In 1970, Cuatrecasas et al showed that healthy individuals could have an isolated deficiency of intestinal lactase.1 Shortly thereafter, it was shown that a large fraction of the world’s adult population became lactase deficient2 owing to a genetically programmed reduction in lactase activity,3 a state now known as lactase non-persistence.

Initial studies4 showed that many lactase non-persistent subjects had easily identifiable symptoms after ingestion of a challenge dose of 50 g lactose (the equivalent of one quart of milk). When early, unblinded studies5 ,6 suggested that physiological quantities of milk (one cup or less) could induce appreciable symptoms, lactose intolerance became a favoured explanation for a variety of what otherwise would have been considered to be functional abdominal symptoms. The widespread dissemination of this information in lay publications has led a sizable fraction of the population of the United States to believe that lactose, in trivial quantities, is the cause of a wide array of abdominal symptoms.

One of the prevailing ideas concerning lactose malabsorbers was that continued ingestion of this …