The Lactose Intolerance Clearinghouse Has Moved.

My old website can be found at www.stevecarper.com/li I am no longer updating the site, so there will be dead links. The static information provided by me is still sound.

For quick offline reference, you can purchase Planet Lactose: The Best of the Blog as an ebook on Smashwords.com or Amazon.com or BarnesandNoble.com or a whole lot of other places that Smashwords is suppose to distribute the book to. Almost 100,000 words on LI, allergies, milk products, milk-free products, and the genetics of intolerance, along with large helpings of the weirdness that is the Net.

I suffer the universal malady of spam and adbots, so I moderate comments here. That may mean you'll see a long lag before I remember to check the site and approve them. Despite the gap, you'll always get your say. I read every single one, and every legitimate one gets posted.


Wednesday, March 10, 2010

Report from the LI Conference, part 8

From the overview talks of Doctors Neu, Krebs, Sibley, Grand, and Chang, the panel pulled together the following summary.

Introduction

Lactose intolerance is the syndrome of diarrhea, abdominal pain, flatulence, and/or bloating occurring after lactose ingestion. These symptoms—produced by malabsorption of lactose, a sugar found in milk and other dairy products—often result in afflicted individuals avoiding dairy products in their diets. Lactose malabsorption occurs because of a decreased ability to digest lactose, due to a deficiency in the levels of the enzyme lactase. Lactase breaks lactose down into two 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.

Infants of every racial and ethnic group worldwide produce lactase and successfully digest lactose provided by human milk or by infant formulas. However, sometime after weaning, in the majority of the world’s children, there is a genetically programmed decrease in lactase (lactase nonpersisters). Lactase nonpersistence variably affects diverse populations in the United States, including Asian Americans, African Americans, Hispanic Americans, Native Americans, Alaska Natives, and Pacific Islanders.

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 finding elevated levels of breath hydrogen, which is produced by bacterial fermentation of undigested lactose in the colon. Other diagnostic tools include measuring the 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 be symptomatic. 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, lactase nonpersisters may tolerate moderate amounts of dairy products ingested with other foods. However, many individuals mistakenly ascribe symptoms of a variety of 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 they will develop symptoms if given lactose.

The public health burden from deficiencies attributable to lactose intolerance has not been established. However, many adults and children who avoid dairy products—which constitute a readily accessible source of calcium, vitamin D, and other nutrients—are not ingesting adequate amounts of these essential nutrients. For example, most African American adolescents consume inadequate amounts of calcium and vitamin D because they avoid dairy products. Deficient intakes of calcium and vitamin D are risk factors for decreased bone mineral density. This may increase the risk of fracture throughout the life cycle, especially in postmenopausal women. Very low intake of vitamin D can lead to the development of rickets, especially in children of African descent and other highly pigmented individuals. Although reduced-lactose dairy and nondairy alternative products are typically fortified with calcium, vitamin D, and other nutrients, they may be more expensive and less widely available than conventional dairy products. The bioequivalence of these and other calcium supplements is uncertain.

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