We conducted blinded, controlled crossover studies to determine the effect of daily lactose feeding on colonic adaptation and intolerance symptoms. The initial study with nine lactose maldigesters showed a threefold increase in fecal beta-galactosidase activity after 16 d of lactose feeding. To determine the effects of this adaptation on breath hydrogen and intolerance symptoms, 20 lactose-maldigesting adults were randomly assigned to lactose or dextrose supplementation for 10 d (days 1-10), crossing over to the other period for days 12-21. The sugar dosage was increased from 0.6 to 1.0 g.kg-1.d-1, subdivided into three equal doses, by adjusting the dose every other day. Symptoms during lactose supplementation and comparison of symptoms during the lactose and dextrose feeding periods showed no significant differences. On days 11 and 22, challenge doses of lactose (0.35 g/kg) were administered after an overnight fast, and breath hydrogen and intolerance symptoms (abdominal pain, flatulence, and diarrhea) were carefully monitored for 8 h. Frequency of flatus passage and flatus severity ratings after the lactose challenge decreased 50% when studied at the end of the lactose period compared with the dextrose period. The sum of hourly breath-hydrogen concentrations (1-8 h) was significantly reduced after the lactose feeding period (9 +/- 38 ppm.h) compared with after the dextrose period (385 +/- 52 ppm.h, P < 0.001). We conclude that there is colonic adaptation to regular lactose ingestion and this adaptation reduces lactose intolerance symptoms.

Directed modulation of the colonic bacteria to metabolize lactose effectively is a potentially useful approach to improve lactose digestion and tolerance. A randomized, double-blind, multisite placebo-controlled trial conducted in human subjects demonstrated that administration of a highly purified (>95%) short-chain galactooligosaccharide (GOS), designated "RP-G28," significantly improved clinical outcomes for lactose digestion and tolerance. In these individuals, stool samples were collected pretreatment (day 0), after GOS treatment (day 36), and 30 d after GOS feeding stopped and consumption of dairy products was encouraged (day 66). In this study, changes in the fecal microbiome were investigated using 16S rRNA amplicon pyrosequencing and high-throughput quantitative PCR. At day 36, bifidobacterial populations were increased in 27 of 30 of GOS subjects (90%), demonstrating a bifidogenic response in vivo. Relative abundance of lactose-fermenting Bifidobacterium, Faecalibacterium, and Lactobacillus were significantly increased in response to GOS. When dairy was introduced into the diet, lactosefermenting Roseburia species increased from day 36 to day 66. The results indicated a definitive change in the fecal microbiome of lactose-intolerant individuals, increasing the abundance of lactosemetabolizing bacteria that were responsive to dietary adaptation to GOS. This change correlated with clinical outcomes of improved lactose tolerance.A limited ability to digest lactose occurs when the intestinal lactase enzyme is reduced in the brush border of the small bowel mucosa. Consumption of dairy foods by lactose-intolerant individuals may result in clinical symptoms including abdominal pain, diarrhea, bloating, flatulence, and abdominal cramping. In these cases, lactose travels through the gastrointestinal tract and is fermented in the colon, producing acetate, carbon dioxide, hydrogen gas, and methane by gas-producing microbes. Approximately 75% of the global human population are lactose maladsorbers (1, 2). In the United States, it is estimated that up to 80 million Americans are at risk for lactose intolerance.Efforts to address lactose intolerance include avoidance of dairy foods, reduction in the lactose content of milk through treatment with microbial lactases, and the use of lactase enzymes to process milk before dairy consumption (3). Savaiano et al. conducted a randomized, double-blind, parallel-group, placebocontrolled study at two sites in the United States (4). A high purity (>95%) galactooligosaccharide (GOS/RP-G28) or a placebo (Sweetose; Tate & Lyle Ingredients) was administered in increasing doses to 62 lactose-intolerant subjects for 36 d. Subjects refrained from consuming lactose during the GOS treatment period. After GOS treatment, subjects reintroduced dairy products into their diets for an additional 30 d and then were challenged for lactose digestion and were evaluated for symptoms improvement via a Likert scale. Subjects consuming GOS trended toward improvement in overall symptoms after 36 d of ...

The use of fermented dairy foods is common in areas of the world where lactase deficiency is prevalent. Recently, we have shown that the digestion of lactose from yogurt is enhanced as compared to that from milk. This enhanced digestion is apparently due to inherent B-galactosidase in yogurt which is active in the gastrointestinal tract after consumption of the yogurt. Furthermore, yogurt is well tolerated by lactase-deficient subjects resulting in little or no gastrointestinal distress. Since other fermented and microbial-containing dairy foods are consumed worldwide and may also contain some "lactase" activity, we chose to evaluate the digestion of lactose from three of these products: pasteurized yogurt, cultured milk (buttermilk), and sweet acidophilus milk. Breath hydrogen techniques were used to evaluate lactose malabsorption in nine lactase-deficient subjects. The studies demonstrated that yogurt is unique among the products tested in enhancing the digestion of lactose. Furthermore, pasteurization of yogurt eliminated the enhanced digestion of lactose, reduced the inherent lactase activity of the yogurt by 10-fold and reduced cell counts by 100-fold. Interestingly, eight of nine subjects fed cultured milk experienced gastrointestinal distress, whereas all subjects fed pasteurized yogurt were symptom free, even though the amount of malabsorbed lactose was similar.

We reported previously that consumption of one cup of milk (240 mL) per day produced negligible symptoms in lactase-nonpersistent (LNP) individuals self-described as being severely lactose intolerant. We hypothesized that such LNP individuals could also tolerate two cups of milk per day if taken in two widely divided doses with food, and that psychologic factors play a role in perceptions of lactose intolerance. The Minnesota Multiphasic Personality Inventory 2 (MMPI-2) was administered to 19 LNP subjects self-described as markedly lactose intolerant (S-LNP), 13 LNP subjects who denied lactose intolerance (A-LNP), and 10 lactase-persistent individuals who believed they were lactose intolerant (S-LP). Symptoms were recorded when LNP subjects ingested 240 mL regular or lactose-hydrolyzed milk twice daily for 7 d in a double-blind crossover study. The results showed that neither LNP group had a significant increase in symptoms (P < 0.05) during the regular compared with the lactose-hydrolyzed milk periods. However, S-LNP subjects reported significantly greater gaseous symptoms than did the A-LNP subjects during both treatment periods. The MMPI-2 showed a high score on the "lie" validity scale for S-LNP subjects. We conclude that LNP subjects tolerate two cups of milk per day without appreciable symptoms. S-LNP subjects have underlying flatulence that is misattributed to lactose intolerance. MMPI-2 results were of questionable validity because of the high rate of dissimulation by LNP subjects.