin appear to be tolerated by individuals with fructose intolerance.

A barrier to managing fructose intolerance is figuring out the fructose content in foods and beverages. (Table 5) Determining fructose content in gluten-free grains can be difficult. Labels usually list total carbohydrate content rather than individual sugars such as fructose. Hidden sources of fructose include foods with added sugar that may not be obvious such as cured meats, commercial baked goods, sauces, and condiments. To find fructose content in foods and beverages try contacting manufacturers or using the USDA Nutrient Database.

Summary

Gastrointestinal symptoms are a hallmark of celiac disease even though not all individuals have obvious symptoms. Once a strict gluten-free diet and lifestyle are started the expected outcome is gastrointestinal healing and resolution of symptoms.

It may take as long as a year or more after becoming gluten-free for symptoms to improve or resolve. If gastrointestinal symptoms persist, do not improve, or improve and then reoccur consider consulting a physician regarding carbohydrate intolerance. Prompt diagnosis and treatment contributes to improved health status and quality of life.

USDA National Nutrient Database for Standard Reference, Release 24

References

  1. Anderson JW, Baird P, Davis RH Jr, et al. Health benefits of dietary fiber. Nutrition Reviews® 2009;67(4):188–205.
  2. Beyer PL, Caviar EM, McCallum RW. Fructose intake at current levels in the United States may cause gastrointestinal distress in normal adults. JADA. 2005;105(10):1559-66.
  3. Bharadia L, Shivpuri D. Non responsive celiac disease due to coexisting hereditary fructose intolerance. Indian J Gastroenterol. 2012;31(2):83-4.
  4. Ciacci C, Gennarelli D, Esposito G, Tortora R, Salvatore F, Sacchetti L. Hereditary fructose intolerance and celiac disease: a novel genetic association. Clin Gastroenterol Hepatol. 2006;4(5):635-8.
  5. Hessels J, Eidhof HH, Steggink J, et al. Assessment of hypolactasia and site-specific intestinal permeability by differential sugar absorption of raffinose, lactose, sucrose and mannitol. Clin Chem Lab Med. 2003;41(8):1056-63.
  6. Latulippe ME, Skoog SM. Fructose Malabsorption and Intolerance: Effects of Fructose with and without Simultaneous Glucose Ingestion. Critical Reviews in Food Science and Nutrition, 51:583–592 (2011).
  7. National Digestive Diseases Information Clearinghouse, National Institutes of Health. http://digestive. niddk.nih.gov/ddisease/pubs/lactoseintolerance/ index.htm. Accessed June 24, 2009.
  8. Newcomer AD, Thomas PJ, McGill DB, Hofmann AF. Lactase deficiency: a common genetic trait of the American Indian. Gastroenterology. 1977;72(2):234- 7.
  9. Ojetti V, Nucera G, Migneco A, et al. High prevalence of celiac disease in patients with lactose intolerance. Digestion. 2005;71(2):106-10.
  10. Skoog SM, Bharucha AE. Dietary fructose and gastrointestinal symptoms: a review. Am J Gastroenterol. 2004;99(10):2046-50.
  11. Skoog SM, Bharucha AE, Zinsmeister. Comparison of breath testing with fructose and high fructose corn syrups in health and IBS. Neurogastroenterol Motil. 2008;20(5): 505–511.
  12. United States Department of Agriculture National Nutrient Database for Standard Reference 24. http:// ndb.nal.usda.gov. Accessed June 21, 2012.
  13. United States Department of Agriculture Economic Research Service. www.ers.usda.gov/data/ foodconsumption/ FoodAvailablespreadsheets. htm#sweets. Accessed June 24, 2012.

Reviewed 2/19/2013