Probiotics—compensation for lactase insufficiency

Probiotics—compensation for lactase insufficiency1–3 Michael de Vrese, Anna Stegelmann, Bernd Richter, Susanne Fenselau, Christiane Laue, and Jürgen Schrezenmeir ABSTRACT Yogurt and other conventional starter cultures and probiotic bacteria in fermented and unfermented milk products improve lactose digestion and eliminate symptoms of intolerance in lactose maldigesters. These beneficial effects are due to microbial -galactosidase in the (fermented) milk product, delayed gastrointestinal transit, positive effects on intestinal functions and colonic microflora, and reduced sensitivity to symptoms. Intact bacterial cell walls, which act as a mechanical protection of lactase during gastric transit, and the release of the enzyme into the small intestine are determinants of efficiency. There is a poor correlation between lactose maldigestion and intolerance; in some studies, low hydrogen exhalation without significant improvement of clinical symptoms was observed. Probiotic bacteria, which by definition target the colon, normally promote lactose digestion in the small intestine less efficiently than do yogurt cultures. They may, however, alleviate clinical symptoms brought about by undigested lactose or other reasons. Am J Clin Nutr 2001;73(suppl):421S–9S. KEY WORDS Probiotic, lactose digestion, lactose maldigestion, lactose intolerance, lactase INTRODUCTION Improvement of lactose digestion and avoidance of symptoms of intolerance in lactose malabsorbers are the most profoundly studied health-relevant effects of fermented milk products. However, these are not specifically probiotic effects, which are defined as being exerted by living microorganisms surviving gastrointestinal transit and affecting the indiginous microflora (1). Lactose digestion, on the other hand, is most improved by bacteria if the -galactosidase of the bacteria is released by destruction of the bacterial cell wall. Those probiotic bacteria that improve lactose digestion do so, if at all, mostly to a lesser degree than do conventional yogurt cultures. The lack of a strong correlation between lactose maldigestion and the incidence of symptoms of intolerance, such as flatulence, abdominal pain, and diarrhea, suggests that probiotic baceria act by preventing symptoms of intolerance in the large intestine in addition to or rather than by improving lactose digestion in the small intestine. LACTOSE MALDIGESTION AND INTOLERANCE Lactase insufficiency means that the concentration of the lactosecleaving enzyme -galactosidase, also called lactase, in the brush border membrane of the mucosa of the small intestine is too small. This hypolactasia causes insufficient digestion of the disaccharide lactose, a phenomenon called lactose malabsorption or, more precisely, lactose maldigestion. Lactose maldigestion is defined by an increase in blood glucose concentration of < 1.12 mmol/L or in breath hydrogen of > 20 ppm after ingestion of 1g/kg body wt0.75 or 50 g lactose (2). In addition to intestinal lactase activity and its determinants, ethnic origin, age, and possibly sex, other factors are known to influence lactose digestion or maldigestion: the lactose load, dietary components ingested together with lactose (meal effect), the rate of gastric emptying, gastrointestinal transit time, and interactions among these factors (3, 4). There are several forms of lactose maldigestion. In primary or adult-type lactose malabsorption, lactase activity is high at birth, decreases in childhood and adolescence, and remains low in adulthood. This primary hypolactasia is also called lactase nonpersistence and is the normal (physiologic) situation for mammals and humans (5). With the exception of the population of Northern and Central Europe and its offspring in America and Australia, 70–100% of adults worldwide are lactose malabsorbers. The prevalence of primary lactose maldigestion is 3–5% in Scandinavia, 17% in Finland, 5–15% in Great Britain, 15% in Germany, 15–20% in Austria, 17% in northern France, 65% in southern France, 20–70% in Italy, 55% in the Balkans, 70–90% in Africa (exeptions: Bedouins, 25%; Tuareg, 13%; Fulani, 22%), 80% in Central Asia, 90–100% in Eastern Asia, 30% in northern India, 70% in southern India, 15% in North American whites, 80% in North American blacks, 53% in North American Hispanics, and 65–75% in South America (2, 4). In population groups with predominant primary lactase deficiency, loss of lactase activity begins between the ages of 2 and 6 y. In white populations with a low prevalence of lactase maldigestion it starts later, in some cases after adulthood (20 y). The frequencies of lactose maldigestion at ages 2–3 y, 6 y, and 9–10 y, respectively, are 0%, 0%, and 6% in white Americans; 18%, 30%, and 47% in Americans of Mexican descent; 25%, 45%, and 60% in black South Africans; 30%, 80%, and 85% in Chinese and Japanese; and 30–55%, 90%, and > 90% in Mestizos of Peru (6, 7). Secondary forms of lactose malabsorption may be due to inflammation or functional loss of the small intestinal mucosa 1 From the Institute of Physiology and Biochemistry of Nutrition, Federal Dairy Research Center, Hermann-Weigmann-Straße 1, D-24103 Kiel, Germany. 2 Presented at the symposium Probiotics and Prebiotics, held in Kiel, Germany, June 11–12, 1998. 3 Address reprint requests to M de Vrese, Federal Dairy Research Center, Institute of Physiology and Biochemistry of Nutrition, Hermann-WeigmannStraße 1, D-24103 Kiel, Germany. E-mail: . Am J Clin Nutr 2001;73(suppl):421S–9S. Printed in USA. © 2001 American Society for Clinical Nutrition 421 422S DE VRESE ET AL TABLE 1 Frequency of lactose maldigestion and intolerance in residents of northern Germany Status according to breath hydrogen test Digesters Maldigesters 1 Total 173 (85.7)1 29 (14.3) Gastrointestinal symptoms during test No Yes 159 (91.9) 15 (51.7 ) 14 (8.1) 14 (48.3) Percentage in parentheses. (enteritis, Morbus Crohn, bacterial or parasitic infections, sprue, or small bowel syndrome) and by protein-energy malnutrition. Although some forms are transient, disappearing after recovery from the original disease, others are irreversible (8). Congenital lactose malabsorption, a rare autosomal-recessive heritable genetic defect, is evident immediately after birth. Afflicted newborns respond to their first milk feed with diarrhea (4). Hypolactasia and lactase maldigestion accompanied by clinical symptoms such as bloating, flatulence, nausea, diarrhea, and abdominal pain is termed lactose intolerance. Symptoms are caused by undigested lactose in the large intestine, where the lactose serves as a fermentable substrate for the bacterial flora and osmotically increases water flow into the lumen. Whether and to what extent undigested lactose causes the above-mentioned symptoms depends first on the amount of lactose ingested but also on individual sensitivity, the rate of gastric emptying, gastrointestinal transit time, and the pattern of the flora in the large in (...truncated)