National Institutes of Health Consensus Development Conference: lactose intolerance and health.

National Institutes of Health (NIH) consensus and stateof-the-science statements are prepared by independent panels of health professionals and public representatives on the basis of 1) the results of a systematic literature review prepared under contract with the Agency for Healthcare Research and Quality; 2) presentations by investigators working in areas relevant to the conference questions during a 2-day public session; 3) questions and statements from conference attendees during open discussion periods that are part of the public session; and 4) closed deliberations by the panel during the remainder of the second day and morning of the third. This statement is an independent report of the panel and is not a policy statement of the National Institutes of Health or the U.S. government. The following statement is an abridged version of the panel’s report, which is available in full at http: //consensus.nih.gov/2010/lactosestatement.htm. Lactose intolerance is the syndrome of diarrhea, abdominal pain, flatulence, or bloating occurring after lactose ingestion. These symptoms, which are produced by malabsorption of lactose, a sugar found in milk and other dairy products, often cause afflicted individuals to avoid dairy products in their diets. Lactose malabsorption is caused by a decreased ability to digest lactose that is due to a deficiency in the levels of the enzyme lactase. Lactase breaks lactose down into 2 simpler sugars, glucose and galactose, which are readily absorbed into the bloodstream. This enzyme is produced by expression of the lactase–phlorizin hydrolase gene in the cells lining the small intestine. All infants produce lactase and successfully digest lactose provided by human milk or by infant formulas. However, sometime after weaning, a genetically programmed decrease in lactase (lactase nonpersistence) occurs in most children worldwide. The symptoms of lactose intolerance result from bacterial fermentation of undigested lactose in the colon. Lactose malabsorption can be diagnosed by having individuals ingest a standard dose of lactose after fasting and measuring breath hydrogen; elevated breath hydrogen levels are caused by bacterial fermentation of undigested lactose in the colon. Other diagnostic tools include measuring lactase activity in an intestinal biopsy sample or genetic testing for the common polymorphism that is linked to lactase nonpersistence. The demonstration of lactose malabsorption does not necessarily indicate that an individual will have symptoms. Many variables determine whether a person who malabsorbs lactose develops symptoms, including the dose of lactose ingested, the residual intestinal lactase activity, the ingestion of food along with lactose, the ability of the colonic flora to ferment lactose, and individual sensitivity to the products of lactose fermentation. Current management often relies on reducing lactose exposure by avoiding milk and milk-containing products or by drinking milk in which the lactose has been prehydrolyzed with lactase. Alternatively, persons with lactase nonpersistence may tolerate moderate amounts of dairy products ingested with other foods. Many individuals, however, mistakenly ascribe symptoms of diverse intestinal disorders to lactose intolerance without undergoing testing. This misconception becomes intergenerational, when parents with self-diagnosed lactose intolerance place their children on lactose-restricted diets (even in the absence of symptoms) in the mistaken belief that the children will develop symptoms if given lactose. The public health burden from deficiencies attributable to lactose intolerance has not been established. Many adults and children who avoid dairy products—which con-