Differential impact of lactose/lactase phenotype on colonic microflora

Abstract

Background: The ability to digest lactose divides the world's population into two phenotypes that may be risk variability markers for several diseases. Prebiotic effects likely favour lactose maldigesters who experience lactose spilling into their colon.

Objective: To evaluate the effects of fixed-dose lactose solutions on fecal bifidobacteria and lactobacilli in digesters and maldigesters, and to determine whether the concept of a difference in ability to digest lactose is supported.

Methods: A four-week study was performed in 23 lactose maldigesters and 18 digesters. Following two weeks of dairy food withdrawal, subjects ingested 25 g of lactose twice a day for two weeks. Stool bifidobacteria and lactobacilli counts pre- and postintervention were measured as the primary outcome. For secondary outcomes, total anaerobes, Enterobacteriaceae, beta-galactosidase and N-acetyl-beta-D-glucosaminidase activity in stool, as well as breath hydrogen and symptoms following lactose challenge tests, were measured.

Results: Lactose maldigesters had a mean change difference (0.72 log10 colony forming unitsg stool; P=0.04) in bifidobacteria counts compared with lactose digesters. Lactobacilli counts were increased, but not significantly. Nevertheless, reduced breath hydrogen after lactose ingestion correlated with lactobacilli (r=-0.5; P<0.001). Reduced total breath hydrogen and symptom scorestogether, with a rise in fecal enzymes after intervention, were appropriate, but not significant.

Conclusions: Despite failure to achieve full colonic adaptation, the present study provided evidence for a differential impact of lactose on microflora depending on genetic lactase status. A prebiotic effect was evident in lactose maldigesters but not in lactose digesters. This may play a role in modifying the mechanisms of certain disease risks related to dairy food consumption between the two phenotypes.

Figure 1)

Diagram depicting the flow of recruited participants and their genetic/phenotypic classification. The number of participants at each phase is shown with a summary of the reasons for dropping out of the study. *Lactase nonpersistent (LNP) and lactase persistent (LP) status was defined by genetic analysis. **The reasons for dropping out were as follows: time constraints (seven LP, two LNP subjects); personal (one LNP subject); tests too symptomatic (four LNP subjects) and could not get accustomed to taking regular lactose after test 2 (two LNP subjects). BID Twice daily

Figure 2)

Scatter plot showing the change in the primary outcomes: bifidobacteria and lactobacilli counts (log₁₀ [colony forming units (CFU)/g stool]) between test 3 and test 2. Lactase nonpersistent (LNP) subjects are represented by open circles (genotype CC). Lactase persistent (LP) subjects are represented by solid circles (genotype TT) and open diamonds (genotype CT). In addition, the mean change for the respective LNP/LP groups is shown with a line and the exact value. No comparisons were made with test 1 (baseline)

Figure 3)

Scatter plot showing the change in total breath hydrogen (TBH₂) between test 3 and test 2, with the change in bacterial counts (colony forming units [CFU]) for the primary outcomes for bifidobacteria (left panel) and lactobacilli (right panel) in lactase nonpersistent subjects only (lactase persistent subjects have almost no TBH₂ to begin with). The P value, r² and slope are indicated in each panel. No comparisons were made with test 1 (baseline)