Effects of a beverage containing an enzymatically induced-viscosity dietary fiber, with or without fructose, on the postprandial glycemic response to a high glycemic index food in humans.

OBJECTIVE: Dietary supplementation with guar gum or fructose has been reported to reduce the postprandial glycemic response to an oral glucose challenge. As a result of the poor palatability of most foods containing guar gum, a novel low-viscosity beverage with guar gum was developed that becomes viscous in vivo through an enzymatic induction. The primary study objective was to determine the effect of an amylase-induced viscosity (I-V) product, with or without supplemental fructose, on the postprandial glycemic response to a high glycemic index test meal in healthy nondiabetic subjects. DESIGN: The study was a four-treatment, placebo-controlled, double-blind, randomized block protocol. SETTING: The study was performed at Glycaemic Index Testing, Inc., Toronto, Ontario, Canada. SUBJECTS: A total of 30 healthy nondiabetic volunteers (13 male, 17 female, mean+/-s.e.m. age of 51+/-3 y and body mass index of 24.2+/-0.4 kg/m(2)) participated in the study. INTERVENTION: In the morning after an overnight fast, subjects participated in four 3-h meal glucose tolerance tests on separate occasions. The test meals contained 50 g of available carbohydrate from maltodextrin and white bread (control) or the same meal with either 5 g of guar gum (3.6 g galactomannan), 5 g of fructose, or 5 g of guar gum +5 g of fructose. RESULTS: Treatments containing guar gum had a reduced (P<0.01) baseline-adjusted peak glucose response and incremental area under the glucose curve. In contrast to previous studies, fructose increased (P<0.05) the baseline-adjusted peak glucose concentration. CONCLUSIONS: Guar gum incorporated into an amylase I-V product provided a means to stabilize blood glucose levels by reducing the early phase excursion and then by appropriately maintaining the later phase excursion in healthy nondiabetic humans.

Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet.

OBJECTIVE: To determine whether African-American adolescent girls who were fed a dairy-rich diet for 21 days could adapt to lactose, experiencing an overall improvement in lactose tolerance as well as a decrease in hydrogen gas production. DESIGN: Twenty-one-day dietary intervention study. SUBJECTS/SETTING: Seventeen of 21 African-American girls (aged 11 to 15 years) enrolled in a calcium metabolism study chose to participate in the lactose tolerance study. Subjects were screened for any diseases, conditions, or medications that might alter calcium metabolism or colonic fermentation. Subjects were housed in a fraternity on the Purdue University, West Lafayette, Ind, campus, and were supervised 24 hours a day. INTERVENTION: Subjects consumed a dairy-based diet averaging 1,200 mg calcium and 33 g lactose per day for 21 days. Lactose digestion was assessed by an 8-hour breath hydrogen test on days 1 and 21, and symptoms of intolerance (abdominal pain, bloating, flatulence, and diarrhea) were evaluated hourly on a ranked scale during the breath hydrogen tests and once each evening during the 21-day feeding period. MAIN OUTCOME MEASURES: A comparison of breath hydrogen production and gastrointestinal symptoms at the beginning and end of the study. STATISTICAL ANALYSES PERFORMED: The Wilcoxon signed ranks test was used to compare the area under the curve for the 2 breath hydrogen tests. Spearman's p test for trend was used to determine whether there was a change in symptoms. All statistical analyses were 2-tailed and significance was set at P = .05. RESULTS: Fourteen of the 17 subjects had lactose maldigestion. Breath hydrogen excretion decreased significantly (P < .03) from the beginning (148.3 +/- 27.0 ppm x hours) to the end (100.7 +/- 19.3 ppm x hours) of the 21-day period. Gastrointestinal symptoms were negligible during both the breath hydrogen tests as were symptoms during the 21-day period. APPLICATIONS/CONCLUSIONS: The diet was well tolerated by the subjects. Furthermore, the decrease in breath hydrogen suggests colonic adaptation to the high-lactose diet. The results indicate that lactose maldigestion should not be a restricting factor in developing adequate calcium diets for this population. The existence of lactose maldigestion does not result in lactose intolerance in this population when it is fed a dairy-rich diet.

Fecal hydrogen production and consumption measurements. Response to daily lactose ingestion by lactose maldigesters.

The alteration of hydrogen (H2) metabolism, which accounts for the large decrease in breath H2 excretion following prolonged ingestion of malabsorbed carbohydrate (lactulose, lactose in lactose maldigesters) was studied in six lactose-maldigesting adults. Metabolic inhibitors of the three main H2-consuming reactions (methanogenesis, sulfate reduction, and acetogenesis) were used to independently measure H2 production and consumption in fecal samples obtained after 10 days of either dextrose or lactose feeding. Absolute fecal H2 production (net of production minus consumption) after 3 hr of incubation with lactose was approximately threefold lower after lactose adaptation (242 +/- 54 microliters) compared to dextrose adaptation (680 +/- 79 microliters, P = 0.006). Fecal H2 consumption was not affected by either feeding period. We conclude that decreased absolute H2 production, rather than increased H2 consumption, is responsible for the decrease in breath H2 observed with lactose feeding.

Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance.

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.

How much lactose is low lactose?

OBJECTIVE: To test the hypothesis that complete elimination of lactose is not necessary to ensure tolerance by lactose maldigesters. DESIGN: Double-blind, randomized protocol in which challenge doses of 0, 2, 6, 12, and 20 g lactose in water were fed to subjects after a 12-hour fast. SUBJECTS: 13 healthy, free-living adults who were lactose maldigesters. MAIN OUTCOME MEASURES: Breath hydrogen production (a measure of maldigestion) and symptom response to each challenge dose. STATISTICAL ANALYSIS: Analysis of variance was done to determine overall differences in mean hydrogen gas production (peak and sum of hours 1 through 8). Friedman's test was used to determine overall differences in the mean ranks for each symptom. Fisher's least significant difference test was used for multiple comparisons for hydrogen and symptom and data. RESULTS: Hydrogen production after consumption of the 0- and 2-g lactose doses was not significantly different. Hydrogen production increased with the 6-g dose. Intensity of abdominal pain increased when the dose of lactose was 12 g. Episodes of flatulence did not increase until the dose reached 20 g. No significant differences in the occurrence of diarrhea were observed after the five treatments. CONCLUSIONS: No significant increase in breath hydrogen production or intolerance symptoms occurred after consumption of a 2-g dose of lactose. Up to 6 g was tolerated, even though maldigestion could be measured at the 6-g dose. Thus, lactose maldigesters may be able to tolerate foods containing 6 g lactose or less per serving, such as hard cheeses and small servings (120 mL or less) of milk.