A common problem for the undiagnosed celiac is lactose intolerance. Lactose is the sugar in diary products. It must be broken down by an enzyme, lactase, before it can be absorbed. This enzyme is produced on the tips of the villi which line the small intestine. When the villi are destroyed, as in celiac disease, lactose from diary products is not absorbed normally. When lactose reaches the colon, bacteria 'eat' the lactose and produce acid and gas. Water rushes into the intestine to dilute the lactose. The result is watery, acid diarrhea, bloating, and excessive gas.

There are two ways by which lactose intolerance can be acquired. Primary lactase deficiency/non-persistence is a genetically inherited, age-related decrease in lactase activity, which normally becomes apparent between the ages of 5-20 years. It is not a condition of early childhood. The loss of lactase activity is rarely total, but decreases to 10-30% of the initial level of the enzyme activity. In primary lactase deficiency, the decrease in enzyme activity is permanent and cannot be induced by large quantities of lactose (by lactose ingestion).

Secondary lactase deficiency is a transient state of lactase deficiency due to damage to the lining of the intestine where the lactase is produced. This damage can be caused by a severe bout of gastroenteritis, malnutrition, uncontrolled coeliac disease, inflammatory bowel disease, cancer or toxins. Although lactose intolerance is mainly present in the adult population, temporary secondary lactose intolerance can occur in babies and young children following gastroenteritis or other forms of infection affecting the intestinal tract. The symptoms of secondary lactose intolerance normally disappear when the intestinal wall has recovered from the injury, normally within 2-4 weeks.