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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.

Section I: Basic Principles and Concepts Examining the Relationship between Diet, Nutrition and Disease: Dietary Assessment Methodology. Energy Requirement Methodology. Physical Assessment. Overview of Nutritional Epidemiology. Analysis, Presentation, and Interpretation of Dietary Data. Nutrition Intervention: Current Theoretical Bases for Nutrition Intervention and Their Uses. Nutrition Intervention: Lessons from Clinical Trials. Tools and Techniques to Facilitate Eating Behavior Change. Evaluation of Nutrition Interventions. Biomarkers and Biological Indicators of Change. Genetic Influence on Nutritional Health: Genetic Influences on Blood Lipids and Cardiovascular Disease Risk. Genetics of Human Obesity. Genetic Influence on Cancer Risk. Inborn Errors of Metabolism. Supplements and Food Replacements: Role of Liquid Dietary Supplements. Composite Foods and Formulas, Parenteral and Enteral Nutrition. Herbs and Other Botanical Supplements: Principles and Concepts. Section II: Disease-Specific Intervention: Prevention and Treatment Cardiovascular Disease: Dietary Macronutrients and Cardiovascular Risk. Other Dietary Components and Cardiovascular Risk. Nutrition, Diet & Hypertension. Nutrition and Congestive Heart Failure. Cancer Prevention and Therapy: Nutrition and Breast Cancer. Nutrition and Colon Cancer. Nutrition and Prostate Cancer. Nutrition and Lung Cancer. Nutrition and the Patient with Cancer. Diabetes Melitus: Obesity and the Risk for Diabetes. Nutrition Management for Type 1 Diabetes. Nutritional Management of Type 2 Diabetes. Nutrition Management for Gestational Diabetes. Obesity: Overview of Treatments and Interventions. Role of Physical Activity. Micronutrient Intake and Body Weight. Behavioral Risk Factors for Obesity: Diet and Physical Activity. Role of Taste and Appetite in Body Weight Regulation. Gastrointestinal Diseases: Nutrition in the Prevention and Treatment of Common Gastrointestinal Symptoms. Nutrient Considerations in Lactose Intolerance. Nutrient Considerations in Inflammatory Bowel Disease and Short Bowel Syndrome. Nutrition and Liver Disease. Other Major Diseases: Nutrition and Renal Disease. Nutritional Management of Parkinson's Disease and Other Conditions Like Alzheimer's Disease. Osteoporosis. Eating Disorders: Anorexia Nervosa, Bulimia Nervosa and Binge Eating Disorder. Nutrition and Food Allergy. Nutrition and Cystic Fibrosis. Osteomalacia. Nutrition and Immunodeficiency Syndromes. Disease Prevention Strategy: Nutrition Guidelines to Maintain Health. Epilogue.

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

Ingestion of a large, single dose of lactose by lactose maldigesters commonly results in diarrhea, bloating, and flatulence. However, multiple factors affect the ability of lactose to induce perceptible symptoms. These factors include residual lactase activity, gastrointestinal transit time, lactose consumed with other foods, lactose load, and colonic fermentation. This chapter reviews the pathophysiology of lactose maldigestion, attempts to correct common misconceptions concerning the frequency and severity of lactose intolerance symptoms, and provides dietary strategies to minimize symptoms of intolerance. In addition to food sources of lactose, small amounts of lactose are found in a wide variety of medications due to the excellent tablet-forming properties of lactose. Avoidance of milk and milk products is unnecessary since moderate lactose consumption does not produce a symptomatic response in maldigesters. Additionally, various dietary strategies effectively manage lactose intolerance by reducing or eliminating gastrointestinal symptoms. Dairy food consumption is possible for individuals who are lactose intolerant if simple dietary management strategies are incorporated into daily living.

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.Twenty-one-day dietary intervention study.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.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.A comparison of breath hydrogen production and gastrointestinal symptoms at the beginning and end of the study.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.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.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.

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.