SIX CASES OF LACTOSE INTOLERANCE. LACTOSE INTOLERANCE AND COELIAC DISEASE. DISACCHARIDASES ACTIVITY IN THE INTESTINAL MUCOSA ASCERTAINED WITH THE PERORAL BIOPSY.
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Of 40 patients with a partial gastrectomy (Billroth-II) 10 developed a milk intolerance and 11 had a lactase deficiency, the latter in 4 cases appearing together with a decrease in other disaccharidases. Only 2 of the 11 lactase-deficient patients complained of milk intolerance. The Ethanol lactose tolerance test (ELTT) was performed in 21 patients and was found to be abnormal in 6. Whereas cases of abnormal ELTT usually (4 of 6 cases) showed a lactase deficiency, only 2 patients with milk intolerance showed an abnormal ELTT and lactase deficiency. Milk intolerance can therefore only exceptionally be explained by lactase deficiency, and lack of lactase in the upper jejunum usually does not produce intolerance symptoms. Moreover, in comparable determinations from the afferent and efferent jejunal loop no differences in enzyme activities could be observed.
Lactose intolerance affects more than 50 million Americans. It is one of the most common gastrointestinal disorders seen by primary care physicians. When this disorder is properly diagnosed, the patient is easily treated with education and dietary modifications. Lactose intolerance is commonly misdiagnosed because of its overlapping symptoms of diarrhea and abdominal bloating. This article reviews the etiology, diagnosis, and treatment of lactose intolerance.
Lactose intolerance is a concern for the majority of the world's population. Persons who experience symptoms following the consumption of milk should consult with their physician. Symptoms may be eliminated or reduced with good dietary management that includes: Limiting milk consumption to one glass at a time. Drinking milk with other foods rather than alone. Eating yogurts instead of fluid milk. Using enzyme tablets to predigest the lactose in milk or to supplement the body's own lactase. Possibly eating small amounts of dairy foods each day to adapt the colonic bacteria. For an additional review of the research findings on lactose intolerance and milk drinking, the reader is directed to reference 4, a very recent and complete review by Scrimshaw and Murray. For information on dietary management of lactose intolerance suitable for the consumer, contact your local affiliate of the National Dairy Council.
Lactose intolerance is a concern for the majority of the world's population. Persons who experience symptoms following the consumption of milk should consult with their physician. Symptoms may be eliminated or reduced with good dietary management that includes: 1. limiting milk consumption to one glass at a time; 2. drinking milk with other foods rather than alone; 3. eating yogurts instead of fluid milk; 4. using enzyme tablets to predigest the lactose in milk or to supplement the body's own lactase; 5. possibly eating small amounts of dairy foods each day to adapt the colonic bacteria. For an additional review of the research findings on lactose intolerance and milk drinking, the reader is directed to reference 4, a very recent and complete review by Scrimshaw and Murray. For information on dietary management of lactose intolerance suitable for the consumer, contact your local affiliate of the National Dairy Council.
Lactose intolerance may give rise to a variety of gastro enterological symptoms depending on the degree of lactase deficiency present. A percentage of patients may be asymtomatic, but the presence of lactose in their diet leads to inadequate absorption of a variety of important nutrients resulting in deficiency disorders or less than optimal weight gain. The increase in migration from southern Europe and of late from Indo-China significantly increases the Australian population likely to be lactase-deficient. Many immigrants keen to adapt to the Australian way of life see milk as a new essential part of their diet. This, accompanied with a lack of basic English as a language, may compound the problem of diagnosis in these patients particularly if the medical practitioner is unaware of the syndrome. The ready availability of lactose-hydrolyzed milk powder as a Pharmaceutical Benefit should allow all patients to gain the nutritional advantage of milk without suffering the complications associated with lactose intolerance.
