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Evidence has been accumulating that except where dairying has been carried on for centuries, postweaning inability to digest milk is the norm for humans as well as other land mammals. Given the ethnic diversity of the U.S., there may well be 30 million Americans who cannot drink milk without developing symptoms and many instinctively learn to avoid it. A simple lactose tolerance test is described that establishes the diagnosis.
The adult lactase phenotype, lactose absorber or malabsorber, was determined using the lactose tolerance test with breath hydrogen assay in a group of Tuareg, a traditionally nomadic pastoralist population in the central Sahara. Out of a total of 118 subjects, 103 (87.3%) were lactose absorbers and 15 (12.7%) lactose malabsorbers. The frequency of the "lactase suppression gene" in this population sample was .357 (SD .043). The low frequency of lactase suppression in the Tuareg supports the hypothesis of natural selection in favor of the "lactase persistence gene" in milk-dependent nomadic pastoralist.
Physiological bases of digestion and absorption of carbohydrates are reviewed, as a preliminary step, in order to draw a general scheme of its patholophysiology. Clasification of different types of carbohydrate malabsorption is presented. Various exploration methods are discussed in terms of autors' own experiences. Relationship between a sugar screening test, faecal lactic acid contents and a simplified lactose tolerance test, is described in detail. Systematic diagnoses of these diseases are established. Different clinical pictures are reviewed. It is not yet well defined if a starch malabsorption can be caused by either a primary or secondary duodenal amylase deficiency. The clinical forms of congenital sucrose-isomaltose intolerance may be more attenuated than its classical form; incertain cases, secondary sucrose intolerance may also be present due to mucosa anatomic lesions. Maltose malabsorption has no clinical implications. As compared to other alpha-glycosidades, the trehalase activity has been not more affected by not using trehalose in feeding. Primary congenital lactase deficiency is not frequent, whereas secondary forms as much more usual and appear, in primary malabsorption syndromes and in the coeliac disease, very often along with clinical tolerance to lactose. In Spain, lactose nonabsorbers in 16.5% for adults 11.2% for adolescents and 18.3% for children, meaning, that it is being favored by environmental factors in the latter. The unspecified sugar malabsorption during the child's first year is still the most frequent cause of carbohydrate intolerance in children and, although certain progress has been achieved in its diagnosis and therapy, its pathogenic mechanism is not satisfactorily known yet.
One hundred sixteen healthy black children ages 13 to 59 months, representing high and low socioeconomic deciles, were studied for lactose malabsorption. A fasting lactose tolerance test using 2 g of lactose/kg of body weight was carried out. Glucose was determined at 0, 15, 30, and 60 min. Of the 116 preschoolers 34 (29%) evidenced lactose malabsorption as determined by a blood glucose rise of less than 26 mg/100 ml. Clinical signs of diarrhea, gas, and cramps were noted singly or in combination in 18% of the 34 lactose-malabsorbing children. Of the 82 lactose absorbers, 12% demonstrated similar signs. The nature and length of the initial infant milk feeding failed to show any relationship to the onset of malabsorption. Current milk drinking patterns were reported as being similar. Eight-seven percent of the malabsorbers and 92% of the absorbers report drinking 240 ml or more of milk/day. Socioeconomic status, education, marital status, and medical assistance of the parent is similarly distributed between lactose absorbers and malabsorbers.
A female stumptail macaque had signs of intermittant diarrhea and chronic weight loss over a 2-year period during which she was fed a commercial laboratory maintenance diet. Intolerance of this individual to lactose, a ubiquitous constituent of most commercial primate diets, was diagnosed on the basis of lactose tolerance tests and favorable clinical response to dietary carbohydrate substitution with glucose. Oral administration of varying doses of glucose to this animal consistently produced elevations in plasma glucose concentrations exceeding 20 mg/dl, while orally-administered doses of lactose did not cause significant elevations in blood glucose concentrations.
Intestinal biopsy is an essential procedure in the diagnosis of cow's milk protein-sensitive enteropathy. The number and timing of biopsies, however, is still controversial. Twenty-two infants who were clinically suspected of having cow's milk protein intolerance were put on a milk-free diet, during which they all improved. In the first 14 infants (Group I), milk withdrawal lasted 6-8 weeks; in the following 8 infants (Group II), milk withdrawal lasted 3.5-4 months. At the end of the withdrawal period, each patient was submitted to an oral lactose tolerance test and then to a first jejunal biopsy, followed by a cow's milk challenge, and a second biopsy (1-2 days later). None of the infants showed evidence of lactose intolerance, but they all reacted adversely to milk reintroduction. In Group I, the distribution of mucosae from grade 0 (normal) to III was almost the same before and after challenge (p greater than 0.5); this is considered to be due to the severe mucosal damage still present in prechallenge biopsies. In Group II, however, a significant difference was found in the distribution of mucosae before and after challenge (p less than 0.05), and a deterioration could be observed in each case after challenge. Intraepithelial lymphocyte counts and mitotic index determinations before and after milk reintroduction were of no diagnostic value in either group. It is suggested that the diagnosis of cow's milk protein-sensitive enteropathy may rely on two biopsies, the first after a period of 3.5-4 months on milk-free diet and the second following milk challenge.
