Response of lactose-intolerant children to different lactose levels.
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Age Factors↗
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[Lactose intolerance (incapacity to hydrolyze lactose)].
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Child↗
Management of lactose intolerance.
The management of lactose intolerance comprises two parts: (1) the basic principles of treatment in persons intolerant to a dietary dose of lactose, and (2) main manoeuvres to reduce the lactose content in food, and/or consumption of special products of milk or exogenous lactase enzyme. The tactics of management depend on the type of hypolactasia, the severity of intolerance, and on the age of the patient. Special attention is paid to the development of lactose intolerance in some patients via iatrogenic mechanisms such as certain drugs, gastric surgery and ionizing radiation.
Age of Onset↗
The molecular basis of lactose intolerance.
A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else--the key to our own evolution--the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.
Animals↗
Cows' milk protein intolerance: a possible association with gastroenteritis, lactose intolerance, and IgA deficiency.
Twenty-five children with cows' milk protein intolerance were studied. Twenty had presented with an illness clinically indistinguishable from infantile gastroenteritis; an enteropathogenic Escherichia coli was isolated from the stools in two children, and in six another member of the family simultaneously developed acute diarrhoea and vomiting. Twenty-three children had lactose intolerance secondary to cows' milk protein intolerance. Eight out of 20 children were found to be partially IgA deficient. An acute attack of gastroenteritis, in damaging the small mucosa, may act as a triggering mechanism in cows' milk protein intolerance, and a deficiency in IgA may be a predisposing factor in so far as it allows the patient to become sensitised to foreign protein.
Animals↗
Lactose intolerance: diagnosis and management.
Lactose intolerance affects hundreds of millions of people worldwide. Although the presentation is frequently atypical, it should be part of the differential diagnosis when evaluating nonspecific gastrointestinal symptoms. We review the terminology, types of lactase deficiencies, diagnostic procedures, and management.
Ethnicity↗
Primary lactose intolerance in Zulu adults.
The incidence of lactose intolerance in a sample of 47 Zulu patients from a general medical ward and 14 healthy members of the Zulu population in Durban was investigated. Eighty-nine percent of patients and 93% of control subjects were diagnosed as having lactose intolerance because of failure to increase blood glucose more than 1,1 mmol/l during the 2 hours following 50 g lactose ingestion. Ninety-two per cent of the female and 64% of the male patients complained of symptoms of lactose intolerance, and 61% of the female and 75% of the male patients passed stools with a pH of less than 6. Glucose tolerance (50 g) was normal in 87% of patients and 92% of controls; 2 patients had a diabetic response while 5 patients and 1 control had 'flat' glucose and lactose responses, suggesting delayed absorption. Analysis of nutritional status showed that male patients were significantly more malnourished than female patients, and patients more so than controls. The results indicate that lactose intolerance is a normal observation in the Zulu and that it is primary in origin since there was no association between intolerance, sickness or malnutrition. Practical implications that arise from the study are that milk-based diets should be avoided in refeeding malnourished Zulu patients and that lactose may find a useful place in the treatment of constipation and liver failure in such patients.
Adult↗
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 administration of either lactose or sucrose on clinical tolerance and bacterial adaptation to lactose. METHODS: Forty six lactose intolerant subjects underwent two 50 g lactose challenges on days 1 and 15. Between these days they were given 34 g of lactose or sucrose per day, in a double blind protocol. Stool samples were obtained on days 0 and 14, to measure faecal beta-galactosidase and pH. Symptoms, breath H2 excretion, faecal weight and electrolytes, and orofaecal transit time were assessed. RESULTS: Except for faecal weight, symptoms were significantly milder during the second challenge in both groups, and covariance analysis showed no statistical difference between them. In the lactose group, but not in the sucrose group, faecal beta-galactosidase activity increased, pH dropped, and breath H2 excretion decreased. CONCLUSION: Bacterial adaptation occurred when lactose intolerant subjects ingested lactose for 13 days, and all symptoms except diarrhoea regressed. Clinical improvement was also observed in the control group which displayed no signs of metabolic adaptation. This suggests that improved clinical tolerance may be just a placebo effect.
Adult↗
Lactose intolerance in a calf.
