ABSTRACT
Lactose is the primary carbohydrate in milk. To be digested, lactose must be hydrolyzed in the intestinal brush border by an enzyme, lactase, into two monosaccharides, glucose and galactose, which are rapidly absorbed in the small intestine (Paige 2005). Lactose is the most important energy source for infants and supplies one of the few sources of galactose in the human diet. Once past the weaning stage, humans’ ability to secrete lactase diminishes, leading to the development of lactase deficiency (or lactase nonpersistence) (Silanikove et al. 2015). Lactase deficiency can lead to undigested lactose reaching the colon (lactose malabsorption) and possibly lactose intolerance (lactose malabsorption accompanied by gastrointestinal symptoms). Due to inconsistent definitions and use of the term lactose intolerance, in 2010, the National Institutes of Health (NIH) developed a consensus statement on a formal definition of lactose intolerance: “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 an individual ingests an indistinguishable placebo” (Suchy et al. 2010). Despite this consensus definition, it should be noted that the terms lactase deficiency, lactose malabsorption, and lactose intolerance are still used interchangeably and inconsistently, which continues to cause confusion about the true prevalence of lactose intolerance versus lactase deficiency. The difference between lactose absorption and lactase malabsorption is illustrated in Figure 8.1 and the difference between lactose malabsorption and lactose intolerance is illustrated in Figure 8.2.