Lactose (milk sugar) is a fermentable substrate. It can be fermented outside of the body to produce cheeses, yoghurts and acidified milks. It can be fermented within the large intestine in those people who have insufficient expression of lactase enzyme on the intestinal mucosa to ferment this disaccharide to its absorbable, simple hexose sugars: glucose and galactose. In this way, the issues of lactose intolerance and of fermented foods are joined. It is only at the extremes of life, in infancy and old age, in which severe and life-threatening consequences from lactose maldigestion may occur. Fermentation as part of food processing can be used for preservation, for liberation of pre-digested nutrients, or to create ethanolic beverages. Almost all cultures and ethnic groups have developed some typical forms of fermented foods. Lessons from fermentation of non-dairy items may be applicable to fermentation of milk, and vice versa.
Lactose maldigestion has been under intensive research since its discovery in the 1960's. We know the prevalence of lactose maldigestion in a great number of countries and ethnic groups. However, there is often no provision made for the secondary type of maldigestion, and the study populations have sometimes been selected rather than picked at random. New methods for the measurement of lactose digestion have been developed, and its genetic mechanisms have received a great deal of attention during the last few years. However, in many studies the measurement and/or reporting of symptoms has quite often been overlooked. In this review, various topics related to lactose intolerance are discussed with a special emphasis on its symptoms.
Lactose intolerance is a prevalent clinical problem. Low lactase levels result either from intestinal injury, or as in the majority of the world's adult population, from alterations in the genetic expression of lactase-phlorizin hydrolase. Progress is being made in the basic understanding of the molecular and cellular biology of this enzyme and of the scientific basis of clinical syndromes involving low lactase activity.
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Milk intolerance, lactose intolerance and non-ulcer dyspepsia are common among Ethiopians. This study, therefore, was designed to find out if milk intolerance associated with lactase deficiency account for non-ulcer dyspepsia. Ninety-eight patients with non-ulcer dyspepsia and 95 controls were examined and interviewed for demographic data and milk drinking habits. Then each had a lactose tolerance test (LTT), stool examination for pH, ova and parasites. The demographic characteristics and the number of milk drinkers were comparable in the 2 groups. However, milk intolerance and lactose intolerance were significantly higher among the patients with non-ulcer dyspepsia than among the control group (p less than 0.01, p less than 0.05 respectively). The combination of milk intolerance, lactose intolerance and LTT was also significantly different (p less than 0.01). The mean stool pH was markedly reduced after lactose ingestion and there were more ova and parasites in the stools of the control group. These observations suggest that milk intolerance and/or lactose intolerance account significantly for the symptoms of the patients with non-ulcer dyspepsia. However, since lactose intolerance and abnormal LTT are very common among adult Ethiopians symptoms related to the drinking of milk should be interpreted with caution vis-a-vis the results of the lactose loading test.
Lactose digestion and tolerance were evaluated in 164 African Americans ranging in age from 12 to 40 y who claimed intolerance to one cup (240 mL) or less of milk. With use of a breath-hydrogen test with 25 g lactose as test dose and the presence or absence of symptoms, 50% of the subjects were classified as lactose maldigesters and intolerant, 8% were maldigesters but tolerant, 15% were digesters but intolerant, and 27% were digesters and tolerant. Forty-five subjects from the lactose maldigesting and intolerant group were further tested for milk intolerance in a double-blind study. Sixty-seven percent of the subjects reacted appropriately to the presence or absence of lactose in ingested milk whereas 33% reported symptoms to both low-lactose milk and milk containing lactose. The results suggest that the cause of milk intolerance in as many as one-third of African Americans claiming symptoms after ingestion of a moderate amount of milk cannot be its lactose content.