In 1969--1970, a simple random sample of 129 Finnish school-aged children was examined to study selective adult-type lactose malabsorption (SLM) in this age category. SLM was found in 8 children. All subjects were reexamined 5 years later. SLM was reconfirmed in these 8 persons and found in 3 additional subjects who had normal lactose absorption in the first examination. The prevalence of SLM was 9.3%, being 8.5% in the age category 12--15 years and 9.9% in that 16--20 years. Low rise of blood glucose in the lactose tolerance test of the first examination, very low milk consumption, milk intolerance, and history of gastrointestinal symptoms were found to be of low predictive value as indicators of SLM. It was also concluded that information about dietetic sources of lactose is important to persons with SLM, but categorical exclusion of lactose from the diet is not necessary, at least in the Finnish population.
Endoscopic biopsies at the inferior duodenal flexure from 36 patients were assayed for disaccharidases. Comparative studies in 8 patients were carried out from this location and from the duodenojejunal flexure. 16 patients with lactase values under 20 U/g protein and normal histology also underwent a lactose tolerance test. Evidence is presented that the easily performed duodenal biopsies give the same information as those from the angle of Treitz, at a level about 40% under the latter. Tolerance to lactose was in close relation with the lactase level in 16 patients, the limit being at about 5 U/g protein.
This study aims to estimate the tolerable lactose intake which can be utilized in the digestion by lactase and in the fermentation by intestinal microbes in Japanese female adults. The first, the maximum permissive dosage of lactose not to induce transitory diarrhea was estimated based on the oral ingestion of lactose at several dose levels in all the subjects, and compared with that of lactitol which is not hydrolyzed by digestive enzymes. A second lactose tolerance test involving 10 g and 30 g of lactose was carried out in 10 subjects showing resistance to diarrhea, and serum glucose and insulin levels and the amount of hydrogen excreted in the breath were measured for comparison with those of glucose and lactitol. Subjects were 43 Japanese female adults (average: age 20.5+/-2.1 y, weight 51.3+/-5.1 kg) who had not been diagnosed as having either hypolactasia or being lactose intolerant. Serum glucose and insulin levels were scarcely elevated following the ingestion of both 10 g and 30 g of lactose, while the amount of hydrogen excreted in the breath was greatly increased following the ingestion of 30 g of lactose, but these levels were less following the ingestion of 10 g of lactose. In contrast, the ingestion of 15 g of glucose significantly increased blood glucose and insulin levels, while no hydrogen was detected in the breath. The maximum permissive dosage of lactose not to induce transitory diarrhea was 0.72 g/kg of body weight and that of lactitol was 0.36 g/kg of body weight in Japanese adults. The digestive capacity of lactase is less than 10 g of lactose by single ingestion, while intestinal microflora are able to ferment approximately 20-30 g of lactose. In addition, the ingestion of more than 10 g of lactose might be contributed as prebiotics.
A standard oral lactose tolerance test (LTT) was performed in 32 white and 18 non-white hospitalized Brazilian adults. A flat LTT was found in 22 (68,75%) white and in 17 (97,45%) non-white patients indicating a 78% overall rate of lactose malabsorption, Both lactose absorbers and malabsorbers showed a modal milk ingestion of less than a 1 glass/day. Symptoms related to milk consumption or lactose administration were more common among lactose malabsorbers. Estimations of disaccharidase activity in intestinal mucosa specimens obtained by peroral biopsy in 28 patients confirmed a high prevalence of lactose deficiency, and disclosed only one false result, in the patient with a flat LTT and high intestinal lactase levels.
The ability of the horse to digest and absorb soluble carbohydrates was assessed using a series of oral disaccharide tolerance tests followed in the same animals by tolerance tests with the constituent monosaccharides. In horses older than three years, lactose did not produce an increase in the plasma glucose levels but induced the passing of soft faeces, indicating that adult horses are lactose intolerant. Horses of all ages could absorb the glucose: galactose mixture without any change in the faeces. The tolerance is due to a failure to hydrolyse lactose and does not involve the monosaccharide transport systems. These findings correspond to the known development pattern of brush border lactase activity in the equine small intestine. Both sucrose and maltose were rapidly hydrolysed, the resulting tolerance curves closely approximating to those for the constituent monosaccharides. Galactose was absorbed at a similar rate to glucose, although a dose of 1g/kg was necessary to produce galactosaemia. An oral lactose tolerance test (1 g/kg as a 20 per cent solution) could be of clinical value to determine small intestinal mucosal damage in diarrhoeic foals when the continued ingestion of lactose might be detrimental.
