Dairy Products and Lactose Intolerance

Lactose intolerance refers to inefficient digestion of lactose, the main carbohydrate present in milk and dairy products. A p-galactosidase, known as lactase, is an enzyme able to hydrolyze lactose in glucose and galactose, this enzyme is connected to small intestine mucosa membrane. When lactose is hydrolyzed, the two monosaccharides, glucose, and galactose, are absorbed and transported to the liver through the portal vein, where galactose is converted into glucose (Lomer et al., 2008). Lactose malabsorption is due to reduced expression or impaired activity of enzyme lactase. The most frequent cause of lactose malabsorption is lactase nonpersistence, a common condition in which lactase expression decreases during infancy. Congenital lactase deficiency, due to complete lack of the enzyme, is a rare condition that presents with severe symptoms in newborns. Lactose malabsorption may be also due to acquired conditions, including small bowel bacterial overgrowth, infectious enteritis (i.e., giardiasis), or mucosal damage due to coeliac disease, inflammatory bowel disease, drugs, gastrointestinal surgery, short bowel syndrome, or radiation enteritis, conditions that lead to down regulation of lactase expression in the small intestine (Misselwitz et al., 2013).

Studies suggest the world populations have a different percentage of p-galactosidase persistence. Individuals with p-galactosidase nonpersistence often do not develop lactose intolerance because several nutritional and genetic factors can influence its absorption (Cavalli-Sforza 1973; Hertzler and Savaiano 1996). In fact, it is important to realize that lactose malabsorption (lactase nonpersistence) is not equivalent to or synonymous of lactose intolerance. Lactose malabsorption in many cases will not come to clinical attention. Development of symptoms depends on several individual factors, including diet, oro-cecal transit time, distribution and fermentation capacity of gut flora, (Zhao et al., 2010) sensitivity toward chemical and mechanical stimulation of the gut, and psychological factors (Tomba et al., 2012). Lactose intolerance itself causes several gastrointestinal symptoms provoked by lactose and sugar fermentation in the colon. Inadequate lactase activity allows lactose to reach the large intestine, where the gut flora provides a salvage pathway for lactose digestion by cleaving lactose into short-chain fatty acids (SCFA) and gas, mainly hydrogen (H2), carbon dioxide (CO2), and methane (CH4) that affect intestinal motility causing constipation, increased bowel internal pressure, and increased bowel transit time. Abdominal cramps and bloating, flatulence, diarrhea, nausea, and vomiting are frequent adverse events (Berkey et al., 2009). Treatment of lactose intolerance should not be aimed at reducing malabsorption but rather, at improving digestive symptoms. It is recommended that lactose be reduced rather than excluded. Some studies suggest that individuals with nonpersistent p-galactosidase can consume up to 11 g/day of lactose without adverse symptoms. It has also been shown that lactose digestion is improved by combination with other foods in small amounts and throughout the day (Shaukat et al., 2010). Colon bacteria can adapt their metabolic activity to improve lactose tolerance (He et al., 2006; He et al., 2008), such as through the consumption of lactic bacteria or specific probiotics (Kalliomaki et al., 2010).

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