Lactose intolerance was identified as the cause of bovine neonatal diarrhea. Glucose and xylose oral absorptions were normal whereas lactose absorption was reduced relative to normal calves. Lactase deficiency is common in people but rarely reported in animals. The treatment of whole milk with lactase alleviated the diarrhea.
Absorption↗
Association of Clostridium difficile with enterocolitis and lactose intolerance in a foal.
Diagnoses of Clostridium difficile enterocolitis and lactose intolerance were made in a neonatal foal with persistent diarrhea. It was determined that the foal had lactose intolerance on the basis of the results of a lactose tolerance test, and a diagnosis of C difficile enterocolitis was subsequently made. The foal responded to oral administration of metronidazole and lactase. Lactose intolerance is a secondary problem most commonly associated with rotavirus infection, but it can be caused by any condition affecting the small intestine. Because C difficile can affect the small intestine in foals, it was presumably the cause of the lactose intolerance in this foal with persistent diarrhea. Oral administration of lactase was not initially successful in this foal, most likely because of ongoing C difficile enterocolitis. Presumably, metronidazole was an effective treatment for C difficile enterocolitis and administration of lactase allowed for normal digestion of milk until endogenous lactose production returned. Clostridium difficile enterocolitis and lactose intolerance should be considered as differential diagnoses in neonatal foals with diarrhea, especially when the foal is bright and alert.
Animals↗
[Study on the expired gas of subjects with lactose intolerance by using H2/13CO2 breath test].
The relationship between breath gas and lactose intolerance symptoms is studied in the subjects with lactose intolerance and lactose mal-absorption. The breath gas samples are collected for 6 hours after consumption of 25 g 13C-lactose. Expired H2 concentration and 13CO2 abundance at each detecting time point is measured by gas chromatography and continuous flow Gas Isotope Mass Spectrometry respectively. The cumulative amount of breath H2 and 13CO2 for 6 hours are calculated, and the abdominal symptoms are recorded by the questionnaire for 12 hours. The results show that the H2 peak is significantly higher in the intolerance group than that in the mal-absorption group(P < 0.01). The cumulative amount of breath H2 during 6 hours is significantly higher in the intolerance group than that in the mal-absorption group (P < 0.01). The oral-colon transit time (OCTT) is negatively related to the lactose intolerance symptom scores (r = -0.705). There are no significant differences for the amount of 13CO2 excretion at each detecting time point and cumulative percentage of the expired 13CO2 between the intolerance and the mal-absorption groups. It is suggested that the cumulative breath H2 amount is associated with the severity of lactose intolerance, which can reflect the degree of lactose hydrolysis in the small intestine, while there is no such relationship between the amount of expired 13CO2 and the severity of lactose intolerance.
Adult↗
Relationship of lactose intolerance to milk intolerance in young children.
The prevalence of lactose intolerance as revealed by the standard lactose tolerance test was compared with the occurrence of intolerance to graded amounts of milk in 69 black and 30 white children. Of the black children studied, 11% of those 4 to 5 years old, 50% of those 6 to 7 years old, and 72% of those 8 to 9 years old were found to be lactose-intolerant, yet no child was intolerant to 240 ml of milk. Symptom responses to greater amounts of milk did not suggest that the frequency of primary lactose intolerance might be a reason for limiting existing milk programs for young children. No significant differences were found between the milk intakes of black lactose-tolerant and black lactose-intolerant children, nor between milk intakes of 6- and 7-year-old black and white children in Boston. However, 8- to 9-year-old black children drank significantly less milk than 8- to 9-year-old white children did. The blood glucose response at 0, 20, and 45 min after the ingestion of 2 g lactose/kg (maximum 50 g) was unreliable as an indicator of an individual's symptomatic response to lactose.
Age Factors↗
Comparison of symptoms after the consumption of milk or lactose-hydrolysed milk by people with self-reported severe lactose intolerance.
