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Sunday, March 21, 2010

Report from the LI Conference, part 13a: Question 1 Summary

The Draft Report summarized the presentations that looked at Question 1 (Tishkoff; Wooten; Wood; and Wilt) as follows:

1. What Is the Prevalence of Lactose Intolerance, and How Does This Prevalence Differ by Race, Ethnicity, and Age?

The prevalence of lactose intolerance is difficult to discern because studies have varied in their interpretation of what constitutes this condition. To estimate accurately the prevalence of lactose intolerance, one first must define lactose intolerance to permit the identification of those individuals with the condition and the exclusion of those without the condition. By applying this definition to a representative population sample, one can then estimate the prevalence in the general population and assess how this prevalence differs by age and race/ethnicity. We define lactose intolerance as the onset of gastrointestinal symptoms following a blinded, single-dose challenge of ingested lactose by an individual with lactose malabsorption, which are not observed when the person ingests an indistinguishable placebo. Although lactose malabsorption and lactase nonpersistence can be easily identified, they are not equivalent to lactose intolerance.


The prevalence of lactose intolerance in the United States cannot be estimated, despite a systematic evidence review that identified 54 articles, including 15 studies in the United States with a total of 4,817 participants. None of the studies used this definition or evaluated a representative sample of the U.S. population. Seven studies that assessed self-reported lactose intolerance provide limited insight because the self-diagnoses were not confirmed by testing for lactose malabsorption, and the symptoms seen in true lactose intolerance may result from several other conditions such as irritable bowel syndrome. Nine studies evaluated only the genetic predisposition to lower than expected levels of lactase in adults (lactase nonpersistence) without assessing lactose malabsorption or intolerance directly. Five studies reported decreased intestinal tissue lactase activity, and 31 studies addressed lactose malabsorption directly (as evidenced by a positive hydrogen breath test after ingestion of lactose).


Although these studies shed some light on the epidemiology of lactose intolerance (discussed below), they cannot be used to estimate the prevalence of lactose intolerance. Many individuals who have the biologic underpinnings for lactose malabsorption (low lactase levels or a genetic profile associated with low lactase) or who have demonstrated lactose malabsorption do not experience the onset of or an increase in the severity of gastrointestinal symptoms following a blinded lactose challenge. Complicating this further, evidence demonstrates that many who self report lactose intolerance show no evidence of lactose malabsorption. Thus, the cause of their gastrointestinal symptoms is unlikely to be related to lactose.


Despite the limitations in the available studies discussed above, several trends are noteworthy across the studies regarding lactose intolerance, lactose malabsorption, lactase nonpersistence, age, and race/ethnicity. First, lactose intolerance determined by self-report or nonblinded lactose challenge is less frequent across all ethnic groups than is lactose malabsorption determined by breath hydrogen tests or lactase nonpersistence determined by biopsy or genetic testing. Second, lactose intolerance, lactose malabsorption, and lactase nonpersistence vary across racial and ethnic groups with the lowest reported occurrence in European Americans and higher although variable occurrence in African Americans, Hispanic Americans, Asian Americans, and Native Americans. The systematic evidence review notes that the racial and ethnic variability in lactose intolerance following nonblinded lactose challenge was not as extreme as that reported in lactose malabsorption and lactase nonpersistence. Third, lactose intolerance with nonblinded lactose challenge and lactose malabsorption was low in young children, but increased with age. In children younger than 6 years, lactose malabsorption was low in all the studies and peaked between ages 10 and 16 years. Little evidence suggests that lactose intolerance increases in older persons. These trends need to be verified by representative population studies using the case definition of lactose intolerance

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