Lactose intolerance.

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.

Role of irritable bowel syndrome in subjective lactose intolerance.

It has been suggested that the symptoms of irritable bowel syndrome (IBS) may be wrongly attributed to lactose intolerance. We examined the relations among IBS, demographic factors, living habits, and lactose intolerance. On the basis of a lactose tolerance test with ethanol, 101 of the 427 healthy subjects studied were lactose maldigesters and 326 were lactose digesters. IBS was diagnosed by means of the Bowel Disease Questionnaire, according to the Rome criteria. The use of dairy products and symptoms experienced after their consumption were recorded. IBS was found in 15% of both the lactose maldigesters and lactose digesters. One-third of the subjects reported intolerance to dairy products containing < or = 20 g lactose. About half of this third were lactose maldigesters and about half were lactose digesters. As explanations for this subjective lactose intolerance, the logistic regression model estimated lactose maldigestion (odds ratio: 10.3; 95% CI: 5.2, 20.4), IBS (4.6; 2.1, 10.1), experience of symptoms other than gastrointestinal ones (2.3; 1.2, 4.5), and female sex (2.1; 1.1, 4.0). Characteristics common to both subjective lactose intolerance and IBS were female sex and the experience of abdominal pain in childhood (P < 0.01). Age, regularity of meals, and the amount of physical activity were not associated with either subjective lactose intolerance or IBS. Of the subjects with IBS, the percentage of lactose maldigesters was the same as in the whole study group (24%) but the number who reported lactose intolerance was higher (60% compared with 27%, P < 0.001). We showed a strong relation among subjective lactose intolerance, IBS, the experience of abdominal pain in childhood, and female sex.

Milk fat does not affect the symptoms of lactose intolerance.

OBJECTIVE: This study investigated the role of the fat content of milk on symptoms of lactose intolerance. DESIGN: Subjects recorded intolerance symptoms using a visual analogue scale (VAS) following ingestion of three test milks for varying fat content for a two-day period. SUBJECTS/SETTING: The subjects were thirty adult volunteers, patients of two Estonian out-patient clinics with diagnosed lactose intolerance. The study milks were drunk at home or at work. All thirty subjects completed the study protocol. INTERVENTION: Each subject drank, in random order, fat-free milk (4.9% lactose), high-fat milk (8% fat, 4.9% lactose), and a lactose-free and fat-free control milk. They drank 200 ml of the milk twice a day for two days, one milk type per session, with five days between sessions. The subjects noted their gastrointestinal symptoms during the test periods and during a 5 d milk-free period at the beginning of the study. The occurrence and severity of symptoms were compared. A global measure of the severity of symptoms was defined by computing the sum of the symptoms scores. RESULTS: The sum of symptoms was higher during all milk periods than during the milk-free period (P < 0.01). There were no statistically significant differences in the occurrence or severity of symptoms during the fat-free milk period compared with the high-fat milk period. CONCLUSIONS: Even a marked difference in the fat content of milk did not affect the symptoms of lactose intolerance. Consequently, there seems to be no case for recommending full-fat milk products in the treatment of lactose intolerance.

Effects of milk viscosity on gastric emptying and lactose intolerance in lactose maldigesters.

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.

Raising milk energy content retards gastric emptying of lactose in lactose-intolerant humans with little effect on lactose digestion.