BACKGROUND: Ingestion of a large dose of the milk sugar lactose--for example, the 50 g load in 1 liter of milk--causes symptoms such as abdominal pain, diarrhoea, bloating and flatulence in the majority of people with lactose malabsorption. It is uncertain whether the ingestion of more common doses of lactose, such as the amount in 240 mol (8 oz) of milk, causes symptoms. Some people insist that even smaller quantities of milk, such as the amount used with cereal or coffee, cause severe gastrointestinal distress. METHODS: In a randomized, double-blind, cross-over trial, we evaluated gastrointestinal symptoms in 30 people (mean age, 29.4 years; range 18-50) who reported severe lactose intolerance after ingesting less than 240 ml of milk. The ability to digest lactose was assessed by the subjects' end-alveolar hydrogen concentration after they ingested 15 g of lactose in 250 ml of water. Subjects then received either 240 ml of lactose-hydrolysed milk containing 2% fat or 240 ml of milk containing 2% fat and sweetened with aspartame to approximate the taste of the lactose-hydrolysed milk; each type of milk was administered daily with breakfast for a 1-week period. Using a standardized scale, subjects rated the occurrence and severity of bloating, abdominal pain, diarrhoea, and flatus and recorded each passage of flatus. RESULTS: Twenty-one participants were classified as having lactose malabsorption and nine as being able to absorb lactose. During the study periods, gastrointestinal symptoms were minimal (mean symptom-severity scores for bloating, abdominal pain, diarrhoea, and flatus between 0.1 and 1.2 [1 indicated trivial symptoms, 2 indicated mild symptoms]). When the periods were compared, there were no statistically significant differences in the severity of these four gastrointestinal symptoms. For the lactose malabsorption group, the mean (+/- SEM) difference in episodes of flatus per day was 2.5 +/- 1.1 (95% confidence interval, 0.2-4.8). Daily dietary records indicated a high degree of compliance, with no additional sources of lactose reported. CONCLUSIONS: People who identify themselves as severely lactose-intolerant may mistakenly attribute a variety of abdominal symptoms to lactose intolerance. When lactose intolerance is limited to the equivalent of 240 ml of milk or less a day, symptoms are likely to be negligible and the use of lactose digestive aids unnecessary.
Journal Article↗
When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues.
Lactose intolerance is widespread, with adult-type hypolactasia being the predominant cause of lactose malabsorption. Daily ingestion of less than 240 mL of milk is well tolerated by most lactose-intolerant adults. Some persons with normal lactase activity may become symptomatic on consumption of products containing lactose. Lactose maldigestion may coexist in adults with irritable bowel syndrome and in children with recurrent abdominal pain. Management consists primarily of dietary changes. People who avoid dairy products should receive calcium supplementation and should be advised to read ingredient labels carefully. Several lactase replacement products are available, but their efficacy varies.
Adolescent↗
Chemotherapy-induced lactose intolerance in adults.
BACKGROUND: Anorexia and weight loss contribute to the morbidity and mortality from cancer. This study was designed to test the hypothesis that chemotherapy produces lactose intolerance which could have an adverse effect on the nutritional status of patients receiving cytotoxic drugs. METHODS: Twenty-seven patients were evaluated for the development of lactose intolerance during chemotherapy. Lactose breath hydrogen testing (LBHT) was used to assess lactose malabsorption objectively. This test is based on the principle that in patients with lactase deficiency, lactose is not hydrolyzed in the small intestine and ultimately is degraded by colonic bacteria. This results in the production of hydrogen gas, which is excreted by the lungs and can be quantified with a breath hydrogen analyzer. RESULTS: Of the 27 patients studied, 8 (30%) had an abnormal postchemotherapy LBHT results, and for the population as a whole, postchemotherapy LBHT values were significantly greater than prechemotherapy values (P = 0.04). However, only three patients (11%) showed clinical symptoms of lactose intolerance during the post-chemotherapy LBHT. Five patients had asymptomatic elevations in breath hydrogen excretion on prechemotherapy testing. One of these patients had a further increase in hydrogen excretion on Day 8 after chemotherapy, which was accompanied by symptoms of lactose intolerance. Twenty-two patients had normal prechemotherapy LBHT results. Two of these patients had abnormal post-chemotherapy LBHT results, which were associated with symptoms of lactose intolerance. CONCLUSION: Although chemotherapy may interfere with lactose metabolism, the development of symptomatic lactose intolerance is uncommon. Dietary restriction of milk products in patients receiving chemotherapy therefore is not warranted unless clinical symptoms of lactose intolerance are observed.
