The ability to digest lactose depends on the expression and activity of intestinal enzyme, lactase. In Finland, 17% of the population suffers from hypolactasia, resulting in lactose maldigestion. Symptomatic lactose maldigestion is called lactose intolerance. The aim of this study was to investigate factors which may either improve or impair the digestibility of lactose and will thus affect the development of maldigestion symptoms, and also the reliability of lactose intolerance diagnosis.
The possible regulatory role of gastric emptying in the digestibility of lactose was studied in 18 maldigesters. In an oral lactose tolerance test, delaying gastric emptying with propantheline improved tolerance to lactose by 26% (p=0.03), as measured by the reduced area under the 12-h gastrointestinal symptoms score curve, compared to the placebo. In a study with 9 lactose maldigesters, the temperature of the test solution used in the test modified symptoms but had only minor effects on the other maldigestion indicators. The effects of a cold test solution were more intense than those of a hot one, and the former reduced flatulence (p=0.01) and abdominal bloating (p=0.04) compared with the room temperature solution.
Inflammation markers were investigated in eight lactose maldigesters. In the urinary excretion of prostacyclin metabolite (6-keto-prostaglandin F1α) a moderate increase of about 30% (p=0.17), was seen following lactose intake. Ibuprofen, a nonselective inhibitor of cyclo-oxygenases, tended to inhibit this increase (p= 0.02). In none of the other indicators of inflammation used (e.g. nitric oxide production, blood leucocyte count) were any differences observed compared with the controls.
In an experimental model, the effect of dietary lactose on the expression or activity of lactase was tested for seven days with 8-week-old rats on a lactose-containing diet. About 40% induction of lactase was noticed in the lactose-fed rats compared with the controls (p=0.04), especially in the proximal and middle parts of the jejunum.
In the diagnosis of lactose intolerance, it was found that any one of the laboratory variables used (breath hydrogen, blood glucose and urine galactose tests) was more reliable than self-diagnosis. Only a third of the self-diagnosed subjects proved to be real lactose maldigesters, and about the same proportion of the previously tested subjects were, in reality, lactose digesters, indicating either a high incidence of secondary hypolactasia or incorrect previous diagnoses.
It was thus shown that rather than being of inflammatory origin, lactose intolerance is caused, at least partly, by motility disorders. This reduction of motility could be the result of any factors, dietary or otherwise, which retard gastric emptying and/or reduce intestinal motility. The continuous intake of lactose further improves tolerance to lactose by increasing the expression and activity of the lactase, at least in rats. Finally, we suggest that practical details, such as the temperature of the test solutions, should be re-estimated in testing tolerance to lactose.