Lactose digestion improves when the energy content of a meal is raised, perhaps due to delayed gastric emptying; however, this has not been demonstrated directly. It is not known whether lactose-intolerant subjects should consume full-fat or high energy milk instead of half-skimmed milk. In this study, breath 13CO2 and hydrogen (H2) measurements were combined to assess simultaneously the effect of increasing milk energy content on gastric emptying, digestion, and tolerance of lactose. On two separate days, 11 adult lactose maldigesters ingested, in the fasting state, a single dose of 710 kJ half-skimmed milk or 1970 kJ high energy milk. Both contained 18 g lactose and were supplemented with 100 mg 13C-glycine for breath 13CO2 measurement. For 6 h after milk ingestion, samples of expired breath were collected, and subjects scored their symptoms on a four-grade questionnaire. Gastric emptying was measured from excretion of breath 13CO2. The mean gastric emptying half-time was significantly longer after ingestion of high energy milk than after half-skimmed milk (84 +/- 4 vs. 64 +/- 4 min, P = 0.004). The mean area under the breath H2 excretion curve measured for 6 h was 330 +/- 61 microL/L after subjects consumed high energy milk vs. 470 +/- 82 microL/L after they consumed half-skimmed milk (P = 0.07). Mean symptom scores did not differ after ingestion of the two milks, but only two subjects experienced disturbing symptoms after high energy milk ingestion compared with five subjects after ingestion of half-skimmed milk (P = 0.56). Although ingestion of high energy milk delayed the gastric emptying of lactose for significantly longer than the ingestion of half-skimmed milk (P < 0.01), it did not lead to significant improvement in symptoms and reflected only a trend toward improved lactose digestion (P = 0.07), as measured by the area under the breath H2 excretion curve. These results indicate that it is not beneficial for most lactose-intolerant subjects to replace consumption of half-skimmed milk by milk with a higher energy content.

Digestion and tolerance of lactose from yoghurt and different semi-solid fermented dairy products containing Lactobacillus acidophilus and bifidobacteria in lactose maldigesters--is bacterial lactase important?

OBJECTIVE: To compare the digestibility and tolerance of lactose from three semi-solid fermented dairy products with the same amount of lactose but different lactase contents and bacterial cultures in lactase deficient adults. DESIGN: Measurement of breath hydrogen (H2) concentration and of clinical symptoms after consumption of the test meals. SETTING: Metabolic ward for healthy volunteers, INSERM U290, Hôpital St. Lazare, Paris. SUBJECTS: Fifteen lactase-deficient healthy adult volunteers (20-45 y) started the study. One subject became a non-H2-producer during the study; therefore the results of 14 subjects are presented. INTERVENTION: Each subject consumed, on four different days and in random order, after a 12 h fast, three semisolid test meals containing 18 g of lactose, and a 10 g dose of lactulose which allowed calculation of lactose malabsorption. The three meals were: traditional yoghurt, fermented milk (Ofilus) that contained Lactobacillus acidophilus and Bifidobacterium sp., and a similar product 'Bulgofilus' enriched with Lactobacillus bulgaricus to increase the lactase content. RESULTS: Compared with lactulose, the sum of symptoms was significantly lower for Bulgofilus (P = 0.05), and bloating was less severe for Ofilus (P = 0.06). Between the fermented milks, there were no differences. The area under the breath H2 curve was significantly lower for each fermented milk when compared to lactulose (P < 0.0001). The degree of maldigestion of lactose did not differ significantly between the products; it was 21 +/- 3% (range 6-52) for Ofilus, 21 +/- 3% (range 6-44) for Bulgofilus, and 18 +/- 3% (range 3-43) for yoghurt. CONCLUSION: Despite the differences in the lactase and bacterial content, lactose was as well digested and tolerated from the three different semi-sold fermented dairy products. This could be due to a slow gastric emptying of the semi-solid milk.

Tolerance to small amounts of lactose in lactose maldigesters.

In this study we examined whether small doses of lactose induced symptoms in 39 lactose maldigesters and 15 lactose digesters in a randomized, crossover, double-blind design. The test doses were 200 mL fat-free, lactose-free milk to which 0, 0.5, 1.5, and 7 g lactose was added. Every third day of a lactose-free diet, after an overnight fast, the subjects drank one of the test milks in random order and registered the occurrence and severity of gastrointestinal symptoms in the next 12 h. During the study, the maldigesters reported significantly more abdominal bloating (P = 0.0003) and abdominal pain (P = 0.006) than the digesters. There was no difference in the mean severity of the reported symptoms between the test milks and the lactose-free milk in the group of lactose maldigesters, of whom one-third did not experience any symptoms from any of the test doses. The same proportion (64%) of the maldigesters experienced symptoms after both the lactose-free milk and the milk with 7 g lactose. However, the symptoms occurred inconsistently with the different test doses in 59% of the maldigesters. Thus, it can be concluded that the gastrointestinal symptoms in most lactose maldigesters are not induced by lactose when small amounts (0.5-7.0 g) of lactose are included in the diet.