Lactose Challenge Research Articles

Lactose malabsorption and rate of bone loss in older women.

to study the prevalence of lactose malabsorption with increasing age and to determine whether lactose malabsorbers consume less dietary calcium, have lower bone mineral density or display faster bone loss than lactose absorbers. 80 healthy Caucasian women aged 40-79 years (20 per decade) were studied for 1 year. breath hydrogen exhalation was measured for 3 after a 50 g oral lactose challenge. Bone density was assessed in the radius, femoral neck, lumbar spine and total body by dual energy x-ray absorptiometry and dietary calcium intake was estimated by 4-day diet records and food-frequency questionnaires. lactose malabsorption rose with age (15% in those aged 40-59 years versus 50% in those aged 60-79; P < 0.01). Malabsorbers aged 70-79 years consumed significantly less calcium than lactose absorbers of this age (P < 0.05). Baseline total body calcium values were lower in lactose malabsorbers (n=26) than in lactose absorbers (n=54) but age-adjustment eliminated this difference. Bone change (% per year) was correlated with dietary calcium intake at the femoral neck and trochanter (P < 0.05) but was not statistically greater in malabsorbers than in absorbers. the ability to absorb lactose declines in the 7th decade. This may contribute to decreased dietary intakes of milk products and calcium in elderly women. However, lactose malabsorption without reduction in calcium intake has little effect on bone mineral density or the rate of bone loss.

Improved clinical tolerance to chronic lactose ingestion in subjects with lactose intolerance: a placebo effect?

Background—Uncontrolled studies of lactose intolerant subjects have shown that symptom severity decreases after chronic lactose consumption. Adaptation of the colonic flora might explain this improvement.Aims—To compare the effects of regular...

Recurrent abdominal pain and lactose maldigestion in school-aged children.

Recurrent abdominal pain of childhood affects 10 to 15% of school-aged children and leads to disability and learning difficulties. Lactose maldigestion may be a causative or contributory factor that when identified may lead to improvement. Thus, formal diagnostic testing using breath hydrogen lactose challenge methods is encouraged. This review focuses on this important condition and management options.

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.

Lactose and galactose intake and metabolism in relation to the risk of epithelial ovarian cancer.

It has been suggested that aspects of lactose consumption and metabolism favoring a relatively high tissue level of galactose-1-phosphate may predispose women to ovarian cancer. The authors sought to examine this hypothesis in a study of 108 18- to 74-year-old Caucasian residents of a three-county area of western Washington who were diagnosed with stage I ovarian cancer during 1989-1991, and 108 age- and race-matched controls. Lactose and galactose intake, measured using a food frequency questionnaire, had been hypothesized to increase risk, but were somewhat lower among the cases than among the controls (75th percentile of lactose intake vs. 25th: odds ratio (OR) = 0.80, 95% confidence interval (Cl) 0.52-1.2; of galactose intake: OR = 0.71, 95% Cl 0.48-1.1). Intestinal lactase activity, also hypothesized to have a positive relation with ovarian cancer occurrence, was measured with an oral lactose challenge followed by determination of urinary galactose; no evidence that it was related to the disease was found (75th percentile of excreted galactose vs. 25th: OR = 0.87, 95% Cl 0.62-1.2). Galactose-1-phosphate uridyltransferase (transferase), the enzyme responsible for the metabolism of galactose-1-phosphate, was measured in erythrocytes; no deficit in cases was observed (75th percentile of transferase activity vs. 25th: OR = 1.3, 95% Cl 0.80-2.1). There was also no excess of cases carrying low-activity genetic variants of the transferase enzyme (lower-activity variants vs. higher-activity variants: OR = 0.61, 95% Cl 0.21-1.7). These results do not support the hypothesis that aspects of lactose and galactose intake and metabolism have a bearing on the etiology of ovarian cancer.

The status of lactose absorption in Hong Kong Chinese children.

Lactose malabsorption was investigated in 169 Chinese children aged between two and 16 years using the breath hydrogen test. The challenge was either lactose solution (1 g/kg) or cow's milk (10 ml/kg). Overall, 68% of the children showed a significant increase in breath hydrogen following the lactose challenge while only 17% showed an increase after the cow's milk challenge and 13% after both challenges. The number of malabsorbers increased significantly (p less than 0.001) with age and no associated gastrointestinal symptoms or signs were found in any of the children following the challenges, suggesting a gradual and partial loss of intestinal lactase activity. We conclude that the prevalence of lactose malabsorption in Hong Kong children is very high using the standard lactose tolerance test but when a more realistic amount of lactose and a natural medium such as a glass of milk is used as the challenge, the number of malabsorbers becomes small and clinically insignificant.

