Lactose is a disaccharide consisting of glucose and galactose. It is found in milk and other dairy products. The concentration of lactose in human milk is about 7% whereas in cow's milk it is about 5% (Palmiter 1969). The ability to digest lactose depends on the presence of an enzyme (lactase) located in the small intestinal brush border. The monosaccharides are then absorbed by active transport.
If the activity of lactase is low in the relation to the amount of lactose ingested, the lactose cannot be hydrolysed to its components, resulting in maldigestion. This situation is called hypolactasia (lactase nonpersistence, lactase restriction) and means that there is low lactase activity in the jejunal mucosa. The term for the opposite of hypolactasia is normolactasia (lactase persistence), and is applied to those with moderate or high ('normal') lactase activity. Lactose maldigestion and lactose malabsorption are terms to describe a poor lactose hydrolysing capacity. The term lactose intolerance should only be used for a clinical entity, describing symptomatic lactose maldigestion.
Reasons for lactose maldigestion can be classified as congenital lactase deficiency (almost total lack of lactase, alactasia), hypolactasia ('general' lactose maldigestion) and secondary hypolactasia (due to reversible injury in the gastrointestinal tract).
Lactase activity has a typical genetically-determined pattern during mammalian life. This activity increases in late gestation and remains at a high level during early childhood, whereafter it declines to the lower adult level (Sahi and Launiala 1978, Flatz 1987). Hypolactasia may develop as a secondary condition in people already suffering from other gastrointestinal diseases such as celiac disease or enteritis (see Ushijima et al 1995, Gudmand-Høyer and Skovbjerg 1996).
The decline of lactase activity from the high infant level to the lower adult level is the normal physiological pattern in about 75% of the world adult population, as reviewed by Sahi (1994). The maintenance of high lactase levels occurs in only a few populations, mainly in northern Europe. In Europe the incidence of hypolactasia ranges from about 10% up to 70%. In Finland the incidence is less than 20% (see Sahi 1994).
The inability to digest lactose will not always result in symptoms of intolerance (abdominal pain, bloating, flatulence and diarrhoea) if lactose is consumed. The terms lactose intolerance and lactose maldigestion are often used as if they were synonymous, but they are not, in fact, the same. There are subjects who have a low lactase hydrolysing capacity, i.e. they are hypolactasians but are still asymptomatic after an oral dose of lactose (Rosado et al 1987, Scrimshaw and Murray 1988, Carraccio et al 1998, Teuri et al 1999, Peuhkuri et al 2000b).
The most commonly used methods of diagnosing hypolactasia are the indirect measurements of the breakdown products of lactose following an oral dose. Reduced increase in blood glucose concentration, increase in exhaled breath hydrogen or excreted urinary galactose all indicate hypolactasia (reviewed by Arola 1994).
The use of laboratory methods for diagnosing lactose intolerance (i.e. symptomatic lactose maldigestion) is not sufficient. During a lactose tolerance test the development of gastrointestinal symptoms must always be recorded side by side with the laboratory results. Unhydrolysed lactose is transported to the colon and fermented by colonic bacteria into short-chain fatty acids and gases (hydrogen, carbon dioxide, and methane). The development of gastrointestinal symptoms depends on the balance between the production and the removal of these fermentation products. If the disposal capacity is exceeded, excessive rectal gas and/or abdominal distension occur, as reviewed by Villako and Maaroos (1994). A hypolactasian subject who suffers no gastrointestinal symptoms during the test is not lactose intolerant.
In the study of Teuri et al (1999) we showed the correlation between the blood glucose concentration and gastrointestinal symptoms to be fair, between the concentration of expired breath hydrogen and symptoms to be moderate, and between the concentration of urinary galactose and symptoms to be good. In practice, this means that if the blood glucose concentration alone is measured during the tolerance test, as is the case in most Finnish health care centres (Peuhkuri et al 2000a), the number of incorrect diagnoses is likely to be significant.
In oral lactose tolerance tests the most widely used test dose in Finland is 50 g lactose dissolved in 200 - 400 ml water (Peuhkuri et al 2000a). Newcomer et al (1978) demonstrated that the majority of hypolactasian subjects develop gastrointestinal symptoms following this dose. This equals the lactose found in a whole litre of milk, and even normolactasians may suffer gastrointestinal symptoms after such a large dose. The minimum dose of lactose needed to cause notable symptoms differs between individuals. Most maldigesters are reportedly able to tolerate 12 g lactose if it is consumed with a meal (Suarez et al 1995, Vesa et al 1996). However, there appear to be no well-controlled trials in which a more natural dose of lactose (20-50 g) has been consumed in smaller doses divided between the meals, which is the usual pattern of lactose intake.
The prevalence of lactose intolerance seems to be overestimated, and many people who describe themselves as intolerant, whether tested by professionals in official health care or not, are actually lactose digesters (Peuhkuri et al 2000b). Similar results have been shown by other authors, too (Johnson et al 1993a, Suarez et al 1995, Saltzman et al 1999). Discussion of the principles for testing lactose tolerance and possible affecting factors is very much needed.
Even though hypolactasia is fairly common in Finland, milk and other dairy products are essential part of the Finnish food culture. This has inspired to several series of studies on lactose intolerance, for example, of genetics (Sahi 1974a), diagnostic methods (Arola 1988a) and gastrointestinal symptoms (Vesa 1997).
The aim of this study was to investigate factors which might possibly improve the digestibility of lactose in the small intestine, thus affecting the development of maldigestion symptoms, and also affecting the reliable diagnosis of lactose intolerance.