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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.

There are only limited published data on the glycemic index (GI) and insulin index of raisins. Further, the GI and insulin index of raisins have not been determined in endurance athletes or in persons with prediabetes. The objective of this study was to determine both the GI and the insulin index of raisins, and to evaluate if these indexes are similar when measured in different populations. The study groups consisted of 10 healthy sedentary subjects (S, 25.7±1.3 y, BMI=23.3±1.7 kg/m2), 11 endurance athletes (A, 23.1±1.0 y, BMI=24.1±0.3 kg/m2), and 10 prediabetic individuals (P, 50±2.6 y, BMI=32.6±1.9 kg/m2). Subjects consumed 50 g of available carbohydrates from raisins and from a glucose solution (reference food) on two separate occasions. Serum glucose and insulin concentrations were measured from capillary finger-stick blood samples at baseline and at 15, 30, 45, 60, 90, and 120 min (& 150 and 180 min for P) postprandially. The GI of raisins was low (GI≤55) in the S (49.4±7.4) and P (49.6±4.8) groups and was moderate (GI 55-69) in the A group (62.3±10.5), but there were no differences among the groups (P=0.437). The insulin index values of raisins were 47.3±9.4, 51.9±6.5, and 54.4±8.9 for the S, A, and P groups, respectively. On average, the A group secreted 2-2.5-fold less insulin per gram of carbohydrate compared with the S and P groups, respectively (P

Background: Many laboratories offer glycemic index (GI) services. Objective: We assessed the performance of the method used to measure GI. Design: The GI of cheese-puffs and fruit-leather (centrally provided) was measured in 28 laboratories (n = 311 subjects) by using the FAO/WHO method. The laboratories reported the results of their calculations and sent the raw data for recalculation centrally. Results: Values for the incremental area under the curve (AUC) reported by 54% of the laboratories differed from central calculations. Because of this and other differences in data analysis, 19% of reported food GI values differed by > 5 units from those calculated centrally. GI values in individual subjects were unrelated to age, sex, ethnicity, body mass index, or AUC but were negatively related to within-individual variation (P = 0.033) expressed as the CV of the AUC for repeated reference food tests (refCV). The between-laboratory GI values (mean +/- SD) for cheese-puffs and fruit-leather were 74.3 +/- 10.5 and 33.2 +/- 7.2, respectively. The mean laboratory GI was related to refCV (P = 0.003) and the type of restrictions on alcohol consumption before the test (P = 0.006, r(2) = 0.509 for model). The within-laboratory SD of GI was related to refCV (P < 0.001), the glucose analysis method (P = 0.010), whether glucose measures were duplicated (P = 0.008), and restrictions on dinner the night before (P = 0.013, r(2) = 0.810 for model). Conclusions: The between-laboratory SD of the GI values is approximate to 9. Standardized data analysis and low within-subject variation (refCV < 30%) are required for accuracy. The results suggest that common misconceptions exist about which factors do and do not need to be controlled to improve precision. Controlled studies and cost-benefit analyses are needed to optimize GI methodology. The trial was registered at clinicaltrials.gov as NCT00260858.