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The possibility of delaying gastric emptying and improving lactose digestion and tolerance by increasing milk viscosity was studied in 13 lactose maldigesters who ingested three test milks with different viscosities (range: 33-1892 mPa.s) in random order at intervals of 1 wk. Each test portion was 500 mL and provided approximately equal to 1900 kJ and 18 g lactose. The different viscosities were obtained by adding varying proportions of rice starch and maltodextrin to a basic milk formula. A combined [13C]glycine-hydrogen breath test was used to measure gastric emptying and lactose digestion simultaneously. Participants reported their gastrointestinal symptoms by using a four-grade scale. Mean (+/- SEM) gastric-emptying half times were 78 +/- 5.7 min for low-viscosity milk (30 mPa.s), 86 +/- 5.0 min for moderate-viscosity milk (80 mPa.s), and 78 +/- 4.5 min for high-viscosity milk (1.9.10(3) mPa.s). Mean orocecal transit times (180 +/- 24, 163 +/- 23, and 180 +/- 24 min, respectively) were not significantly different. There were no milk-dependent differences in breath-hydrogen excretion or in the severity of gastrointestinal symptoms. The milks were well tolerated; > 50% of the subjects reported nondisturbing symptoms or none. We conclude that gastric emptying, orocecal transit time, and lactose digestion and tolerance were not affected by altering milk viscosity. This may have been due to the high energy content of the test milks, which in itself led to slow gastric emptying.
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Thirty children on a lactose-free diet aged from 2-38 months who had previously been diagnosed as having secondary lactose intolerance were reinvestigated on 32 occasions by an oral lactose tolerance test, small intestinal biopsy, and measurement of disaccharidase activity in order to detect the presence of continuing lactose intolerance before reintroduction of milk. No correlation was found between continuing lactose intolerance, as diagnosed by the development of watery stools containing excess reducing substances after an oral load of lactose, and maximum blood glucose rise during a lactose tolerance test, lactase levels, and small intestinal morphology.
BACKGROUND: Lactose intolerance is the most common disorder of intestinal carbohydrate digestion. Lactobacillus acidophilus BG2FO4 is a strain of lactobacilli with properties of marked intestinal adherence and high beta-galactosidase activity. OBJECTIVE: This study was designed to determine whether oral feeding of Lactobacillus acidophilus BG2FO4 leads to a lactose-tolerant state. DESIGN: We studied 42 subjects with self-reported lactose intolerance and performed breath-hydrogen tests to determine whether they were lactose maldigesters. Subjects with established lactose maldigestion (n = 24) were invited to be randomly assigned to an omeprazole-treated (hypochlorhydric) group or a non-omeprazole-treated group, but 6 subjects chose not to participate. All randomly assigned subjects (n = 18) ingested Lactobacillus acidophilus BG2FO4 twice per day for 7 d and stool samples were collected. Breath-hydrogen tests were performed and symptom scores were recorded at baseline and after lactobacilli ingestion. RESULTS: Lactose maldigestion was established in 24 of 42 subjects (57%) with self-reported lactose intolerance. In 18 lactose-maldigesting subjects, overall hydrogen production and symptom scores after ingestion of Lactobacillus acidophilus BG2FO4 were not significantly different from baseline values. Live Lactobacillus acidophilus BG2FO4 was recovered in stool samples from 7 subjects. CONCLUSIONS: Lactose intolerance is overreported in subjects with gastrointestinal symptoms after lactose ingestion. Treatment of lactose-maldigesting subjects with and without hypochlorhydria with Lactobacillus acidophilus BG2FO4 for 7 d failed to change breath-hydrogen excretion significantly after lactose ingestion.
Lactose intolerant populations are heterogeneous with respect to their milk-drinking habits. A gradation of lactase activity in the intolerant population may result in sufficient lactose hydrolysis to obviate symptoms and lead to continued milk consumption. This paper reports on differences in maximum blood sugar rise in lactose intolerant children who are observed to consume or reject milk. Of the 89 black elementary school children, 48 (54 per cent) evidenced a flat lactose tolerance curve. Twenty-eight of these 48 children (58 per cent) were defined as nonmilk drinkers. The maximum blood sugar rise was 12.3 mg/100 in the 20 lactose malabsorbers who were defined as milk drinkers. It appears that some lactose malabsorbing children may have sufficient, albeit lower, levels of lactase to hydrolyze moderate amounts of milk.