β-Galactosidase Tablets in the Treatment of Lactose Intolerance in Pediatrics

Lactose-intolerant children manifest diminished or nonexistent intestinal lactase activity, resulting in flatulence, abdominal pain, and diarrhea. To assess the hydrolytic capability of lactase-containing tablets taken immediately before oral lactose challenge, we studied 18 children previously identified as being lactose intolerant and having no underlying organic gastrointestinal disease. Subjects had a mean (+/- SEM) age of 11.4 +/- 3.4 years; 72% were male. At time of the study, lactase-containing tablets or placebo tablets were ingested (double-blind) immediately before drinking a solution of lactose. Breath samples were obtained for hydrogen analysis at 30-minute intervals during a 2-hour period, and clinical symptoms were monitored. In lactose-intolerant patients, hydrogen production was significantly greater following placebo (maximum hydrogen excretion, approximately 60 ppm) compared with lactase-containing tablets (maximum hydrogen excretion, 7 ppm). Increased hydrogen production was associated with clinical symptoms including abdominal pain (89% of subjects following placebo ingestion), bloating (83%), diarrhea (61%), and flatulence (44%). These results indicate, therefore, that coingestion of lactose and lactase-containing tablets significantly reduces both breath hydrogen excretion and clinical symptoms associated with lactose intolerance.

Enzyme Replacement for Lactose Malabsorption Using a Beta-D-Galactosidase

We evaluated 10 healthy symptomatic lactose malabsorbers for effect of an oral beta-D-galactosidase derived from Aspergillus oryzae (Lactrase, Kremers Urban Company, Milwaukee, WI, U.S.A.) on symptom and breath hydrogen response to challenge with 50 g lactose. Basally and at 30-min intervals for 8 h after lactose challenge, end-alveolar breath samples were collected and analyzed for hydrogen using gas chromatography. Symptoms were scored at 30 min and hourly for 8 h, rating bloating, cramps, nausea, pain, diarrhea, and flatulence. Four challenges were performed on 4 separate days with at least 3 days between challenges. The first two challenges served as baselines. Just before ingestion of 50 g powdered lactose dissolved in 200 ml water, beta-D-galactosidase capsules were given orally as a 250-mg dose for the third challenge and a 500-mg dose for challenge 4. Hydrogen excretion, quantified by using a trapezoidal method for computing area under the discontinuous curve of breath hydrogen concentration, was decreased in subjects receiving beta-D-galactosidase (base-line I, 346.0 ppm/h; baseline II, 367.2 ppm/h; 250-mg galactosidase 208.2 ppm/h; 500-mg galactosidase, 178.0 ppm/h; p less than or equal to 0.05). Other analyzed parameters of H2 excretion were also decreased. Analysis of symptom response scores showed a dose-related decrease for bloating and flatus (p less than or equal to 0.05) and no statistical difference in the other assessed symptoms. We conclude that beta-D-galactosidase from Aspergillus oryzae, when given just before ingestion of lactose by lactose malabsorbers, can produce a dose-dependent reduction (statistically significant for the 500-mg dose) in breath hydrogen excretion, bloating, and flatus.

Lactase insufficiency in Chinese children detected by oral milk and lactose challenge

A study to determine the incidence of late-onset lactose intolerance was undertaken in 68 normal Chinese children in Singapore using measurements of breath hydrogen concentrations, following a lactose or milk challenge, as indicator of lactose malabsorption. Evidence of lactose malabsorption was detected in 26% of children given a lactose challenge, and in 21% of those given a milk challenge. It is concluded that late-onset lactase insufficiency is common in Chinese children in Singapore.

Lactose tolerance despite hypolactasia in adult coeliac disease

Although symptoms of milk intolerance are common in primary (genetically determined) hypolactasia it is a clinical impression that such symptoms are infrequent in adult patients with hypolactasia secondary to damage of the mucosa of the small intestine. This study was designed to determine whether a lactose (50 g) challenge is better tolerated by patients with coeliac disease and secondary hypolactasia than patients with primary hypolactasia. Based on intestinal histology and disaccharidase levels, three groups of adults were studied: controls (n= 20), patients with primary hypolactasia (n= 20) and patients with hypolactasia secondary to newly diagnosed coeliac disease (n= 15). The response to a challenge with 50 g lactose was assessed by a score of five symptoms and breath hydrogen production. Despite an equivalent level of hypolactasia, symptoms affected fewer patients with coeliac disease (33%) than subjects with primary hypolactasia (90%). Further, a positive lactose breath hydrogen test was noted in all (100%) patients with primary hypolactasia but in only six (40%) of those patients with newly diagnosed coeliac disease. These results suggest the presence of a considerable absorptive reserve for lactose in the distal small bowel of many patients with coeliac disease.

Blood glucose rise after lactose tolerance testing in infants1–2

Lactose tolerance tests are used clinically to screen children and infants. It is assumed that absorption of a lactose challenge in infants would occur in a predictable pattern prior to weaning. Twenty-one infants from 3 to 12 months of age were studied. The maximum blood glucose rise over fasting levels ranged from 11.0 to 62.0 mg/100 ml; the mean was 32.6 mg/100 ml. Six infants had a maximum rise of less than 20 mg/100 ml. Eleven infants (52%) had a maximum rise of greater than 30 mg/100 ml. Signs of intolerance were not noted in any subject. Weight and length were normally distributed. Results indicate the variance in glucose rise existing within a population of infants growing normally and consuming milk. Gastric emptying, digestion, and absorption may influence the blood glucose rise after a lactose test. Established glucose levels used as an index to lactose absorption in older children and adults may not accurately reflect lactase activity in infants.