Lactose malabsorption and nutrition

© 2014 John Wiley & Sons, Ltd. Published 2014 by John Wiley & Sons, Ltd. The consumption of milk and dairy products varies considerably in different regions of the world. Indeed, according to the statistics of the Food and Agriculture Organization of the United Nations (FAO), in 2007 the consumption of milk and dairy products averaged 240 kg and 360 kg per capita in the UK and Sweden, respectively, while in China it was about 29 kg per capita. Milk is a complex and nutrient-dense food [1] that may have positive or negative effects on adult health [2]. The major carbohydrate component in milk is lactose, a disaccharide whose concentration in bovine milk has been reported to range between 45 and 55 g/L [2–4]. Lactose needs to be digested by the small intestinal enzyme lactase into its constituent monosaccharides, glucose and galactose, before transport across the epithelial cell membranes. Lactase activity is therefore essential for the development of young mammals, since their sole source of nourishment is their mother’s milk. In most mammals, including most humans, lactase expression decreases after the weaning period is over [5]. In humans, this condition is termed lactase non-persistence and is observed in around 65% of adults worldwide [6,7]. Lactase non-persistent individuals are sometimes described as having primary adult hypolactasia and are lactose maldigesters, while adults who have the genetically determined trait of lactase persistence (LP) and continue to produce lactase throughout life are termed lactose digesters. The range of timing of lactase downregulation varies from one population to another; for example, most Chinese and Japanese become lactase nonpersistent between 1 and 5 years old, while on average lactase non-persistence does not manifest in Finns and Estonians until somewhat later [8]. Even though the mechanisms of developmental lactase downregulation are not well understood, it is clear that it is not reversible [9,10]. Lactase production can also be lost through non-genetic mechanisms; this is called secondary hypolactasia and it can occur, for example, after any condition that damages the small intestinal mucosa brush border [11]. Adults with either primary or secondary hypolactasia are lactose malabsorbers and may exhibit symptoms of lactose intolerance after ingestion of lactose. Genetically determined lactase non-persistence is quite normal in the majority of humans worldwide and is distinct from congenital alactasia, the absence of lactase from birth. This, in contrast, is an extremely rare and potentially fatal condition. A number of mutations that affect the structure of the protein, and consequently its function, have been identified in Finnish patients suffering from this condition [12,13]. Two types of tests are available for determining lactase production status at the phenotypic level. Duodenal or jejunal biopsies can be taken by endoscopy and allow direct determination of lactase activity. A lactase assay is usually combined with routine histology and an assay of another enzyme such as sucrase, so that secondary deficiency of lactase can be readily identified. This procedure is the most accurate available, but it is invasive and performed routinely only if a pathological condition such as coeliac disease is indicated. Other methods Chapter 3.15