3Address correspondence and reprint requests to DA Savaiano, Purdue University, Stone Hall, 700 West State Street, West Lafayette, IN 47907-7829. E-mail: savaiano
The American Journal of Clinical Nutrition, Volume 99, Issue 5, May 2014, Pages 1251S–1255S, https://doi.org/10.3945/ajcn.113.073023
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Yogurt is traditionally consumed throughout the world among populations who are seemingly unable to digest lactose. This review provides a historical overview of the studies that show lactose digestion and tolerance from yogurt by lactose-intolerant people. The lactose in yogurt is digested more efficiently than other dairy sources of lactose because the bacteria inherent in yogurt assist with its digestion. The bacterial lactase survives the acidic conditions of the stomach, apparently being physically protected within the bacterial cells and facilitated by the buffering capacity of yogurt. The increasing pH as the yogurt enters the small intestine and a slower gastrointestinal transit time allow the bacterial lactase to be active, digesting lactose from yogurt sufficiently to prevent symptoms in lactose-intolerant people. There is little difference in the lactase capability of different commercial yogurts, because they apparently contain Lactobacillus bulgaricus and Streptococcus thermophilus in sufficient quantities (108 bacteria/mL). However, Lactobacillus acidophilus appears to require cell membrane disruption to physically release the lactase. Compared with unflavored yogurts, flavored yogurts appear to exhibit somewhat reduced lactase activity but are still well tolerated.

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People with lactose intolerance experience gastrointestinal symptoms when consuming milk or milk products because they lack sufficient small intestinal lactase (β-galactosidase) activity to adequately digest the milk sugar lactose (which comprises galactose and glucose linked by a β-galactoside bond). Undigested lactose consequently enters the colon where it is fermented by the resident microflora, resulting in symptoms including abdominal pain, bloating, diarrhea, and flatulence. Lactase deficiency is common in nonwhite adults, with a prevalence of 50–70% or higher (1–3), because of a genetically programmed loss of lactase after weaning.

Yogurt is produced by incubating concentrated milk with Lactobacillus bulgaricus and Streptococcus thermophilus (4). The bacteria ferment the milk, reducing the pH and creating the tangy taste associated with yogurt. The lactose content of the finished product is approximately similar to that of unconcentrated milk (4), although there may be small differences (perhaps ∼5%) between products and brands according to manufacturing processes. Traditionally, lactose-intolerant populations have consumed yogurt without experiencing symptoms; however, because yogurt contains lactose, this would appear to be counterintuitive. This review provides an overview of the studies that reported on how yogurt is well tolerated by people with lactose intolerance.


It was suggested as early as 1974 that fermented dairy foods would be beneficial for lactose intolerance, although, at the time, this was hypothesized to be attributable to a low lactose content (5). However, when natural (live culture) yogurt was fed to rats, they absorbed galactose more efficiently and had greater intestinal lactase activity than rats fed pasteurized yogurt or a simulated yogurt formulation (6). Furthermore, the yogurt bacteria survived for 3 h in the gastrointestinal tract of the rats, and the authors hypothesized that the bacteria contributed to the hydrolysis of lactose (6). These data from experimental animals suggested that there was something more going on than a simple lactose dose effect.

The first human study followed in 1982, although it was not designed to determine the mechanism. In contrast to low-fat milk, a test drink of yogurt or acidophilus milk resulted in no symptoms in lactose-intolerant individuals (1). The reduced lactose quantity in the yogurt/fermented milk was implicated, because the dose of lactose in the test drinks was greater in the low-fat milk (24.6 g) than in the acidophilus milk (18.1 g) or yogurt (11.4 g) (1). The author suggested that lactase-containing microorganisms within the yogurt and fermented milk could continue to be active in the intestinal tract, participating in the hydrolysis of lactose (1). However, with the confounding effect of dose it was not possible to establish the mechanism.

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The dose question was settled with a controlled study that showed that the lactose in yogurt is better digested than that in milk, apparently as a result of its lactase activity (4). In this study, the 10 participants were confirmed to be lactose-intolerant on the basis of elevated breath-hydrogen concentrations after a lactose challenge (4). This technique measures the hydrogen produced when undigested lactose is fermented by the colonic microflora from individuals who have low levels of gastrointestinal lactase activity. The subjects were given test drinks, each containing similar lactose loads, which comprised lactose in water (20 g lactose), milk (18 g lactose), commercial unflavored yogurt (18 g lactose), or lactulose (a nonabsorbable disaccharide, 10 g in water); and breath-hydrogen concentration was measured for 8 h afterward (4). The ingestion of 18 g of lactose in yogurt resulted in only approximately one-third as much hydrogen excretion as a similar load of lactose in milk or water, indicating a much better digestion of lactose from yogurt (4). The breath-hydrogen curves (Figure 1) showed a significantly smaller (P 4). The consumption of yogurt also resulted in fewer symptoms than did a similar quantity of lactose in milk or water, with diarrhea or flatulence reported by 20% of participants after yogurt and 80% of participants after milk (4). The lactase activity of duodenal contents was assessed indirectly in 3 individuals, by measuring lactose disappearance and galactose appearance. It was negligible before the yogurt test, but for at least 1 h afterward there was sufficient lactase activity to digest 50–100% of the lactose in 4 h (4), supporting the findings of the rat study (6). The measured lactase activity of yogurt decreased faster than would be expected from the measured rate of galactose appearance (4). This study suggested that the enhanced absorption of lactose in yogurt resulted from the intraintestinal digestion of lactose by yogurt-derived microbial lactase, with the survival of yogurt-derived lactase in the duodenum. The role of lactase-digesting bacteria in yogurt was further supported by findings that less breath hydrogen was produced by lactose-intolerant individuals after consuming unheated yogurt than when the product had been heated (7, 8).