Lactose Digestion and Gastrointestinal Function

Lactose is hydrolyzed at the intestinal jejunal brush border by the enzyme lactase into its absorbable monosaccharides glucose and galactose. Lactase activity is robust during infancy and, as is the case in humans and most mammals, declines after weaning. Accordingly, the general pattern of lactase non-persistence is a continuous decline in genetically programmed populations. A shifting pattern of lactose digestion and gastrointestinal function is a result of lactase nonpersistence. The pattern can be described and monitored during three distinct clinical phases.

First, there is a decreasing ability to digest the large lactose load consumed during the screening test. It is important to recognize that this is not an all-or-none phenomenon but rather a slowly progressive decline in available lactase activity, and that this decline, as noted previously, can be influenced by transit time, the vehicle in which the lactose is consumed, and/or the intake of additional foods along with lactose.

Next, with the continued decline of lactase activity, a point is reached when available lactase activity is no longer sufficient to hydrolyze more modest levels of lactose. Therefore, the consumption of a glass of milk or another product containing the equivalent level of lactose will result in incomplete hydrolysis of the lactose consumed. The individuals so tested frequently do not recognize signs or symptoms associated with the incomplete digestion of lactose.

Finally, with the continued decline of lactase activity with increasing age, individuals become symptomatic as a result of the undigested lactose. The decline in available lactase activity reaches a recognizable clinical threshold with increasing age (Figure 1).

Initially, many reports treated the population studied as a single unit and paid incomplete attention to age-specific considerations. Distinctions between secondary lactose malabsorption due to short-term intestinal injury and primary lactose malabsorption that has a genetic basis were not always made. This introduced additional confounding variables. Differences in an individual's capacity to hydrolyze and tolerate a lactose challenge dose compared to his or her ability to utilize lesser amounts of lactose found


Figure 1 Symptoms associated with lactose maldigestion result from the decline in lactase levels with age and increase with the amount of lactose consumed.

Figure 1 Symptoms associated with lactose maldigestion result from the decline in lactase levels with age and increase with the amount of lactose consumed.

in usually consumed amounts of milk created additional areas of confusion.

When attention is paid to the many factors associated with lactose digestion from infancy to old age, it is possible to place many of the seeming contradictions into perspective. What may have appeared to be incongruities in reported data appear to merge into a relatively predictable pattern of lactose digestion.

Lactose maldigestion and intolerance are influenced by age, infection, size of the lactose bolus, gastric emptying time, intestinal transit time, individual sensitivities, eating habits, genetics, environment, food ideologies, and cultural patterns. Furthermore, symptoms of lactose malabsorption may also be the result of bacterial fermentation of undigested carbohydrate in the colon. The type and extent of the colonic bacterial profile and the absorption of hydrogen and the volatile fatty acids will influence individual reports of symptoms associated with lactose intolerance. Clearly, lactose malabsorption is not a homogeneous event. Neither is it an all-or-none phenomenon having its origins in a single etiology. Clinical expressions of lactose malabsorption, lactose intolerance, and milk rejection find their origins in one or more of the causes outlined previously (Table 1).

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