Clinical Review

Understanding Lactose Intolerance

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Among US adults, 30 million may be affected by lactose intolerance (LI), and older patients are particularly susceptible. How is LI best investigated in patients who report its troublesome symptoms? And for those with a confirmed diagnosis, how can clinicians provide optimal management—minimizing symptoms without placing patients’ bone health at risk?


 

References

Lactose intolerance (LI), a term closely associated with hypolactasia (lactase deficiency) and lactose malabsorption,1 is a common syndrome composed of diarrhea, abdominal pain, flatulence and/or bloating, and sometimes nausea and vomiting in severe cases, after ingestion of dairy products.2 This common disorder results from a deficiency in the enzyme lactase, which makes affected patients unable to digest lactose, a sugar found in milk and other dairy products.3 Malabsorption of lactose produces the symptoms associated with LI.

The level of LI varies among affected individuals, depending on many nutritional and genetic factors, the amount of lactose consumed, the patient’s degree of lactase deficiency, and the substance in which the lactose is ingested.4

Epidemiology
LI prevalence is difficult to ascertain because the symptoms are vague and can be attributed to a number of conditions; additionally, there is no gold standard for diagnosis of LI. It is estimated that about 70% of the world population is affected by LI—with great variation among ethnicities and races.5,6 Some degree of LI is reported in up to 80% of African-Americans and Latinos, and almost 100% of Native Americans and Asian Americans. LI is least common in people of northern European descent (and is unlikely to develop before adulthood7), although it has been suggested that 30 million American adults experienced lactose malabsorption to some degree by age 20.3,8 Heyman4 estimates that approximately 2% of people of northern European descent have LI.

Regardless of ethnicity or race, older patients are more susceptible to LI than are younger adults, largely as a result of the normal processes of aging.2

Pathophysiology and Patient Presentation
Cells of the inner lumen of the small intestines, enterocytes, are covered with a membrane that has a brush border composed of microvilli.9 The microvilli produce lactase, the enzyme necessary to split and hydrolyze dietary lactose into glucose and galactose for transport across the cell membrane.6 Unfortunately, lactase is produced in the upper, most shallow section of the villi, which is exceedingly prone to damage by secondary insult.

If the lactase enzymes are absent or deficient, unabsorbed sugars osmotically attract fluid into the bowel lumen. The amount of fluid influx into the bowel is approximately triple the normal amount, based on the osmolality of sugar alone. In addition, the unabsorbed lactose entering the colon is fermented by bacteria, producing gas and resulting in the cleavage of lactose into monosaccharides. Monosaccharides cannot be absorbed by the colonic mucosa; as a result, osmotic pressure increases, and fluid levels rise in the bowel. This process explains the most common symptoms of flatulence, diarrhea, abdominal pain, and bloating.6

Most mammalian babies, including human infants, produce enough lactase to digest milk, including breast milk. This ability persists until the child is weaned. In humans, lactase activity drops at age 2 to 3 years and may cease altogether by age 5 to 10.9 Worldwide, most humans lose 90% to 95% of birth lactase levels by early childhood, followed by a continuing decline during the course of a lifetime.6 This may help explain why many elderly people are affected by LI.

Typically, development of LI progresses subtly over many years, but onset can also be relatively acute.4

Lactose Malabsorption
The three main types of lactose malabsorption are primary, secondary, and congenital. The latter is a rare, genetic form of LI in which the lactase enzyme is entirely absent; for the purposes of this article, congenital lactose malabsorption will not be discussed.

Primary lactase deficiency is the most common form and the focus of this article. It is the normal, gradual reduction in lactase enzyme that a maturing individual experiences through adulthood, and the rate of reduction is genetically determined. Secondary lactose malabsorption occurs following an insult to the small bowel, as in severe diarrhea, infection (eg, rotavirus), chemotherapy, or acute gastroenteritis.4 In these situations, lactase is the first enzyme to be negatively affected and the last to return as the insult resolves.10 Secondary hypolactasia is transient and reversible.11,12

LI is not to be confused with cow’s milk allergy—an immune response to the protein in cow’s milk, which can be a life-threatening event. A true milk allergy most commonly appears within the first year of life, whereas LI occurs more often in adulthood.5,8

LI is not considered life threatening, but its symptoms can severely affect a person’s quality of life and productivity. In addition to ethnicity and age, the type and amount of lactose ingested and the amount that the patient is unable to digest all affect the severity of LI symptoms.13

Lactose makes up between 2% and 8% of the solids in milk; 1 mL of milk (0.03 fl oz) contains 47.2 mg of lactose. No amount of lactose has been specified to produce symptoms, but most adults can tolerate as much as 8 fl oz of milk without problems,1 and patients can tolerate more lactose if the food containing it is consumed with a meal.11 Some adults may be able to ingest only 2 to 4 fl oz before symptoms appear4; in highly sensitive adults, as little as 200 mg of lactose (0.13 fl oz of milk) can produce symptoms.5

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