Effects of Lactose on Gastro-Intestinal Motility: A Review

Summary The literature dealing with the effects of lactose on the rate of movement of food residues in the gastro-intestinal tract has been reviewed. Species, strain, age and individual differences in susceptibility to lactose-induced laxation have been reported. A lactose feeding level of 20 per cent of the diet often induces diarrhea in weanling rats of the Sprague-Dawley strain. When lactose in sufficient amounts to produce diarrhea is fed, the animals exhibit pot-bellies, slow growth and reduced feed consumption. These symptoms become progressively more severe and persistent as the percentage of lactose in the ration is increased. The lowest levels of lactose feeding which will initiate diarrhea in species other than the rat have not been carefully determined, although the occurrence of diarrhea has been reported in all species studied. Early death in rats fed rations containing 61.8 to 100 per cent lactose has been reported by several investigators. The lactose linkage apparently is responsible for the diarrhea and some of the other symptoms noted when moderate to large amounts of lactose are fed. The literature reports, based generally upon case studies rather than upon carefully controlled experiments, indicate that more than about 12 to 19 per cent of lactose in the formula is apt to cause diarrhea in human infants. This may be compared with 10 to 15 per cent for puppies, and 20 per cent for weanling rats. Other reports suggest that smaller amounts of lactose may be valuable in controlling or preventing diarrheal conditions. The available evidence indicates that lactose in large amounts (20 per cent or more of the ration) tends to produce diarrhea in chickens and to lower the pH of the contents of the ceca markedly and of the large intestine somewhat less. The ceca are distended by a frothy liquid material. Water consumption is increased. When lactose constitutes about 40 per cent of the ration of young chicks, extreme inflammation of intestinal mucous membranes may result, and death often may ensue. The evidence seems to show that the purgative action of large amounts of skim milk and whey is due partly, but not entirely, to lactose. Lactose may act to produce diarrhea in several possible ways, for example: (a) Direct stimulation of intestinal muscles, (b) Hydragogue action; interfering with absorption of water and organic nutrients, (c) Alteration of intestinal flora to an aciduric type, the aciduric flora then acting in several different possible ways, (d) Alteration of pH enough to stimulate the intestinal musculature, (e) Maintenance of a positive oxidation-reduction potential, (f) Stimulation of intestinal muscle through its nerve supply by small amounts of unhydro-lyzed lactose in the blood. Of these possibilities, the first, third and sixth are contraindicated by the available evidence, while the fourth appears to be an effect rather than a cause of the diarrhea. The possible relation, if any, of the positive oxidation-reduction potential to lactose diarrhea is not clear. Thus, at the present time, the second possibility, that of a hydragogue type of action, seems most plausible. However, some evidence does not support the idea that tissue dehydration is accomplished by persistent lactose diarrhea. Dehydration would be expected if a continuous hydragogue action were involved, unless water consumption were increased or urine volume decreased. It has been shown that water intake sometimes is increased, at least on rations consisting solely or largely of lactose. On such high-lactose rations, urine volume also increases as a result of the urinary excretion of galactose, whereas urine volume decreases in many diarrheal conditions. However, the work of one investigator does indicate decreased diuresis when lactose is given. Water balance experiments at lower lactose feeding levels seem to be desirable in order to better evaluate the possibility of a hydragogue type of action. Other dietary constituents seem to influence the occurrence, severity and persistence of lactose-produced diarrhea. Certain calcium salts may decrease the severity of the diarrhea to some extent, while both calcium gluconate and sodium gluconate seem to increase the severity of the diarrhea and prevent adaptation to lactose feeding. It has been demonstrated that calcium chloride decreases the rate of lactose hydrolysis and galactose absorption. A certain portion of the salts of whey intensifies and prolongs lactose diarrhea. Increasing the amounts of fat in the diet tends to decrease the diarrhea, and there is some indication that butter fat may be more valuable in this respect than certain other food fats. The feeding of liver may postpone but not prevent the appearance of lactose-feeding symptoms on a high-lactose diet. Lactose has been used successfully in conjunction with and for prolonging the effect of L. acidophilus in transforming the intestinal flora to a predominantly aciduric type. The use of lactose without L. acidophilus seems to have definite therapeutic possibilities as yet little investigated. Evidence indicates that the permanent transformation of the flora by lactose depends upon sufficient amounts of the sugar continually arriving in the lower bowel, for the flora reverts to the normal mixed type when lactose feeding is discontinued or when intestinal stasis is produced. Adaptation to lactose feeding is evidenced by the diarrheal condition becoming less conspicuous or disappearing completely. Lactase occurs in the mucosal cells of the intestines of mammals, but not to any extent in the intestinal juice. Therefore, lactose hydrolysis must be mainly an intracellular process, occurring during absorption. Since lactose diarrhea probably is the result of slight lactose hydrolysis and the resulting hydragogue effect, then the species, strain, age and individual differences in the severity of lactose feeding symptoms might be due to differences in intestinal lactase activity. Also, it seems likely that adaptation to lactose feeding is brought about by increased intestinal lactase activity. The results of one early investigator indicate that increased lactase activity does not result from continued milk or lactose feeding, but these experiments have not been confirmed.