A prospective follow-up was conducted of 29 patients with celiac disease 3 to 10 years in duration. Of these, 8 were on a spare agluten diet, in whom the time-related course of clinical manifestations of the illness was characterized by stabilization of the primary symptoms of disturbed intestinal absorption, improvement in the psychoemotional state at year of their prophylactic management. The glucose tolerance test had gotten normalized after two years of being on a spare diet, lactose tolerance test remaining below the normal range in 37.5 percent of cases at year 3 of the observation, with the content of IgG antibodies to gliadine exceeding the threshold values in 33.3% on an average three times as much as the norm. In those patients having not been on a spare diet, retardation in physical development was recordable together with bone abnormalities manifested by pathologic fractures of the tubular bones. The level of anti-gliadine antibodies of both classes was found to be augmented in 71.4 percent of cases, their values having been fifty times as much as the norm. Glucose tolerance test suggested to us a steady decline in the absorption that was still to be seen at year 10 of the prospective follow-up. Lactase intolerance was somewhat less, remaining at lower values in the half of the patient population.
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.
Milk intolerance was investigated in 87 healthy elderly individuals with a mean age of 77 years who were given 240 ml of a chocolate dairy drink twice in one week with a light lunch. No significant differences in symptomatic responses distinguished the subjects consuming a lactose-free (LF) drink from those consuming a drink containing 4.5% lactose (LC) under double-blind study conditions. Breath hydrogen analysis during lactose tolerance testing identified 23 malabsorbers, none of whom responded exclusively to the LC drink, although five were symptomatic on both days, and two had symptoms only on the day the LF drink was served. A similar percentage of absorbers (72%) and malabsorbers (70%) were asymptomatic on both days. Factors other than lactose malabsorption appeared to be responsible for the symptoms of intolerance reported, and most may have been psychosomatic in origin.
20 g lactose load test, BHT and LTT done simultaneously were examined in 32 Crohn's disease patients and 51 healthy volunteers. Hypolactasia frequency were examined. A rise in hydrogen concentration > 20 parts per million (ppm) above the base line during breath hydrogen test and maximum blood sugar rise during lactose tolerance test were considered to indicated Hypolactasia. High rates, 50% by BHT and 72.5% by LTT, of primary adult hypolactasia were found in healthy volunteers as previously reported. Higher rates, 83.3% by BHT and by LTT (p < 0.05), were observed in Crohn's disease patients. There were higher rates in small intestine type Crohn's disease (91.6% by BHT, 92.3% by LTT) compare with healthy volunteers but no difference were found with large intestine type Crohn's disease.
A family with combined heterozygosity for "classical" galactosemia (deficiency of uridyl-transferase) and for galactokinase deficiency is reported. The proband, who had this genetic combination was detected as newborn in the ordinary screening for galactosemia. A lactose tolerance test at the age of three months proved normal and he has no symptoms or signs on ordinary diet. The mother of the proband was not only heterozygote for "classical" galactosemia and galactokinase deficiency but also for the Durarte variant. She had a substantial urine excretion of galactose and high serum galactose after an oral lactose load. She had no clinical symptoms or signs. Patients with combined heterozygosity for galactosemia may develop cataracts and should be followed by clinical examinations.
Sixty newborn infants with normal birth weight suffering from uncomplicated hyperbilirubinemia were studied. They were fed human mature milk from which lactose had been eliminated, whereafter either sucrose ("sucrose milk") or lactose ("lactose milk") was added. 30 infants received ordinary phototherapy and 30 intensive phototherapy (blue double light). 15 in each group had "sucrose milk" and 15 "lactose milk". There was no significant difference between the increase in blood glucose (delta BS) by lactose tolerance tests performed before phototherapy (LTT1) and by those performed during phototherapy (LTT11), neither in infants treated with ordinary nor with intensive phototherapy. All infants had normal delta BS-LTT11, except one receiving ordinary phototherapy. There was no significant difference in gut transit time between infants having "sucrose milk" and infants having "lactose milk", neither in those treated with ordinary nor with intensive phototherapy. Gut transit time was significantly shorter in infants treated with intensive phototherapy than in infants treated with ordinary phototherapy without there being any significant difference in delta BS-LTT11. The infant with flat LTT11 may have developed lactose malabsorption during the phototherapy. Thus, lactose malabsorption is not the usual cause of the reduced gut transit time during phototherapy and must be a rare complication in phototherapy.
One hundred and fifty subjects were studied in a double blind fashion to determine the relationship between lactose malabsorption and milk lactose intolerance. Each participant received 250 ml of a different type of milk on 3 consecutive days. Milk A contained no lactose, milk B had 12.5 g, and milk C contained 37.5 g of lactose. After the experiment was completed each subject was classified with a lactose tolerance test as having "sufficient" or "insufficient" lactase activity. Milk A produced no gastrointestinal symptoms in either sufficient or in insufficient persons. Milk B produced symptoms in 3.8% of sufficient and 37.1% of insufficient individuals, and Milk C induced symptoms in 7.6% of sufficient and 83.5% of insufficient subjects. These differences are very highly significant (P less than 0.0001). It is concluded that lactose-intolerant subjects are indeed milk-intolerant and that the frequency with which symptoms occur in persons with lactose malabsorption increases in direct relation to the lactose content of the milk.