CARBOHYDRATE MALABSORPTION, INCLUDING LACTOSE MALABSORPTION - pediagenosis
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Thursday, February 19, 2026

CARBOHYDRATE MALABSORPTION, INCLUDING LACTOSE MALABSORPTION

CARBOHYDRATE MALABSORPTION, INCLUDING LACTOSE MALABSORPTION


CARBOHYDRATE MALABSORPTION, INCLUDING LACTOSE MALABSORPTION


Carbohydrate malabsorption is a frequent clinical condition caused by fermentation of unabsorbed carbohydrates by colonic flora and giving rise to symptoms. Although lactose is the most commonly malabsorbed sugar, other carbohydrates, including oligosaccharides, disaccharides, and monosaccharides such as fructose, can cause symptoms related to malabsorption.

 

Lactose Malabsorption

Lactose intolerance refers to the development of abdominal pain, flatulence, nausea, bloating, and diarrhea after ingestion of lactose, whereas malabsorption refers to the inefficient digestion of lactose, a disorder that might not cause symptoms. Lactose is the main source of sugar from milk and milk products from all mammals except the sea lion. It is hydrolyzed by lactase, an intestinal brush-border enzyme that cleaves lactose into glucose and galactose.

Intestinal lactase activity is maximal at birth but starts to decline after 2 years of age, a process that might help weaning. Most people in the world (70%) have low lactase activity after childhood (lactase nonpersistence). The proportion is higher in Native Americans and some populations of Southeast Asia and Africa, where it reaches 90% to 95%. Low activity should be distinguished from congenital lactase deficiency, a rare autosomal recessive disease that affects infants from birth, and acquired lactose intolerance, which is a consequence of loss of intestinal brush-border enzyme activity associated with infectious enteritis or celiac disease. In approximately 30% of the population, the lactase activity level does not decline and continues at the maximal neonatal level well into adulthood (lactase persistence). This occurs mainly in people of Northern European descent and may indicate a natural selection in those populations who relied on mammalian milk in times of poor harvest. Individuals with lactase nonpersistence are able to tolerate low doses of lactose. Studies indicate that symptoms are likely to be negligible if lactose intake is limited to 12.5 g, equivalent to 240 mL of milk per day.

The average adult with a western diet consumes approximately 15 g of lactose per day.

Lactose that is not absorbed by the small intestine rapidly reaches the colon and is fermented to short-chain fatty acids and hydrogen gas, which are responsible for the ensuing symptoms. Symptoms, however, are variable and may depend on the fat content of the food, the intestinal transit time, and the composition of the colonic flora. Furthermore, short-chain fatty acids can be used up as an energy source by colonocytes, and this is one mechanism whereby lactose-deficient individuals adapt to ingestion of lactose.

The presence of lactose intolerance is usually suggested by the patient’s history; however, testing may be necessary to confirm the diagnosis. Lactose tolerance testing and breath testing after ingestion of a standard dose of lactose are easy, noninvasive tests of lactose malabsorption.

Complete restriction of foods containing lactose may be recommended for a short period of time to alleviate symptoms and confirm the diagnosis. After this period, however, strict elimination may not be necessary, and small quantities may slowly be reintroduced. Preparations containing bacterial or yeast β-galactosidases are commercially available and can be added to foods containing lactose or ingested with meals to prevent symptoms. Products containing predigested milk or other dairy substances or nondairy milk products such as almond milk are possible alternatives. Live culture yogurt, which contains endogenous β-galactosidase, is well tolerated and can be a good source of calcium. Avoidance of dairy products has been associated with low calcium and vitamin D levels; therefore, these levels should be monitored and properly supplemented.

 

Fructose Malabsorption

One fourth of the general population is estimated to suffer from varying degrees of fructose malabsorption. This should not be confused with hereditary fructose intolerance, in which infants develop hypoglycemia owing to a deficiency of the enzyme fructose-1-phosphate aldolase. Fructose is naturally present in fruits such as apples but can also be produced from corn and is a major ingredient in high-fructose corn syrup. Fructose is not efficiently absorbed, as glucose or galactose is, and the capacity of the gut to absorb fructose can be easily over-whelmed when large quantities are ingested. Unabsorbed fructose can reach the colon, where fermentation by colonic bacteria leads to abdominal symptoms. Fructose malabsorption seems more common in patients with functional bowel disease and can be present in up to 80% of cases. Avoidance of fructose from the diet or even reduction of intake eliminates symptoms.

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