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Institute of Biomedicine, Department of Pharmacology and Toxicology, University of Helsinki, PO Box 8, Helsinki FIN-00014, Finland
Foundation for Nutrition Research, PO Box 390, Helsinki FIN-00101, Finland, E-mail: riitta.korpela{at}valio.fi
Valio Ltd, R&D Centre, PO Box 30, Helsinki FIN-00039, Finland
Dear Sir:
We read with interest the paper published recently by Saltzman et al (1) concerning lactose intolerance. We consider it to be of great significance that >40% of the subjects with self-reported lactose intolerance were, according to Saltzman et al (1), lactose digesters.
In Finland, 17% of the population has hypolactasia (2). The Finnish population is very much aware of lactose intolerance because of media coverage. Because milk and milk products are a large part of the Finnish diet, gastrointestinal problems are easily assumed to be caused by milk. Because many lactose maldigesters tolerate small amounts of lactose in their diet without experiencing any gastrointestinal symptoms (3), the concept of lactose intolerance becomes confusing.
Inspired by the interesting results of Saltzman et al (1), we combined our existing data from 4 different studies (4–7). Over the last few years, 68 subjects (mean age: 35 y; range: 18–65 y; 60 females and 10 males) participated in our blinded crossover trials set up to investigate the biochemical background of lactose intolerance (4–7). We used the 3 most commonly used lactose tolerance tests in these subjects. The diagnostic variables were as follows: increased blood glucose 1.1 mmol/L, increased excretion of breath hydrogen 20 ppm, and excreted urinary galactose 20 mg/3 h. Thirty-one subjects had previously received a diagnosis of lactose intolerance by a health care professional and the remaining 37 subjects were self-diagnosed. Using our gold standard of 2 of the 3 diagnostic variables being positive after ingestion of 50 g lactose in 250 or 300 mL water after an overnight fast (10 h), we found only half of the 31 subjects with a previous diagnosis of lactose tolerance and 40% of the 37 self-diagnosed subjects to be lactose maldigesters (Figure 1).
FIGURE 1. . Distribution of subjects with a previous diagnosis of lactose maldigestion and those self-diagnosed as lactose intolerant according to symptoms and laboratory findings after ingestion of 50 g lactose in a blinded crossover study design in our laboratory. *Positive findings for 2 of the 3 variables (increase in blood glucose, breath hydrogen, or urinary galactose excretion).
Surprisingly, one-third of the 29 subjects diagnosed by us as lactose maldigesters had no clinically significant gastrointestinal symptoms for 3 h after ingesting 50 g lactose. At the same time, one-fourth of the 39 lactose digesters experienced clinically significant gastrointestinal symptoms after ingesting the same amount of lactose. However, the gastrointestinal symptoms differed between the lactose maldigesters and the digesters. Flatulence was the most severe symptom in the maldigesters (40% of the individual maximum scores) and abdominal bloating was the most severe symptom in the symptomatic digesters (>40% of the individual scores). In both of these groups, the severity of the other symptoms was roughly the same (20%). Clearly, there is a danger that those lactose digesters who experienced symptoms could receive an incorrect diagnosis of lactose intolerance. Thus, it is essential that the diagnostic tests be conducted carefully.
It is obvious that secondary lactose intolerance due to epithelial damage (secondary hypolactasia) is common. Therefore, the diagnosis of lactose intolerance needs to be made with carefully controlled clinical lactose tolerance tests, preferably more than one. In cases in which values are borderline, a repeat test should be conducted, preferably with use of a different diagnostic method after a period of time. It is hoped that more studies concerning the problems related to the diagnosis of lactose intolerance, like that by Saltzman et al (1), will be carried out.
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