Adult↗
Lactose intolerance: a risk factor for reduced bone mineral density and vertebral fractures?
BACKGROUND: The purpose of the present study was to determine differences, if any, in bone mineral density, the risk of fracture, and clinical behavior in patients with lactose intolerance investigated by hydrogen breath test. METHODS: The study population (n = 218; age, mean +/- SD, 58.2 +/- 11.5 years) consisted of 103 healthy individuals negative hydrogen breath test (Delta H2 0-20 ppm; group I), and 115 individuals with evidence of lactose intolerance according to the hydrogen breath test (Delta H2 > 20 ppm), of whom 40 individuals had test results of 20 ppm < Delta H2 < 59 ppm (group II). The remaining 75 individuals were strongly positive on the hydrogen breath test (Delta H2 > 60 ppm; group III). The entire study population was measured for bone mineral density in the nondominant forearm and in the vertebra (quantitative computed tomography [qCT]). Radiographs of the spine were studied for fractures. RESULTS: In healthy individuals, bone mineral density in the vertebra assessed by qCT (mean +/- SD, 111.2 +/- 31 mg/cc) did not significantly differ between those with mild (qCT, mean +/- SD, 109.8 +/- 35 mg/cc) and those with severe (qCT, mean +/- SD, 107.7 +/- 36 mg/cc) lactose intolerance. Lactose-intolerant individuals had more vertebral fractures per patient when compared with those with mild lactose intolerance or controls ( P < 0.05). Considering vertebral and self-reported non-vertebral fractures, no statistically significant differences were found. In the entire group, the overall occurrences of fracture in the presence of lactose intolerance and in controls were comparable after correction for age and body mass index (BMI). CONCLUSIONS: Individuals with lactose intolerance verified by the hydrogen breath test appear not to be at risk for accelerated bone loss. Nevertheless, a relationship between vertebral fractures and an apparent lactose intolerance cannot be excluded, as a few individuals with severe lactose intolerance had a large number of vertebral fractures.
Absorptiometry, Photon↗
The role of colonic microbiota in lactose intolerance.
In a previous study we observed a clear difference in lactose intolerance symptoms after a 25-g lactose load in two groups of persons with lactase nonpersistence and similar small intestinal lactase activity. From this observation we hypothesized a colon resistance factor. To identify this factor, the microbial composition of fecal samples of the two lactose intolerant groups (one with mild symptoms, n = 16, and one with diarrhea-predominant symptoms, n = 11) was compared using the fluorescent in situ hybridization technique. Large interindividual differences were found in the numbers of total bacteria and main groups of bacteria (CV: 0.65 and 0.64-0.82 respectively). The bacterial numbers were not significantly different between the two groups. A significant negative correlation, however, was found between the individual symptom scores of the intolerant persons and the numbers of total hybridizable bacteria (r(s) = -0.42, P = 0.03). The results suggest that an increased number of bacteria might contribute--by means of a higher fermentative capacity--to the reduction of lactose intolerance symptoms.
Adult↗
Review article: the treatment of lactose intolerance.
While about 50 million Americans malabsorb lactose, the colonic metabolism of this disaccharide may prevent the symptomatic state known as lactose intolerance. Elucidation of the clinical importance of lactose malabsorption requires comparison of symptoms after ingestion of lactose with those following an identical appearing lactose-free control. This paper reviews the extensive literature concerning lactose-induced symptoms and the value of lactose digestive aids. Poorly controlled studies have suggested that a cup of milk results in appreciable symptoms in the majority of lactase-deficient subjects. In contrast, controlled trials in unselected lactose malabsorbers of subjects claiming severe lactose intolerance indicate that symptoms from a cup of milk are no greater than that with a lactose-hydrolyzed control. An increasing fraction of subjects experience symptoms as the lactose load is increased, with the majority having symptoms when the equivalent of 1 L of milk is ingested as a single dose. Further studies are required to determine the tolerance to several cups of milk taken throughout the day. Available digestive aids include pre-hydrolyzed milk and lactase preparations that can be added to milk (which is then incubated) or ingested with milk. While these products are effective in reducing symptoms, it should be emphasized that there appears to be no need for these preparations when the dosage of milk is limited to one cup per day.
Humans↗